SRB’s Manual of Surgery

Contents 1. General Surgery A. Wounds and Wound Healing  1

Wounds  1; Classification of Wounds  1; Wound Healing  6; Compartment Syndrome  10; Crush Injury  11; Crush Syndrome  11; Degloving injuries  12; Scar  12; Keloid  12; Hypertrophic Scar  13; Problems with Wound Healing  14

B. Ulcer 15

Ulcer  15; Granulation Tissue  18; Investigations for an Ulcer  9; Management of an Ulcer  20; Traumatic Ulcer  22; Trophic Ulcer (Pressure Sore/Decubitus Ulcer)  22; Ulcer Due to Chilblains  23; Ulcer Due to Frostbite  24; Martorell’s Ulcer  24; Arterial/Ischaemic Ulcer  24; Bairnsdale Ulcer  24; Carcinomatous Ulcer (Epithelioma, Squamous Cell Carcinoma)  24; Marjolin’s Ulcer  25; Rodent Ulcer  25; Melanotic Ulcer  25; Diabetic Ulcer  26; Meleney’s Ulcer (Postoperative Synergistic Gangrene)  27; Lupus Vulgaris 27; Tuberculous Ulcer  28; Bazin’s Disease (Erythrocyanosis Frigida/Erythema Induratum)  28; Tropical Ulcer  28; Venous Ulcer (Gravitational Ulcer)  29; Syphilitic Ulcer  29; Soft Chancre/Soft Sore/Ducrey’s Ulcer/Chancroid/Bubo  29; Climatic Bubo/Tropical Bubo  29

C. Sinus and Fistula  31

Sinus  31; Fistula  31; Median Mental Sinus  33; Sequestrum  34; Preauricular Sinus  35

D. Infectious Diseases  36

Surgical Infection  36; Cellulitis  36; Erysipelas  39; Erysipeloid Disease  39; Lymphangitis  39; Abscess  40; Metastatic and Pyaemic Abscess  45; Bacteraemia  45; Septicaemia  45; Pyaemia  45; Boil (Furuncle)  46; Hidradenitis Suppurativa  46; Carbuncle  47; Pott’s Puffy Tumour  48; Pyogenic Granuloma (Granuloma Pyogenicum)  48; Impetigo  49; Erythrasma  49; Scrum Pox  49; Tetanus  49; Gas Gangrene  53; Tuberculosis  55; Leprosy  56; Syphilis (Great Pox) (French Disease)  56; Actinomycosis  57; Madura Foot (Mycetoma Pedis)  58; Rabies (Hydrophobia)  59; Rabies in Dogs  61; Anthrax  62; Nosocomial and Opportunistic Infections  62; Necrotising Fasciitis  63; Acute Pyomyositis  64; Surgical Site infection (SSI)  65; HIV Infection and AIDS  67

E. Swellings 71

Lipoma  71; Cysts  74; Dermoids  75; Sebaceous Cyst (Wen, Epidermoid Cyst)  78; Glomus Tumour  81; Papilloma  81; Warts  82; Fibroma  82; Bursae  83; Semimembranosus Bursa  85; Morrant Baker’s Cyst  85; Lymph Cyst (Lymphatic Cyst)  86; Lymphangioma  86; Calcinosis Cutis  86; Neuroma  87; Neurofibroma  87; Neurilemmoma (Schwannoma)  89; Ganglion  90; Chordoma  90; Epignathus  90

F. Electrolyte and Nutrition  92

Normal Physiology  92; Water Loss (Volume Loss)  92; Water Excess (ECF Volume Excess)  92; ECF Loss  93; ECF Excess  93; Hyponatraemia  93; Hypernatraemia  94; Hypokalaemia  94; Hyperkala­ emia  94; Hypermagnesaemia  95; Hypomagnesaemia  95; Acid-Base Balance  95; Metabolic Alkalosis  96; Respiratory Alkalosis  96; Metabolic Acidosis  96; Respiratory Acidosis  97; Anion Gap  97; Fluid Therapy  97; Nutrition  101; Gastrostomy  102; Jejunostomy  103; Total Parenteral Nutrition (TPN)  104; Refeeding Syndrome  105; Obesity and Morbid Obesity  105; Different Surgeries  106

G. Shock  110

Shock  110; Stages of Shock  111; Effects of Shock  111; Clinical Features of Shock (Hypovolaemic Shock)  114; Assessment, Investigations and Monitoring   114; Central Venous Pressure (CVP)  115; Pulmonary Capillary Wedge Pressure (PCWP)  116; Systemic Inflammatory Response Syndrome (SIRS)  116; Multiple Organ Dysfunction Syndrome (MODS)  117; Oxygen Therapy  117; Topical O2 Therapy  117;

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SRB's Manual of Surgery Cardiac Arrest  117

H. Haemorrhage and Blood Transfusion  119

Haemorrhage  119; Blood Transfusion  122; Massive Blood Transfusion  124; Autologous Blood Transfusion  124; Artificial Blood  124; Erythropoietin  125; Tourniquets  125; Disseminated intravascular Coagulation  126; Mechanism of Blood Coagulation (Haemostasis)  126

I. Burns 128

Burns  128; Management of Burns  132; Eschar  134; Contracture in Burn Wound  135; Electrical Burns  136; Inhalation injury  137; Chemical Burns  138

J. Trauma 139

Triage  139; Concepts in Trauma Management  141; Spinal Injury  142; Neck injuries  142; Bullet Injuries  142; Blast Injuries  143; Penetrating Injuries  143; Abdominal Trauma  144; Blunt Trauma of Abdomen  146; Duodenal Injury  148; Pancreatic Injury  148; Small Bowel Injury  148; Colonic Injury  149; Liver Injury  149; Splenic Injury  149; Renal Injury  150; Urinary Bladder Injury  150; Abdominal Compartment Syndrome  150; Seat-Belt Injuries  151

K. Hand and Foot  152

Hand  152; Hand Infections  153; Acute Paronychia  156; Chronic Paronychia  156; Apical Subungual Infection  156; Terminal Pulp Space Infection (Felon)  157; Infection of Web Spaces  158; Deep Palmar Space Infection  158; Space of Parona Infection  160; Acute Suppurative Tenosynovitis  160; Compound Palmar Ganglion  161; ORF  161; Milker’s Nodes/Nodules (Milkmaid Blisters)  161; Hand Injuries  161; Dupuytren’s Contracture  163; Volkmann’s Ischaemic Contracture  164; Syndactyly  164; Mallet Finger (Base Ball Finger)  165; Heberden’s Nodes  165; Spina Ventosa  165; Foot  165; Callosity  165; Corn  166; Plantar Fasciitis (Policeman’s Heel)  166; Ingrowing Toe Nail (Onychocryptosis)  166; Onychogryphosis  167; Onychomycosis  167; Athlete’s Foot  167; Hallux Valgus  167

L. Arterial Diseases  169

Surgical Anatomy of Thoracic Outlet  169; Arteries of Upper Limb  169; Arteries of Lower Limb  169; Arterial Diseases  170 ; Intermittent Claudication  170 ; Rest Pain  170 ; Limb Ischaemia  171 ; Pregangrene  171; Gangrene  171; Different Levels of Arterial Obstruction  172; Other Features of Poor Circul­ation  173; Investigations for Arterial Diseases  174; Diseases of the Arteries  176; Atherosclerosis  176; Thromboangiitis Obliterans (TAO) Syn. Buerger’s Disease  178; Takayasu’s Pulseless Arteritis  182; Raynaud’s Phenomenon  182; Temporal Arteritis  184; Treatment of Arterial Diseases  184; Subclavian Steal Syndrome  189; Acute Arterial Occlusion  189; Traumatic Acute Arterial Occlusion  190; Embolism  190; Reperfusion Injury  192; Saddle Embolus  193; Embolectomy  193; Fat Embolism  194; Air/Gas Embolism  195; Therapeutic Embolisation  195; Caisson’s Disease or Decompression Disease  195; Aneurysm  195; Mycotic Aneurysm  197; Abdominal Aneurysm  197; Abdominal Aortic Aneurysm (AAA)  198; Peripheral Aneurysm  201; Carotid Artery Aneurysm (Extracranial)  202; Dissecting Aneurysm  203; Erythromelalgia (Erythralgia)  204; Livedo Reticularis  204; Polyarteritis Nodosa  204; Scleroderma/Systemic Sclerosis  204; Acrocyanosis (Crurum Puellarum Frigidum)  204; Gangrene  205; Diabetic Foot and Diabetic Gangrene  206; Trophic Ulcer  207; Bedsores (Decubitus Ulcer) (Pressure Sores)  208; Frostbite  208; Ainhum  208; Endovascular Surgeries  208; Upper Limb Ischaemia  209; Arterial Substitutes  211

M. Vascular Lesions and Hamartoma  213

Vascular Anomalies  213; Haemangioma  213; Vascular Malformations  216; Cirsoid Aneurysm  217; Arteriovenous Fistula (AVF)  217; Campbell De Morgan Spots  220; Parry-Romberg Disease  220; Hamartomata  220

N. Venous Diseases  221

Anatomy of Veins of Lower Limb  221; Physiology of Venous Blood Flow in Lower Limb  222; Deep Vein Thrombosis  222; Varicose Veins  226; Venous Ulcer (Gravitational Ulcer)  238; Compression Therapy for Varicose Veins  241; Thrombophlebitis  241; Klippel-Trenaunay Syndrome  242; Anticoagulants  242; Heparin (Unfractionated/UFH)  242; Low Molecular Weight Heparin (LMWH)  242; Oral Anticoagulants  242; Warfarin  243; Direct Thrombin Inhibitors  243; Antiplatelet Drugs  243; Pulmonary Embolism  243

O. Lymphatics  245

Contents Surgical Anatomy  245; Lymphangiography  246; Isotope Lymphoscintigraphy  247; Lymphoedema  247; Lymphomas  253; Hodgkin’s Lymphoma (HL)  254; Non-Hodgkin’s Lymphoma (NHL)  258; Mantle Cell Lymphoma  259; Malt Lymphoma (Maltoma)  259; Burkitt’s Lymphoma (Malignant Lymphoma of Africa)  260; Cutaneous T Cell Lymphoma  260; Chylous Ascites  261; Chylothorax  261; Chyluria  261; Sarcoidosis  262

P. Peripheral Nerves  263

Peripheral Nerve Injuries  263; Tinel’s Sign  265; Brachial Plexus Injuries  265; Causalgia  265; Median Nerve Injury  266; Carpal Tunnel Syndrome  266; Ulnar Nerve Injury  268; Claw Hand  268; Radial Nerve Injury  269; Common Peroneal Nerve Injury  270; Foot Drop  270; Medial Popliteal Nerve Injury  270; Axillary Nerve Injury  271; Long Thoracic Nerve Injury (Nerve of Bell)  271; Meralgia Paraesthetica  271

Q. Neoplasm  272

Definition  272; Dysplasia  273; Carcinoma In Situ  273; Aetiologic Factors  273; Spread of Malignant Tumours  274; Grading of Tumour  274; Staging of the Tumour  275; Paraneoplastic Syndromes  275; Investigations for Neoplasm  275; Management Strategy for Cancers  280

R. Skin Tumours  282

Anatomy  282; Classification of Skin Tumours  283; Skin Adnexal Tumours  283; Dermatofibroma (Sclerosing Angioma or Subepithelial Benign Nodular Fibrosis)  284 ; Dermatofibrosarcoma Protuberans  285; Keratoacanthoma (Molluscum Sebaceum)  285; Rhinophyma (Potato Nose) (Bottle Nose)  286; Seborrhoeic Keratosis (Seborrhoeic Wart, Basal Cell Papilloma)  286; Squamous Cell Carcinoma (Epithelioma)  287; Marjolin’s Ulcer  290; Basal Cell Carcinoma (Rodent Ulcer)  290; Turban Tumour  292; Naevi  292; Melanoma  294

S. Sarcomas  302

Sarcoma  302; Liposarcoma  308; Fibrosarcoma (11%)  308; Malignant Fibrous Histiocytoma (MFH)  310; Leiomyosarcoma  310; Rhabdomyosarcoma  310; Chondrosarcoma  310; Haemangiosarcoma  310; Lymphangiosarcoma  311; Synovial Sarcoma (7%)  311; Malignant Peripheral Nerve Sheath Tumour (MPNST) (3%)  311; Kaposi’s Sarcoma  311

T. Amputations  312

Amputation  312; Complications of Amputations  318; Prosthesis  320

U. Reconstruction  321

Graft  321; Skin Grafts  321; Flaps  324; Tendon  330; Tendon Repair  331; Tendon Transfer  331; Tendon Graft  331

V. Transplantation  332

Preoperative Evaluation  332; Organ Procurement  332; Graft Rejection (Transplant Rejection)  333; Immunosuppressive Agents  334; Renal Transplantation  335; Liver Transplantation  336; Bone Marrow Transplantation  338; Pancreatic Transplantation  338; Small Bowel Transplantation  338; Dialysis  339; Cimino Fistula (Cimino-Brescia)  340

W. Stings and Bites  341

Snake Bite  341; Spider Bite  341; Bee Bite  342; Mammalian Bite  342

X. Pain  343

Gate Control Theory  343

2. Faciomaxillary Diseases

346

Diseases of the Palate  346; Orthopantomogram (OPG)  346; Cleft Lip and Cleft Palate  347; Maxillofacial Injuries  350; Primary Care (Early Care) in Maxillofacial Injuries  351; Fracture Middle Third Area  352; Zygomatic Complex Fracture  353; Fracture of the Mandible  355; Dislocation of the Mandible  357; Jaw Tumours  358; Epulis  358; Ameloblastoma (Adamantinoma, Eve’s Disease, Multilocular Cystic Disease of the Jaw)  359; Dentigerous Cyst (Follicular Odontome)  360; Dental Cyst (Radicular Cyst, Periapical Cyst)  361; Osteomyelitis of Jaw  361; Alveolar Abscess (Dental Abscess)  362; Fibrous Dysplasia of Bone/Jaw  362; Cherubism  364

3. Oral Cavity

365

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SRB's Manual of Surgery Ranula  365; Sublingual Dermoids  366; Stomatitis  367; Cancrum Oris (Noma)  367; Syphilitic Lesions of Oral Cavity  368; Leukoplakia  368; Erythroplakia  369; Oral Submucosal Fibrosis  369; Premalignant Conditions of Oral Cavity  369; Oral and Upper Aerodigestive Cancers  370; Cheek  372; Carcinoma Cheek/Buccal Mucosa  372; Lip  383; Neoplasm of Lip  384; Carcinoma Lip  384; Tongue  387; Tongue Ulcers  388; Benign Tumours of Tongue  389; Tongue Fissure  389; Glossitis  390; Tongue Tie  391; Carcinoma Tongue  391; Carcinoma of Posterior One-third/Base of the Tongue  394; Nasopharyngeal Carcinoma  395; Maxillary Tumours  395; Malignant Tumours of Tonsil  398; Carcinoma Hard Palate  398; Laryngeal Tumours  399; Malignant Tumours of Larynx  399; Trismus  402

4. Salivary Glands

403

Anatomy  403; Saliva  406; Sialography  406; Salivary Calculus and Sialadenitis  406; Sialosis  409; Sialectasis  409; Recurrent Childhood Parotitis  409; Parotid Abscess (Suppurative Parotitis)  409; Parotid Fistula  410; Sjögren’s Syndrome  411; Mikulicz Disease  412; Salivary Neoplasms  412; Pleomorphic Adenoma (Mixed Salivary Tumour)  413; Adenolymphoma (Warthin’s Tumour, Papillary Cystadenoma Lymphomatosum)  415; Oncocytoma (Oxyphil Adenoma)  416; Basal Cell Adenoma  416; Mucoepidermoid Tumour  416; Adenoid Cystic Carcinoma (10% of Salivary Tumours)  417; Acinic Cell Tumour  417; Malignant Mixed Tumour (MMT)  417; Adenocarcinoma of Salivary Glands  417; Squamous Cell Carcinoma of Salivary Glands  417; Submandibular Salivary Gland Tumours  417; Management of Malignant Salivary Tumours  418; Minor Salivary Gland Tumours  420; Parotid Lymphoma  421; Parotidectomy  421; Frey’s Syndrome (Auriculotemporal Syndrome, Gustatory Sweating)  423; Facial Nerve Injury (Lower Motor Nerve Lesion, Surgically Related)  424

5. Neck

426

Anatomy of Lymphatics of Head and Neck  426; Thoracic Outlet Syndrome (TOS)  427; Cervical Rib  428; Branchial Cyst  431; Branchial Fistula  432; Pharyngeal Pouch (Zenker's)  433; Laryngocele  434; Cystic Hygroma (Cavernous Lymphangioma)  435; Ludwig’s Angina  436; Parapharyngeal Abscess  437; Retropharyngeal Abscess  437; Subhyoid Bursitis (Retrohyoid Bursa/Boyer’s Bursa)  438; Carotid Body Tumour (Potato Tumour, Chemodectoma, Nonchromaffin Paraganglioma)  438; Torticollis (Wry Neck)  440; Sternomastoid Tumour  440; Tuberculous Lymphadenitis  441; Cold Abscess  444; Secondaries in Neck Lymph Nodes  445; Chemotherapy for Head and Neck Cancers  452

6. Thyroid

453

Development  453; Anatomy  453; Physiology  455; Congenital Anomalies  455; Thyroid Function Tests  458; FNAC of Thyroid  458; Classification of Goitre  459; Diffuse Hyperplastic Goitre  460; Multinodular Goitre (MNG)  460; Discrete Thyroid Nodule  462; Solitary Thyroid Nodule  463; Retrosternal Goitre  466; Thyrotoxicosis and Hyperthyroidism  467; Radioactive Iodine  477; Thyroid Neoplasms  478; Differentiated Thyroid Carcinoma (DTC)  478; Papillary Carcinoma of Thyroid (PCT)  480; Follicular Carcinoma of Thyroid (FCT)  482; Anaplastic Carcinoma of Thyroid  485; Medullary Carcinoma of Thyroid (MCT)  486; Malignant Lymphoma  488; Hashimoto’s Thyroiditis (Struma Lymphomatosa)  488; De-Quervain’s Subacute Granulomatous Thyroiditis  489; Riedel’s Thyroiditis (0.5% Common)  489; Thyroid incidentaloma  489; Thyroidectomy  490; Emil Theodor Kocher  495; Kocher’s Test  495; Hypothyroidism  495; Recurrent Laryngeal Nerve Palsy  496

7. Parathyroids and Adrenals

499

Anatomy  499; Calcium  499; Hyperparathyroidism (HPT)  500; Parathyroidectomy  503; MEN Syndrome (MEA Syndrome)  505; Apudomas  505; Hypoparathyroidism  505; Tetany  506; Adrenals  507; Adrenal Cortical Tumours  507; Adrenocortical Carcinoma  507; Cushing’s Syndrome  508; Conn’s Syndrome  508; Virilising Syndrome or Adrenogenital Syndrome  509; Neuroblastoma  509; Phaeochromocytoma  510

8. Breast Anatomy  512; Mammography  515; Aberration of Normal Development and Involution (ANDI) of The Breast  516; Fibroadenoma  516; Fibrocystadenosis (Fibrocystic Disease of the Breast/Mammary Dysplasia/Cyclical Mastalgia with Nodularity)  518; Sclerosing Adenosis  519; Phylloides Tumour (Cystosarcoma Phylloides/Serocystic Disease of Brodie)  520; Mastalgia (“Pain in the Breast”)  521; Traumatic Fat Necrosis  521; Galactocele  522; Mastitis  522; Antibioma  524; Duct Ectasia  525; Mondor’s Disease  525; Tuberculosis of the Breast  525; Breast Cysts  526; Galactorrhoea  527; Gynaecomastia  527;

512

Contents Duct Papilloma  528; Zuska-Atkins Disease  529; Mammary Fistula of Atkins  529; Carcinoma Breast  529; TNM Staging of Carcinoma Breast  539; Management of Early Carcinoma Breast  553; Advanced Carcinoma Breast  557; Prognostic Factors in Carcinoma Breast  559; Prophylactic Mastectomy  560; Carcinoma of Male Breast  560; Breast Reconstruction  561; Breast Implants  563; Nipple Retraction  564

9. Peritoneum

565

Anatomy  565; Physiology  565; Acute Peritonitis  566; Primary Peritonitis  566; Secondary Peritonitis  566; Tertiary Peritonitis  566; Spontaneous Bacterial Peritonitis  572; Sclerosing Peritonitis  573; Biliary Peritonitis  573; Postoperative Peritonitis  573; Other Forms of Peritonitis  573; Pelvic Abscess  574; Subphrenic Spaces and Subphrenic Abscess  575; Mesenteric Cysts  577; Mesenteric Panniculitis  578; Acute Mesenteric Lymphadenitis  578; Mesenteric Malignancy  578; Mesenteric Trauma  579; Peritoneal Malignancy  579; Omental Cyst  580; Omental Torsion  580; Omental Tumour  580

10. Abdominal Tuberculosis

581

Abdominal Tuberculosis  581; Ileocaecal Tuberculosis  582; Ileal Tuberculosis  587; Peritoneal Tuberculosis  587; Tuberculous Mesenteric Lymphadenitis  590; Ano-recto-sigmoidal Tuberculosis  591; Tuberculosis of the Omentum  591

11. Liver

592

Surgical Anatomy of Liver  592; Liver Function Tests (LFT)  593; Alpha Fetoprotein (AFP)  594; Liver Biopsy  594; Liver injury  594; Infections of Liver  596; Liver Tumours  605; Liver Cysts  613; Congenital Liver Cysts  613; Portal Hypertension  614; Oesophageal Varices  617; Emergency Management in Severe Haemorrhage  619; Portal Hypertensive Gastropathy  624; Ascites  624; Ascites in Portal Hypertension  626; Budd-Chiari’s Syndrome  626; Hepatic Failure  627; Hepatic Encephalopathy  627; Hepatorenal Syndrome  628; Hepatic Resection  628; Portal Biliopathy  630

12. Gallbladder

631

Surgical Anatomy  631; Oral Cholecystogram (OCG; Graham-Cole Test)  633; IV Cholangiogram  633; Endoscopic Retrograde Cholangio-pancreatography (ERCP)  633 ; Percutaneous Transhepatic Cholangiography (PTC)  634 ; Magnetic Resonance Cholangio-pancreato­g raphy (MRCP)  634 ; Radioisotope Scan Study  635; Peroperative Cholangiogram  635; Postoperative T-tube Cholangiogram  635; Congenital Anomalies of Gallbladder  635; Choledochal Cysts  636; Caroli’s Disease  638; Biliary Atresia  638; Gallstones  640; Acute Cholecystitis  643; Acute Acalculous Cholecystitis (5%)  645; Mirizzi Syndrome  645; Empyema Gallbladder  646; Mucocele of The Gallbladder  647; Chronic Cholecystitis  647; Murphy’s Sign  648; Gallstone Ileus  648; Cholecystoses  649; Dissolution Therapy for Gallstones  650; Choledocholithiasis  650; Sump Syndrome  653; Courvoisier’s Law (Sign)  654; Surgical Jaundice (Obstructive Jaundice)  654; CBD Strictures (Biliary Strictures)  657; Sclerosing Cholangitis  658; Gallbladder Polyp  658; Benign Biliary Papilloma  658; Carcinoma Gallbladder  659; Cholangiocarcinoma (Bile Duct Carcinoma)  661; Klatskin Tumour  661; Biliary Fistulas  662; Hemobilia  662; White Bile  663; Cholecystectomy  663; Open Approach Cholecystectomy  663; Laparoscopic Cholecystectomy  664; Single Incision Laparoscopic Surgery (SILS) in Cholecystectomy  665; Bile Duct Injuries  666; Postcholecystectomy Syndrome (15%)  667; Biliary Dyskinesia  667

13. Spleen

668

Surgical Anatomy  668; Functions of the Spleen  668; Splenunculi (30%)  669; Splenic Injury (Rupture Spleen)  669; Splenomegaly  672; Hereditary Spherocytosis  673; Immune Haemolytic Anaemia  673; Thalassaemia (Mediterranean Anaemia/Cooley’s Anaemia/Erythroblastic Target Cell Anaemia)  674; Sickle Cell Disease  674; Idiopathic (Immune) Thrombocytopaenic Purpura (ITP)  674; Thrombotic Thrombocytopaenic Purpura (TTP)  675; Splenectomy  676; Overwhelming Post-splenectomy Infection (OPSI)  677; Splenic Artery Aneurysm  677; Splenic Abscess  678; Hypersplenism  678; Splenic Cyst  678; Atraumatic Rupture of Spleen  679

14. Pancreas

680

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SRB's Manual of Surgery Anatomy  680; Serum Amylase  681; Serum Lipase  682; Magnetic Resonance Cholangio-pancreatography (MRCP)  682; Pancreatitis  682; Acute Pancreatitis  683; Complications of Acute Pancreatitis  689; Pseudocyst of Pancreas  690; Chronic Pancreatitis  692; Pancreatic Tumours  700; Exocrine Pancreatic Tumours  700; Carcinoma Pancreas  702; Endocrine Pancreatic Tumours  708; Insulinomas  709; Gastrinomas  709; Glucagonomas  710; Zollinger-Ellison Syndrome  711; Cystic Fibrosis  711; Annular Pancreas  711; Ectopic (Accessory) Pancreatic Tissue  712; Pancreatic Divisum  712; Pancreatic Calculus  712; Pancreatic Ascites  713; Pancreatic Fistulae  713; Pancreatic Necrosis  714; Pancreatic Trauma  714; Cystic Lesions of Pancreas  715; Pancreatic Exocrine Insufficiency (Exocrine Pancreatic Disease)  715

15. Retroperitoneal Space Anatomy of Retroperitoneum  717; Retroperitoneal Fibrosis  717; Retroperitoneal Tumours  718; Psoas Abscess  722

717 Retroperitoneal Swellings  718;

16. Differential Diagnosis of Mass Abdomen

724

Mass in the Right Hypochondrium  726; Mass in the Epigastrium  727; Mass in the Left Hypochondrium  728; Mass in the Lumbar Region  729; Mass in the Umbilical Region  730; Mass in the Right Iliac Fossa  731; Mass in the Left Iliac Fossa  731; Mass in the Hypogastrium  731; Digital Rectal Examination for Prostate and Other Conditions  733

17. Abdominal Wall and Umbilicus

736

Diseases of the Umbilicus  736; Omphalitis  737; Umbilical Granuloma  737; Anomalies of Vitellointestinal Duct  738; Umbilical Sinus  738; Umbilical Adenoma (Raspberry Tumour)  739; Umbilical Fistula  739; Patent Urachus  739; Burst Abdomen (Abdominal Wound Dehiscence) (Acute Wound Failure)  740; Abdominal Wall Tumours  742; Desmoid Tumour  742; Exomphalos (Omphalocele)  743; Gastroschisis (Belly Cleft)  744; Rectus Sheath Haematoma  744; Abdominal Wall Abscess  745; Meleney’s Progressive Synergistic Bacterial Gangrene of Abdominal Wall  745; Divarication of Recti (Diastasis Recti)  746

18. Hernia

747

Aetiology  748; Parts of Hernia  749; Classification of Hernia  750; Inguinal Hernia  751; Surgical Anatomy of Inguinal Canal  751; Classification of Inguinal Hernia (Earlier)  753; Indirect (Oblique) Inguinal Hernia  754; Direct Inguinal Hernia  762; Incarcerated Hernia  768; Strangulated Hernia  768; Sliding Hernia (Hernia-En-Glissade)  770; Pantaloon Hernia (Double Hernia, Saddle Hernia, Romberg Hernia)  771; Femoral Hernia  771; Ventral Hernia  774; Incisional Hernia  775; Umbilical Hernia  778; Paraumbilical Hernia (Supra- and Infraumbilical Hernia)  779; Epigastric Hernia (Fatty Hernia of Linea Alba)  780; Spigelian Hernia  781; Obturator Hernia  782; Richter’s Hernia  782; Lumbar Hernia  783; Phantom Hernia  783; Sciatic Hernia  783; Complications of Hernia Surgery  783; Parastomal Hernia  784

19. Oesophagus

786

Anatomy  786; Lower Oesophageal Sphincter (LOS)  788; Dysphagia  788; Contrast Study of Oesophagus  789 ; Oesophagoscopy  790 ; Oesophageal Endosonography  790 ; Third Space Endoscopy  790; Gastro-Oesophageal Reflux Disease (GORD/GERD)  790; Hiatus Hernia  795; Rolling Hernia (Paraoesophageal Hernia)  795; Reflux Oesophagitis  796; Barrett’s Oesophagus  796; Barrett’s Ulcer  797; Oesophageal Motility Disorders  797; Achalasia Cardia (Cardiospasm)  797; Plummer-Vinson Syndrome (Paterson-Kelly Syndrome)  800; Corrosive Stricture of Oesophagus  800; Schatzki’s Rings  802; Boerhaave’s Syndrome  802; Mallory-Weiss Syndrome  803; Tracheo-oesophageal Fistula (Oesophageal Atresia)  803; Oesophageal Diverticulum  804; Carcinoma Oesophagus  804; Benign Tumours of the Oesophagus  811; Oesophageal Perforation  812

20. Stomach Anatomy  814; Blood Supply of Stomach  815; Nerve Supply of Stomach  815; Histology  815; Lymphatic Drainage of Stomach  815; Duodenum  816; Gastric Physiology  816; Gastric Function Tests  817; Gastrin  817; Barium Meal Study  818; Gastroscopy  818; Helicobacter pylori  819; Congenital (Infantile) Hypertrophic Pyloric Stenosis  820; Gastritis  822; Acute Peptic Ulcer (Duodenal or Gastric Ulcer)  822;

814

Contents Gastric Ulcer  823; Duodenal Ulcer  825; Pyloric Stenosis Due to Chronic Duodenal Ulcer  828; Perforated Peptic Ulcer  830; Bleeding Peptic Ulcer  833; Haematemesis  836; Complications of Gastric Surgery  837; Trichobezoar (Rapunzel Syndrome)  840; Chronic Duodenal Ileus (Wilkie’s Syndrome)  841; Dunbar ‘s (MALS) Syndrome (Harjola—Marable Syndrome)  841; Acute Gastric Dilatation  842; Gastric Volvulus  842; Gastric Polyp  843; Menetrier’s Disease  843; Duodenal Diverticula  844; Carcinoma Stomach  844; Gastric Lymphoma  855; Gastric Sarcomas  857; Gastrointestinal Stromal Tumours (GISTS)  857; Pyloroplasty  858; Gastrostomy  858; Gastrectomy  859; Gastrojejunostomy (GJ)  860; Retrograde Jejunogastric Intussusception  860; Vagotomy  860

21. Small Intestine

862

Anatomy  862; Meckel’s Diverticulum  863; Regional Enteritis (Crohn’s Disease)  865; Surgical Complications of Typhoid  868; Surgical Complications of Roundworm (Ascaris lumbricoides)  869; Pneumatosis Cystoides Intestinalis  870; Mesenteric Vessel Ischaemia  871; Necrotising Enterocolitis  872; Small Bowel Tumours  873; Benign Tumours of Small Bowel  874; Malignant Tumours of Small Bowel  876; Carcinoid Tumour  877; Short Bowel Syndrome (Short Gut Syndrome)  879; Small Bowel Enema (Enteroclysis)  880; Capsule Endoscopy  881; Small Bowel Enteroscopy  881; Enteric/Gastrointestinal Fistula  881

22. Large Intestine

885

Anatomy  885; Hirschsprung’s Disease (Congenital Megacolon)  886; Diverticular Disease of the Colon  888; Ulcerative Colitis  891; Ischaemic Colitis  896; Pseudomembranous Colitis  896; Surgical Complications of Intestinal Amoebiasis  896; Tumours of Colon  897; Benign Tumours/Polyp of the Colon  897; Juvenile Polyps  898; Metaplastic/Hyperplastic Polyp  898; Peutz-Jeghers Polyp  898; Adenoma of Colon  898; Familial Adenomatous Polyp (FAP)  899; Carcinoma Colon  900; Angiodysplasia of Colon  909; Ogilvie’s Syndrome  909; Colostomy  910; Stoma Care  912; Stoma Appliances  913; Faecal Fistula  913; Preparation of Large Bowel for Surgery  914; Surgical Pouches  915; Barium Enema  915

23. Intestinal Obstruction

917

Intestinal Obstruction: Types  917; Dynamic Obstruction  918; Duodenal Atresia  924; Small Intestine Atresia (Intestinal Atresia)  925; Malrotation  926; Meconium Ileus  927; Intussusception (ISS)  928; Volvulus  931; Sigmoid Volvulus (Volvulus of Pelvic Colon)  931; Paralytic Ileus (Adynamic Intestinal Obstruction)  933; Adhesions and Bands  933; Internal Hernias  936

24. Appendix

937

Surgical Anatomy  937; Acute Appendicitis  938; Incidental Appendicectomy  945; Appendicular Mass (Periappendicular Phlegmon)  946; Appendicular Abscess  946; Faecal Fistula After Appendicectomy  947; Mucocele of Appendix  948; Neoplasms of the Appendix  948; Laparoscopic Appendicectomy  949

25. Rectum and Anal Canal

951

Anatomy  951; Per-rectal Examination (Digital Examination of the Rectum)  952; Proctoscopy (Kelly’s)  953; Sigmoidoscopy  953; Colonoscopy  953; Carcinoma Rectum  954; Solitary Ulcer Syndrome  960; Rectal Prolapse  961; Anorectal Malformations (ARM)  965; Pilonidal Sinus/Disease (Jeep Bottom; Driver’s Bottom)  967; Piles/Haemorrhoids  969; Anal Fissure (Fissure-in-Ano)  976; Anorectal Abscess  978; Fistula-in-Ano  980; Anorectal Strictures  985; Condyloma Acuminata  986; Anal Intraepithelial Neoplasia (AIN)  986; Malignant Tumours of Anal Area  986; Sacrococcygeal Teratoma  987; Anal incontinence  988; Descending Perineal Syndrome  988; Proctitis  989; Proctalgia Fugax  989; Hidradenitis Suppurativa of Anal Region  989; Pruritus Ani  989; Gastrointestinal Haemorrhage (GI Bleed)  989

26. Urology A. Kidney  993

Anatomy of Kidney and Ureter  993; Kidney—Anatomy  993; Ureter—Anatomy  994; Plain X-ray—Kidney, Ureter and Bladder (KUB)  994; Intravenous Urogram (IVU)  995; Retrograde Pyelography (RGP)  996; Renal Angiogram  997; Micturating Cystourethrography (MCU)  997; Ascending Urethrogram  997; Isotope Renography  998; Cystoscopy  998; Catheters  999; Foley’s Catheter  1000; Malecot’s Catheter  1000;

993

xxiii

xxiv

SRB's Manual of Surgery Red Rubber Catheter  1001; Nephrostomy  1001; Suprapubic Cystostomy (SPC)  1002; Haematuria  1002; Horseshoe Kidney  1003; Cystic Diseases of the Kidney  1004; Polycystic Kidney Disease (PCKD)  1004; Duplication of Renal Pelvis and Ureter  1005; Retrocaval Ureter  1006; Ureterocele  1006; Injuries to Kidney  1007; Renal Tuberculosis  1008; Hydronephrosis (HN)  1010; Pyonephrosis  1014; Carbuncle of Kidney (Renal Carbuncle)  1014; Perinephric Abscess  1015; Renal Calculus  1015; Ureteric Calculi  1019; Staghorn Calculus  1021; Benign Tumours of Kidney  1022; Wilms’ Tumour (Nephroblastoma)  1022; Renal Cell Carcinoma (RCC)  1024

B. Urinary Bladder  1028

Anatomy  1028; Ectopia Vesicae (Extrophy of the Bladder)  1029; Urachal Anomalies  1029; Vesical Calculus  1029; Cystitis  1031; Recurrent Cystitis  1032; Interstitial Cystitis (Hunner’s Ulcer, Elusive Ulcer)  1032; Schistosoma Haematobium (Endemic Haematuria, Urinary Bilharziasis) (Swimmer’s Itch)  1032; Thimble or Systolic Bladder  1033; Bladder Tumours  1033; Transitional Cell Carcinoma (TCC)  1033; Ureterosigmoidostomy  1036; Rupture Bladder (Bladder Injury)  1037; Residual Urine  1038; Malakoplakia  1038; Neurogenic Bladder  1038; Vesicoureteric Reflux  1039; Bladder Diverticula  1039; Urinary Diversion  1040; Urinary Fistulas  1041

C. Prostate 1043

Anatomy  1043; Acid Phosphatase  1043; Prostate Specific Antigen (PSA)  1043; Benign Prostatic Hyperplasia (BPH)  1044; Prostatitis  1047; Bladder Outlet Obstruction (BOO)  1047; Carcinoma Prostate  1048

D. Urethra 1051

Anatomy  1051; Urethral Injury  1051; Rupture of Membranous Urethra and/or Prostatic Urethra (Posterior Urethra)  1051; Rupture of Bulbous Urethra (Anterior Urethra)  1052; Stricture Urethra  1053; Hypospadias  1055; Epispadias  1056; Posterior Urethral Valve  1056; Urethral Calculi  1056; Urethritis  1057; Extravasation of Urine  1057; Retention of Urine  1058

E. Penis 1060

Phimosis  1060; Paraphimosis  1061; Circumcision  1061; Balanoposthitis  1062; Chordee (Cordee)  1062; Priapism  1063; Peyronie’s Disease (Induratio-Penis Plastica)  1063; Ram’s Horn Penis  1063; Carcinoma Penis  1063; Buschke-Löwenstein Tumour  1067

F. Scrotum 1068

Anatomy  1068; Fournier’s Gangrene  1068; Hydrocele  1069; Primary Vaginal Hydrocele  1070; Secondary Vaginal Hydrocele  1071; Haematocele  1073; Pyocele  1074; Cyst of Epididymis  1074; Spermatocele  1075; Varicocele  1075

G. Testis  1078

Anatomy  1078; Undescended Testis  1078; Ectopic Testis  1081; Retractile Testis  1081; Torsion of the Testis  1081; Testicular Tumours  1083; Paratesticular Tumours  1087; Orchitis  1087; Epididymitis  1088

27. Neurosurgery

1090

Head Injuries  1090; Extradural Haematoma  1095; Subdural Haematoma  1096; Subarachnoid Haemorrhage (SAH)  1097; Fracture Skull  1098; Depressed Skull Fracture  1099; CSF Rhinorrhoea  1099; Hydrocephalus  1100; Intracranial Abscess  1101; Intracranial Aneurysms  1102; Intracranial Tumours  1102; Pituitary Tumours  1105; Craniopharyngiomas  1106; Spinal Dysraphism  1106; Meningocele  1106; Spina Bifida  1107; Intervertebral Disc Prolapse (IVDP)  1108; Tuberculosis of Spine (Caries Spine)  1109; Spinal Tumours  1111

28A. Thorax Chest Injuries  1112; Fracture Ribs  1114; Flail Chest and Stove in Chest  1115; Pneumothorax  1116; Tension Pneumothorax  1116; Haemothorax  1117; Pleural Tap  1117; Bronchoscopy  1118; Empyema Thoracis  1118; Empyema Necessitans  1119; Lung Abscess  1120; Intercostal Tube Drainage  1121; Shock Lung (Stiff Lung)  1123; Pulmonary Embolism (PE)  1123; Surgical Emphysema  1124; Lung Cysts  1124; Mediastinal Tumours  1125; Thymomas  1127; Lung Cancers  1127; Pancoast Tumours (Superior Sulcus Tumour)  1128; Chest Wall Tumours  1128; Pericarditis  1129; Acute Pericarditis  1129;

1112

Contents Chronic Constrictive Pericarditis (Pick’s Disease)  1129; Pericardial Tap  1129; Cardiac (Pericardial) Tamponade  1130; Diaphragmatic Hernia  1130; Pulmonary Complications During Postoperative Period  1133; Surgical Management of Pulmonary Tuberculosis  1133; Video-assisted Thoracoscopic Surgery (VATS)  1133

B. Cardiac Surgery  1134

Anatomy  1134; Preoperative Assessment and Preparation of the Cardiac Patient  1135; Cardiopulmonary Bypass  1135; Congenital Heart Diseases  1136; Patent Ductus Arteriosus (PDA)—10%  1136; Coarctation of Aorta—5%  1136; Atrial Septal Defect (ASD)—7%  1137; Ventricular Septal Defect (VSD)—15%  1137; Pulmonary Stenosis  1138; Transposition of Great Vessels  1138; Tetralogy of Fallot  1138; Acquired Heart Disease  1139; Mitral Regurgitation  1139; Aortic Stenosis  1140; Aortic Regurgitation  1140; Valve Replacement Surgery  1140; Ischaemic Heart Disease (IHD)  1140; Cardiac Pacemakers  1141; Postoperative Care  1141

29. Adjuvant Therapy

1142

Radiotherapy  1142; Chemotherapy  1144; Cell Cycle  1145; Antimalignancy Drugs  1145; Hormone Therapy in Cancer  1145; Immunosuppression  1146; Immunotherapy  1147; Hybridoma  1147; Gene Therapy  1147

30. Anaesthesia

1148

Preoperative Assessment  1148; General Anaesthesia  1149; Anaesthetic Agents  1149; Oxygen  1149; Muscle Relaxants  1149; Reversal Agents  1149; Instruments in Anaesthesia  1149; Complications of General Anaesthesia  1151; Postoperative Care  1151; Monitoring the Postoperative Patient  1151; Regional Anaesthesia  1152; Topical Anaesthesia  1152; Infiltration Block  1152; Field Block  1152; Nerve Block  1152; Intravenous Regional Anaesthesia (Bier’s Block)  1152; Spinal Anaesthesia  1152; Saddle Block  1153; Epidural Anaesthesia  1153; Caudal Anaesthesia  1153

31. Advanced Imaging Methods

1154

Ultrasound  1154; Doppler  1156; CT Scan  1156; Magnetic Resonance Imaging (MRI)  1158; Radionuclide Imaging  1159; Positron-Emission Tomography (PET Scan)  1159

32. Operative Surgery A. Asepsis and Sterilisation  1160

Sterilisation  1160; Disinfection  1160; Antisepsis  1160; Asepsis  1160; Different Methods of Disinfection/ Sterilisation  1160

B. Instruments 1163

Cheatle’s Forceps  1163; Sponge Holding Forceps (Rampley’s)  1163; Mayo’s Towel Clip  1163; Artery Forceps (Haemostat)  1163; Right Angle Forceps  1164; Kocher’s Forceps  1164; Allis’ Tissue Holding Forceps  1164; Babcock’s Forceps  1164; Lane’s Tissue Holding Forceps  1165; Morant-Baker’s Appendix Holding Forceps  1165; Volkmann’s Retractor  1165; Langenbeck’s Retractor  1165; Czerny’s Retractor (Hernia Retractor)  1165; Morris’ Retractor  1165; Deaver’s Retractor  1165; Doyen’s Retractor  1166; Self-retaining Retractor  1166; Single Hook Retractor  1166; Plain Non-toothed Dissecting Forceps  1166; Toothed Dissecting Forceps  1166; Surgical Needles  1166; Needle Holder  1167; Joll’s Thyroid Retractor  1167; Moynihan’s Occlusion Clamp  1167; Payr’s Crushing Clamp (Gastric)  1167; Desjardin’s Choledocholithotomy Forceps  1167; Bake’s Dilator  1167; Sinus Forceps (Lister’s)  1168; Scissors  1168; Volkmann’s Scoop  1168; Tracheostomy Tube  1168; Drains  1168; Foley’s Catheter  1170; Malecot’s Catheter  1170; Simple Red Rubber Catheter  1170; Lister’s Urethral Dilator  1170; Ryle’s Tube  1170; Infant Feeding Tube  1171; Kehr’s ‘T’ Tube  1171; Proctoscope  1171; Flatus Tube  1171

C. Suture Materials  1172

Classification I  1172; Classification II  1173; Classification III  1173; Classification IV  1173; Classification V  1173

D. Diathermy (Electrocautery)  1174 Types  1174

E. Operative Procedure  1175

1160

xxv

xxvi

SRB's Manual of Surgery Abdominal Incisions  1175; Vasectomy  1176; Circumcision  1176; Hydrocele  1177; Inguinal Hernia  1177; Appendicectomy  1178; Thyroidectomy  1178; Tracheostomy  1179; Cryosurgery  1180; Lasers in Surgery  1180; Staplers in Surgery  1181; Nasojejunal Tube Feeding  1182; Gossypiboma 1182

F. Laparoscopic Surgery  1183

Advantages of Laparoscopic Surgery  1183; Laparoscopic Cholecystectomy  1184; Laparoscopic Appendicectomy  1185; Advanced Laparoscopic Surgeries  1185; Diagnostic Laparoscopy  1185; Retroperitoneoscopy  1186 Natural Orifice Transluminal Endoscopic Surgery (Notes)  1186

G. Dressings and Bandages  1187 Dressings  1187; Bandages  1187

H. Day Care Surgery  1189

Day Care Surgery  1189; Surgical Audit  1190; Surgeon and Law  1191

33. Miscellaneous

1192

A. Fascinating Signs in Surgery  1192 B. Triads in Surgery  1201 C. Misnomers in Surgery  1202 D. Triangles in Surgery  1203 E. Drugs at a Glance  1204

Antibacterials  1204; Sulfonamides  1204; Quinolones  1204; Penicillin  1204; Ampicillin/Amoxycillin/ Talampicillin/ Pivampicillin  1205; Methicillin  1205; Cloxacillin/Dicloxacillin/Flucloxacillin  1205; Carbenicillin/ Ticarcillin  1205; Piperacillin/Azocillin/Mezlocillin  1205; Clavulanic Acid  1205; Sulbactum  1205; Tazobactum  1205 ; Carbapenem/Imipenem/Meropenem  1205 ; Lincomycin/Clindamycin  1205 ; Vancomycin/Teicoplanin  1205; Cephalosporins  1206; Macrolides  1206; Aminoglycosides  1206; Tetracyclines  1206; Chloramphenicol/Thiamphenicol  1207; Drugs for Tuberculosis  1207; Antiamoebic Drugs  1207; Important Antihelminthics  1208; Anticoagulants  1208; Other Drugs  1209

Further Reading Appendix

1211 1213

Index

1217

Chapter

1

General Surgery A. Wounds and Wound Healing One having a wound in his eyebrow. An ailment which I will treat. Treatment [of a wound in the eyebrow]: Now after thou hast stitched it, [thou shouldst bind] fresh meat upon [it] the first day. If thou findest that the stitching of this wound is loose, thou shouldst draw it together for him with two strips (of plaster), and thou shouldst treat it with grease and honey every day until he recovers. —[Anonymous], circa 2500 BC

CHAPTER OUTLINE ™™ ™™ ™™ ™™

Wounds Classification of Wounds Wound Healing Compartment Syndrome

™™ ™™ ™™ ™™

Crush Injury Crush Syndrome Degloving Injuries Keloid

™™ Hypertrophic Scar ™™ Problems with Wound Healing

WoundS Wound Definition A wound is a break in the integrity of the skin or tissues often, which may be associated with disruption of the structure and function. Wound is simply a disruption of any tissues—soft tissue or bone or internal organs. Ulcer is disruption or break in the continuity of any lining—may be skin, mucous membrane or others. Ulcer is one of the types of wounds.

CLASSIFICATION OF WOUNDS I. Rank and Wakefield classification a. Tidy wounds  They are wounds like surgical incisions and wounds caused by sharp objects.

Fig. 1.1A: Tidy wound

 It is incised, clean, healthy wound without any tissue loss.  Usually primary suturing is done. Healing is by primary

intention.

I dressed him and God healed him.— Ambroise Pare

2

SRB's Manual of Surgery b. Untidy wounds  They are due to: –– Crushing. –– Tearing. –– Avulsion. –– Devitalised injury. –– Vascular injury. –– Multiple irregular wounds. –– Burns.  Fracture of the underlying bone may be present. Wound dehiscence, infection, delayed healing are common.  Liberal excision of devitalised tissue and allowing to heal by secondary intention is the management.  Secondary suturing, skin graft or flap may be needed.

A

B Fig. 1.1B: Untidy wound

II. Classification based on the type of the wound Clean incised wound: It is a tidy, simple, clean cut wound with linear cut edges; usually due to a sharp object like blade, glass piece or knife. It is treated by primary suturing.

Fig. 1.2: Clean incised wound.

Lacerated wound: It has ragged edges with some part of the tissues getting devitalized; viability of the tissues may be impaired; depth of the injury and tissue damage should be carefully assessed. Proper adequate wound excision, thorough warm saline wash and suturing of the wound layer-by-layer is required.

Figs 1.3A and B: Lacerated wounds.

Bruise or contusion: It is due to blow or blunt force to the skin and tissues underneath wherein blood vessels or capillaries are damaged underneath. There is skin discolouration without breaking of the skin; broken vessels cause seepage of blood underneath; minor soft tissue injury crushes small vessels without breaking the skin accumulating trapped blood underneath. It is more on the skin over the bones; lax area like face, scrotum, eyes; vascular areas; children, old aged, fair skin people. Haematoma: It is a localized collection of blood after blunt trauma or after surgery. Collected fluid blood in few minutes to hours gets clotted; later eventually it gets liquefied and shows discoloured fluid. It may be subcutaneous/ intramuscular/subfascial/intra-articular. Large haematoma may get infected to form an abscess; so large haematoma needs drainage under general or regional anaesthesia. Small haematoma usually gets absorbed (like scalp haematoma). Often haematoma contains reddish plasmatic fluid which should be aspirated using wide bore needle. Complications are—pressure effects and abscess formation; both needs incision and drainage under anaesthesia. Haematoma causing cosmetic problems may require needle aspiration. Haematoma can occur spontaneously in coagulation disorders (haemophilia) or in individuals who are on anticoagulant drug therapy.

Wounds and Wound Healing

Fig. 1.4: Haematoma of eyelid.

Fig. 1.7: Typical look of abrasion in face.

Fig. 1.5: Haematoma in the groin being aspirated. Haematoma may get infected or can compress adjacent structures.

Fig. 1.8: Multiple abrasions.

Fig. 1.6: Subungual haematoma. Often nail may need to be removed to evacuate the blood clot.

Abrasion: It is superficial injury (scratch/graze/pressure/ contact) and is due to shearing of the skin where the surface is rubbed off. This tangential force causes loss of epidermis exposing dermal vessels and nerves leading into profuse painful oozing. Abrasion heals by epithelialisation. Any dirt or foreign body on the abrasion should be removed to avoid formation of poor tattoo like scar. Puncture wounds and bites: It is usually a stab wound with a pointed object; here depth of the wound is more than the width. Deeper vital structures or organs may be injured, so should be assessed; foreign body or object may be present in the depth of the wound. Wound should be explored under general or regional anaesthesia to assess the depth and severity of the injury and sutured layer by layer after through saline wash.

Fig. 1.9: Penetrating wound of the abdomen.

Penetrating wounds: They are similar like puncture wounds; due to stab. Abdomen and chest are common sites. Liver, bowel, spleen, major vessels and other visceral organs may be

A great part, I believe, of the art of medicine is the ability to observe.—Hippocrates, Father of Medicine

3

4

SRB's Manual of Surgery involved. Ultrasound and CT scan should be done to evaluate deeper organ injuries. Under general anaesthesia wound should be explored properly. Traction and avulsion injuries: these are complex injuries with tissues getting displaced from its normal anatomical position and alignment. It can occur in single plane like in subcutaneous tissue or in multiple planes like in machinery injuries, major injuries or degloving injuries. Ischaemia, bleeding, sepsis, loss of wide tissue area are common problems. Open traction injury occurs on the surface. Closed traction injury can occur in deeper plane like brachial plexus injury or traction bowel injury. After initial resuscitation, definitive treatment like skin graft or nerve repair should be done.

III. Classification based on thickness of the wound xx Superficial wound involving only epidermis and dermal papillae. xx Partial thickness wound with skin loss up to deep dermis with only deepest part of the dermis, hair follicle shafts and sweat glands are left behind. xx Full thickness wound with loss of entire skin and subcutaneous tissue causing spacing out of the skin edges. xx Deep wounds are the one extending deeper, across deep fascia into muscles or deeper structures. xx Complicated wounds are one associated with injury to vessels or nerves. xx Penetrating wound is one which penetrates into either natural cavities or organs. IV. Classification based on involvement of structures xx Simple wounds are one involving only one organ or tissue. xx Combined/complex wounds are one involving mixed tissues.

Crush injury: It is due to major wounds, war wounds, natural disaster like earth quake injuries, tourniquet injury. It leads into—compartment syndrome; muscle ischaemia; loss of tissues; gangrene; sepsis. Muscle will lose its viability which is identified by its colour (dark coloured with loss of shining); loss of contractility; turgid, and will not bleed on cutting.

Fig. 1.11: Complex wound exposed tendons. Fig. 1.10: Severe crush injury leg.

Gunshot injuries: These injuries may be superficial or deep. Usually entry wound and exit wound will be present. It causes explosive and destructive injuries along with burn injuries in the deeper planes and organs. It can be high velocity injuries with massive bleeding and major organ injuries. Injuries to bones and joints: It is common in all major injuries; should be identified clinically and confirmed radiologically. It needs specialized management like reduction, plating etc. Injuries to nerves, arteries, veins (major vessels), deeper organs: It needs initial resuscitation, later staged management as per individual patient basis depending on the severity and extent of injury and loss of function. Closed blunt injury: It may be due to fall, blunt injury wherein no obvious external injury may be seen but deeper injury occurs; it may be often severe enough to cause major injury like in blunt abdominal injury causing bowel/liver/spleen/ renal injuries. Note:

wound may be closed (bruise, haematoma, blunt injury); open (abrasion, incised, lacerated, penetrating) or complex (traction/avulsion, crush or gunshot injuries).

V. Classification based on the time elapsed Acute wounds are generally defined as those that progress through the normal phases of healing and typically show signs of healing in less than 4 weeks; examples are—surgical or traumatic or burn wounds; progress through the healing phases in a timely and orderly fashion - haemostasis, inflammation, proliferation, and remodeling or maturation. Chronic wounds are defined as those that do not follow the normal healing process and show no signs of healing in 4 weeks. It fails to progress through the normal phases of healing but with prolonged inflammatory phase. Diabetes, venous/arterial diseases, nutritional deficiencies are the causes. Hypoxia initially is a potent stimulus for fibroblast activity and angiogenesis; persisting hypoxia impedes fibroblast and collagen activity and also allows bacterial invasion to make wounds chronic. Chronic wounds are chronically infected with biofilms which interfere mainly with the inflammatory phase of healing, contributing to the non-healing. A biofilm is a complex structure of microorganisms contained in an extracellular matrix of proteins and polysaccharides that adhere to a surface, creating a protected environment for the organisms. Chronic ulcers are unresponsive to dressing treatment; it requires biopsy, culture study, definitive treatment like wound debridement, VAC (Vacuum Assisted Closure) therapy, skin grafting or flap. Specific conditions like tuberculosis if present should be treated. Malignancy if confirmed is treated by wide local excision and skin graft.

Wounds and Wound Healing

Fig. 1.14: Appendicectomy wound, which is a clean contaminated wound. Fig. 1.12: Chronic wounds over the scalp vi. Classification of surgical wounds a. Clean wound  Herniorrhaphy.  Excisions.  Surgeries of the brain, joints, heart, transplant.  Infective rate is less than 2%. b. Clean contaminated wound  Appendicectomy.  Bowel surgeries, gastrojejunostomy.  Gallbladder, biliary and pancreatic surgeries.  Infective rate is 10%. c. Contaminated wound  Acute abdominal conditions.  Open fresh accidental wounds.  Infective rate is 15–30%. d. Dirty infected wound  Abscess drainage.  Pyocele.  Empyema gallbladder.  Faecal peritonitis.  Infective rate is 40–70%.

Fig. 1.15: Contaminated wound—burst appendicitis.

Wound classifications • Simple wounds: Only skin is involved

• Tidy wounds

• Complex wounds: Vessels, nerves, tendons or bones are involved

• Untidy wounds

• Closed wounds:

• Clean wound.

–– Contusion

• Clean contaminated wound

–– Abrasion

• Contaminated wound

–– Haematoma

• Dirty wound

• Open wounds: –– Incised wounds –– Lacerated wounds –– Crush injuries

Fig. 1.13: Clean wound of thyroidectomy surgery.

–– Penetrating wounds

Start by doing what’s necessary, then do what’s possible and suddenly you are doing the impossible.

5

6

SRB's Manual of Surgery Wound healing is complex method to achieve anatomical and functional integrity of disrupted tissue by various components like neutrophils, macrophages, lymphocytes, fibroblasts, collagen; in an organised staged pathways—haemostasis → inflammation → proliferation → matrix synthesis (collagen and proteoglycan ground substance) → maturation → remodelling → epithelialisation → wound contraction (by myofibroblasts).

Types of Wound Healing Primary Healing (First Intention) xx It occurs in a clean incised wound or surgical wound.

Wound edges are approximated with sutures. There is more epithelial regeneration than fibrosis. Wound heals rapidly with complete closure. Scar will be linear, smooth, and supple.

A

Secondary Healing (Second Intention) xx It occurs in a wound with extensive soft tissue loss like in

major trauma, burns and wound with sepsis. It heals slowly with fibrosis. It leads into a wide scar, often hypertrophied and contracted. It may lead into disability. xx Re-epithelialisation occurs from remaining dermal elements or wound margins.

B Figs 1.16A and B: Acute peritonitis with frank pus in peritoneal cavity due to bowel perforation is a dirty wound.

Fig. 1.17: Wound causing extensive skin loss and necrosis.

WOUND HEALING A scab is a beautiful thing—a coin the body has minted, with an invisible motto: In God We Trust. Our body loves us, and, even while the spirit drifts dreaming, works at mending the damage that we do. —John Updike, 1984

Fig. 1.18: Wound in the abdomen healing with second intention which requires secondary suturing once it granulates well. Secondary suturing is done after 10–14 days, once wound granulates well with proper control of infection. Scar in such type is prone to form incisional hernia.

Healing by Third Intention (Tertiary Wound Healing or Delayed Primary Closure) After wound debridement and control of local infection, wound is closed with sutures or covered using skin graft. Primary contaminated or mixed tissue wounds heal by tertiary intention.

Wounds and Wound Healing Stages of wound healing Stage of inflammation. Stage of granulation tissue formation and organi­sation. Here due to fibroblastic activity synthesi­sation of collagen and ground substance occurs. ™™ Stage of epithelialisation. ™™ Stage of scar formation and resorption. ™™ Stage of maturation. ™™ ™™

Phases of Wound Healing Inflammatory phase (Lag or Substrate or Exudative Phase) xx It begins immediately after formation and lasts for 72 hours. xx There is initial arteriolar vasoconstriction, thrombus formation, platelet aggregation due to endothelial damage and release of adenosine diphosphate (ADP). xx Later vasodilatation and increased vascular permeability develops. xx Here haemostasis, coagulation and chemotaxis occur. Note:

Coagulation begins at wound haematoma → formation of platelet fibrin thrombus → release of cytokines, PDGF (platelet-derived growth factor), epidermal growth factor (EGF), transforming growth factor β (TGF – β), platelet activating factor and platelet factor IV, fibrin, serotonin. Chemotaxis causes first neutrophil migration, and then activation of macrophages, lymphocytes leading into phagocytosis, wound debridement, matrix activation, angiogenesis. Chemotaxis factors are complement factors, interleukin-1, TNF-α (tumour necrosis factor-α) TGF–β and platelet factor. Activated macrophages produce free radicals and nitric oxide; release cytokine to activate lymphocytes which release interferon and interleukin (called as lymphokines). These factors attract polymorpho nuclear leucocytes (PMN—poly morphonuclear cells–neutrophills) in 48 hours secreting inflammatory mediators and bactericidal oxygen derived-free radicals. Injured tissues and platelet release histamine, serotonin and prostaglandins which increases the vascular permeability by vasodilatation. These actions are reduced in diabetes mellitus, Cushing’s syndrome and immunosuppression increasing the sepsis rate.

Remodelling phase (Maturation Phase) xx It begins at 6 weeks and lasts for 6 months to 1 or 2 years. xx There is maturation of collagen by cross linking and realignment of collagen fibers along the line of tension, which is responsible for tensile strength of the scar. There is reduced wound vascularity. Fibroblast and myofibroblast activity causes wound contraction. Type III collagen is replaced by type I collagen causing maturation of the collagen. Ratio of type I collagen to type III collagen becomes 4:1. xx Early extracellular matrix contains fibronectin and collagen type III; eventually it contains glycosaminoglycans and proteoglycans; final matrix contains type I collagen. xx Scar strength is 3% in 1 week; 20% in 3 weeks; 80% in 12 weeks. Final matured scar is acellular and avascular. Note: Initially fibrin, fibronectin, proteoglycans deposition occurs; later collagen protein develops to form scar. Normal dermal skin contains 80% type I (20% type III) collagen; granulation tissue contains mainly type III collagen; scar contains both type I and III collagen, initially in equal proportion, later becomes 4:1. Basic essential components of collagen are proline and lysine. Hydroxylation of lysine and later glycosylation of this hydroxylysine decides the type of collagen molecule. Hydroxylation of both proline and lysine as essential step needs adequate concentration of vitamin C, iron and α ketogluteric acid. Collagen deposition in the wound is assessed by quantity of hydroxyproline excreted in urine. There is a balanced activity of collagen production and degradation of collagen (collagenolysis). Collagen is broken down by collagenase and MMPs (matrix metalloproteinases). Procollagen through procollagenase → collagen fibril → cross linking → collagen fiber → deposition. Deposited collagen → through collagenase → degradation and collagenolysis.

Points to be remembered ™™

™™

xx All these cause features of acute inflammation—rubor, calor, tumour, dolor and loss of function.

Proliferative phase (Collagen/fibroblastic phase) xx It begins from 3rd day and lasts for 3–6 weeks. There will be formation of granulation tissue and repair of the wound. Granulation tissue contains fibroblasts, neocapillaries, collagen, fibronectin and hyaluronic acid. xx (1) Initial angiogenesis (growth of new blood vessels) occurs by release of vascular endothelial cell growth factor (VEGF) by keratinocytes; by release of TNF-α, TGF–β, PDGF, FGF by macrophages. (2) Eventual fibroplasia develops by fibroblast activity with formation of the collagen and ground substance/ glycosaminoglycans. Type III collagen is deposited initially in a random fashion. (3) Later re-epithelialisation of the wound surface occurs by migration of basal layer of the retained epidermis which proliferates, differentiates and stratifies to form wound closure.

™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

PMN cells survive only for 24 hours; so after 48 hours PMNs won’t be found in the wound significantly; PMNs are not needed for wound healing. Activated monocytes called macrophages predominate after 48 hours which will persist until completion of the wound healing. Macrophages are the main cells of wound healing. Macrophages secrete TNF - α, interleukin -1, fibroblast growth factor (FGF), proteinases (MMPs – matrix metallo proteinases). B lymphocyte will not have any role in wound healing; T lymphocytes produce stimulatory cytokines like interleukin – 1 supporting the fibroblast activity. Collagen and glycosamines are produced by fibroblasts. Tropocollagen is produced which aggregates to form collagen fibrils. Hydroxyproline and hydroxylysine are synthesized by specific enzymes using iron, α ketoglutarate and vitamin C. Fibroblast requires vitamin C to produce collagen. Granulation tissue and early scar contains type III collagen. Final scar contains type I collagen mainly. Final extra cellular matrix contains type I collagen and proteoglycans. Collagen production decreases after 4 weeks of wound healing (declines in 28-42 days). Eighty per cent of tensile strength of normal skin will be achieved finally but not 100%

Clinical diagnosis is an art, and the mastery of an art has no end: you can always be a better diagnostician —Logan Clendening

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SRB's Manual of Surgery Wound infection: Infection prolongs inflammatory phase, releases toxins and utilizes vital nutrients thereby prevents wound epithelialisation. The β-haemolytic streptococci more than 105 per gram of tissue prevent wounds healing. Formation of biofilms on the wound surface by microorganisms prevents wound healing. Anaemia: Haemoglobin less than 8g % causes poor oxygenation of tissues preventing healing of the wounds. Hypoxia: Hypoxia prevents fibroblast proliferation and collagen synthesis; it also promotes bacterial invasion into the wound. Causes of hypoxia are—arterial diseases, cardiac failure, respiratory causes, hypotension, smoking, tobacco, infection, diabetes mellitus and radiation. Fig. 1.19: Healing ulcer with healthy granulation tissue which is ready for skin grafting.

Factors affecting Wound Healing Age: In younger age group wound healing is faster and better. In elderly healing is delayed due to reduction in collagen synthesis, epithelialisation, growth factors and angiogenesis. But final scar will be excellent in old individuals. Nutrition: Adequate vitamin, trace elements, fatty acids and proteins are essential for wound healing. Vitamin A deficiency affects monocyte activation, inflammatory phase, collagen synthesis and growth factor actions. Vitamin K deficiency affects synthesis of prothrombin (II), factors VII, IX and X. Vitamin E, being an antioxidant stabilizes the cell membrane. Vitamin C deficiency impairs collagen synthesis, fibroblast proliferation and angiogenesis; increases the capillary fragility and susceptibility for infection. Zinc is an essential cofactor for RNA and DNA polymerase; magnesium is a co-factor for synthesis of proteins and collagen; copper is a required co-factor for cytochrome oxidase, for cytosolic anti-oxidant superoxide dismutase, and for the optimal cross-linking of collagen; Iron is required for the hydroxylation of proline and lysine. Glutamine is the most abundant amino acid in plasma; is a major source of energy for rapidly proliferating cells such as fibroblasts, lymphocytes, epithelial cells, and macrophages. The serum concentration of glutamine is reduced after major surgery, trauma, and sepsis, and supplementation of this amino acid improves nitrogen balance and diminishes immunosuppression. Glutamine stimulates the inflammatory immune response in early wound healing. Oral glutamine supplementation improves wound breaking strength and of mature collagen. Arginine is a semi-essential amino acid that is required in growth, severe stress, and injury. Arginine modulates immune function, wound healing, hormone secretion, vascular tone, and endothelial function. Arginine is a precursor to proline; supports collagen deposition, angiogenesis, and wound contraction. Under psychological stress situations, the metabolic demand of arginine increases, and its supplementation hastens the wound healing. Serum albumin level less than 2 g/dl causes prolonged inflammatory phase, decreased fibroplasia, neovascularisation and cell synthesis and wound remodeling and hence decreased wound healing. Wounds in patients who remain in catabolic state will not heal. Collagen is the major protein component of connective tissue; it contains mainly glycine, proline, and hydroxyproline. Collagen synthesis requires hydroxylation of lysine and proline, and co-factors such as ferrous iron and vitamin C. Polyunsaturated fatty acids which cannot be synthesized de novo by mammals, consist mainly of omega-6 (found in soybean oil) and omega-3 (found in fish oil—fatty acids such as eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]). They affect pro-inflammatory cytokine production, cell metabolism, gene expression and angiogenesis; improve the systemic immune function of the host, thus reducing infectious complications.

Radiotherapy: Both external radiotherapy or ionizing radiation cause endarteritis, fibrosis and delay in wound healing. Radiation may itself cause local tissue necrosis, sepsis and hypoxia. Systemic and metabolic causes: Diabetes mellitus affects all stages of wound healing. Cardiac, renal, hepatic, respiratory diseases prevent wound healing. Tissue oedema impairs wound healing. HIV and immunosuppression of varying causes, malignancy leads into poor wound healing. Jaundice interferes with wound healing. Obesity causes hypoperfusion, reduced microcirculation, increased wound tension and hence prevents wound healing. Drugs: Steroids interfere with activation of macrophages, fibroblasts and angiogenesis in the early phase of healing (proliferative). Non-steroidal anti-inflammatory drugs (NSAIDs) decrease collagen production. Chemotherapeutic agents used in oncology inhibit cellular proliferation, protein synthesis. Alcohol consumption decreases the phagocyte response and pro-inflammatory cytokine release; diminishes host response and thus increasing the infection rate. Local factors ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Infection Presence of necrotic tissue and foreign body Poor blood supply Venous or lymph stasis Tissue tension Haematoma Large defect or poor apposition Recurrent trauma X-ray irradiated area Site of wound, e.g. wound over the joints and back has poor healing Underlying diseases like osteomyelitis and malig­nancy Mechanism and type of wound—incised/lacerated/crush/ avulsion Tissue hypoxia locally reduces macrophage and fibroblast activity

General Factors ™™ Age, obesity, smoking, alcohol, stress ™™ Malnutrition, zinc, copper, manganese ™™ Vitamin deficiency (Vit C, Vit A) ™™ Anaemia, hypoxia ™™ Malignancy ™™ Uraemia ™™ Jaundice ™™ Diabetes, metabolic diseases ™™ HIV and immunosuppressive diseases ™™ Steroids and cytotoxic drugs ™™ Neuropathies of different causes

Wounds and Wound Healing Management of Wounds Wound cleaning Wound cleaning is needed to optimize the healing environment. It is achieved by removing visible devitalized tissues or dressing materials or excess exudates or crusts. Absolute aseptic technique should be used while cleaning the wound; warm sterile isotonic normal saline (37°C—this is optimum temperature to support cellular activity) is ideal; normal exudates in the wound should be removed; gentle cleaning of the wound is important to minimize the interference of the wound-healing process. Cleaning agent should be of neutral pH and nontoxic; delipidising agents, antiseptics, alkaline soaps should be avoided. Gentle irrigation of warm saline using a sterile syringe on the wound surface is ideal; rubbing with undue force using cotton or gauze may cause mechanical damage on the process of wound healing. Wound is measured either in two dimensions (length and width) or in three dimensions (length, width and depth).

has to be dealt with accordingly. Fractured bone is also identified and properly dealt with. xx Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid (0.5 ml intramuscular to deltoid muscle), or antitetanus globulin (ATG) injection. Later definitive management is done with: Wound debridement (wound toilet, or wound excision) is liberal excision of all devitalised tissue at regular intervals (of 48-72 hours) until healthy, bleeding, vascular tidy wound is created. Types of wound suturing Primary suturing means suturing the wound immedia­tely within 6 hours. It is done in clean incised wounds. ™™ Delayed primary suturing means suturing the wound in 48 hours to 10 days. It is done in lacerated wounds. This time is allowed for the oedema to subside. ™™ Secondary suturing means suturing the wound in 10–14 days or later. It is done in infected wounds. After the control of infection, once healthy granulation tissue appears, secondary suturing is done. ™™

Specific management xx Wound is inspected and classified as per the type of wounds. xx If it is in the vital area, then:

The airway should be maintained. The bleeding, if present, should be controlled. Intravenous fluids are started. Oxygen, if required, may be given. Deeper communicating injuries and fractures, etc. should be looked for. xx If it is an incised wound then primary suturing is done after thorough cleaning. xx If it is a lacerated wound then the wound is excised and primary suturing is done. xx If it is a crushed or devitalised wound there will be oedema and tension in the wound. So after wound debridement or wound excision by excising all devitalised tissue, the oedema is allowed to subside for 2–6 days. Then delayed primary suturing is done. xx If it is a deep devitalised wound, after wound debridement it is allowed to granulate completely. Later, if the wound is small secondary suturing is done. If the wound is large a split skin graft (Thiersch graft) is used to cover the defect. xx In a wound with tension, fasciotomy is done so as to prevent the development of compartment syndrome. xx Vascular or nerve injuries are dealt with accordingly. Vessels are sutured with 6-zero polypropylene nonabsorbable suture material. If the nerves are having clean cut wounds it can be sutured primarily with polypropylene 6-zero or 7-zero suture material. If there is difficulty in identifying the nerve ends or if there are crushed cut ends of nerves then marker stitches are placed using silk at the site and later secondary repair of the nerve is done. xx Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube drainage, intra-abdominal by laparotomy)     

A

B Figs 1.20A and B: Delayed primary suturing is done once oedema over the wound subsides. It is done as single layer interrupted deep sutures using monofilament polypropylene or polyethylene.

A Fig. 1.21A

When you smile world smiles with you. When you cry, it will be your alone.

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SRB's Manual of Surgery Features are—It compromises circulation and function mainly of muscles and nerves. It often maintains the normal colour and temperature of the fingers and distal pulses may not be obliterated in spite of severe muscle ischaemia. Muscle ischaemia more than 4 hours causes muscle death and myoglobinuria. Irreversible nerve damage develops if ischaemia persists for 8 hours. Progressive, persistent severe pain which is aggravated by passive muscle stretching is the diagnostic sign. Tense tender regional lymph node is typical. Pulse will be usually normally felt in compartment syndrome; but may become absent if there is associated arterial injury. Compartment pressure more than 30 mmHg is an indication for fasciotomy.

B Fig. 1.21B

Figs 1.21A and B: Secondary suturing is done once wound is healthy after control of wound infection. Principles of wound suturing ™™ ™™

™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Primary suturing should not be done if there is oedema/infection/devitalised tissues/haematoma Always associated injuries to deeper structures like vessels/ nerves or tendons should be looked for before closure of the wound Wound should be widened by extending the incision whenever needed to have proper evaluation of the deeper structures— proper exploration Proper cleaning, asepsis, wound excision/debridement Any foreign body in the wound should be removed Skin closure if it is possible without tension Skin cover by graft/flap—immediate or delayed Untidy wound should be made tidy and clean before suturing Proper aseptic precautions should be undertaken Antibiotics/analgesics are needed Sutured wound should be inspected in 48 hours Sutures are removed after 7 days

Remember Wound toilet is washing the wound thoroughly using normal saline—ideal ™™ Wound debridement (french-letting loose) is allowing content to come out by release incisions or facio­tomies. But commonly debridement is used for wound excision ™™ Wound excision is actually correct terminology for excision of devitalised tissues once or serially ™™ Radical wound excision is (pseudotumour approach) is excising entire devitalised tissues leaving tissues with visible bleeding from all layers ™™

COMPARTMENT SYNDROME Compartment syndrome is a special entity; common in leg, forearm, thigh and arm; is a syndrome due to increased intracompartmental pressure within a limited space area. Causes are—narrowed space due to tight dressings/plaster cast, lying on one limb in comatous patient; increased content within the compartment due to trauma like fractures, oedema, ischaemic injury, haematoma, positioning after trauma, burn injury, etc.; high pressure injection injuries like gun injury, oil based material injury, extravasation of chemotherapeutic drugs; snake bite.

Fig. 1.22: Necrotizing fasciitis with extensive skin involvement which requires adequate wound excision and eventual skin coverage.

Fig. 1.23: Fasciotomy for compartment syndrome should be longitudinal, deep and lengthy and should decompress the compartment to expose the underlying muscle. It should be done early.

It is common in calf and forearm. Closed injuries cause haematoma leading to increased pressure. It is often associated with fracture of the underlying bone which in turn compresses the major vessel further aggravating the ischaemia causing pallor, pulseless­ness, pain, paraesthesia, diffuse swelling and cold limb. If allowed to progress it may eventually lead to gangrene or chronic ischaemic contracture with deformed, disabled limb. Problems with the compartment syndrome ™™ ™™ ™™ ™™ ™™

Infection, septicaemia and abscess formation Renal failure Gangrene of the limb Chronic ischaemic contracture Disabled limb, Volkmann's ischaemic contracture

Muscle necrosis releases myoglobulin which is excreted in the urine, damages the kidneys leading into renal failure. Note:

Affected muscle when passively stretched worsens the pain—the most reliable clinical sign.

Wounds and Wound Healing Treatment xx Compartment pressure will be persistently more than 30 mm

Hg. It can be measured by placing a fine catheter in the compartment and using a pressure monitor. This is an indication for fasciotomy. Adequate lengthy incision involving skin, fat and deep fascia should be done until underneath muscle bulges out properly. Multiple incisions should be made if needed. Separate incision in each compartment should be done.

Fasciotomy done in forearm anterior compartment is a specific method. Carpal tunnel should be released by cutting flexor retinaculum. Incision begins at the junction of the thenar and hypothenar area; extends proximally initially transverse across flexion crease of the wrist at the ulnar border; then across forearm towards radial side of forearm; then in proximal forearm towards medial side creating convex flap towards lateral side. In the elbow it crosses along the medial border to reach the arm where it runs in arm along the medial part of the anterior arm. Injury to major nerves, palmar cutaneous branch of median nerve should be avoided while placing the incision. Incision should be deepened by cutting the deep fascia along the entire length of the incision. Dorsal fasciotomy should be added by placing longitudinal lengthy incision in the midline. Two longitudinal incisions on the dorsum of the hand also should be made.

B Fig. 1.25B

Figs 1.25A and B: Traumatic crush injury pelvis exposing testis and iliac vessels. Patient underwent hemipelvectomy.

CRUSH SYNDROME It is due to crushing of muscles causing extravasation of blood and release of myohaemoglobin into the circulation leading to acute tubular necrosis and acute renal failure.

Causes xx xx xx xx Fig. 1.24: Incision for fasciotomy in upper limb begins at flexor retinaculum extending into the forearm with a convex flap towards radial side eventually leading towards medial epicondyle of the elbow joint. xx xx xx xx xx

Antibiotics. Catheterisation. Mannitol or diuretics to cause diuresis, so as to flush the kidney. Fresh blood transfusion. Hyperbaric oxygen.

CRUSH INJURY Crush injury is one where a part of the body is being squeezed/ compressed between two high force or pressure systems. It causes extensive lacerations, bruising, compartment syndrome, crush syndrome, fractures, haemorrhage, etc. with extensive tissue destruction and devitalisation. Renal failure, hypovolaemic shock and sepsis are the most dreaded problems in crush injuries.

A Fig. 1.25A

Earthquakes. Mining and industrial accidents. Air crash. Tourniquet. Initially tension increases in the muscle compart­ment commonly in the limb, which itself impedes the circulation and increases the ischaemic damage. In 3 days, urine becomes discoloured and scanty, patient becomes restless, apathy and delirious with onset of uraemia. Crush syndrome is often lifethreatening. Injury is much worser than initial look. Effects of crush syndrome ™™ ™™ ™™ ™™ ™™

Renal failure Toxaemia Septicaemia Disability with extensive tissue loss Gas gangrene

Treatment xx Tension in the muscle compartment is relieved by placing

multiple parallel deep incisions in the limb so as to prevent further damage—Fasciotomy. xx Rheomacrodex, or mannitol is given to improve the urine output by improving the renal function. xx Alkalisation of urine is done by giving sodium citrate or sodium bicarbonate. It increases the solubility of acid haematin in the urine and so promotes its excretion. Urinary pH should be above 6.5 until urine does not show any myoglobin. Mannitol-alkaline diuresis should be 8 litre/day. xx Initial aggressive volume load using saline about 1-1.5 litres/ hour is ideal in these patients. xx Haemodialysis is done sometimes as a life-saving procedure.

Success is getting what you want. Happiness is liking what you get.

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SRB's Manual of Surgery xx Other measures:

Catheterization. Oxygen therapy. Antibiotics. Blood transfusion.  Correction of severe hyperkalaemia.    

Note:

Doing fasciotomy several days after crush injury may not be safe as it may lead to sudden release of myoglobulin causing myoglobulinuria and renal failure.

DEGLOVING INJURIES xx It occurs due to shearing force between tissue planes as traction— avulsion injury. It usually occurs between subcutaneous tissue and deep fascia or between muscle and bone. It can be localised or circumferential. xx Avulsion injury strips off the superficial tissues exposing the neurovascular bundle, muscles, tendons, and bone. Degloving injury can be open or closed.

Types of scar A mature scar is paler, acellular, softer, flat, with reduced blood vessels and fibroblasts, without itching (diminishes). ™™ An atrophic scar is pale, flat and stretched. ™™ A hypertrophic scar is excess scar but will not extend beyond the margin of the scar of the original wound; there is prolonged inflammatory phase of wound healing. It develops in 1 to 3 months after trauma. It improves spontaneously. ™™ Keloid is persistent excessive growth of the scar beyond its margin into the adjacent skin; occurs in a triangular area between two shoulder points and xiphisternum. It develops 3 months to years after the trauma; progressive. Presternal area is the commonest site. Note: ™™ A linear scar is supple, thin, soft occurs after healing by primary intention. ™™ A wide, irregular firm scar occurs after healing by secondary intention or when there is infection ™™

|

KELOID: ‘Like a claw’ xx Keloid is common in blacks. Common in females. xx Genetically predisposed. Often familial. Very rare in Cauca-

sians. xx There is defect in maturation and stabilization of collagen

fibrils. Normal collagen bundles are absent.

xx Keloid continues to grow even after 6 months, may be for many

Fig. 1.26: Degloving injury wherein skin often with soft tissues gets avulsed off the deeper plane to create extensive raw area which may bleed/get infected. xx It can be in one plane or multiple planes. xx It is commonly observed in machinery injuries or major road traffic accidents. It is much more extensive than of on initial presentation. xx Under anaesthesia fluoroscein is injected intravenously and viable skin is visible as fluorescent yellowish—green colour under ultraviolet light. As injection of fluoroscein is not fully safer, serial excision is better to look for dermal punctate bleeding. xx It needs examination under general anaesthesia, wound excision/ radical excision, flap coverage, microflap surgeries, skin grafting, with proper asepsis, and blood transfusion as there is significant blood loss in these injuries.

SCAR Initially immature scar is formed during remodeling phase; this scar is disorganized contains type III collagen. Such scar is itchy, raised, hard and pink in colour. Over the pan of 12 months scar gets matured fully by making disorganised collagen getting aligned along the stress lines and formation of more type I collagen. This matured scar is soft, supple, pale and flat without any itch. Hypertrophic scar and keloid persists to have more type III collagen than type I collagen unlike in matured scar.

years. It extends into adjacent normal skin. It is brownish black/ pinkish black (due to vascularity) in colour, painful, tender and sometimes hyperaesthetic; spreads and causes itching. xx Keloid may be associated with Ehlers-Danlos syndrome or scleroderma. xx When keloid occurs following an unnoticed trauma without scar formation is called as spontaneous keloid, commonly seen in Negroes. xx Some keloids occasionally become non-progressive after initial growth. xx Pathologically keloid contains proliferating immature fibroblasts, proliferating immature blood vessels and type III thick collagen stroma. Site: Common over the sternum. Other sites are upper arm, chest wall, lower neck in front. Differential diagnosis: Hypertrophic scar. Treatment: Controversial. xx Steroid injection—intrakeloidal triamcinolone, is injected at regular intervals, may be once in 7–10 days, of 6–8 injections. xx Steroid injection—excision—steroid injection. xx Triamcinolone reduces the fibroblast proliferation and collagen synthesis; it is the first line of therapy for keloid xx Methotrexate and vitamin A therapy into the keloid. xx Silicone gel sheeting; topical retinoids. xx Laser therapy. xx Vitamin E/palm oil massage. xx Intralesional excision retaining the scar margin may prevent recurrence. It is ideal and better than just excision.

Wounds and Wound Healing xx Excision and irradiation or irradiation alone. xx Excision and skin grafting may be done. Note:

Excision and primary suturing has got high recurrence rate; hence it is not usually practiced.

Recurrence rate is very high—more than 50%.

HYPERTROPHIC SCAR xx xx xx xx

Occurs anywhere in the body. Not genetically predisposed. Not familial. Growth usually limits up to 6 months. It is limited to the scar tissue only. It will not extend to normal skin. xx Spontaneous improvement with time occurs commonly.

B

A

Figs 1.27A and B: Keloid over the sternum (butterfly shaped; commonest site) and upper part of the arm near shoulder—common sites of occurrence.

Fig. 1.30: Diagrammatic representation of linear, hypertrophic and keloid scar. xx It is pale brown in colour, not painful, nontender. xx Often self-limiting also. It responds very well for steroid

injection. xx Recurrence is uncommon. xx It is common in wounds crossing tension lines, deep dermal

burns, wounds healed by secondary intention.

Complications A

B Figs 1.28A and B: Keloid in the ear lobule and chest wall near shoulder.

xx Often this scar breaks repeatedly and causes infection,

pain. xx After repeated breakdown it may turn into Marjolin’s

ulcer.

Treatment xx It is controlled by pressure garments or often revision exci-

sion of scar and closure, if required with skin graft. xx Triamcinolone injection is the 2nd line of therapy for hyper-

trophic scar.

Fig. 1.29: Keloid in the upper part of the scar. It is the previous parotidectomy scar.

A Fig. 1.31A

It is not how much we have, but how we enjoy, that makes us happy.

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SRB's Manual of Surgery Differences between keloid and hypertrophic scar Keloid Yes Chest wall, upper arm, lower neck, ear

a. b.

Genetic predisposition Site of occurrence

c.

Growth

d. e. f.

Treatment Recurrence Collagen synthesis

g. h. i. j. k.

Relation of size of injury and lesion Age Sex Race Structure

l. m. n.

Features Natural history Problems

Continues to grow without time limit Extends to normal skin Poor response Very high 20 times more than normal skin (Type III thick) No relation. Small healed scar can form large keloid Adolescents, middle age Common in females More in blacks (15 times) Thick collagen with increased epidermal hyaluronic acid Vascular, tender, itching Progressive Hyperaesthesia, ulceration

Hypertrophic scar No Anywhere in the body, common in flexor surfaces Growth limits for 6 months Limited to scar tissue only Good response to steroids Is uncommon 3-6 times more than normal skin (Type III fine collagen) Related to size of injury and duration of healing Children Equal in both No racial relation Fine collagen with increased alpha actin Not vascular, nontender, no itching Shows regression Not much

B Fig. 1.31B

Figs 1.31A and B: Different contractures in hypertrophic scars over forearm, finger and neck. Fig. 1.33: ‘Z’ plasty is very useful method to release small contractures.

PROBLEMS WITH WOUND HEALING

Fig. 1.32: Hypertrophied scar in the abdominal healed wound

xx Wound infection is common in devitalized deep difficult wounds. Diabetes, immunosuppression, cytotoxic drugs, anaemia, malnutrition, malignancy increases the chances of wound infection. xx Wound dehiscence is common in all above said adverse factors. Wound suddenly gives away with pain causing copious serosanguineous discharge. After laparotomy when done specially as an emergency in trauma, acute abdomen and also in malignancy, abdominal closed wound may burst in 5–7 days. Usually all layers of abdomen give away causing discharge, occasionally bowel will extrude out. It needs emergency closure of the abdominal wound using specialized sutures or retention sutures. xx Hypertrophic scar or keloid formation due to altered collagen synthesis in the wound healing process. Collagen synthesis is increased 3–6 times in hypertrophic scar and 20 times in keloid. xx Deeper wound will cause specified problems like paraesthesia, ischaemia, paralysis, etc.

B. Ulcer CHAPTER OUTLINE ™™ Ulcer

™™ Bairnsdale Ulcer

™™ Bazin’s Disease

™™ Granulation Tissue

™™ C  arcinomatous Ulcer

™™ Tropical Ulcer

™™ Investigations for an Ulcer

™™ Marjolin's Ulcer

™™ Venous Ulcer

™™ Traumatic Ulcer

™™ Rodent Ulcer

™™ Syphilitic Ulcer

™™ Trophic Ulcer

™™ Melanotic Ulcer

™™ S oft Chancre/Soft Sore/Ducrey’s

™™ Ulcer due to Chilblains

™™ Diabetic Ulcer

™™ Ulcer due to Frostbite

™™ Meleney’s Ulcer

™™ Martorell’s Ulcer

™™ Lupus Vulgaris

™™ Arterial/Ischaemic Ulcer

™™ Tuberculous Ulcer

Ulcer/Chancroid/Bubo ™™ Climatic Bubo/Tropical Bubo

ULCER Definition An ulcer is a break in the continuity of the covering epithelium, either skin or mucous membrane due to molecular death.

Parts of an Ulcer a. Margin: It may be regular or irregular. It may be rounded or oval. b. Edge: Edge is the one which connects floor of the ulcer to the margin. Different edges are: Sloping edge. It is seen in a healing ulcer.   Its inner part is red because of red, healthy granulation tissue.   Its outer part is white due to scar/fibrous tissue.   Its middle part is blue due to epithelial prolife­ration. Undermined edge is seen in a tuberculous ulcer. Disease process advances in deeper plane (in subcutaneous tissue) whereas (skin) epidermis proliferates inwards. Punched out edge is seen in a gummatous (syphilitic) ulcer and trophic ulcer. It is due to endarteritis. Raised and beaded edge (pearly white) is seen in a rodent ulcer (BCC). Beads are due to proliferating active cells. Everted edge (rolled out edge): It is seen in a carcino­matous ulcer due to spill of the proliferating malignant tissues over the normal skin. c. Floor: It is the one which is seen. Floor may contain discharge, granulation tissue or slough. d. Base: Base is the one on which ulcer rests. It may be bone or soft tissue.

Fig. 1.35: Ulcer edges.

Induration of an Ulcer Induration is a clinical palpatory sign which means a specific type of hardness in the diseased tissue. It is obvious in well-differentiated carcinomas. It is better felt in squamous cell carcinoma. It is also observed in long standing ulcer with underlying fibrosis. It is absent or less in poorly differentiated carcinomas and malignant melanoma. Less indurated carcinoma is more aggressive. Specific types of indurations are observed in venous diseases and chronic deep venous thrombosis. Brawny induration is a feature of an abscess. Induration is felt at edge, base and surrounding area of an ulcer. Induration at surrounding area signifies the extent of disease (tumour). Outermost part of the indurated area is taken as the point from where clearance of wide excision is planned.

Classifications Classification I (Clinical)

Fig. 1.34: Parts of an ulcer.

1. Spreading ulcer: Here edge is inflamed, irregular and oedematous. It is an acute painful ulcer; floor does not contain healthy granulation tissue (or granulation tissue is absent) but with profuse purulent discharge and slough; surrounding area is red and edematous. Regional (draining)

Happiness is never found until we have the grace to stop looking for it.

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SRB's Manual of Surgery lymph nodes are enlarged and tender due to inflammation. There will be associated fever, pain, impairment of functions with local tissue destruction and with little evidence of regeneration.

Fig. 1.38: Non-healing ulcer with pale unhealthy granulation tissue with slough.

Fig. 1.36: Spreading ulcer copious purulent discharge with slough.

2. Healing ulcer: Edge is sloping with healthy pink/red healthy granulation tissue with scanty/minimal serous discharge in the floor; slough is absent; regional lymph nodes may or may not be enlarged but when enlarged always non-tender. Surrounding area does not show any signs of inflammation or induration; base is not indurated. Three zones are observed in healing ulcer. Innermost red zone of healthy granulation tissue; middle bluish zone of growing epithelium; outer whitish zone of fibrosis and scar formation.

4. Callous (stationary) ulcer: It is also a chronic non-healing ulcer; floor contains pale unhealthy, flabby, whitish yellow granulation tissue and thin scanty serous discharge or often with copious serosanguinous discharge, with indurated nontender edge; base is indurated, nontender and often fixed. Ulcer does not show any tendency to heal. It lasts for many months to years. Tissue destruction is more with absence of or only minimal regeneration. Induration and pigmentation may be seen in the surrounding area. There is no/less discharge. Regional lymph nodes may be enlarged; are firm/ hard and nontender. It is callousness towards healing; word callous means—insensitive and cruel; and also it means— hard skinned.

Fig. 1.39: Callous ulcer without any sign of healing and, without any granulation tissue.

Classification II (Based on Duration) Fig. 1.37: Healing ulcer with healthy granulation tissue in the floor.

3. Non-healing ulcer: It may be a chronic ulcer depending on the cause of the ulcer; here edge will be depending on the cause—punched out (trophic), undermined (tuberculous), rolled out (carcinomatous ulcer), beaded (rodent ulcer); floor contains unhealthy granulation tissue and slough, and serosanguineous/purulent/bloody discharge; regional draining lymph nodes may be enlarged but non-tender.

1. Acute ulcer—duration is less than 2 weeks. 2. Chronic ulcer—duration is more than 2 weeks (long).

Classification III (Pathological) 1. Specific ulcers:  Tuberculous ulcer.  Syphilitic ulcer: It is punched out, deep, with “wash-leather” slough in the floor and with indurated base.  Actinomycosis.  Meleney’s ulcer.

Ulcer

A

Fig. 1.42: Basal cell carcinoma of face (rodent ulcer). Ulcer edge is raised and beaded in appearance.

B Figs 1.40A and B: Maggots seen in a chronic ulcer

Fig. 1.41: Tuberculous ulcer ankle area. Note the undermined edge. Discharge study, biopsy and later antituberculous drugs are the treatment. They are usually painless. 2. Malignant ulcers:  Carcinomatous ulcer  Rodent ulcer.  Melanotic ulcer. 3. Non-specific ulcers:  Traumatic ulcer: It may be mechanical, physical, chemical— common.  Arterial ulcer: Atherosclerosis, TAO

Fig. 1.43: Squamous cell carcinoma (SCC/epithelioma) leg with typical everted edge. SCC can be ulcerative, ulceroproliferative or proliferative ulcer on clinical look.

Fig. 1.44: Squamous cell carcinoma in the arm with secondaries in the axillary lymph node. Friable tumour tissues in the floor cause bleeding after trauma. Secondaries are fixed with ulceration. It is advanced disease.    

Venous ulcer: Gravitational ulcer, post-phlebitic ulcer. Trophic ulcer/Pressure sore. Infective ulcers: Pyogenic ulcer. Tropical ulcers: It occurs in tropical countries. It is callous type of ulcer, e.g. Vincent’s ulcer.  Ulcers due to chilblains and frostbite (cryopathic ulcer).  Martorell’s hypertensive ulcer.

Excellence is never granted to man but given as the reward of labour.

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SRB's Manual of Surgery  Bazin’s ulcer.  Diabetic ulcer.  Ulcers due to leucaemia, polycythemia, jaundice, collagen

diseases, lymphoedema.  Cortisol ulcers are due to long-time application of cortisol

(steroid) creams to certain skin diseases. These ulcers are callous ulcers last for long time and require excision and skin grafting.

Fig. 1.48: Large ulcer in the foot and leg with exposed tendon.

Fig. 1.45: Ischaemic ulcer foot. Middle three toes are already amputated because of gangrene.

Fig. 1.49: Nonhealing ulcer foot in a diabetic patient with Pseudomonas infection. Note the greenish discharge in the wound. Pseudomonas infection is commonly hospital acquired.

Wagner’s Grading/Classification of Ulcer Grade 0  –  Preulcerative lesion/healed ulcer Grade 1  –  Superficial ulcer Grade 2  – Ulcer deeper to subcutaneous tissue exposing soft tissues or bone Grade 3  –  Abscess formation underneath/osteomyelitis Grade 4  –  Gangrene of part of the tissues/limb/foot Grade 5  –  Gangrene of entire one area/foot Stages of ulcer healing 1. Stage of extension: Ulcer floor is covered with slough, purulent discharge and inflamed edge and margin. 2. Stage of transition: Floor shows separated slough; healthy granulation tissue; serous discharge.

Fig. 1.46: Venous ulcers in both feet. Site is around ankle (Gaiter’s zone). There are healthy granulation tissues. It needs skin grafting and definitive procedure for varicose veins after evaluation.

3. Stage of repair: Fibrosis, collagen deposition, scar formation occurs.

GRANULATION TISSUE It is proliferation of new capillaries and fibroblasts intermingled with red blood cells and white blood cells with thin fibrin cover over it.

Types Fig. 1.47: Infective ulcer in the foot. Note the quantity of slough, exposed tendon and gangrenous toes. Patient requires below or above knee amputation.

xx Healthy granulation tissue: It occurs in a healing ulcer. It has got sloping edge. It bleeds on touch. It has got serous discharge. 5 Ps of granulation tissue—Pink, Punctate haemorrhages, Pulseful,

Ulcer Painless, Pin head granulation. Skin grafting takes up well with healthy granulation tissue. Streptococci growth in culture should be less than 105/gram of tissue before skin grafting. Different discharges in an ulcer (as well as from a sinus) a. Serous: In healing ulcer b. Purulent: In infected ulcer Staphylococci: Yellowish and creamy Streptococci: Bloody and opalescent Pseudomonas: Greenish colour due to pseudocyanin c. Bloody: Malignant ulcer, healing ulcer from healthy granulation tissue d. Seropurulent e. Serosanguinous: Serous and blood f. Serous with sulphur granules: Actinomycosis g. Yellowish: Tuberculous ulcer

Fig. 1.52: Pyogenic granuloma.

INVESTIGATIONS FOR AN ULCER xx Study of discharge: Culture and sensitivity, AFB study,

cytology. Fig. 1.50: Healing ulcer with healthy granulation tissue. Note the sloping edge. xx Unhealthy granulation tissue: It is pale with purulent discharge. Its floor is covered with slough. Its edge is inflamed and oedematous. It is a spreading ulcer. xx Unhealthy, pale, flat granulation tissue: It is seen in chronic nonhealing ulcer (callous ulcer). xx Exuberant granulation tissue (Proud flesh): It occurs in a sinus or ulcer wherein granulation tissue protrudes out of the sinus opening or ulcer bed like a proliferating mass. It is commonly associated with a retained foreign body in the sinus cavity. Fig. 1.53: Typical greenish coloured ulcer due to Pseudomonas infection.

Fig. 1.51: Exuberant granulation tissue (proud flesh) in an ulcer. It should be scooped out using Volkmann’s scoop prior to skin grafting. xx Sprouting granulation tissue of sinus. xx Pyogenic granuloma: It is a type of exuberant granu­lation tissue. Here granulation tissue from an infected wound or ulcer bed protrudes out, presenting as a well-localised, red swelling which bleeds on touching. Differential diagnosis: Papilloma, skin adnexal tumours. Treatment: Antibiotics, excision and sent for biopsy.

Fig. 1.54: X-ray showing osteomyelitis with sequestrum inside. Osteomyelitis prevents ulcer healing. Bone thickening on clinical examination is typical.

The wards are the greatest of all research laboratories.— Sir Henry Wade

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SRB's Manual of Surgery xx Wedge biopsy: Biopsy is taken from the edge because edge

contains multiplying cells. Usually two biopsies are taken. Biopsy taken from the centre may be inadequate because of central necrosis. xx X-ray of the part to look for periostitis/osteomyelitis. xx FNAC of the lymph node. xx Chest X-ray, Mantoux test in suspected case of tuberculous ulcer. xx Haemoglobin, ESR, total WBC count, serum protein estimation (albumin).

xx xx

Note: Ulcer will not granulate if haemoglobin is less than 8 gm% and serum albumin is 3 L fluid loss). xx Only pure water loss occurs due to poor fluid intake and diabetes insipidus. It causes dehydration with proportionate decrease in total body water (2/3rd ICF, 1/3rd ECF). As ECF including intravascular fluid loss is less, hypotension is less. Features here are—severe thirst, confusion and convulsions due to hypernatraemia; blood pressure is relatively normal. Dehydration can be mild (weight loss 5%); moderate (10%); severe (15%).

xx Evaluation is done by doing serum sodium, urinary sodium, and blood urea. xx Isotonic volume depletion is corrected by 0.9% normal saline. xx Pure water depletion is corrected by more water intake/ intravenous 5% dextrose. xx Monitoring fluid therapy by skin and tongue examination, weight gain, pulse, blood pressure, CVP, PCWP.

WATER EXCESS (ECF VOLUME EXCESS) It can be divided into water and salt excess or predominantly water excess called as water intoxication. Water and salt excess occurs in CCF, cirrhosis, nephrotic syndrome, hypoproteinaemia, renal failure, excessive saline infusion. Water intoxication occurs in TURP, excess infusion of 5% dextrose only, SIADH secretion, psychogenic polydypsia. It is managed by stopping fluid infusion or procedure (TURP); fluid restriction, and treating the cause.

Causes xx Excessive amount of intravenous dextrose (5%). xx During colorectal bowel wash for preparation of large bowel for surgery, if water is used instead of saline, especially in children. xx In TURP (Transurethral resection of prostate) when excess irrigating fluid water or glycine is used (commonly used). xx In syndrome of inappropriate antidiuretic hor­mone (SIADH) which is commonly associated with lobar pneumonia, empyema, oat cell carcinoma and head injury. Clinical features Drowsiness, weakness Convulsions and coma Nausea, vomiting Passage of dilute urine Distended neck veins Pedal oedema Gain in body weight—most sensitive and consistent sign Circulatory overload—tachycardia, pulmonary oedema, hypertension ™™ Bilateral basal crepitations, ascites ™™ Raised CVP, PCWP ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Electrolyte and Nutrition Investigations xx Haematocrit and sodium level (will show fall in level). xx Low potassium. Low blood urea.

Treatment xx xx xx xx

Water and salt restriction and observation. Monitoring in ICU. Management of fluid and electrolyte balance. Infusion of hypotonic sodium chloride. Administration of diuretics and hypertonic saline should be avoided, as it may cause rapid changes in serum sodium and water level which will lead to neuronal demyelination and fatal outcome.

ECF LOSS xx Here only ECF loss is present with normal ICF. xx It is seen in vomiting, diarrhoea, intestinal obstruction. xx Treatment is infusion of normal saline.

ECF EXCESS

diarrhoea, vomiting, wherein urine sodium level is less than 20 mmol/l; due to diuresis or renal causes wherein urine sodium level is more than 20 mmol/l or it may be due to correction of hypovolaemia using hypotonic fluid like 5% dextrose. Condition can be treated well using isotonic normal saline. xx Normovolaemic hyponatraemia: It may be due to renal failure or syndrome of inappropriate ADH secretion (SIADH). In mild asymptomatic patients it is corrected by fluid restriction (1 l/day will raise the serum Na). Vasopressin antagonist demeclocycline which increases the diluting ability of kidney is used in severe cases. xx Pseudohyponatraemia: Plasma osmolality is mainly achieved by serum sodium; but small proportion, i.e. 25% of osmolality is due to other solutes like glucose, lipids, plasma proteins, urea which will not move easily between intracellular and extracellular spaces. When concentration of these molecules raise due to some pathology, proportionately relative concentration of sodium will drop causing pseudohyponatraemia. Here condition causing related to specific solutes mentioned above is treated, than hyponatraemia.

Causes

xx Only ECF excess without an ICF excess. xx Excessive infusion of saline with impaired excretion. xx Raised JVP (earliest and best clinical sign), cardiac failure and peripheral oedema. xx Treatment is fluid restriction and diuretics like frusemide.

HYPONATRAEMIA Sodium level less than 130 mEq/l. Hyponatraemia is said to be severe if serum sodium becomes lesser than 100 mEq/l in acute type; and lesser than 115 mEq/l in chronic type. It can be due to water overload (dilutional) or sodium loss.

Types of Hyponatraemia xx Acute—presents as neurological manifestations. xx Chronic—causes pontine myelinolysis. It presents as

behavioural changes, progressive weakness, and cranial nerve palsies. Types also may be: xx Hypervolaemic hyponatraemia wherein rapid absorption of fluid occurs into intravascular compartment leading into pulmonary and cerebral oedema. It is due to decreased osmolality causing movement of ECF into the cells. Serum sodium level lesser than 100 mmol/l is called as severe hyponatraemia, causes convulsions. Here urinary sodium will be less than 15 mmol/l. Acute hyponatraemia is corrected by fluid restriction, hypertonic saline, loop diuretics like frusemide. Monitoring the serum sodium level of the patient is essential. Sodium should be corrected up to above the level of 125 mmol/l. Correction should be slow and gradual at a rate of 2 mEq/l/h with up to 20 mEq/l correction in 24 hours with 4th hourly assessment of serum sodium. Overcorrection of sodium should not be done. Rapid correction can lead into irreversible myelin lysis of pontine. xx Hypovolaemic hyponatraemia: It is due to hypovolaemia by

xx xx xx xx xx

Intestinal obstruction. Intestinal fistulas—biliary, duodenal, gastric, pancreatic. Gastric outlet obstruction with severe vomiting. Ryle’s tube aspiration. Severe diarrhoea due to viral cause, in colitis, colorectal polyps. xx Syndrome of inappropriate antidiuretic hormone (SIADH). xx Immediately after surgery and trauma, sodium depletion occurs. xx Stroke. Clinical features ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Dry coated tongue Sunken eyes Dry wrinkled skin Hypotension Dark scanty urine Irritability, disorientation and neurological manifestations Convulsions In chronic hyponatraemia—hypothermia, reduced tendon reflexes, pseudobulbar pasly

Investigations xx Serum electrolytes. Urinary sodium is low. xx Sodium deficit is calculated by: (125 – present serum

sodium) × body weight in kg × 0.6.

Treatment xx Intravenous infusion of normal saline as a slow and gradual

correction at a rate of 2 mEq/L/hour in acute cases and < 1 mEq/L/hour in chronic cases. Correction should not exceed more than 20 mEq/L/day in acute cases and more than 10 mEq/L/day in chronic cases. Hypertonic saline of 1.6% or 3% also can be used in severe cases. 0.9% normal saline contains 154 mEq of NaCl; 3% saline contains 500 mEq of NaCl. xx The cause is treated.

You cannot harm a bandaged wound.— Croatian Proverb

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SRB's Manual of Surgery HYPERNATRAEMIA Serum sodium level > 150 mEq/L. Excess infusion of normal saline causes overload in circulating salt and water. It is usually due to water deficit.

Causes xx Renal dysfunction. xx Cardiac failure. xx Drug induced like NSAID, corticosteroids.

It may be either primary sodium excess or primary potassium excess or primary water deficit.

Types of Hypernatraemia xx Euvolemic (pure water loss): It is due to failure of water

intake like in comatous patients, bedridden people, postoperative patients and in patients with high fever leading into extrarenal loss of water. It can occur in diabetes insipidus or chronic renal failure as renal loss of water. xx Hypovolaemic (among loss of water and sodium, more water is lost than sodium): It is due to vomiting, diarrhoea, more undue sweating (extrarenal); osmotic diuresis by glucose/ mannitol (renal). xx Hypervolaemic (both sodium and water gain but sodium gain is more than water gain) as seen in more salt intake, excess steroids, sodium bicarbonate/hypertonic saline infusion (salt gain).

Clinical Features xx xx xx xx xx

Pitting oedema. Puffiness of face. Increased urination. Often dilated jugular veins. Features of pulmonary oedema.

It occurs in patients in diabetic coma treated by insulin and saline infusion.

Gradual Hypokalaemia Causes xx Diarrhoea of any causes, villous tumour of the rectum,

ulcerative colitis. xx After trauma or surgery. xx Pyloric stenosis with gastric outlet obstruction. xx Duodenal fistula, ileostomy. xx After ureterosigmoidostomy. xx Insulin therapy. xx Poisoning. xx Drugs like beta agonists. xx Familial periodic paralysis.

Clinical Features xx xx xx xx xx xx xx

Slurred speech. Muscular hypotonia—physical sign. Depressed reflexes. Paralytic ileus. Weakness of respiratory muscles. Cardiac arrhythmias. Inability to produce concentrated urine and so causes nocturia and polyuria. ECG shows prolonged QT interval, depression of the ST segment and inversion of T wave, prominent U wave. Often hypokalaemia is associated with alkalosis. Serum potassium will be decreased.

Treatment xx Oral potassium 2 g 6th hourly, 15 ml potassium chloride

syrup (20 mmol of K).

Investigation xx Serum electrolytes, plasma and urine osmolality, renal func-

tion tests, haematocrit.

Management

xx IV KCl 40 mmol/litre given in 5% dextrose or nor­mal saline

slowly, often under ECG monitoring [Total dose is 40 mmol (0.2 mmol /kg/hour). Maximum dose per hour is 20 mmol]. xx Hypokalaemic alkalosis which occurs in pyloric stenosis should be treated carefully by IV potassium as there will be severe potassium loss.

xx Restriction of saline and sodium. Treatment of pulmonary

HYPERKALAEMIA

oedema. xx Hypernatraemia should be corrected slowly as follows:  Initial infusion of normal saline, then infusion of half

strength saline (0.45%) and later with 5% dextrose, i.e. gradual controlled correction is done. Otherwise cerebral oedema and hyperglycaemia can develop.  Oral and nasogastric administration of water/fluids.

HYPOKALAEMIA Sudden Hypokalaemia Serum potassium level less than 3.5 mEq/l.

Normal range of potassium is 4.0 to 4.5 mEq/l. Hyperkalaemia manifests when potassium exceeds 6 mEq/l.

Causes xx xx xx xx xx xx xx

Renal failure. Rapid infusion of potassium. Transfusion of stored blood. Diabetic ketoacidosis. Adrenal insufficiency. Potassium sparing diuretics, cyclosporine, beta blockers. Metabolic acidosis.

Electrolyte and Nutrition xx Insulin deficiency. xx Tissue destruction, burns, trauma, tumour necrosis, crush injury. xx In vitro haemolysis, thrombocytosis, tourniquet application,

exercise—pseudohyperkalaemia. xx Familial hyperkalaemic periodic paralysis.

Potassium excess is a dangerous condition which can cause sudden cardiac arrest.

Investigations High serum potassium level. Peak ‘T’ wave in an ECG.

Treatment xx IV administration of 50 ml of 50% glucose with 10 units of

soluble insulin, slowly. xx Infusion of 10% calcium gluconate (as cardio­protection)

intravenously. xx Calcium chloride is given in severe cases as calcium in this form is released immediately without hepatic metabolism. xx Diuresis using frusemide injection. xx Haemodialysis when required—very useful. xx Continuous ECG monitoring is a must. xx Polyesterene sulphonate ion exchange resin 30 g/hour in 50 ml of 70% sorbitol as an enema. xx Salbutamol nebulisation or intravenously 0.5 mg in 4 ml of saline/Albuterol nebulisation. xx IV sodium bicarbonate—shifts potassium in to cells. 7.5%, with 50–100 ml intravenously in 10 minutes.

HYPERMAGNESAEMIA It is rare. Serum magnesium > 2.5 mEq/l. Normal serum magnesium is 1.5–2.5 mEq/l and intra-cellular magnesium which is more (2nd higher) is 26 mEq/l. Magnesium is mainly deposited in bone (60%). It is a cofactor for many enzymes necessary in phosphorylation of glucose in the cell and ATP utilisation in muscle fiber. Daily required dietary intake of magnesium is 0.4 gram. It is reabsorbed well in proximal renal tubule.

Causes xx Advanced renal failure treated with magnesium containing antacids, diabetic ketoacidosis. xx Intentionally produced hypermagnesaemia while treating pre­eclampsia.

Clinical Features xx xx xx xx xx xx

Loss of tendon reflexes (most common). Neuromuscular depression. Flaccid quadriplegia. Respiratory paralysis. Somnolence. Hypotension.

HYPOMAGNESAEMIA xx Serum magnesium 50; 30 ml if BMI is 40–50). It is usually carried out through linear stapler. Jejunum is transected 45 cm from ligament of Treitz. A side to side jejunojejunal anastomosis is done using stapler 75 cm distal to the distal cut end. Proximal Roux part of the distal jejunal cut part (75–150 cm, based on patient’s preoperative weight) is brought out through the transverse mesocolon towards the created proximal gastric pouch and gastrojejunostomy is done to this proximal gastric pouch. Mesenteric defect is closed. Stomal integrity is checked on table by air distension and methylene blue infusion. Gastrograffin study is done in 24 hours to assess pouch size, stomal patency and distal obstruction. Oral food is started in 24 hours and patient is discharged in 4 days. RYGB is more useful in weight loss compared to purely restrictive types. 5 years weight loss is 60–75%. It also prevents progression of noninsulin dependent diabetes mellitus, controls hypertension, sleep apnoea, hyperlipidaemia, asthma, arthritis, GERD. Complications are—Roux obstruction, anastomotic leak, acute distal gastric dilatation, stomal stenosis, marginal ulcer, dumping syndrome, internal hernias, vitamin B12 deficiency, iron deficiency anaemia. Distal gastric dilatation needs emergency intervention which is usually due to jejunojejunal obstruction.

Laparoscopic RYGB (1994, Wittgrove, Clark, Trembly) Technique is similar to open RYGB. Anastomoses are done using endoscopic stapler. GJ between gastric pouch and Roux jejunum is done either using linear stapler through laparoscopic port after making a gastrotomy in the pouch which is later sutured after staple firing; or using circular stapler anastomosis is done wherein anvil is initially passed transorally often under endoscopic guidance across the pouch into the

The lazy man is always occupied with his laziness.

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SRB's Manual of Surgery Roux jejunum; or using hand sewing with absorbable sutures. Omentum is released from the colon and is covered over the GJ. Mesenteric defect and Patterson Brown defect are closed. A Bronlin antiobstructive stitch is placed between Roux and biliopancreatic limbs. Integrity of anastomosis is checked using insufflation of air, methylene blue. Complications are similar to open RYBG. Conversion rate is 9%. Advantages of LRYBG to open RYBG are—faster recovery, less post-operative pain, less wound related complications, less morbid one. Disadvantage of LRYBG is availability of facility, technical expertise, and steep learning curve. Now technique is modified to antegastric, antecolic one which has become popular (Gagner).

Biliopancreatic Diversion (BPD) (Nicola Scopinaro, Italy)

Fig. 1.203: Jejunoileal bypass procedure (JIB).

It is done in patients who had failed restrictive procedure or who are superobese. Distal subtotal gastrectomy is done with formation of proximal gastric pouch (of 400 ml in BMI 40–50; 200 ml in BMI >50). Ileum is transected 250 cm proximal to ileocaecal valve; distal ileal segment is brought up to anastomose into the proximal gastric pouch. Proximal biliopancreatic jejunoileal limb is anastomosed into distal ileal segment 50 cm proximal to ileocaecal valve as end to side stoma. Additionally cholecystectomy should be done. Modification of BPD with duodenal switch (BPD-DS) has become more popular. Here sleeve gastrectomy along the greater curvature is done to create gastric reservoir (200 ml) along lesser curve. Duodenum just distal to first part is divided using stapler; proximal cut end is sutured to proximal upward pulled end of the distal ileal segment of earlier transected ileum, 250 cm from ileocaecal valve. Biliopancreaticoduodenal with proximal jejunoileal segment is later stapled to distal ileum 50 cm proximal to ileocaecal valve. Duodenal switch reduces the rate of marginal ulcer and dumping syndrome. Results of BPD/BPD-DS are—excellent for weight reduction compared to restrictive procedures. But they need lifelong supplement of vitamins, fat-soluble vitamins, calcium, and iron. Technically BPD is easier to do when compared to BPD-DS. Complications of BPD/BPD-DS are—anemia (30%); protein deficiency (20%); dumping syndrome; marginal ulcer (in BPD 10%; in BPD-DS it is 1%); osteoporosis; night blindness; biliopancreatic

Fig. 1.204: Roux-en-Y gastric bypass procedure (RYBG).

Fig. 1.205: Biliopancreatic diversion procedure (BPD).

Fig. 1.202: Laparoscopic adjustable gastric banding (LAGB).

Electrolyte and Nutrition cm from duodenojejunal flexure. Isolated 170 cm ileal segment is interposed 50 cm distal to DJ junction with end-to-end anastomosis on both ends. Type 2: After doing sleeve gastrectomy, gastroduodenal junction is transected; cut proximal end of duodenum is closed. 170 cm ileal segment with mesentry is isolated and interposed between cut end of stomach and side of jejunum 50 cm distal to DJ flexure.

Cholecystolithiasis After Bariatric Surgery

Fig. 1.206: Biliopancreatic diversion with duodenal switch procedure (BPD-DS). limb obstruction; staple line leak; staple line bleed; DVT; subphrenic abscess. Vitamin B12 deficiency is specific.

Ileal Interposition with Sleeve Gastrectomy It is done mainly in type II diabetes. Often they are associated with obesity, dyslipidaemia, hypertension, nephropathy and neuropathy. Two types of ileal interposition with sleeve gastrectomy are done. Type 1: Sleeve gastrectomy is done. 170 cm of ileum with mesentery is isolated 30 cm from ileocaecal junction. Jejunum is transected 50

Gallstone formation is common after bariatric surgery (50%). It is due to rapid weight loss. If gallstones are present at the time of bariatric surgery it is essential to do laparoscopic cholecystectomy during bariatric procedure. It is controversial about doing prophylactic cholecystectomy during bariatric surgery even though it is practiced in many places. Advantages are—it prevents future gallstone formation at the time of bariatric surgery (loss of access); it prevents difficulties in approaching CBD in case needed endoscopically due to surgery. Disadvantage is cholecystectomy adds additional 1 hour time for bariatric surgery increasing the risk of immediate complications. Patients who are not having gallstones at the time of bariatric surgery, should receive ursodeoxycholic acid 300 mg twice daily for 6-12 months of post-bariatric surgery period. Often stomach is anchored to abdominal wall as access part to biliary system for future need. Note:

Many of these patients after bariatric surgery require plastic surgery for abdominal contour (panniculectomy, abdominoplasty) after weight reduction due to bariatric surgery.

It is what a man thinks of himself that really determines his fate.

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G. Shock The first noteworthy characteristic of the blood in shock is a high capillary red count…. When haemorrhage as a complicating factor tending to reduce the blood count is considered, these high counts are striking. They indicate that in shock a concentration of the blood occurs, at least in the superficial capillaries. —Walter Bradford Cannon, J Fraser, AN Hooper, 1918

CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™

Shock Stages of Shock Effects of Shock Clinical Features of Shock Assessment, Investigations and Monitoring

™™ Investigations in Shock ™™ Central Venous Pressure ™™ Pulmonary Capillary Wedge Pres­ sure ™™ Systemic Inflammatory Response Syndrome

Shock

™™ M  ultiple Organ Dysfunction Syndrome ™™ Oxygen Therapy ™™ Topical O2 Therapy ™™ Cardiac Arrest

Contd...

Shock is a state of poor perfusion with impaired cellular metabolism manifesting with severe patho­physiological abnormalities. It is due to circulatory collapse and tissue hypoxia. Normal aerobic metabolism is not maintained due to hypoperfusion. Shock is meant by ‘inadequate perfusion’ to maintain normal organ function. At cellular level hypoxia causes change of normal aerobic to anaerobic metabolism causing lactic acidosis. Intracellular potassium is released into circulation. Lysosomes from cells get released into blood causing cell lysis. Hypoxia and acidosis through complements release free oxygen radicals and cytokines which damage capillary endothelium. Eventually cardiovascular, respiratory, renal, endocrine and GIT will be affected presenting as systemic features. Causes of shock 1. Hypovolaemic shock—due to reduction in total blood volume. It may be due to: a. Haemorrhage –  External from wounds, open fractures – Internal from injury to spleen, liver, mesentery or pelvis b. Severe burns, which results in loss of plasma c.  Peritonitis, intestinal obstruction d.  Vomiting and diarrhoea of any cause 2. Cardiac causes a.  Acute myocardial infarction, acute carditis b. Acute pulmonary embolism wherein embolus blocks the pulmonary artery at bifurcation or one of the major branches c.  Drug induced d.  Toxaemia of any causes e. Cardiac surgical conditions like valvular diseases, congenital heart diseases f.  Cardiac compression causes i. Cardiac tamponade due to collection of blood, pus, fluid in the pericardial space which prevents the heart to expand leading to shock. ii.  Trauma to heart 3. Septic shock—is due to bacterial infections which release toxins leading to shock

Contd...

4. Neurogenic shock—due to sudden anxious or painful stimuli causing severe splanchnic vessel vasodilatation. Here, patient either goes for cardiac arrest and dies or recovers fully spon­ taneously—spinal cord injury/anaesthesia can cause neurogenic shock 5. Anaphylactic shock—is due to Type 1 hyper­sensitivity reaction 6. Respiratory causes a.  Atelectasis (collapse) of lung b.  Thoracic injuries c.  Tension pneumothorax d.  Anaesthetic complications 7. Other causes a.  Acute adrenal insufficiency (Addison‘s disease) b. Myxoedema

Shock may be hypovolaemic, cardiogenic, obstructive, distributive or of endocrine variety.

Pathophysiology of Shock Any cause of shock ↓ Low cardiac output ↓ Vasoconstriction occurs as a compensation to perfuse vital organs like brain, heart, kidneys, liver ↓ Because of vasoconstriction and tachycardia ↓ Dynamic circulation increases ↓ Tachypnoea occurs to increase the oxygen saturation ↓ Peripheral veins (capacitance vessels) constrict diverting blood from splanchnic system towards essential vital organs ↓

Shock Decreased renal blood flow reduces the GFR and thereby the urine output ↓ Renin angiotensin mechanism gets activated causing further vasoconstriction and aldosterone release ↓ Causes salt and water retention ↓ ADH is released ↓ Further concentration of urine occurs When shock persists cardiac output falls further ↓ Hypotension and tachycardia occurs leading to poor perfusion of coronaries ↓ Hypoxia—metabolic acidosis ↓ Release of cardiac depressants ↓ Cardiac (pump) failure Hypoxia ↓ Anaerobic metabolism ↓ Lactic acidosis ↓ Cell wall damage ↓ Sodium and calcium enter the cell ↓ Potassium leaks out of the cell ↓ Causes hyperkalaemia, hyponatraemia and hypocalcaemia ↓ Intracellular lysosomes break down releasing powerful enzymes which destroy own cell ↓ SICK CELL SYNDROME Platelets are activated forming small clots in many places ↓ Disseminated intravascular coagulation (DIC) (Consumption coagulopathy) ↓ Further bleeding.

STAGES OF SHOCK Factors like infection, trauma, burns, haemorrhage, hypovolaemia ↓

Hypoxia and its effects. ↓ SIRS (Systemic inflammatory response syndrome) is due to vasodilatation, increased endothelial per­meability, thrombosis, leucocyte migration and activation. ↓ All these lead to altered cytokines level, abnormal NO (nitric oxide) synthesis, abnormal arachidonic acid metabolism, neutrophil activation, free radical production, altered complement activation, failure to have a localisation of inflammation. It is severe type of reversible shock. ↓ Which will lead to established microvascular occlusion, cellular dysfunction, sick cell syndrome, DIC and PUMP failure. ↓ MODS (Multiorgan dysfunction syndrome) (Irrever­sible shock)—of lungs, kidneys, liver, clotting system and brain. Stages of shock Stage 1

Stage of compensatory shock by neuroendocrine response to maintain the perfusion of the vital organs like brain, heart, kidney, liver.

Stage 2

Stage of decompensatory shock where there is progressive shock causing persistent shock with severe hypotension (with mean arterial pressure < 65 mmHg); oliguria, tachycardia.

Stage 3

Stage of irreversible shock with severe hypoxia and MODS.

Note:

•

•

Distributive shock is one in which there is vasodilatation, decreased vascular resistance, hypotension, altered micro-vascular perfusion with arteriovenous shunting, altered cellular oxygen metabo­ lism. It is seen in septic shock, spinal trauma, adrenal crisis and anaphylaxis. Obstructive shock occurs due to mechanical impediment of circula­ tion due to pulmonary embolism, tension pneumothorax or cardiac tamponade.

Effects of Shock Heart: Low perfusion → low venous return → decreased cardiac output → hypotension → tachycardia. Persistent shock causes hypoxia and release of myocardial depressants leading to further cardiac damage. Lung: Interstitial oedema → decreased gaseous exchange → pulmonary arteriovenous shunting → tachypnoea → Adult/Acute respiratory distress syndrome (ARDS) and pulmonary oedema. Metabolic: Shock leads to hypoxia, which activates anaerobic metabolism leading to lactic acidosis. Antidiuretic hormone (ADH) is released which increases the reabsorption of water from renal tubules. Other hormones released are ACTH, prostaglandins, histamine, bradykinin, and serotonin to compensate the effects of shock to increase the perfusion of vital organs like heart, brain and lungs. Cellular changes occur in persistent shock due to release of lysosomal enzymes, which alters the cell membrane permeability causing cell death—sick cell syndrome.

Ideas have a short shelf life—that’s why we must act before the expiry date.

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SRB's Manual of Surgery Sympathetic overactivity alters the microcirculation leading to capillary dysfunction. Brain perfusion, when decreases the patient becomes drowsy. Brain is the last organ to get underperfused in shock. Kidneys: GFR decreases and tubular reabsorption of salt and water increases for compensatory response. But in severe cases tubular necrosis sets in leading into irreversible damage. Blood: Alteration in cellular components including platelets leads to Disseminated intravascular coagulation (DIC). It causes bleeding from all organs. Gastrointestinal tract: Mucosal ischaemia develops causing bleeding from GIT with haematemesis and malaena. It is aggravated by DIC. Hepatic ischaemia leads into increased enzyme levels.

Types of Shock 1. Vasovagal shock

It is sudden dilatation of peripheral and splanchnic vessels causing reduced cardiac output and shock. Often it may be life-threatening due to hypoxia.

2. Neurogenic shock xx It is usually due to spinal cord injury, which causes dilatation of splanchnic vessels.  This type can safely be treated with vasoconstrictor drugs to bring up the blood pressure. There will be bradycardia, hypotension, arrhythmias, and decreased cardiac output. Blood pressure control, oxygen delivery, maintenance of haemodynamics, airway, fluid therapy, intravenous methylprednisolone therapy should be done. Dopamine and or phenylephrine (α agonist) can be used.

3. Hypovolaemic shock—most common type xx Haemorrhage, may be due to injury to the liver, spleen, bone fractures, haemo­thorax, vascular injury, severe bleeding on table during surgeries of thyroid, liver, portal vein or major vessels. xx Vomiting, diarrhoea due to any cause. xx Burns. Types of Hypovolaemia a. Covert compensated hypovolaemia (Mild 40%): Here all features of hypovolaemia are present like hypotension, tachy­cardia, sweating, tachypnoea, oliguria, drowsiness, eventually features of SIRS is seen and often if not treated on time leads to MODS, i.e. irreversible shock.

4. Cardiogenic shock xx Cardiogenic shock is defined as circulatory failure causing diminished forward flow leading into tissue hypoxia in the setting of adequate intravascular volume with systolic blood pressure 50%.  Cardiogenic shock develops within 24 hours of MI. it occurs when 50% of left ventricular wall is damaged by infarction.  It leads to pulmonary oedema and severe hypoxia. Ischaemic necrosis of left ventricular wall causes failure of pump thereby decreasing stroke volume. Diagnosis is established by ECG, echocardiography, arterial blood gas analysis, cardiac enzymes, PCWP and electrolyte estimation (hypokalaemia and hypomagnesaemia are common) are the essential investigations.

Management xx Proper oxygenation with intubation, ventilator support, cardioversion, pacing, antiarrhythmic drugs, correction of electrolytes, avoiding fluid overload, prevention of pulmonary oedema as immediate measures. xx Dobutamine (β1 receptor agonist) is used to raise cardiac output provided there is adequate preload and intravascular volume (it is peripheral vasodilator and reduces BP). Dopamine is preferred in patients with hypotension. But it may increase peripheral resistance and heart rate worsening cardiac ischaemia. Often both dopamine and dobutamine combination may be required. xx Careful judicial use of epinephrine, norepinephrine, phosphodiesterase inhibitors (amrinone, milrinone) are often needed. Anticoagulants and aspirin are given. Thrombolytics can be used. b blockers, nitrates (nitroglycerine causes coronary arterial dilatation), ACE inhibitors are also used. xx Intra-aortic balloon pump (IABP) may need to be introduced transfemorally as a mechanical circulatory support to raise cardiac output and coronary blood flow. xx Relief of pain, preserving of remaining myocardium and its function, maintaining adequate preload, oxygenation, minimizing sympathetic stimulation, correction of electrolytes should be the priorities. xx Percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) are the final choices.

5. Cardiac compression shock xx It is probably due to pericardial tamponade of any cause or kinking of great vessels, massive pulmonary embolism, tension pneumothorax, air embolism causes obstructive shock with reduced preload to heart. xx Acute massive pulmonary embolism from a thrombus or an air embolism (50 ml of air), obstructing more than 50% of pulmonary vasculature leads to severe shock and sudden death. xx Tachycardia, hypotension, pulmonary oedema, raised JVP, gallop rhythm are the features.

6. Septic shock xx Septic shock may be due to gram-positive organisms, gram

negative organisms, fungi, viruses or protozoal origin. xx Gram-negative septicaemia/gram-negative septic shock is

called as endotoxic shock. It occurs due to gram-negative bacterial infections, commonly seen in strangulated intestines, peritonitis, gastrointestinal fistulas, biliary and urinary infections, pancreatitis, major surgical wounds, diabetic wounds and crush injuries.

Shock Gram-positive septic shock

Gram-negative septic shock

• Due to exotoxin by gram +ve bacteraemia like Clostridium tetani/welchii, staphylococci, streptococci pneumococci • Fluid loss, hypotension is common; with normal cardiac output

Gram negative bacteria cause endotoxaemia and its effects. Urinary/gastrointestinal/ biliary and respiratory foci are common

Pathophysiology of septic shock Toxins/endotoxins from organisms like E. Coli, Klebsiella, Pseudomonas, and Proteus ↓ Inflammation, cellular activation of macrophages, neutrophils, monocytes ↓ Release of cytokines, free radicals ↓ Chemotaxis of cells, endothelial injury, altered coagulation cascade—SIRS ↓ Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea ↓ Severe circulatory failure with MODS (failure of lungs, kidneys, liver, heart) with DIC ↓ Hypodynamic, irreversible cold stage of septic shock.

Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of sepsis. b. Hypodynamic hypovolaemic septic shock (cold septic shock): Here pyrogenic response is lost. Patient is in decompensated shock. It is an irreversible stage along with MODS (Multi-organ dysfunction syndrome) with anuria, respiratory failure (cyanosis), jaundice (liver failure), cardiac depression, pulmonary oedema, hypoxia, drowsiness, eventually coma and death occurs (Irreversible stage).

Treatment of septic shock xx Correction of fluid and electrolyte by crystalloids, blood transfusion. Perfusion is very/most important. xx Appropriate antibiotics—third generation cephalosporins/ aminoglycosides. xx Treat the cause or focus—drainage of an abscess; laparotomy for peritonitis; resection of gangrenous bowel; wound excision. xx Pus/urine/discharge/bile/blood culture and sensitivity for antibiotics. xx Critical care, oxygen, ventilator support, dobutamine/ dopamine/noradrenaline to maintain blood pressure and urine output. xx Activated C protein prevents the release of inflammatory mediators and blocks the effects of these mediators on cellular function. xx Monitoring the patient by pulse oximetry, cardiac status, urine output, arterial blood gas analysis. xx Short-term (one or two doses) high dose steroid therapy to control and protect cells from effects of endotoxaemia. It improves cardiac, renal and lung functions. Single dose of methylprednisolone or dexamethasone which often may be repeated again after 4 hours is said to be effective in endotoxic shock.

xx Septic shock is typically a vasodilatory shock wherein there

is peripheral vasodilatation causing hypotension which is resistant to vasopressors. This is due to toxin induced release of isoform of nitric oxide synthetase from the vessel wall which causes sustained prolonged release of high levels of nitric oxide. xx Magnitude of infection is quantified as: 1. Sepsis which shows fever, tachycardia, leucocytosis. 2. Severe sepsis which shows low tissue perfusion with organ dysfunction (lactic acidosis, dysfunction of liver, kidney, lungs). 3. Septic shock with systemic hypotension (BP < 90 mmHg in spite adequate fluid therapy), severe organ dysfunction (acute lung, kidney, liver injury), maldistribution of blood flow, shunting in microcirculation.

Septic shock ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Common causes are biliary, urinary, GIT sepsis (peritonitis, stran­ gulation), respiratory (pneumonia) Common bacteria are E. coli, Klebsiella, Pseudomonas Common pathophysiologies are release of toxins, neutrophil activation, cytokine release, and sick cell syndrome, SIRS, MODS Clinical stages are hyperdynamic amd hypodynamic Find out the source of the infection by US, CT scan Do pus/blood/urine culture Start antibiotics of high generations like ceftazidime, amikacin, cefoperazone Dopamine/dobutamine infusion (slow) Monitoring by pulse, BP, respiration, urine output, level of consciousness Ventilator support, ICU management Treat the causes like peritonitis, abscess

Stages of septic shock a. Hyperdynamic (warm) shock: This stage is reversible stage. Patient is still having inflammatory response and so presents with fever, tachycardia, and tachypnoea. Pyrogenic response is still intact. Patient should be treated properly at this stage. Based on blood culture, urine culture (depending on the focus of infection), higher antibiotics like third generation cephalosporins, aminoglycosides, metronidazole are started. The underlying cause is treated like draining the pus, laparotomy for peritonitis, etc.

7. Anaphylactic shock Injections—penicillins, anaes­thetics, stings, venom, shellfish may be having antigens which will combine with IgE of mast cells and basophils, releasing histamine and large amount of SRS-A (Slow releasing substance of anaphylaxis). They cause bronchospasm, laryn­geal oedema, respiratory distress, hypotension and shock. Mortality is 10%. Rashes all over the body are commonly observed.

Tears shed for self are tears of weakness, but tears shed for others is a sign of strength.

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SRB's Manual of Surgery Anaphylactic shock Sudden onset Distributive shock Bronchospasm, laryngeal oedema Generalised rashes and oedema Hypotension, feeble pulse Mortality 10% To start adrenaline 100 ug IV, steroids, IV fluids, oxygen with foot end elevation ™™ Ventilator in severe cases ™™ Cardiac massage, defibrillation ™™ ™™ ™™ ™™ ™™ ™™ ™™

Clinical Features of Shock (hypovolAemic shock)

xx Pus/urine/blood/bile/sputum cultures depending on the focus and need in sepsis. xx Serum lactate estimation is an important prognostic factor. Level >2 mEq/L suggest tissue ischaemia. xx USG of part, CT/MRI of the location of the pathology of the septic focus should be done; often may require repetition of these imaging to assess progress. xx Blood urea, serum creatinine, liver function tests, prothrombin time (PT), activated partial thromboplastin time (APTT), ECG monitoring are also should be done. xx All these tests including platelet count and arterial blood gas analysis (ABG) should be repeated at regular intervals.

Treatment of Shock

xx In early stage—tachycardia, sweating, cold peri­phery,

hypotension, restlessness, air hunger, tachypnoea, oliguria, collapsed veins. xx In late stage—cyanosis, anuria, jaundice, drowsi­ness.

Guidelines ™™ ™™ ™™

To treat the cause To improve cardiac function To improve tissue perfusion

Clinically shock may be: xx Compensated with mild tachycardia, normal blood pressure, urine output, normal respiration and mild lactic acidosis. xx Mild shock with mild lactic acidosis, tachycardia, tachypnoea and anxiousness. xx Moderate shock with significant lactic acidosis, decreased urine, tachycardia, tachypnoea, drowsiness, and mild hypotension. xx Severe shock with severe lactic acidosis, anuria, tachypnoea with gasping, severe tachycardia, profound hypotension and unconsciousness.

Treatment of shock ™™ ™™ ™™

xx Treat the cause, e.g. arrest haemorrhage, drain pus. xx Fluid replacement:  Plasma, normal saline, Ringer’s lactate, plasma expander

Note:

• •

Shock index is ratio of pulse rate to blood pressure; normal shock index is < 1. In shock it reverses. Tachycardia, tachypnoea, oliguria, hypotension are typical features in shock.

Complications of shock Acute respiratory distress syndrome and respiratory failure Acute renal failure Hypoxia, metabolic acidosis Stress ulcers, ileus, liver failure Disseminated intravascular coagulation (DIC) and thrombocy­ topenia ™™ Systemic inflammatory response syndrome and multiorgan dysfunction syndrome (MODS) ™™ ™™ ™™ ™™ ™™

ASSESSMENT, INVESTIGATIONS AND MONITORING xx Regular monitoring with blood pressure, pulse, heart rate, respiratory rate, urine output measurement (hourly) should be done. Urine output should be more than 0.5 ml/kg/hour. Pulse oximetry should be used. xx Central venous pressure (CVP—only have gross assessment), pulmonary capillary wedge pressure (PCWP—an accurate assessment of left ventricular function) monitoring should be done. ICU care is needed during monitor period. But both CVP and PCWP are not accurate method of assessing tissue perfusion. xx Complete blood count, ESR, pH assessment, serum electrolyte estimation, chest x-ray (to rule out ARDS/pulmonary problems).

First stabilize the patient with initial resuscitation Next evaluate the patient for cause and severity Lastly treat the specific cause to achieve cure

(haemaccel) (maximum 1 litre can be given in 24 hours).  Initially crystalloids then colloids are given. Blood

transfusion is done whenever required.

 Fluid therapy is ideally done with crystalloids like

normal saline, Ringer’s lactate, Hartmann’s solution. Blood loss should be corrected by blood transfusion only. Crystalloids and colloids do not have O2 carrying capacity. Hypotonic solutions like dextrose are poor volume expanders and so should not be used in shock.  Dynamic fluid response is studied by infusing 500 ml of fluid rapidly in 10 minutes. Responders show improvement; transient responders show improvement temporarily but revert back to original status probably due to still existing fluid/blood loss or still existing fluid shift from intravascular space; nonresponders will not respond as fluid loss is severe and persistently ongoing. xx Inotropic agents: Dopamine, dobutamine, adrenaline infusions—mainly in distributive shock like septic shock. Note: ™™ ™™ ™™ ™™

Dopamine improves renal and splanchnic blood Dobutamine improves the cardiac output Adrenaline/Levarterenol IV in anaphylaxis Amrinone and milrinone are newer inotropic drugs

xx Correction of acid-base balance: Acidosis is corrected by

using 8.4% sodium bicarbonate intravenously. xx Steroid is often life-saving. 500–1000 mg of hydro­cortisone

can be given. It improves the perfusion, reduces the capillary

Shock

Fig. 1.207: Trendelenburg position—head down position, used in patient in shock.

leakage and systemic inflam­matory effects.

to the SVC (used for TPN purpose). Occasionally a long catheter (60 cm) can be passed through basilic vein (not commonly done). Under radiological guidance, initially a needle is passed 3 cm above the medial end of the clavicle, in the hollow between the two heads of sternomastoid muscles, directing towards the suprasternal notch into the right internal jugular vein. Then through a guide wire, a venous catheter is passed into the SVC through right internal jugular vein, which can also be confirmed by changes in flow during inspiration and expiration. Catheter is connected to saline manometer, taking manubriosternal angle (angle of Louis) as zero point. Normal value is 2–10 cm of saline. If less than 2 cm, more fluid is infused. If more than 10 cm, fluid infusion should be restricted.

xx Antibiotics in patients with sepsis; proper control of blood

sugar and ketosis in diabetic patients. xx Catheterisation to measure urine output (30–50 ml/hour or

>0.5 ml/kg/hour should be maintained). xx Nasal oxygen to improve oxygenation or ventilator support with intensive care unit monitoring has to be done. xx CVP line to perfuse adequately and to monitor fluid balance. TPN is given when required. xx PCWP to monitor very critical patient. xx Haemodialysis may be necessary when kidneys are not functioning. xx Control pain-using morphine (4 mg IV). xx Ventilator and ICU/critical care management. xx Injection ranitidine IV or omeprazole IV or pantoprazole IV. xx Activated C protein even though costly is beneficial as it prevents the release and action of inflammatory response. xx MAST (military antishock trouser): Provides circumferential external pressure of 40 mmHg. It is wrapped around lower limbs and abdomen, and inflated with required pressure. It redistributes the existing blood and fluid towards centre. It should be deflated carefully and gradually.

Fig. 1.208: CVP cannula. Note the location of tip of CVP line in the SVC (or can be in the right atrium).

Remember xx Response to dynamic fluid therapy can be checked in patient in shock by perfusing 500 ml of fluid rapidly in 10 minutes and patient is checked as nonresponder/transient only initial responder or proper responder. xx Vasopressor like dobutamine is used only in distributive shock like due to sepsis (not in hypovolaemic, haemorrhagic shock where there is low preload). xx Intubation and ventilator may be needed in shock. xx The patient is monitored with ECG, pulse oximetry, blood pressure/ invasive blood pressure, CVP/ PCWP, urine output, pupillary reaction (dilated or not), serum electrolytes, arterial PO2 and PCO2 analysis.

CENTRAL VENOUS PRESSURE (CVP) It is a method to measure the right atrial pressure by placing a venous catheter (20 cm) into the SVC (superior vena cava). Commonly for CVP monitoring, a venous catheter is passed through internal jugular vein or infraclavicular subclavian vein

Fig. 1.209: CVP line for monitoring and perfusing the patient in shock.

Complications of CVP ™™ ™™ ™™ ™™ ™™ ™™

Pneumothorax Haemothorax Injury to brachial plexus and vessels Bleeding Sepsis Catheter displacement

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SRB's Manual of Surgery PULMONARY CAPILLARY WEDGE PRESSURE (PCWP) It is a better indicator of circulating blood volume and left ventricular function. Catheter used is Swan Ganz triple channel pulmonary artery balloon catheter. It is used to: Differentiate right and left ventricular failure, pulmonary embolus, septic shock ™™ To measure and monitor cardiac output during the use of inotropic agents, vasodilators and fluid therapy ™™

Procedure Under strict aseptic precaution, using cannula and guide wire, catheter is passed through internal jugular vein, into the right atrium. Balloon is inflated by 1.5 ml of air and then negotiated into pulmonary artery, until it reaches a small branch and wedges it. Pressure at this point is called as pulmonary capillary wedge pressure. PCWP normally is 8–12 mmHg, considering mid axillary point as zero reference point. After that, balloon is deflated to get pulmonary artery pressure which is normally 25 mmHg systolic and 10 mmHg diastolic. PCWP catheter can be kept in situ only for 72 hours. Complications ™™ ™™ ™™ ™™ ™™ ™™ ™™

Arrhythmias Pulmonary artery rupture Balloon rupture Pulmonary infarction Pneumothorax Haemothorax Bleeding, sepsis, thrombosis

Fig. 1.210: Pulmonary capillary wedge pressure. Note the wedged balloon in the tip of the venous catheter in the pulmonary arteriole.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS) xx SIRS is systemic manifestations of inflammation due to variety of causes like infection, pancreatitis, polytrauma, burns, transfusion reaction, and malignancy. So it is often categorised as infectious cause SIRS or noninfectious cause SIRS. It causes either hyperthermia (>38°C) or hypothermia (90/ minute); tachypnoea (>20/minute); total white cell count >12,000/ cu mm, or count 15% of total body

volume in otherwise healthy individuals (liver, spleen, kidney, GIT injuries, fractures, haemothorax, perineal injuries). xx During major surgeries—abdominoperineal surgery, thoracic surgery, hepatobiliary surgery. xx Following burns. xx In septicaemia.

1. Packed cells  I t i s o b t a i n e d b y c e n t r i f u g i n g w h o l e b l o o d a t 2000–2300 g for 15–20 minutes.  It is used in chronic anaemias, in old age, in children.  It minimises the cardiac overload due to trans­fusion.  It can be stored for 35 days at 1°–6°C.  One unit contains 300 ml with haematocrit about 70%. One unit raises Hb% by 1.0 gram. 2. Plasma:  This is obtained in the same way as packed cells by centrifugation.  It is indicated in burns, hypoalbuminaemia, severe protein loss.  It can be fractionalised into different fragments: a. Human albumin 4.5% is obtained after repeated fractionations and can be stored for several months in liquid form at 4°C. b. Fresh frozen plasma (FFP): Fresh plasma obtained, is rapidly frozen and stored at –40°C. It contains all coagulant factors. 1 unit of FFP increases the clotting factors levels by 3%. It can be stored for 2 year. Rhesus D positive FFP can be transfused to Rhesus D negative female. Uses: -- Severe liver disease with abnormal coa­gulation function. -- Congenital clotting factor deficiency. -- Deficiency following warfarin therapy, DIC, massive transfusion.

Haemorrhage and Blood Transfusion -- To maintain prothrombin time at normal level. Dose of

FFP is 15 ml/kg. c. Cryoprecipitate: When fresh frozen plasma is allowed to thaw at 4°C, visible white supernatant layer develops and is called as cryoprecipitate which is rich in Factor VIII and fibrinogen. It is stored at minus 40°C and can be kept for 2 year. Cryoprecipitate is used to raise fibrinogen level at a dose to make plasma fibrinogen level 150 mg/dl. It is also used in inherited deficiency of Factor VIII, fibrinogen, Factor XIII, von Willebrand’s disease.

Advantages This allows good viability of cells ™™ But it is devoid of any protein ™™ It is very useful in anaemias ™™

Precautions

xx For every four units of SAG-M blood, one whole blood has

to be given.

xx Later for every two units of SAG-M blood, one unit (400

ml) of 4.5% human albumin has to be given.

xx Coagulation status and platelet count should be checked

regularly.

Complications of Blood Transfusions (Please also see table for entire list)

Fig. 1.218: Purified freeze dried human coagulation factor VIII is available for use in haemophilia patients. d. Fibrinogen is obtained by organic liquid fractionation of plasma and is stored in dried form. It is very useful in DIC and afibrinoge­naemia. It has risk of transmitting hepatitis. e Factor VIII and IX concentrate: They are freeze dried part from a large pooled plasma used in haemoplhilia and von Willebrand’s disease. 3. Platelet rich plasma: It is obtained by centrifu­gation of freshly donated blood at 150–200 g for 15–20 minutes. Platelet rich plasma contains 5.5 × 109/L platelets in 50 ml plasma. It can be random donor platelet or single donor platelet. Single donor platelet is prepared by plateletapheresis containing 3 × 109/L platelets in 200 ml of plasma. One single donor platelet is equal to 8 units of random donor platelet. 4. Platelet concentrate: It is prepared by centrifu­gation of platelet rich plasma at 1200–1500 g for 15–20 minutes. Used in thrombocytopaenia and drug (aspirin, clopidogrel) induced haemorrhage. Platelet is transfused at a dose of 0.1 unit/kg, when platelet drops below 20,000/or episodes of bleeding. Platelet stored at 4°C should be used within 48 hours; when stored at room temperature can be used up to 5 days. One platelet concentrate can increase up to 10,000 platelet/cumm in one hour. 5. Prothrombin complex concentrate (PCC) are derived from pooled plasma which contains factors II, IX and X; used in emergency reversal of warfarin therapy in uncontrolled haemorrhage.

SAG-M Blood A proportion of donations will have plasma removed and will be replaced by crystalloid solution of SAG-M. S — Sodium chloride. A — Adenine. G — Glucose anhydrate. M — Mannitol.

Febrile reactions: It is the most common complication due to impurities like pyrogens in the blood or in infusion set. Headaches, fever, chills and rigors, tachycardia, nausea are the features. Transfusion is temporarily stopped or the flow is slowed down with administration of antipyretic drug to reduce fever. Often transfusion of that unit needs to be discontinued. Allergic reaction (3%): Utricaria and allergy to specific proteins in the donor’s plasma can occur. Usually it is mild and is treated with steroid and antihistaminics. In severe utricaria that unit of blood is discarded; new washed RBC’s and platelets are used. Acute haemolytic reactions: It is the most dangerous complication. It is due to ABO incompatibility. Usually it is nonfatal but occasionally can be fatal. It is commonly due to technical error at different levels. It amounts for criminal negligence in court of law. Intravascular destruction causes haemoglobinemia, haemoglobinuria, acute renal failure and DIC. Dyspnoea, chest pain, sweating, fever with chills, tachycardia, hypotension, and cardiac arrest occurs in fatal type. Jaundice is a common feature in nonfatal type. Free haemoglobin level in blood will be above 5 mg/dl. Condition is treated as an emergency in critical care unit/ ICU. Transfusion is stopped immediately; blood sample of recipient and transfusing blood is sent immediately for two laboratories for rechecking. Smoky urine of the patient is typical. Injection hydrocortisone/dexamethasone IV is given immediately. Fluid therapy, alkalization of blood is done using sodium lactate and sodium bicarbonate. Mannitol 20 gram in 100 ml is infused in 5 minutes; furosemide 120 mg is injected intravenously. Haemodialysis is needed if there is renal failure. Often ventilator support, defibrillator if cardiac arrest occurs is needed. Correction of acidosis, electrolytes is needed. Transfusion-related acute lung injury: It is due to donor plasma antibody against HLA and leucocyte specific antigens of recipient. Occasionally it is due to recipient’s antibody

Every obstacle introduces a person to himself.

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SRB's Manual of Surgery against donor’s leucocytes. Features are—breathlessness, saturation drop, fever, hypotension which is observed 4 hours after transfusion. Chest x-ray shows bilateral diffuse infiltrate. They need ventilator support for short period with eventual rapid and complete recovery. Transfusion-related graft versus host disease (TGVH): This very serious, very rare complication occurs due to recognition and reaction against host tissues by infused donor lymphocytes. It is common in immunosuppressed, lymphoma, leucaemic patients. Any type of blood products including leukocyte reduced blood can cause the condition. Features are—pancytopaenia, toxic epidermal necrosis, liver dysfunction with more than 90% mortality. It is difficult to treat. Congestive cardiac failure (CCF): It occurs if especially large quantities of whole blood are transfused in chronic severe anaemia, pregnancy, elderly patients, in patients who have cardiac problems. Complications of blood transfusion Congestive cardiac failure Transfusion reactions HBV, HCV – Incompatibility: Major and minor reactions with fever, rigors, pain, hypotension – Pyrexial reactions due to pyrogenic ingredients in the blood – Allergic reactions – Sensitisation to leucocytes and platelets – Immunological sensitisation ™™ Infections –  Serum hepatitis –  HIV infection –  Bacterial infection –  Malaria transmission – Epstein-barr virus infection –  Cytomegalovirus infection – Syphilis, Yersinia – Babesia microti infection – Trypanosoma cruzi infection ™™ Air embolism ™™ Thrombophlebitis ™™ Coagulation failure –  Dilution of clotting factors – DIC – Dilutional thrombocytopenia occurs in patients with massive blood transfusion ™™ Circulatory overload causing heart failure ™™ Haemochromatosis in patients with CRF receiving repeated blood transfusions ™™ Citrate intoxication causes bradycardia and hypo­cal­caemia. For every four units of blood 10 ml of 10% calcium chloride or gluconate should be infused intravenously ™™ Iron overload ™™ ™™

MASSIVE BLOOD TRANSFUSION It is defined as replacement or transfusion of blood equivalent to patient’s blood volume in < 24 hours corresponding to that particular age (In adult it is 5–6 litres, in infants it is 85 ml/kg body weight.) Or single trans­fusion of blood more than 2,500 ml continuously ™™ Massive transfusion is used in severe trauma asso­ciated with liver, vessel, cardiac, pulmonary, pelvic injuries. Often it is required during surgical bleeding (primary haemorrhage on table) of major surgeries ™™ Adverse effects of massive transfusion a. Severe electrolyte imbalance (hypocalcaemia, hyperkalaemia, acidosis) ™™



b. Coagulopathy—altered platelet and coagu­lation factors – Dilutional thrombocytopaenia



c.  Citrate toxicity, hyperammonaemia

d. Hypothermia

e.  Poor oxygen delivery—due to reduced 2,3 DPG

f. Infections

g.  Incompatibility and transfusion reactions



h.  ARDS, DIC, CCF

AUTOLOGOUS BLOOD TRANSFUSION An healthy individual with no infection and haematocrit of > 30% can predonate blood few weeks prior to any elective surgeries, which in turn, can be used at the time of surgery. Autologous blood is used in orthopaedic, gynaecologic and urologic surgeries. Patient donates one unit of blood weekly; last one if at all being 72 hours before the date of surgery.

Recycled Blood In major surgeries if there is significant blood loss, then patient’s bled blood is carefully sucked out through a sterile system and is filtered and reused again to the patient. This will reduce the number of transfusions.

ARTIFICIAL BLOOD 1. Perfluorocarbon (Fluosoleda; perfluoro decalin; Fluosol DA)— abiotic substitute as synthetic oxygen carrier. Its half life is 7 days. It is RBC substitute.  It has got high affinity for O2.  It is inert, colourless, odourless, dense, poorly soluble liquid.  It is biocompatible.  It is emulsified with albumin or lipids before infusion. Its emulsion alone injection can cause pulmonary embolism.  It can bind and release oxygen. But as it reduces the PPO2 quickly, it is a disadvantage. Patient ideally to be kept in hyperbaric place.  It is oily in nature hence has to be emulsified. It releases 1.3 ml of oxygen/100 ml. It should be kept frozen. It can cause anaphylaxis. 2. Stroma-free haemoglobin—biomimetic haemoglobin based substitute. It has more affinity for oxygen as it does not contain 2, 3 DPG but has short half life. It is nephrotoxic. 3. Chelates which reverse bound O2.  Intraoperative­—salvage of blood: On table blood is collected, washed, filtered and transfused. Used in trauma.

Haemorrhage and Blood Transfusion Erythropoietin xx injection 1000–3500 units pre­operatively also used to increase the RBC count. xx It is used in CRF patients who are on haemodialysis. It is given twice weekly but it is costly. Blood substitutes ™™ Human albumin 4.5% There is no risk of transmitting hepatitis. Plasma fractionation is done using organic liquids and heat to extract albumin which is stored at 4°C for many months. It can be used in patients with cirrhosis, burns, nephrotic syndrome, ovarian hyperstimulation syndrome (occurring after ovarian stimulation with gonadotrophin injections during in vitro fertilization (IVF) therapy). One gram of albumin binds with 14 ml of water so it increases the blood volume also. Albumin is infused daily as needed until good response is observed. Albumin is expensive. ™™ Dextrans are useful to improve plasma volume. They are polysaccharides of varying molecular weights. This is derived from leuconostoc mesenteroides bacteria after adding yeast. One gram of dextran binds with 20 ml of water to raise the plasma volume. a. Low molecular weight dextran (40,000 mol wt) (Dextran 40, Rheomacrodex).  Dextran 40 is very effective in restoring blood volume immediately. But small molecules are readily excreted in kidney and so effect is transitory. It may be useful in prevention of sludging in kidney and hence renal shut down. b.  High molecular weight dextran (Dextran 110 and Dextran 70). Less effective but long acting and so useful to have prolonged effect. Precautions 1. Blood samples for blood group and cross-matching should be taken before giving dextrans as it interferes with rouleaux formation of red cells. 2. Dextrans also interfere with platelet function and so may precipitate abnormal bleeding. 3. Total volume of dextrans should not exceed 1000 ml. ™™ Gelatin, in a degraded form of mol. wt. 30,000S, is used as a plasma expander. Up to 1000 ml of 3.4-4% solution containing anions and cations is given intravenously—Haemaccel. But it is less effective than dextran and after 4 hours of its infusion, only 30% remains intravascular. ™™ Hydroxyethystarch: It contains starch, sodium hydroxide, ethylene oxide. It is a good plasma volume expander but lasts only for 6 hours.

Fig. 1.219: Esmarch rubber tourniquet.

Fig. 1.220: Automatic gauged pressure tourniquet.

Uses xx To attain bloodless field in limb surgeries—upper and lower limbs, orthopaedic surgeries, soft tissue tumours, amputations. xx It is used (rubber tourniquet) to access veins for IV injections and IV sampling. xx Tourniquet is used in diagnostic tests for varicose veins, purpura (ITP), carpal tunnel syndrome, tetany. xx It is used as a first aid in bleeding conditions of limbs, snake bite (it is controversial). xx Tourniquets are often used for small procedures in fingers and toes.

Types

TOURNIQUETS Tourner means to turn (Greek). A tourniquet is used to cut off the blood supply to a limb temporarily so that a bloodless field is created while performing the surgery. Limb should be exsanguinated before applying/inflating the cuff of the tourniquet. It is done using a bandage or pressurized Rhys-Davis exsanguinator. A tourniquet is applied in mid-thigh above the knee joint in lower limb and in mid-biceps level above the elbow in upper limb. It should not be closer to joints. It is not applied over the forearm or leg. It is applied over layers of gauze or cotton, not over a bare skin. Pressure used in upper limb is 250 mmHg; lower limb is 300 mmHg (In children, it is 150 and 250 mmHg for upper and lower limbs respectively).

xx Rubber tourniquet: Simple red rubber catheter is used for drawing blood, to have access to veins. xx Martin’s tourniquet made up of India rubber. xx Pneumatic tourniquet: Used in limbs, will give the arterial pressure and also acts as a tourniquet (Sphygmomanometer cuff is simpler and easily available type). xx Esmarch rubber elastic bandage tourniquet. xx Conn pneumatic tourniquet is manually operated tourniquet where air is pumped up to the required pressure. xx Specialised sophisticated tourniquets are available which gauge pressure and time accurately—automatic tourniquet.

The very act of believing creates strength of its own.

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SRB's Manual of Surgery Tourniquet time for upper limb is one hour and for lower limb is two hours.

Contraindications xx xx xx xx xx

In all peripheral vascular diseases and atherosclerosis. Infection. Deep venous thrombosis. Crush injuries. Sickle cell disease.

Complications xx Crushing effect on muscles in thigh occurs leading to crush syndrome. xx Tourniquet palsy in upper limb (radial nerve involvement)— neuropraxia. xx Infection. xx Improper application of tourniquet leads to more bleeding. xx Forgetting the removal of tourniquet or taking more time to release may compromise the blood supply of the limb leading to severe ischaemia and gangrene. It occurs especially when tourniquet is used in finger or toe. xx Skin blistering and necrosis.

DISSEMINATED INTRAVASCULAR COAGULATION Disseminated intravascular coagulation (DIC) is a manifestation due to wide spread intravascular coagulation resulting in microthrombi formation, consumption of platelets and clotting factors and production of breakdown products eventually leading into severe bleeding and tissue ischaemia.

Causes xx Major trauma causes DIC due to release of tissue thrombo-

plastin. Burns, major surgery can also cause DIC. xx Sepsis is the most common cause of DIC. Common sepsis

causing DIC are gram-negative, meningococcal, malarial, histoplasmosis, aspergillosis, etc. xx Acute pancreatitis can cause DIC by releasing proteolytic enzymes which activate prothrombin and factor X. xx Septic abortion, abruption, retained dead foetus, amniotic fluid embolism are obstetric causes of DIC. xx Carcinoma of pancreas, prostate, acute promyelocytic leucaemia often cause DIC. xx Haemolysis, snake bite, liver dysfunction are other causes.

Types of DIC xx Acute DIC presents with bleeding in gums, GIT, venepunc-

ture site, haematuria, petechiae, oozing from surgical or traumatic wounds. Massive bleeding also can occur. xx Chronic DIC is a low grade type with thrombotic features.

Investigations xx In DIC—bleeding time, platelet counts are reduced.

Thrombin time (TT), prothrombin time (PT) and activated partial thromboplastin time (APTT) are prolonged. Fibrin-

ogen degradation product (FDP), D-dimer test are raised. xx Complete haematocrit, investigations relevant to cause, renal

function tests, LFT, electrolyte estimation, blood/discharge/ pus/urine culture.

Treatment of DIC xx Treatment of specific cause as per protocol. Correction of

haemodynamic instability by fluid therapy, transfusion of packed cells or whole blood. Dopamine/dobutamine therapy. xx Factor replacement—specific therapy for DIC—FFP, cryoprecipitate, platelet concentrate transfusions are essential. FFP is given at a dose of 15 ml/kg. Cryoprecipitate is used to raise fibrinogen level at a dose to make plasma fibrinogen level 150 mg/dl. Platelet is transfused at a dose of 0.1 unit/ kg, when platelet drops below 20,000/or with episodes of bleeding. xx Heparin use is often controversial. It is used mainly in chronic DIC, DIC with purpura, DIC of obstetric cause, cancer induced DIC, DIC due to acute antiphospholipid antibody syndrome. xx EACA, tranexamic acid can be used but with questionable benefits.

MECHANISM OF BLOOD COAGULATION (HAEMOSTASIS) Haemostasis is the spontaneous arrest of bleeding. When an injury occurs platelet adhesion occurs to injured vessel/capillary wall which activate the release of ADP (Adenosine diphosphate) which makes more platelet to aggregate (platelet aggregation). These activated platelets release thromboxane A2 which further increases the adhesion and aggregation of platelets. Circulating fibrinogen binds to an activated platelet receptors glycoprotein IIb and IIIa and fibrinogen gets converted into fibrin.

Coagulation cascade system:

Haemorrhage and Blood Transfusion Clotting factors are proteins synthesised by the liver which with a series of cascade reaction activates clotting factors and achieves blood coagulation by a complex mechanism. Factor II, VII, IX and X are vitamin K dependent for their synthesis in liver (carboxylation of glutamic acid). In the process of coagulation each factor gets activated to an enzyme by partial proteolysis, which in turn, activates other needed coagulation factors. Eventually fibrinogen gets converted into soluble fibrin and later into insoluble fibrin.

Contd...

Two types coagulation system are there: xx Intrinsic pathway xx Extrinsic pathway In vitro coagulation occurs by intrinsic coagulation system. Cascade gets activated by vessel wall injury, shear stress of vessel or other factors. It activates the cascade to get final result.

Hemophilia and von Willebrand’s disease

Coagulation cascade system Blood clotting factors Factor No.

Common name

I Fibrinogen II Prothrombin III Thromboplastin IV Ionic calcium V Hereditary labile factor, activator (AC) globulin, proaccelerin VI Accelerin, supposed to be active form of factor V VII Proconvertin; serum prothrombin—conversion accelerator (SPCA) VIII Antihemophilic factor (AHF) IX Plasma thromboplastin component (PTC; Christmas factor) X Stuart-Prower factor XI Plasma thromboplastin antecedent (PTA)

Contd...

XII XIII XIV

Hageman factor Fibrin stabilizing factor, fibrinase Prekallikrein

XV XVI

Kallikrein Platelet factor

They are the two most common inherited bleeding disorders due to deficiency of factor VIII. Factor VIII has two components; smaller one—factor VIII C is needed for activation of factor X in intrinsic coagulation pathway; its deficiency leads to classic hemophilia. It is inherited as an X-linked recessive trait, thus it occurs in males and homozygous females. The larger component of factor VIII called von Willebrand’s factor, facilitates the adhesion of platelets to subendothelial collagen, hence crucial for hemostasis, its absence leads to von Willebrand’s disease. Classic haemophilia is called haemophilia A is caused by deficiency of factor VIII C with X linked recessive trait. It occurs in males or homozygous females. Recurrent haemarthroses is a common presentation. Petechiae and echymoses are absent. Bleeding time is normal but coagulation time is prolonged. Treatment is replacement of factor VIII haemophilic factor. If not known patient may go for a life-threatening bleeding even after dental extraction. Von Willebrand’s disease is deficiency of larger component (99%) of the factor VIII-vWF. It is an autosomal dominant disease with normal bleeding time and normal platelet count. Common presentations are spontaneous bleeding from mucous membrane, excessive bleeding from wounds and severe menorrhagia. Haemarthroses is not common in von Willebrand’s disease. Treatment is replacement of specific factors. Haemophilia B also called as Christmas disease is due to factor IX deficiency is inherited as X linked autosomal recessive trait.

Our greatest glory is not in never falling, but in rising every time we fall.

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I. Burns The infusion of large quantities of fluid, mainly a salt solution, as many as 3–4 litres daily, has proved satisfactory. Sometimes a life is saved if not more than one-quarter of the body surface has received a third-degree burn…. I have given blood transfusions to two patients with severe burns, with recovery in one case and postponement of death in the other. —Gustav Riehl, 1925

CHAPTER OUTLINE ™™ Burns ™™ Management of Burns ™™ Eschar

™™ Contracture in Burn Wound ™™ Electrical Burns ™™ Inhalation Injury

Burns

xx Full thickness burns less than 2%. xx Can be treated on outpatient basis. Types of burns

™™

™™ ™™ ™™ ™™ ™™

™™ Chemical Burns

Thermal injury –  Scald—spillage of hot liquids –  Flame burns – Flash burns due to exposure of natural gas, alcohol, combustible liquids – Contact burns—contact with hot metals/objects/materials Electrical injury Chemical burns—acid/alkali Cold injury—frost bite Ionising radiation Sun burns

Classification of Burns Depending on the Percentage of Burns (Burn Severity Classification) Mild (Minor): xx Partial thickness burns 80%. Take up of cultured graft is 60–75%. Limitations are—time taken to develop cultured graft; more vulnerability for mechanical trauma; costly; time taken to manufacture; scarring.

Synthetic dressings in burn wound xx Vaseline impregnated gauze dressing prevents stiffness of eschar. xx Hydrocolloid dressing (duoderm) helps moist environment, proper epithelialisation. It is useful in mixed deep burns. It is changed once in 3 days.

It is used to cover the wound temporarily as a barrier and also to have some immunologic function. Eventually graft will slough. Later wound is covered with auto-skin graft. It is used for massive burn injuries more than 50%. Possible problem is transmission of viral diseases. Xenograft is of pig skin. Allograft is of cadaver skin (homograft)—it gives all existing normal skin function for temporary period. It may leave a dermal equivalent in the wound later.

ESCHAR xx It is charred, denatured, full thickness, deep burns with contracted dermis. xx It is insensitive, with thrombosed superficial veins. xx Circumferential eschar in the upper limb, lower limb, neck, thorax can cause more oedema which initially causes venous compression and later arterial compres­sion causing ischaemia, gangrene of the distal part. So distal area should be monitored for circulation. xx If required deep longitudinal full thickness incisions are made in different areas so as to prevent collection of oedema fluid and

Burns also to prevent compression over the vessels. This is called as escharotomy. Escharotomy causes large quantity of blood loss and so blood transfusion is needed while doing escharotomy. Incision should be of adequate length and depth during escharotomy. It should be placed in such a way so as to avoid injury to major neurovascular system. Release of muscle compartment is needed often in these patients. xx Multiple incisions or incisions over the joints may be needed. xx Early rapid separation of eschar indicates severe sepsis underneath. xx Eventually eschar should be excised and the area is allowed to granulate and skin grafting should be done. Pseudoeschar is thickened burnt skin due to repeated silver sulphadiazine application.

CONTRACTURE IN BURN WOUND Contracture in burns can occur anywhere. It is more common wherein flexibility and mobility is present like along the joint, eyelids, cheeks, lips, neck, elbow, knee, etc. Contracture can be intrinsic by loss of tissue or extrinsic by pull during healing phase contraction. Contracture proceeds towards position of comfort until it meets or closely reaches opposite surface. There is clearly wound shortening. Disorganised over formation of compact collagen (3 times normal) causes hypertrophic scar leading further contracture. Deficit of neck extension is graded, normal >110°; E1 95–110°; E2 is 85–95°; E3 is 30% Burns should be assessed whether it is accidental or homicidal Relatives should be informed about the duration of stay, problems, repeated surgeries In patients with severe burns who is likely to die, when suspected, dying declaration should be arranged Cost of therapy, long duration of stay and cosmetic problems should be informed to the relatives

J. Trauma CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™

Triage Spinal Injury Neck Injuries Bullet Injuries Blast Injuries Penetrating Injuries Abdominal Trauma

™™ ™™ ™™ ™™ ™™ ™™ ™™

Blunt Trauma of Abdomen Duodenal Injury Pancreatic Injury Small Bowel Injury Colonic Injury Liver Injury Splenic Injury

Trauma is a major public health problem in all countries. It causes death disability and both. 50% die immediately at the time of accident. 25% die in golden hour of trauma, i.e. first 4–6 hours of trauma. 25% may die late during treatment period due to sepsis and complications. Injuries may be penetrating, blunt, blast, chemical, electrical and other injuries.

™™ Renal Injury ™™ Urinary Bladder Injury ™™ A  bdominal Compartment Syndrome ™™ Seat-belt Injuries

Assessment of four components i. ii. iii. iv.

Physiologic response Anatomical injury Biomechanical injury Comorbid factors

Triage algorithm Step One (Assess physiological impact) Measure vital signs and level of consciousness ™™ By Glasgow coma scale ™™ Systolic blood pressure ™™ Respiratory rate ™™ Revised trauma score. It is based on airway, laryngeal injury, spine injury, maxillofacial injury Step Two (Assess anatomical impact) All penetrating injuries to head, neck, thorax, major burns, fracture bones, pelvic fractures, paralysis Step Three (Assess mechanism)

Fig. 1.240: Trauma causing large tissue defect exposing the bone.

Automobile accidents, crash or blast injuries, high energy injuries, fall from more than 20 feet. Bullet injury Step Four (Assess history)

TRIAGE Triage means “To sort” in French. Triage is a system to attend trauma patients, formu­lated by Committee of Trauma of the American College of Surgeons. Advanced trauma life support (ATLS) is essential for first hour care of an injured patient. Pre-hospital trauma life support (PHTLS) is to prevent deaths while injured patients are transported to the hospital.

Types of Triage System xx Multiple casualties: Staff and facilities are sufficient but priority is given to life-threatening injuries. xx Mass casualties: Staff and facilities are not sufficient to manage. Here those who are likely to have highest chance of survival are given priority.

™™ ™™ ™™ ™™ ™™

Patient’s age below 5 years or age more than 55 years Cardiac diseases, respiratory and metabolic diseases Pregnancy Patients with bleeding disorders Immunosuppressed individuals

BASED ON THESE STEPS CONSIDER TO SHIFT THE PATIENT TO TRAUMA CENTER and TRAUMA TEAM SHOULD BE KEPT ALERT. It is important in multiple and mass casualities (fire, blasts, automobile accidents, train accidents).

Management xx xx xx xx xx

Initial evaluation of the patient. Physiologic stabilisation. Control of haemorrhage. Management of thoracic and abdominal injury. Management of cranial injury.

Action, to be effective, must be directed to clearly conceived ends.

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SRB's Manual of Surgery I.  Primary Management xx Airway management (blocked by food, vomitus, clot, fallen tongue). xx Breathing. xx Circulation. xx Disability and level of consciousness assessment by Glasgow coma scale. xx Exposure of the patient from head to toe for final assessment. xx Fingers and tubes: Finger evaluation, Foley’s catheterisation.

Goals xx xx xx xx xx xx

Identify life-threatening conditions. Decide and implement appropriate treatment to the area of trauma. First think to salvage the life, then think to salvage the limb. Rapid assessment, rapid resuscitation, rapid stabilisation. Optimum, complete care. Transport efficiently to higher trauma centre. Categorise the patient

xx Serum electrolytes. xx U/S abdomen.

III.  Secondary Survey Re-evaluate the patient completely again.

IV.  Definitive Care (All discussed under individual topics.)

Mechanism of Trauma xx Blunt trauma—direct or indirect blunt injury can occur. Seat belt reduces the blunt injury in vehicles. xx Penetrating injury—severity depends on the extent of deeper injury. xx Blast injury. xx Crush injury—earthquake, industrial accidents, and train accidents—causes crush syndrome; compartment syndrome. xx Burn injury. xx Injury in alcohol patients.

I: Deceased II: Walking wounded III: Immobile wounded IV: Trapped wounded Tag the patient accordingly Red colour Yellow colour Green colour Blue colour Black colour

: Immediate treatment is required : Urgent treatment is required : Delayed treatment is required : Expectant treatment is required : Deceased

AIRWAY BREATHING Chin lift 100% oxygen Jaw thrust Assess bilateral chest raise Nasal airway Assess breath sounds Oral airway Use pulse oximetry Endotracheal intubation Treat flail chest, pneumothorax Tracheostomy Intercostal tube drainage (assess airway patency) CIRCULATION DISABILITY EVALUATION Monitor vitals Neurological examination Heart sounds Glasgow coma scale ECG Pupillary reaction IV fluids blood transfusion Treatment of shock Control of external bleed Use two IV lines—14G/16G EXPOSE THE PATIENT FINGERS AND TUBES FULLY Examine all orifices like P/R, Undress the patient P/V, etc. Hypothermia assessment Use required tubes like catheter, Assess injuries Ryle’s tube Examine joints, bones, abdomen, other systems Look for identification marks

II. Investigations xx X-ray spine, chest, pelvis, extremities. xx CT scan. xx Blood group and cross-matching. xx Arterial blood gas analysis.

Fig. 1.241: Crush injury leg due to road traffic accident.

Fig. 1.242: Ankle injury with open wound.

Revised Trauma Score (RTS) It is a reliable physiological scoring system in trauma. Here Glasgow coma scale, systolic blood pressure, respiratory rate are used as parameters. RTS = 0.9368 × GCS + 0.7326 × systolic BP + 0.2908 × Resp rate. RTS will come between 0–7.8. Value 89

10–19

4

9–12

76–89

>29

3

6–8

50–75

6–9

2

4–5

1–49

1–5

1

3

0

0

0

CONCEPTS IN TRAUMA MANAGEMENT xx Concept of ‘golden hour’ to treat the trauma patient is

important. xx Multidisciplinary approach. xx Planning, setting up, organizing, team work. xx Assess respiratory system; circulation; bleeding areas—as

priority. xx Assess also whether patient is haemodynamically stable

or unstable.

xx Arrange fluids, blood, catheters, ventilator, etc. xx Further definitive therapy depending on severity and site

of injury.

Damage Control Surgery

Fig. 1.243: Degloving injury involving entire left lower limb, perineum, and left groin. Patient has lost scrotum and both testes. There were no internal injuries and vessels and nerves were intact. Patient underwent wound excision extensively and colostomy was done to promote healing of perineal wound and prevent contamination.

xx Resuscitation and early therapy in operation theatre itself. xx Minimum but essential surgery to control bleeding and prevent contamination. xx Secondary definitive surgery at a later period to have final control. xx Damage control surgery is done when there is inability to control bleeding, complex abdominal injuries like of liver or pancreas, major vascular injuries with or without bowel injuries, retrohepatic IVC injury which is not accessible; decline in physiological reserve like temperature, pH, prothrombin time, serum lactate, systolic blood pressure less than 90 mmHg for 60 minutes; if operating time expected is more than one hour, inability to close the wound or whenever reopening the cavity is needed. xx Principles of damage control surgery apply to injuries of the abdomen, thorax and extremities equally.

Fig. 1.244: Class III dog bite on face in a boy. Fig. 1.246: Hand injury involving all fingers.

Fig. 1.245: Degloving of scalp with bone periosteum exposing the skull bone. Outer table was actually dead and required bone removal and graft after healthy granulation tissue was formed.

A Fig. 1.247A

During an injury, unsuspected lesions of the spinal cord may cause the most excruciating abdominal pain. —Theodore Schrire

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SRB's Manual of Surgery

B Fig. 1.247B

Figs 1.247A and B: A person has bitten this patient during a fight and removed the central part of lower lip. It was repaired primarily by Y repair. Remember human bites are most dangerous.

SPINAL INJURY xx Assess the type, extent and severity of the injury. xx Careful first aid and transfer to prevent further damage to the spinal cord. xx Assess the sensory loss or motor loss properly. xx Assess fractures clinically, by X-ray, CT scan (for fracture) and MRI (for spinal cord injuries). xx Central cord syndrome is common and is due to hyperflexion or hyperextension of the neck in an injured patient causing ischaemia of spinal column due to interfering of spinal artery blood flow. xx Brown-sequard syndrome: It is due to partial transec­tion of the cord causing ipsilateral motor function loss and contralateral sensory function loss. xx High dose of steroid is very useful to prevent further damage. xx Rest, traction to neck. xx Decompression of spinal canal surgically by removing bone, disc, haematoma is useful. xx Spinal stabilisation.

Fig. 1.248: Neck trauma zones.

xx Antibiotics. xx Blood transfusion is given as required. xx Ryle’s tube for 5–7 days. Other injuries like head, thorax, abdomen, maxillofacial area are discussed in respective chapters.

BULLET INJURIES Bullet injury has wound of entry and wound of exit. Extent of damage is not related to the external wounds. It is related to the travel of bullet inside and extent of blast or cavitation effect inside caused by the bullet. It causes burn damage. It can damage vessels, organs like liver, spleen, kidneys, bowel, lungs, heart, cranial structures, soft tissues, bones and joints.

NECK INJURIES Neck is divided into zones for managing neck injuries Zone I: From clavicle to cricoid cartilage Zone II: From cricoid cartilage to angle of the mandible ™™ Zone III: Above the angle of the mandible ™™ ™™

Indications for Neck Exploration in Injuries xx xx xx xx xx xx

Expanding haematoma. Uncontrolled external haemorrhage. Decreased carotid pulse. Stridor, hoarseness, dysphonia, haemoptysis. Severe dysphagia, odynophagia. Blood in oropharynx.

Treatment xx The neck is explored with adequate incision under general anaesthesia. xx The injured structure like vessels, oeso­phagus, trachea, muscles are sutured.

Fig. 1.249: Multiple pellets over elbow region after gunshot.

Trauma Management xx xx xx xx

xx xx xx xx xx xx xx xx xx xx xx xx

The wounds are explored properly under general anaesthesia. All dead tissues and dead muscles are excised. Skin is generously and adequately incised. Injured nerves are cleaned and silk marker stitches are placed to identify for later secondary suturing (Nerve should not be sutured primarily in bullet injury). All foreign bodies are removed. Tendon repair should not be done primarily. Wound should not be closed. It should be left open. Adequate blood transfusion and antibiotics cover­age should be given. Major artery or vein are sutured. Vein graft can be used. But synthetic graft should never be used. Thorough inspection, irrigation and debridement of injured joints is done. Immobilisation is done. Tetanus toxoid, antitetanus globulin (3000 units IM), antigas gangrene serum is given. Second look surgeries at a later period is done once patient has been stabilised. Delayed primary closure in 4–7 days or secondary closure in 14 days is done. Depending on extent of defect, skin grafting or flaps are used. Laparotomy, thoracotomy, craniotomy are done depending on the site of the injury.

BLAST INJURIES Here extent of damage is much more than bullet injuries. It creates complex blast wave which contains blast pressure wave and mass movement of air. This explosion pressure wave is more than 1000 pounds per square inch. This pressure wave has got incident pressure and reflected pressure. Both will cause severe damage.

A

B

Figs 1.251A and B: Crush injury foot with retained skin from plantar aspect was rotated forward (Courtesy: Dr Mayur Rai, Orthopaedician, KMC, Mangaluru). Factors causing the damage ™™ ™™ ™™ ™™ ™™

High pressure wave Mechanical injury Chemical injury Thermal injury Inhalation of toxic gases and smoke

Organs Affected xx Ear drums, lungs. xx GIT, brain. xx Skeletal system. Individual becomes deaf after blast and so rescue work may be delayed.

Management xx xx xx xx xx xx xx

Critical trauma care. Management of shock and triage primary management. Urgent surgeries like laparotomy, thoracotomy, craniotomy. Massive blood transfusion. Antibiotics. Ventilator support. Management of specific organs like eye, ear.

PENETRATING INJURIES xx It can occur in abdomen, thorax, cranial cavity. xx It causes haemorrhage, damage to internal organs like liver, bowel vessels, lung, pericardium and heart, brain.

Fig. 1.250: Degloving injury buttock. It needs colostomy to protect the wound from sepsis. Later once skin coverage is done colostomy is closed.

Fig. 1.252: Penetrating injury. Pole missed all the major vessels. Miraculously the patient survived, after a marathon surgery to tell her tale to her children.

Remember what you do not know. It differs you from others.

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Fig. 1.253: Stab wound on the back communicating into the thoracic cavity. Wound was explored and sutured, with an ICT inserted into the thoracic cavity. xx It is life-threatening and immediate surgical intervention is the only treatment. Patient requires adequate amount of blood transfusion, antibiotics, shock management.

ABDOMINAL TRAUMA It can be: ™™ Blunt trauma ™™ Stab injury ™™ Abdominal wall injury

Abdominal trauma is a major surgical emergency which most surgeons face. It is often associated with head injuries, chest, pelvic and bone injuries. Often patient is unconscious causing difficulty in diagnosing the condition. Often more importance is given to other system injuries like of head, thorax and bones whereas abdominal injury is not addressed properly causing life-threatening consequences. When patient is conscious, history related abdominal trauma is useful. Abrasion over the abdominal skin suggests the possibility of internal injury (London’s sign). Distension, tenderness, rebound tenderness,

fullness and dullness in the flank when present one should presume internal injury. Tachycardia, hypotension, shock may be evident when there is significant haemoperitoneum. Injuries may be organ injury like of liver, spleen, kidney, pancreas, etc. or bowel injury or retroperitoneal injury which is often under diagnosed or missed. Major vessel injury like of inferior vena cava, mesenteric vessels can cause real threat to life unless it is identified and managed early. 25% of entire trauma patients need surgical exploration of the abdomen. Abdominal trauma can be blunt or stab/penetrating or abdominal wall injuries. Spleen is the most common organ involved in blunt trauma. Often in blunt trauma first part of the jejunum or ileocaecal junction gives way (blow out effect) due to traction often causing complete transection of bowel horizontally close to the junction. It is due to force of the mobile part of the bowel over the fixed part. Liver is the most common organ involved in penetrating injuries. Injuries of the abdomen may be closed injuries, compression injuries and penetrating injuries. Penetrating injuries may be low velocity injury like stab injuries or high velocity injury like gunshot injuries. Penetration of blunt weapon causes less deep trauma than sharp weapon (sickle, knife). In sickle injury tip and sharp edge moves in curved pattern and so it is often difficult to predict the depth, track and organs injured. Routinely followed indications for exploration in abdominal trauma are—hypotension without any other cause; bleeding through wound; continuous bleeding in nasogastric tube; evisceration of abdominal content through the open wound except in case of protruded omentum without any hypotension and features of peritoneal irritation; air under diaphragm in blunt abdominal injury (not in penetrating injury as external air gets sucked into the peritoneal cavity through the wound). Types ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Liver injury. Spleen injury. Gastric/small bowel/colonic injuries. Duodenal injuries. Pancreatic injuries. Injuries to kidney/bladder/urethra. Mesenteric injury. Vascular injuries. Associated injuries like of diaphragm, lungs. Abdominal compartment syndrome. Gunshot or blast injuries.

General Clinical Features

Fig. 1.254: Traumatic haemoperitoneum.

xx Features of shock—pallor, tachycardia, hypo­tension, cold periphery, sweating, oliguria. xx Abdominal distension. xx Pain, tenderness, rebound tenderness, guarding and rigidity, dullness in the flank on percussion. xx Respiratory distress, cyanosis depending on the amount of blood loss. xx Bruising over the skin of the abdominal wall. xx Features specific of individual organ injuries.

Trauma

A

C

B

Figs 1.255A to C: Stab injury to LIF by an angry husband to his wife causing left common iliac artery transection injury with aortic partial injury. In spite saphenous vein graft reconstruction patient could not survive (Courtesy: Professor Yogishkumar, MS, KMC, Mangaluru).

Investigations 1. Ultrasound abdomen. FAST is Focused Abdominal Sonar Trauma: It is rapid, noninvasive, portable bedside method of investigation focusing on pericardium, splenic, hepatic and pelvic areas. Blood more than 100 ml in cavities can be identified. It is not reliable for bowel or penetrating injuries. It often needs to be repeated. 2. Diagnostic peritoneal lavage (DPL): It is done in case of blunt injury abdomen. Through a subumbilical lavage catheter one litre of normal s aline/Ringer’s lactate is infused

A

into the peritoneal cavity. Patient is changed to different positions and side-to-side. Fluid content is aspirated from the abdomen for assessment. It has got 98% accuracy rate. One of the criterias signifies positive lavage ™™ ™™ ™™ ™™ ™™

10 ml or more of gross blood RBC count more than 1,00,000/cumm WBC count more than 500/cumm Amylase level in the fluid more than 175 IU/dl Presence of bile, bacteria, food particles or foreign body

B

Figs 1.256 and B: Diagnostic peritoneal lavage—incision and technique. 10 French polyvinyl catheter is used. Urinary bladder is emptied by passing a catheter. After injecting xylocaine local anaesthesia into subumbilical region, 2–3 cm vertical subumbilical midline incision is made. Skin, linea alba is incised. Local anaesthesia is infiltrated into the peritoneum again. Peritoneum is held with two haemostats and a purse string suture is placed using polyglactic acid absorbable suture material. Peritoneum is incised for 3 mm length. Catheter (standard peritoneal dialysis catheter) is introduced into the peritoneal cavity. If blood enters the catheter immediately, it means early laparotomy is needed and carried out without continuing the peritoneal lavage. Otherwise, one litre of normal saline is infused into the peritoneal cavity rapidly in few minutes through the catheter using a drip set with elevation of the fluid bottle/bag. Patient is moved well to mix the fluid in all four quadrants. Now bag is lowered below so that fluid from the peritoneal cavity reenters/siphoned into the bag. Collected fluid is analysed for red cells, leukocytes, etc. DPL may not be useful in bowel injury, retroperitoneal injury, diaphragmatic injury, organ haematoma (subcapsular splenic haematoma). If patient is decided for observation catheter can be left in situ for repeat DPL after 6 hours. One has to remember that DPL is not a substitute for clinical assessment and monitoring. In Lazarus-Nelson approach Teflon catheter with a guide wire is used.

Well done is better than well said.

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SRB's Manual of Surgery It is the procedure of choice in physiologically unstable patient with blunt abdominal injury (like with spinal injury, unconscious patient). Contraindications for DPL ™™ ™™ ™™ ™™

When laparotomy is definitely indicated Previous laparotomy Pregnancy Obesity

3. CT scan is indicated in assessing retroperitoneum, solid organ injuries. It is noninvasive and highly specific. 4. Diagnostic laparoscopy (DL) is valuable method in stable abdominal trauma patient.

Treatment Emergency laparotomy. Indications for laparotomy ™™ ™™ ™™ ™™

Frank haemoperitoneum Significant diagnostic peritoneal lavage Haemodynamically unstable patient U/S or CT scan shows significant intra-­abdominal injuries

BLUNT TRAUMA OF ABDOMEN It is common in accidents. It is often missed or lately diagnosed. Ultrasound/CT abdomen or diagnostic peritoneal lavage (DPL) is useful. In many cases on clinical grounds direct exploratory laparotomy is done. Plain X-ray abdomen may show gas under diaphragm. Difficulty arises in deciding about the need for laparotomy in abdominal trauma in unconscious patients. If severity of external injury is out of proportion to the existing severe shock then exploratory laparotomy is indicated in an unconscious patient. It is also often difficult to diagnose bowel injury in such patients. If it is suspected laparotomy should be undertaken in such patients. Associated spinal injury masks the abdominal findings. Injuries may be of liver, spleen, GIT, pancreas, mesentery, vascular or diaphragm. Associated chest, pelvis, skeletal and head injuries should be remembered.

Features of Blunt Trauma xx Features of profound shock, progressive distension of

abdomen, pain, tenderness, guarding, rigidity, rebound tenderness, dull flank. xx Features specific of individual organ injury like obliteration liver dullness in bowel injury. xx Bruising of skin over the abdomen—London’s sign. xx Respiratory distress, cyanosis. xx Repeated clinical examination is a must in blunt trauma.

Evaluation Ultrasound Abdomen xx It is very useful, simpler, noninvasive method of evaluating the abdomen. Negative ultrasound means no immediate further intervention is needed and also conservative treatment can be undertaken.

Fig. 1.257: Blunt injury abdomen. Note the bruising over abdominal skin—London’s sign. xx Advantages of ultrasound: There is no danger of radiation; it can be done bedside; it can be repeated many times; it is cost-effective. Its sensitivity is 90%; specificity is 98%. Focused abdominal sonar (ultrasound) for trauma (FAST) is very useful method. xx Disadvantages: It is less useful in obesity, with interposition of gas, when fluid is less than 500 ml; retroperitoneal injuries and bowel injuries. xx Focused abdominal sonar trauma (FAST): It is rapid, noninvasive, portable bedside method of investigation focusing on pericardium, splenic, hepatic and pelvic areas. Blood more than 100 ml in cavities can be identified. It is not reliable for bowel or penetrating injuries. It often needs to be repeated.

Diagnostic Peritoneal Lavage (DPL) (by Perry) It is useful in blunt injury abdomen. It is not very useful in penetrating injury, bowel injury, retroperitoneal and pelvic injuries.

CT Scan of Abdomen It is most commonly used and better investigation for abdominal trauma. It is useful in blunt/penetrating trauma, suspected pancreas, spleen, liver, duodenal, retroperitoneal injuries. Smaller injuries, early haemoperitoneum are better detected. It is noninvasive, highly specific, highly accurate (96%), with low false-positive/low falsenegative, noninvasive.

Other Investigations a. Abdominal diagnostic paracentesis (Drapanas and McDonald): Here 18 G short bevel spinal needle is inserted into the peritoneal cavity after injecting local anaesthetic agent into the abdominal wall. With continuous suctioning through syringe, needle is passed at various sites. Positive tap means return of minimum of 0.1 ml of nonclotted blood. False-positive result occasionally can occur due to needle puncture of abdominal wall vessels. Needle should not be inserted close to previous abdominal scar as bowel may be adherent underneath the scar. Change of direction of needle is done by withdrawing the needle tip outer to peritoneum and again

Trauma puncturing the peritoneum. Puncture by 18 G needle of nondistended bowel will seal without any leakage. Peritoneal tap should be avoided if bowel is distended. Bilateral flank tap/four quadrant tap is also done with similar result. Rectus sheath haematoma and false-negative results are the problems. b. Diagnostic laparoscopy is very useful. It can be done under local anaesthesia. Haemoperitoneum, solid organ and diaphragmatic injuries are well assessed. But bowel and retroperitoneal injuries are more likely to be missed. c. Arteriography through Seldinger technique is useful in suspected cases of renal arterial injury (thrombosis/spasm); intimal tears, traumatic aneurysm and aortic occlusion (after seat belt injury) are well diagnosed with arteriography. Often it can be therapeutic also. Pelvic bleed extending into retroperitoneum is not uncommon which can be assessed by arteriography and also the bleeding vessel can be identified. But venous bleed cannot be assessed by this. d. Doppler assessment of major vessels may be beneficial especially for IVC, aorta, iliac vessels, and portal system; but with haemoperitoneum visualisation window may be poor and vessels can be better identified by contrast CT scan.

A

Management Concepts in Abdominal Trauma xx Evaluation of extent of the injury; number of organs injured and severity of injury; haematocrit assessment (haemoglobin drop up to 6 g% is tolerated well with adequate tissue oxygenation. Rapid drop of haemoglobin needs adequate number of blood to be kept ready for transfusion, like 5/10/bottles or more); central line for volume replacement; urinary catheterisation; administration of systemic antibiotics. xx Autotransfusion of blood is very useful as a life-saving procedure in such situation. Blood from the cavity is sucked out into a sterile bottle which contains 150 ml of 3.8% sodium citrate dextrose solution. This blood is strained/filtered through gauze and re-transfused. If there is colonic and small bowel injuries auto transfusion is not possible for fear of sepsis due to contamination. xx Upper midline incision extending down across the left of the umbilicus is the preferred incision. But surgeon should not be hesitant to extend the incision into the thorax or do horizontal T or extend as needed depending on the internal organ injury. xx First priority after opening the abdomen is immediate control of profuse bleeding using finger compression or mop or pressure. Later once the field is clean; area is assessed for the extent of injury without releasing the compressed finger on the bleeding site. A vascular clamp or bulldog clamp is helpful in such situation. Once it is applied over the site of bleeding, compressing finger can be removed. Vascular suturing using 4 zero or 6 zero polypropylene/resection of the tissue; reconstruction of the area; persistent pressure mop in situ with closure of the abdominal wall with an option of second look surgery in 48 hours are the different options. Individual organs are assessed and graded for injuries and managed accordingly. xx During laparotomy, entire abdomen should be inspected/palpated carefully for any additional missed injuries. Lesser sac, retroperitoneum, duodenum, pancreas and diaphragm should be checked. Often peritoneum on the margin of the duodenum and right side colon is incised, duodenum and colon is reflected medially to visualise the retroperitoneum. Pelvic structures need special attention. Rectum, urinary bladder injuries are likely to be missed if proper

B

C Figs 1.258A to C: Traumatic blunt injury abdomen causing small bowel injury which is sutured using interrupted horizontal silk sutures. attention is not given. On catheterization, if urine is clear it means urinary system is normal. Portal venous system should be assessed. xx Resection or repair should be decided later once haemostasis is maintained. Whether the injury is to the bowel or organs (liver/ spleen/kidney, etc.) resection or repair approach is decided depending on the severity of individual organ injury (based on scale or grade). xx Mesenteric tear may be the cause for haemoperitoneum. Tear may be perpendicular or parallel to the bowel. If it is perpendicular, haemostasis and approximation of the mesentery is sufficient; if it is parallel tear, then blood supply to corresponding bowel may be compromised and resection of that part of the bowel is indicated. Mesenteric haematoma is left alone if small

Only bed of thorns can give crown of roses.

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SRB's Manual of Surgery and nonprogressive. Whether there is any colour changes in the adjacent bowel should be observed. If haematoma is large; if it is progressive; if it causes compromised blood supply to the adjacent bowel, then it should be gently evacuated. Mesenteric leaf is opened using curved scissor; clot is evacuated using gentle finger dissection; bleeder is identified and ligated. If there is compromised bowel function, it should be resected. Bleeding from the major vein like superior mesenteric vein is disastrous as tear may not be localised but may be extensive; and even gentle dissection may cause more tear. It is carefully mobilised; vascular clamps are applied and repaired using 5 zero polypropylene sutures. xx Aortic clamping: Catastrophic bleeding found after opening the abdomen which cannot be controlled and bleeding with profound hypotension are the indications for aortic clamping. Profuse intraperitoneal bleed comes under control temporarily by tamponade effect of tense abdominal wall and it itself temporarily helps the patient. The moment abdomen is opened; tamponade effect is released causing further rapid bleed leading into critical catastrophe. If such event is expected prior to opening the abdomen very quick rapid thoracotomy (prelaparotomy thoracotomy) through left 5th intercostal space is done; left lung is deflated and displaced; pleura over the thoracic aorta is incised; aorta is dissected using finger; vascular clamp or soft intestinal occlusion clamp is applied to occlude the thoracic aorta. Later laparotomy is performed to go ahead with management of the bleeding. If profound bleeding is observed after laparotomy necessitating the aortic clamping, it is done by applying the clamp in infradiaphragmatic part of the aorta. Peritoneum is incised on the right of the abdominal oesophagus in infradiaphragmatic area; aorta is dissected using finger high up close to diaphragm to avoid injury to celiac plexus; clamp is applied across (infradiaphragmatic aortic occlusion). xx Usually drainage using tube drains on either side of the abdomen is used even though it is controversial. ICT should be placed if thoracotomy is also undertaken. xx Jejunostomy for enteral nutrition is ideal in all major abdominal injuries. Often gastrostomy is also done along with jejunostomy in case of duodenal and pancreatic injuries. xx Management of individual organs after grading its severity of the injury—duodenum, pancreas, liver, spleen, bowel, kidney, etc. (Please refer individual chapters for detail—highlights of individual organ injury is given below). xx Management as critical care (ICU with intensivist); multiple blood transfusions; management of sepsis, maintenance of respiration, management of electrolyte changes, treatment of renal failure, provision of nutrition, prevention of DVT, management of DIC are very essential part of postoperative treatment.

DUODENAL INJURY xx Its severity depends on the type and extent of the injury. xx It can be haematoma or lacerations. xx Lacerations can cause duodenal disruption, may be < 50% or >50% or 75% or more. xx Laceration may extend into the ampulla, distal CBD, pancreas or with duodenal devascularisation.

Management xx CT scan is more relevant investigation. xx Associated other injuries should be managed accordingly. xx Haematoma without extension is managed conser­vatively with nasogastric aspiration, antibiotics and IV fluids.

xx Lacerations are sutured surgically with a stenting or often with bypass like gastrojejunostomy. xx ERCP stenting or CBD bypass is also often required. Grading of duodenal injury Grade I – Haematoma – Laceration

Involving single portion of the duodenum. Partial thickness injury without perforation.

Grade II – Haematoma – Laceration

Involving more than one portion. Disruption less than 50% circumference.

Grade III – Laceration

Disruption of 50–75% of the circumference of 2nd part of the duodenum; disruption 50–100% of the 1st, 3rd or 4th part of the duodenum.

Grade IV – Laceration

Disruption more than 75% of 2nd part of the duodenum and involving the ampulla or distal common bile duct.

Grade V – Laceration – Vascular

Severe disruption of duodenopancreatic complex. Duodenal devascularisation.

Complications ™™ ™™

Infection, duodenal leak. Peritonitis, haemorrhage.

PANCREATIC INJURY xx It can be in the head or body and tail of the pancreas. xx It may be associated with injury to duodenum or portal or superior mesenteric veins. xx It can be contusion or severe lacerations.

Management xx xx xx xx xx

High resolution CT scan is diagnostic. Distal pancreatectomy for injuries distally. Conservative treatment is useful with antibiotics, IV fluids. Whipple’s operation or total pancreatectomy is done as a last resort. Drainage of the pancreatic bed is simple and often useful method.

Complications xx Pancreatitis, septicaemia. xx Pancreatic fistula, pancreatic abscess formation. Pancreatic injury has got high mortality (>45%).

SMALL BOWEL INJURY xx It can be blunt injury or stab injury. xx Blunt injury causes disruption of either duodenojejunal region or at ileocaecal region. xx Presentation is like haemoperitoneum or features of peritonitis. xx Monks localising zones in the abdomen signify the location of the small bowel injury. xx Presence of pattern bruising over the abdominal wall signifies the small bowel injury and its site. It is called as London’s sign.

Management xx Plain X-ray abdomen shows gas under abdomen with ground-glass appearance.

Trauma Present with features of haemorrhagic shock, dis­tension of the abdomen, tenderness, rebound tenderness, guarding, rigidity. ™™

CT is diagnostic tool

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Liver injury is graded depending on involvement of hepatic veins, portal system, biliary system and duodenum

™™

Often high grade liver injury also can be managed nonoperatively

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Push (direct compression); Pringle (occluding portal triad at foramen Winslow with fingers temporarily); plug by embolisation; pack the liver bed; repair of vena cava or portal vein; stenting of biliary tree and hemihepatectomy—are the treatment strategies

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Management xx Small tear is sutured. For larger tears:  Deep sutures.  Packing.  Debridement.  Haemocoagulants. xx Liver resection is not done (not advisable) usually for injuries. xx Pringle manoeuvre—by compressing the porta near foramen Winslow—to control bleeding (not more than 30 minutes). xx Blood transfusions. xx Treatment of associated injuries like of diaphragm, lung, duodenum, colon. xx Antibiotics.

B Figs 1.259A and B: Assault causing stab injury abdomen. On opening the abdomen, multiple perforations were found in the small bowel and was sutured. Patient recovered well. xx Ultrasound abdomen is useful. xx Laparotomy and closure of the perforation if it is small. xx In presence of extensive bowel injury or multiple injuries, resection and anastomosis is done. xx Any associated injuries should be dealt with accordingly.

COLONIC INJURY xx Left sided injury is treated with proximal colo­stomy with closure of the wound if it is small, or resection and anastomosis if it is wider area. Closure of colostomy is done at later stages after 3–6 months. xx Small wound over right-sided colon can be sutured primarily. xx Ileostomy alone or ileostomy with ileo-transverse anastomosis or right hemicolectomy with ileostomy is indicated in following situations:  Extensive peritoneal contamination.  Colonic vascular injuries.  Haemodynamically unstable patients.  Long-term hypotension after trauma.

LIVER INJURY It can be subcapsular haematoma, lacerations, deeper injuries, lacerations with disruption of hepatic lobes or segments or liver injury with vascular injuries like of inferior vena cava or hepatic veins.

Complications of Liver Injury xx Haemorrhage, septicaemia, bile leak. xx Liver failure, haemobilia. xx Subphrenic abscess, CBD stricture.

SPLENIC INJURY It can be subcapsular haematoma, laceration or hilar injury. It can be associated with other organ injuries like left kidney, left lobe of the liver, splenic flexure of the colon or pancreas. It can cause torrential haemorrhage and shock. It is the most common organ injured in blunt injury abdomen.

Management xx Ultrasound abdomen, diagnostic peritoneal lavage are the investigations. xx Blood transfusions. xx Splenorrhaphy is done in selected patients so as to save the spleen. xx Splenectomy. xx Management of associated injuries.

Complications of Splenectomy xx xx xx xx xx

Left lung atelactasis. Overwhelming postsplenectomy infection (OPSI). Pancreatitis and pancreatic fistula. Gastric bleeding. Subphrenic abscess.

What we need is cup of understanding, barrel of love and an ocean of patience.

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SRB's Manual of Surgery RENAL INJURY xx It is commonly managed conservatively. xx IVU is the investigation of choice in renal injury. xx Surgery is indicated when there is hilar injury, progressive bleeding, failure of conservative treatment or perinephric abscess formation.

URINARY BLADDER INJURY Intraperitoneal bladder injury occurs in distended bladder. It is treated always by surgical exploration through transabdominal approach. Bladder tear is sutured with keeping a suprapubic cystostomy using Malecot’s catheter. Extraperitoneal injury can be treated conser­vatively by placing a Foley’s catheter for 2–3 weeks.

ABDOMINAL COMPARTMENT SYNDROME Abdominal compartment syndrome (ACS; Richards and Krons, 1984) is organ dysfunction caused by increased intra-abdominal pressure more than 12 mmHg (intra-abdominal hypertension/ IAH); organ dysfunction is usually respiratory, cardiovascular and renal but can be any organ; normal intra-abdominal pressure is being considered as 2–7 mmHg. Abdominal perfusion pressure (APP) is the pressure which maintains adequate abdominal blood flow. It is measured by subtracting the intra-abdominal pressure (IAP) from mean arterial pressure (MAP). APP in ACS is usually less than 60 mmHg but should be maintained as more than 60 mmHg.

Effects

xx Retroperitoneal haemorrhages, pancreatitis. xx Laparoscopic procedures. xx Morbid obesity, pregnancy, major burns, continuous ambula-

tory peritoneal dialysis are precipitating causes.

Features and Diagnosis xx Tensely distended abdomen, progressive oliguria, airway

obstruction, occult blood loss. xx Measurement of urinary bladder pressure: Transducer

and manometer methods are available. Bladder acts as a passive reservoir at volume less than 100 ml (now 25 ml saline is used to measure) and it can transmit IAP without imparting any additional pressure from its bladder musculature. Measurement of bladder pressure reflects the IAP pressure. IAP is measured using a urinary catheter in the urinary bladder. Pressure is graded (Burch) as: I—10–15 cm of H2O (will not require decompression); II—16–25 cm of H2O (needs close monitoring); III—26–35 cm H2O (most need decompression); IV—more than 36 cm H2O (all need decompression otherwise will die of cardiac arrest in few hours). Beyond grade III immediate decompression is needed. Initial volume preload is essential otherwise sudden decompression may cause cardiac arrest in asystole due to reduced preload, sudden influx of high potassium, acid and other metabolic by products into the heart. Grade III and IV becomes a surgical emergency. xx Chest X-ray, ECG monitoring, ICU care, electrolytes, haematocrit and serum creatinine estimation, USG abdomen should be done. xx Mortality for ACS is 40%.

xx Cardiovascular system: It is often sudden, rapidly progres-

sive, decreasing the venous return (due to IVC compression) to heart and increasing peripheral resistance, with decreased right atrial pressure and decreased cardiac output. xx Respiratory system: Intrapleural pressure is increased proportionately to the abdominal pressure. Upward displacement of the diaphragm, increased peak inspiratory pressure, hypoxia, hypercapnia, acidosis, respiratory failure, ARDS are other problems. It also causes restrictive lung disease. xx Renal system: Decreased renal blood flow and glomerular filtration causes oliguria, renal failure. xx Gastrointestinal system: Mesenteric venous hypertension; bowel wall oedema and ischaemia. xx Central nervous system: Cerebral oedema and hypoxia, unconsciousness.

Causes xx Major abdominal trauma, postoperative haemorrhages, after

damage control surgery with abdominal packings, are the common causes; ruptured aortic aneurysm. xx Closure of the abdomen under tension; forcible reduction of the massive hernia. xx Bowel wall oedema, mesenteric congestion, acute ascites; profound hypothermia and coagulopathy. xx Acute gastric dilatation, paralytic ileus, gastroparesis, colonic pseudo-obstruction.

Intraabdominal pressure grading

Burch grading in cm of water

World Society of the ACS in mm of Hg (Muckart et al., and Malbrain et al.)

I

10–15 cm of H2O

12–15 mmHg

II

15–25 cm of H2O

16–20

III

25–35 cm of H2O

21–25

IV

>35

≥25

Abdominal compartment syndrome (ACS) Causes Multiple trauma and ICU patients— common Postoperative ileus Acute abdomen Acute gastric dilatation Laparoscopic procedures Intestinal obstruction Major burns

Features Hypoxia, hypercarbia Decreased urine output – anuric renal failure in severe cases Tense abdomen— distended Decreased venous return Refractory hypoxaemia in severe cases Bowel ischaemia Cardiac arrest

Management Bladder pressure assessment Ryle’s tube aspiration Hypotension Resuscitation ICU care Surgical decompression

Trauma Treatment xx Abdominal decompression is the only ideal treatment for

ACS; technique and timings are decided based on the clinical situation. xx Temperature and coagulation profile should be made as possible as normal prior to decompression. xx Silastic sheet created chimneys sutured to fascia around is often used. Pressure free abdominal closure should be the target. Bogota bag, first described by Londoni, chief resident in Bogota, Columbia is cost effective; here irrigation bags are sutured to each other as necessary to get a proper size and is sutured to fascia around using 1 zero nylon suture. Several litres of serosanguineous or ascitic fluid are let out through a plastic stoma bag attached to a closed drainage system. Once patient is haemodynamically stable, definitive closure is performed after 48 hours. Abdominal fascia is closed using nonabsorbable sutures; subcutaneous tissue and skin are closed at a later period. Fluid and electrolyte management, antibiotics, adequate blood or blood product transfusions should be used as needed. xx Other methods of closure: Towel clips, temporary mesh placement; PTFE mesh repair; vacuum assisted closure are all temporary closure methods. Definitive closure methods

– Primary closure of fascia; closure using synthetic mesh if no sepsis in the wound; biological mesh closure; component separation technique; closure using skin graft or flaps.

SEAT-BELT INJURIES xx In an individual with seat-belt, during impact, violent deceleration of human body occurs. Seat-belt impinges heavily on its point of contact with trunk and viscera continue to move forward. It leads into severe contusion of abdominal contents; detachment of bowel from its mesentery due to free forward rapid mobility of the bowel over a relatively fixed mesentery. Solid organ injury occurs only occasionally. xx Two point anchorages causes’ solid organ injuries like of liver/ spleen. Lap-belt causes contusion and bowel injury commonly. xx It is often difficult to identify the injuries due to presence of more obvious other injuries. CT chest and abdomen, diagnostic peritoneal lavage (DPL) are very useful. xx Petechiae around iliac crest or costal margin are signs wherein one can suspect seat-belt injuries. xx Distraction fracture of lumbar spine (chance fracture) with hyperaesthesia of T12 and L1 level is often associated. 10% of such fractures are associated with intra-abdominal injuries. xx Treatment is immediate laparotomy and proceed—bowel suturing/ resection/suturing of the organ injuries/splenorrhaphy/splenectomy.

Happiness is not destination, it is a manner of travelling.

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K. Hand and Foot CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Hand Hand Infections Acute Paronychia Chronic Paronychia Apical Subungual Infection Terminal Pulp Space Infection Infection of Web Spaces Deep Palmar Space Infection Space of Parona Infection Acute Suppurative Tenosynovitis

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Compound Palmar Ganglion Orf Milker’s Nodes/Nodules Hand Injuries Dupuytren’s Contracture Volkmann’s Ischaemic Contracture Syndactyly Mallet Finger Heberden’s Nodes Spina Ventosa

HAND Surgical Anatomy of the Hand Flexor Retinaculum xx It extends medially from pisiform and hook of hamate, laterally to scaphoid tubercle and trapezium crest as a strong fibrous band so as to bridge carpus to create a carpal tunnel. xx Ulnar nerve and vessels, palmar cutaneous branches of median and ulnar nerves, palmaris longus muscle are superficial to the carpal tunnel. xx Median nerve, tendons of flexor digitorum superficialis, profundus and pollicis longus, radial and ulnar bursa are deep to flexor retinaculum.

Palmar Aponeurosis It is a thickened, modified deep fascia in the palm with its apex pointing proximally (as continuation of palmaris longus) and base distally which in turn gets divided into four parts. They extend over deep transverse ligament into lumbrical tunnel.

Blood Supply of the Hand xx Superficial palmar arch is mainly formed by ulnar artery and completed by superficial palmar branch of radial artery. It gives four digital branches to medial three fingers. xx Deep palmar arch is formed by radial artery and is completed by deep branch of ulnar artery. It gives three palmar metacarpal arteries which communicate with superficial palmar arch. It also gives communicating, perforating branches to dorsal metacarpal arteries.

Muscles of the Hand xx Thenar muscles: Abductor pollicis brevis, flexor pollicis brevis, opponens pollicis and adductor pollicis. xx Hypothenar muscles: Palmaris brevis, abductor digiti minimi, flexor digiti minimi and opponens digiti minimi.

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Foot Callosity Corn Plantar Fasciitis Ingrowing Toe Nail Onychographosis Onychomycosis Athlete's Foot Hallux Valgus

xx Lumbricals are four in number—named from lateral to medial. xx Four palmar interossei. xx Four dorsal interossei.

Nerve Supply xx Abductor pollicis brevis, flexor pollicis brevis, opponens pollicis and 1st and 2nd lumbricals are supplied by median nerve (5 muscles). xx Rest of the muscles in hand are supplied by ulnar nerve (15 muscles).

Modified Verdan Zone System in the Hand (Tendon Zones) Zone I From the fingertip up to the attachment of flexor digitorum superficialis (middle of middle phalanx). It contains tendon of flexor digitorum profundus.

Zone II It begins proximal to metacarpophalangeal joint at distal palmar crease and extends up to the attachment of flexor digitorum superficialis at the middle of the middle phalanx. It is called as “No-Man’s-Land.” Here flexors are tightly enclosed within a fibro-osseous tunnel. It is the most dangerous zone in hand injuries (critical zone).

Zone III It begins at the distal end of flexor retinaculum (base of the palm) and ends at the transverse crease of the palm. It contains lumbricals attached to flexor digitorum profundus.

Zone IV It begins at the proximal end of the flexor retinaculum and ends at its distal end.

Hand and Foot Zone V It extends from the proximal end of flexor retinaculum up to distal third of the forearm.

Fig. 1.262: Infection of finger at middle phalanx level. Note the oedema and position of the finger. Precipitating causes ™™ ™™ ™™ ™™ ™™ ™™

Diabetes Immunosuppression Trauma HIV infection Steroid therapy Vascular diseases

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Staphylococcus aureus—most common – 90% Streptococcus Gram-negative organisms like E. coli, Klebsiella, Pseudomonas Occasionally fungal infection causing chronic paronychia, Madura hand due to Nocardia group of fungi, viral infection like orf can occur

Common organisms

Fig. 1.260: Anatomy of flexor retinaculum and palmar aponeurosis.

General Features of Hand Infection xx Infection spreads faster in all areas. xx Causes oedema over the dorsum of hand due to lax skin

and more lymphatic network even though infection per se is more over the volar aspect. It looks like frog hand. xx Restricted movements of fingers and hand. The hand functions like hook, pinch, grip, grasp are lost. xx Severe pain and tenderness, with fever. xx Tender palpable axillary lymph nodes are often present.

Different Types of Hand Infections

Fig. 1.261: Modified Verdan zone system in the hand.

HAND INFECTIONS xx Hand is a compact actively functioning unit. It contains

neurovascular bundles, muscles, bones and ligaments. xx Infection may be due to minor injuries or blood borne.

xx xx xx xx xx xx xx xx xx xx

Acute paronychia. Chronic paronychia. Terminal pulp space infection (felon). Subungual infection. Web space infection. Mid-palmar space infection. Thenar space infection. Deep palmar abscess. Acute suppurative tenosynovitis. Chronic tenosynovitis of flexor tendon sheath of palm and forearm—compound palmar ganglion. xx Lymphangitis of the hand. xx Arthritis of hand joints. xx Subcuticular abscess Hand infection can be superficial or deep; it can be localised or spreading.

An ounce of action is worth a ton of theory.

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SRB's Manual of Surgery

A

C

D

B

E

F Figs 1.263A to F: Different types of hand infections. Note the oedema of hand even on dorsal aspect. Small infective focus can aggravate rapidly and so early proper drainage from deeper plane is important in managing the hand infections. Often it may cause extensive destruction exposing the tendons.

Investigations xx xx xx xx xx

Pus for culture and sensitivity. Blood sugar. Urine sugar and ketone bodies. X-ray of the part. Arterial Doppler of the hand if needed.

General Principles of Managing Hand Infections xx Antibiotic therapy. xx Position of rest with wrist slightly abducted and extended,

thumb and index fingers away (glass-holding position). Position of function is in which thumb and index fingers are pinching firmly with wrist extension.

Hand and Foot

Fig. 1.264: Hand positions.

Fig. 1.267: Infection of little finger with dorsal oedema.

A

Fig. 1.268: Hypertrophic scar and keloid in hand and forearm after burn contracture.

B Figs 1.265A and B: Hand positions in immobilisation and function.

adequate length and adequate depth (deep to palmar fascia, otherwise evacuation of pus is inadequate). Care should be taken not to injure neurovascular bundles. Pus should be sent for culture and sensitivity. Slough, if present should be excised thoroughly. Gauze drain is placed. Regular dressings are done with conti­nuation of antibiotics. Communi­cations into other areas of hand should also be drained. xx Bloodless field (using tourniquet) is better to drain pus from hand. xx Proper measures must be taken after treatment. Initial rest, elevation of hand and later proper physiotherapy and regular exercise of hand and fingers are encouraged to restore normal function. Complications of hand infections Stiffness of digits and hand (ankylosis) Deformity and disability Bacteraemia and septicaemia Osteomyelitis of bones depending on the location of abscess like metacarpal bones, terminal phalanx ™™ Suppurative arthritis of joints ™™ Paralysis of median nerve ™™ ™™ ™™ ™™

Fig. 1.266: Hand infection. Infection of ring finger extending into the palm. xx Elevation of hand reduces the oedema, increases perfusion,

promotes healing. xx Early recognition of localised pus. Once localised, Incision

and Drainage is done ideally under general anaesthesia or regional block (not local anaesthe­sia). Draining incision should not cross the palmar crease. Incision should have

Remember Hand should be flexible and strong; sensitive and pain free and coordinated to show all fine and powerful functions ™™ Pinch (picking a small object); power grip (holding a hammer); key grip (holding a key); chuck grip (holding a pen); hook grip (carrying a bag)—are the functions of hand ™™

Contd...

Early signs of Volkmann’s contracture are pain, pallor, puffiness, pulselessness and paralysis. —David L Griffiths

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SRB's Manual of Surgery Contd... Hand should be properly examined clinically for tendon functions; neurological problems—sensations (sweat test, two point discrimination test); for circulation (Allen’s test); joint movements; examination of entire upper limb; opposite hand; axillary lymph nodes and other relevant systemic examinations ™™ Nerve conduction studies; electrophysiology; MRI hand; radioisotope bone scan; selective angiograms; X-ray hand are the relevant investigations other than systemic investigations ™™ Principles of treatment—elevation to reduce oedema; splintage to prevent contracture; early movements once inflammation subsides; early exploration of wound or surgical drainage of infective area; regional anaesthesia; usage of tourniquet; incisions when done across the flexor creases, should be at 45° angle ™™

A

ACUTE PARONYCHIA xx xx xx xx xx

It is the most common hand infection. It occurs in subcuticular area under the eponychium. Minor injury to finger is the common cause. Suppuration occurs very rapidly. It tracks around the skin margin and spreads under the nail causing hang nail or floating nail. xx Organisms are Staphylococcus aureus and Streptococcus pyogenes. xx Quantity of pus is very less around 0.5 ml but it should be drained to relieve sympotoms.

B

Clinical Features

Figs 1.270A and B: Paronychia showing pointing pus in one picture and sloughed area granulating in another picture.

Severe throbbing pain and tenderness (dependent throbbing) with visible pus under the nail root. Nail on touch is very tender (paronychia means “Run around”).

xx Analgesics. xx The pus is drained by making an incision over the eponychium.

Treatment xx Pus is sent for culture and sensitivity. xx Antibiotics like cloxacillin, amoxicillin.

Digital block using xylocaine 2% plain (without adrenaline as end artery supply to digits can develop arterospasm) is given as anaesthesia. xx If there is a floating nail, then the nail is dead and it has to be removed. xx Recovery is fast.

CHRONIC PARONYCHIA It is commonly due to fungal infection—due to candida infection commonly.

Features A

xx xx xx xx xx xx

It is common in females. Nail is diseased with ridges and pigmentation. Itching in the nail bed. Recurrent pain, discharge Secondary bacterial infection may supervene. Investigation: Culture of scrapings for fungus and other causative agents.

xx Treatment  Long-term antifungal therapy—local and systemic.  Antibiotics for secondary infection.  In severe cases removal of nail is required.

B Figs 1.269A and B: Pointing pus in acute paronychia. Quantity of pus is very less usually around 0.5 ml.

APICAL SUBUNGUAL INFECTION xx It is infection of the space between subungual epithelium and the periosteum.

Hand and Foot xx It occurs after minor trauma or rarely after formation of subungual haematoma. xx Beneath the free edge of the nail, pus comes to the surface. xx Excruciating tenderness with small visible pus under the tip (summit) of the nail is the feature. xx Drainage with ‘V’ incision over the summit is the treatment along with antibiotics. xx Osteomyelitis is not common.

Fig. 1.272: Anatomy of the terminal pulp space.

Fig. 1.273: Pulp space infection. Fig. 1.271: Apical subungual infection and pus formation. Note the ‘V’ shaped incision to drain the same.

TERMINAL PULP SPACE INFECTION (FELON) xx It is the second most common hand infection (25%). xx Index and thumb are commonly affected. xx Usually by a minor injury like finger prick.

Surgical Anatomy xx Terminal pulp space contains fat and is partitioned by septae which is attached from periosteum of terminal phalanx to skin. xx Proximally deep fascia is attached to the periosteum distal to the base of terminal phalanx, i.e. distal to the attachment of flexor tendon. xx So, terminal space is a closed compartment, as the result of which pressure increases when there is infection, compressing terminal artery leading to thrombosis, resulting in osteomyelitis of terminal phalanx.

Bacteria xx Staphylococcus—most common. xx Streptococcus, Gram-negative organisms.

Clinical Features xx Pain, tenderness, swelling in the terminal phalanx. xx Fever. xx Tender axillary lymph nodes.

Often suppuration is severe, forming collar stud abscess which eventually may burst.

Fig. 1.274: Incision for pulp space drainage.

Causes of collar-stud abscess ™™ ™™ ™™

Tuberculous cold abscess Terminal pulp space infection (Felon) Deep palmar space infection

Investigations xx X-ray of the part is required often to rule out osteomyelitis

of terminal phalanx. xx Pus for culture and sensitivity.

Treatment xx Antibiotics and analgesics. xx Drainage of terminal pulp space by an oblique deep incision. xx If there is osteomyelitis of the terminal phalanx, it has to

be amputated.

Dupuytren’s contracture typically affects the ring finger and years later the little finger becomes implicated. In 30% cases little finger is primarily affected. —Peter F Early

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SRB's Manual of Surgery Complications

Treatment

xx Osteomyelitis of the terminal phalanx. xx Pyogenic arthritis of distal interphalangeal joint and teno-

xx Elevation of hand. xx Antibiotics and analgesics. xx Drainage under regional or general anaesthesia. A horizontal incision is placed on volar skin of the web and deepened to reach the space by dividing fibres of palmar fascia. Pus is drained and sent for culture and sensitivity. If other web spaces are involved they should be drained through a separate incision. Edges of the wound are cut to leave a diamond shaped opening in front. Often counter-incision over dorsal skin of web is needed.

synovitis of flexor sheath.

xx Septicaemia—in immunosuppressed individuals.

INFECTION OF WEB SPACES Surgical Anatomy There are three triangular web spaces filled with fat between the dorsal and volar skin. When the space is filled with pus it straddles the deep transverse ligament. Even though pus is volar, it points out dorsally. Infection of originates from: xx Abrasion. xx Infection of proximal volar space of finger. xx Callosities. xx Infection of proximal spaces. xx Trauma. xx Spread from other palmar spaces and from flexor sheaths through lumbrical canal.

DEEP PALMAR SPACE INFECTION Surgical Anatomy

Bacteria xx Staphylococcus. xx Streptococcus. xx Gram-negative organisms.

A

Clinical Features xx xx xx xx xx xx

Fever. Pain and tenderness. Oedema of dorsum of hand. Maximum tenderness is on the volar aspect. ‘V’ sign—separation of fingers. If untreated, infection may spread into other web spaces and hand spaces. B

C Fig. 1.275: Incision for web space drainage.

Figs 1.276A to C: Anatomy of palmar spaces of the hand and forearm. Midpalmar space is on the medial aspect; thenar space is on the lateral aspect. Space of Parona is on the lower forearm.

Hand and Foot Two deep palmar spaces are present xx Midpalmar space. xx Thenar space. Midpalmar space is bound in front by palmar aponeurosis, behind by medial three metacarpals, laterally by a vertical line from lateral margin of the middle finger. It contains flexor tendons, neurovas­cular bundles and lumbricals. It is the common site of the infection. Thenar space is located anterior to lateral two metacarpals. Infection here is usually due to extension from midpalmar space.

Midpalmar Space Infection Causes xx xx xx xx

Trauma. Spread from infection of finger spaces and web spaces. Haematogenous spread. Spread from tenosynovitis.

Clinical Features xx xx xx xx

Pain and tenderness in the palm. Oedema of dorsum of hand (frog hand). Loss of concavity of palm. Painful movement of metacarpophalangeal joint (but interphalangeal joint movements are normal and painfree). xx Fever. xx Palpable tender axillary lymph nodes. xx Eventually pus may come out of palmar aponeurosis forming collar stud abscess and later sinus formation. X-ray of the part is required.

Treatment xx Elevation of the affected limb. xx Antibiotics and analgesics.

Fig. 1.277: Incisions to drain midpalmar space infection.



xx Drainage: It is drained under regional/general anaesthesia by placing horizontal/oblique incision parallel to the palmar crease. One should avoid crossing the crease line as much as possible. Palmar aponeurosis is carefully incised vertically to avoid injury of the neurovascular bundles. Alternatively one of the interdigital web spaces is incised horizontally; lumbrical canal (3rd or 4th) is opened to reach the deep palmar space. Pus is drained and sent for culture and sensitivity. Thorough saline irrigation is very essential. Drain is placed through the wound. Complications Osteomyelitis of metacarpals Stiffness of hand ™™ Suppurative arthritis ™™ Extension of infection into other spaces ™™ ™™

Thenar Space Infection xx Thenar space (triangular shape) is located anterior to the lateral two metacarpals and fascia over transverse head of adductor pollicis; behind the short muscles of thumb, flexor tendons of index finger and 1st and 2nd lumbricals. Thenar muscles and flexor pollicis longus are lateral to it; fibrous vertical septum from palmar aponeurosis to 3rd metacarpal bone is medial to it. It is on the outer half of the hollow of the palm. Proximally it extends from flexor retinaculum; distally it extends to transverse palmar crease. It communicates to fascial sheath of 1st lumbrical. It is often associated with midpalmar space infection. xx It is drained similarly by placing incision on the lateral aspect of the palm or through the first web space incision is done along the first lumbrical canal on the radial side of the index finger. Often incision is made parallel to cleft between index and thumb on the posterior aspect. xx In some patients, thenar space infection may spread distally to the first web and then dorsally over the first dorsal interosseous muscle, referred to as a pantaloon abscess. In such situation an additional counter incision over the dorsal aspect of the hand is needed while draining.

Fig. 1.278: Incision and drainage of thenar space abscess.

When a hand is seriously inflamed it takes up the position of greatest ease, which is, in fact, the position of rest. — Frederic Wood Jone

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SRB's Manual of Surgery SPACE OF PARONA INFECTION Forearm space of Parona is a rectangular space situated in the lower part of the forearm above the wrist, in front of pronator quadrates and deep to long flexor tendons. Above it extends up to oblique origin of flexor digitorum superficialis, below up to flexor retinaculum communicating with midpalmar space. Flexor tendon sheath proximally extends into this space. Pus in this space is drained through lateral incisions in the lower part of the forearm.

ACUTE SUPPURATIVE TENOSYNOVITIS It is the bacterial infection of flexor tendon sheaths.

Surgical Anatomy

Kanavel signs ™™ ™™ ™™ ™™

Swollen finger held in flexion Exquisite pain on passive extension Tenderness precisely over the tendon sheath Area of greatest tenderness over the part of ulnar bursa lying between transverse palmar creases

xx In infection of radial bursa thumb is swollen with pain and

tenderness over the sheath of the flexor pollicis longus and there is inextensibility of interphalangeal joint. xx Swelling just above the flexor retinaculum is common.

Treatment

xx Radial bursa is synovial sheath of flexor tendon of thumb which extends to the digit. xx Ulnar bursa is synovial sheaths of medial four flexor tendons of hand which extends into the digit of the fifth (little) finger.

A

Fig. 1.279: Bursae hand. xx Extensor tendons are devoid of sheaths. xx Radial and ulnar bursa communicate with each other in 80% of cases.

Common bacteria: xx Staphylococcus aureus, Strepto­coccus pyogenes.

Clinical Features Symmetrical swelling of entire finger. Flexion of finger—Hook sign. Severe pain on extension. Tenderness over the sheath. Oedema of whole hand, both palm and dorsum (due to lymphatic spread). xx As ulnar bursa extends into the little finger its infection results in pain and tenderness extending up to little finger but not much to other fingers. xx xx xx xx xx

B Figs 1.280A and B: Suppurative tenosynovitis is drained through incision at proximal part and another at digital sheath. Often by placing fine polythene catheter into the sheath, saline wash is given into the area.

Hand and Foot xx xx xx xx

Elevation of the affected limb. Antibiotics and analgesics. Position of rest. Drainage under general anaesthesia. Incisions are placed over the site of maximum tenderness and flexor sheath should be opened up. Many a times multiple incisions are required.

It is drained through two incisions—one over the proximal part of the sheath; other over the distal part of the sheath in the digit—along the crease lines. A fine catheter is passed into the sheath from proximal incision and irrigated with normal saline through this catheter. This catheter is left in situ for further regular irrigations, splinting of hand is necessary with boxing glove dressing.

xx xx xx xx

MILKER’S NODES/NODULES (Milkmaid Blisters)

Complications ™™ ™™ ™™ ™™ ™™ ™™

Spread of infection proximally into forearm—to space of Parona Stiffness of fingers and hand Suppurative arthritis Osteomyelitis Median nerve palsy Bacteraemia and septicaemia

COMPOUND PALMAR GANGLION xx It is chronic tenosynovitis of flexor tendon sheaths due to tuber-

culosis (tuberculous tenosynovitis) or rheumatoid arthritis. xx It can be unilateral or bilateral.

Pathology xx Flexor tendon sheath on either side of the wrist is involved, i.e. both in the volar surface of palm and lower forearm. xx Swelling contains fluid with typical melon seed bodies. xx Condition is often bilateral in case of rheumatoid arthritis.

Features xx Swelling in the palm and lower forearm which is smooth,

soft, nontender, fluctuant and also cross-fluctuant across flexor retinaculum, nontransillu­minating. xx Wasting of hand and forearm muscles are seen. xx Matted axillary lymph nodes may be palpable. xx Primary focus may be present in lungs. xx Investigations:  ESR, chest X-ray.  FNAC of axillary lymph node and swelling itself.

ecthyma contagiosum or thistle disease or scabby mouth caused by a parapox virus infection. Contracted via direct contact with infected sheep or goats or fomites with orf virus. Human-to-human transmission is not known. It causes a purulent-appearing papule locally and generally without systemic symptoms. Infected locations can include the finger, hand, arm, face and even the penis. It may become progressive and life threatening in immunocompromised host. Treatment—1% cidofovir in progressive disease.

xx It is cutaneous condition caused by Paravaccinia virus; transmitted from udders of infected cows. xx Disease in humans is nearly identical to Orf. xx Usually has got self-limiting course, running from 14–72 days, with infrequent systemic symptoms and little or no scarring.

HAND INJURIES Classification xx Tidy injuries: They are clean incised wounds and are usually treated by primary suturing but depends on the tissues involved like nerves, tendons and muscles. xx Untidy injuries: They are lacerated wounds. Treated by debridement and later by delayed primary or secondary suturing. xx Compartment injuries. xx Degloving injuries xx Indetermined injuries which could not be assessed.

Assessment of Injury It should include: Number, extent, depth, deformity and disability, neurovascular injuries, tendon injuries, muscle injuries bone and joint injuries.

Treatment xx Start antituberculous drugs: INH, rifampicin, ethambutol

and pyrazinamide for 9 months.

xx Excision of flexor tendon sheath is done along with scraping

of caseating material, tubercles, melon seed bodies. xx Care should be taken not to injure median and ulnar nerves.

ORF xx It is a rare, benign, self-limiting exanthematous disease, also known as contagious pustular dermatitis or infectious labial dermatitis or

A

B Figs 1.281A and B: Indeterminate and untidy hand injuries.

Disease is the fate of poor, but also punishment of rich.— Ivo Andrick

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Fig. 1.282: Hand injury exposing tendons. Note the marker stitch in the tendon. It needs local transposition flap or groin flap to cover. Skin grafting is not possible over tendons.

Fig. 1.285: Hand injury which is healing but with severe deformity of fingers.

Fig. 1.283: Stuck finger by a ring. It is removed by applying soap, fat, and wax. String method is winding and unwinding a thread under and across the stuck finger. Sawing is done only when every method fails.

Fig. 1.286: Typical deformity of finger which needs correction for proper function.

xx Antibiotics and antitetanus treatment (toxoid and antitetanus

globulin).

xx Primary suturing if it is a incised wound or delayed primary

suturing if there is odema. Skin grafting or flaps for skin loss. Tendon suturing or tendon graft for tendon injuries. Rest and elevation of the affected parts. Management of fractures by splint, wiring. Nerve repair for nerve injuries. Immobilisation up to 21 days. Later physiotherapy with warm, exercise, was bath active movements. xx Microsurgical restoration of digits. Reimplantation of the digits. xx Amputation of digits or metacarpals only when inevitable. xx xx xx xx xx xx xx

Fig. 1.284: Avulsion injury of finger causing raw area.

Principles of Treatment xx Haemostasis. xx Use of tourniquet. xx Wound debridement and cleaning.

Primary repair of tendons and nerves are of lesser priority in untidy injuries. Priority is wound debridement/wound excision and early skin cover. Cut ends of nerves and tendons are tagged with coloured stitches for future identification purpose.

Hand and Foot In hand Do’s

Don’ts

Do examine hand carefully

Do not incise every infected digit

Do think of other diagnosis

Do not make puncture incisions or over pads

Do wait for abscess to localise

Do not injure the digital nerves or vessels

Do place adequate length and depth of incisions

Do not place incisions crossing the crease line

Do immobilise, elevate the hand

Do not close human bites or lacerated wounds

Do give antibiotics and proper dressings

Do not forget to send pus for culture and sensitivity

Complications and morbidity of hand injuries ™™ ™™ ™™ ™™ ™™

Infection Osteomyelitis Arthritis of joints Stiffness Loss of function due to disability

DUPUYTREN’S CONTRACTURE Individuals pre-disposed to the affection we are describing, observe that it is more difficult to extend the fingers of the affected hand… The first (interphalangeal joint) is flexed at nearly a right angle…the most powerful efforts are insufficient to extend it…. Hence, it was natural to conclude, that the commencement of the disease was in the unusual tension of the palmar aponeurosis. —Guillaume Dupuytren, 1833

A

It refers to localised thickening of palmar aponeurosis and later formation of nodules with severe permanent changes in metacarpophalangeal and proximal interphalangeal joints. Terminal interphalangeal joint is not involved as palmar aponeurosis does not extend to terminal phalanx. It is common in males (10:1). xx It starts in ring and little fingers, with flexion of ring and little fingers. Later involving all fingers. xx There is thickening and nodule formation in the palm with adherent skin. xx It is often familial and bilateral 45%. xx Pads (of fat) develop in knuckles and are called as Garrod’s pads (in proximal IP joints). Conditions often associated with ™™ ™™ ™™ ™™ ™™

Plantar fasciitis 5%—Ledderhose’s disease Mediastinal and retroperitoneal fibrosis Peyronie’s disease of penis 3% Nodules in the face and ear Pellegrini-Stieda’s disease

B Figs 1.287A and B: Dupuytren’s contracture in the hands. Note the involvement of the ring finger. Note the fibrous band on the other hand as early finding. Galezia triad

Aetiology xx xx xx xx xx xx

Repeated minor trauma, use of vibrating tools. Cirrhosis, alcoholism, smoking, Epileptics on treatment with phenytoin sodium. Diabetics, pulmonary tuberculosis, AIDS. Other metabolic conditions. Familial—autosomal dominant.

™™ ™™ ™™

Dupuytren’s contracture Retroperitoneal fibrosis Peyronie’s disease of penis

Complications xx Restriction of hand function and so disability. xx Arthritis of MCP and proximal IP joints.

“Impossible” is a word found only in the dictionary of fools.—Napoleon

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SRB's Manual of Surgery Treatment xx Fasciotomy of palmar aponeurosis and later physio­therapy,

Z plasty.

xx In severe cases fasciectomy partial or complete. xx Treatment of the cause.

Recurrence can occur in 5–50% cases.

xx Pallor. xx Puffiness (due to oedema). xx Pulseless (absence of radial pulse; but its presence does not

rule out the onset of impending contracture). xx Paresis.

Late phase: Deformity Deformity (due to injury to median nerve): xx Wrist joint extended. xx Extended metacarpophalangeal joints. xx Flexed interphalangeal joints. Volkmann’s sign: In early stage, the fingers can be extended at the interphalangeal joints, only when the wrist is flexed fully. The fingers tend to flex if any attempt to extend the wrist is made.

Treatment

Fig. 1.288: Z plasty done for Dupuytren‘s contracture.

In acute phase: xx Removal of plastic cast applied after fracture reduction. xx Correction of fracture. xx Exposure of brachial artery and application of 2.5% papaverine sulphate to relieve the spasm if any. xx Suture of arterial tear if present, often with placement of arterial graft. xx Lateral incision over the deep fascia of forearm is placed to decompress the oedema. In late phase (once deformity occurs):

VOLKMANN’S ISCHAEMIC CONTRACTURE It is a vascular injury leading to muscular infarction and subsequent contracture.

Causes xx xx xx xx xx

Supracondylar fracture of the humerus. IV chemotherapy. Burns. Closed forearm crush injuries. Tight plaster after reduction of fracture.

Pathogenesis Injury of brachial artery (tear, contusion, spasm, compression)

xx Physiotherapy xx Dynamic splints. xx Max-Page operation: Release of flexor muscles (forearm muscles) from their origins from the bone and allowing it slide down until full extension. xx Excision of fibrous tissue and damaged muscles along with tendon transfer. xx Arthrodesis.

SYNDACTYLY It is webbing or fusion of fingers.

Causes xx Congenital and hereditary—common. xx Traumatic like burns.

Types Results in infarction Injury to median nerve of forearm flexor (mainly) and ulnar nerve muscle both by ischaemia and ↓ infarction Aseptic muscle necrosis ↓ Fibrosis of flexor muscle of forearm ↓ Contracture

Clinical Features Acute phase: xx Pain (persistent pain in forearm, hand, fingers—ominous symptom).

xx xx xx xx xx xx xx

Cutaneous—simple. Fibrous. Bony—complex. It can be unilateral or bilateral. Often all four limbs may be involved with webbing of toes. It may be associated with polydactyly or visceral anomalies. If bony type is suspected, X-ray of the part should be taken.

Treatment xx If cutaneous, release of web is done as a staged procedure along with “Z” plasty or skin grafting. xx If fibrous, release can be done. xx If bony type, release is difficult because blood supply may be compromised which leads to gangrene of the digit.

Hand and Foot

Fig. 1.289: Syndactyly.

Fig. 1.292: Spina ventosa.

FOOT Foot contains 7 tarsal bones, 5 metatarsals, 14 phalanges (total 26 bones). Two sesamoid bones of 1st metatarsal bone are common. There are 4 layers of muscles in foot. Ligaments, muscles, joints, maintain the stability of foot complex. Blood supply is by anterior tibial, posterior tibial and peroneal arteries. Nerve supply is by saphenous, sural, posterior tibial, superficial and deep peroneal nerves.

Fig. 1.290: Syndactyly and polydactyly of both hands and both feet.

CALLOSITY xx It is a hard, thickened skin occurs as a protective measure

MALLET FINGER (Base Ball Finger)

seen in wider area usually over heel and heads of metatarsals.

The terminal phalanx can not be extended because of tear at insertion of extensor tendon or avulsion fracture of the base of the terminal phalanx.

HEBERDEN’S NODES These are seen in osteoarthritis, occurring behind the distal interphalangeal joints of index, middle, little and ring fingers.

Fig. 1.293: Callosity in the foot.

Fig. 1.291: Arthritis of joints of hands.

SPINA VENTOSA Refers to phalangeal tuberculosis (Tuberculous dactylitis). It is called as spina ventosa because of its appearance as “air- filled balloon”.

xx A callosity protrudes outwards from the skin. xx It is greyish-brown, raised, protruded outwards, thickened, hypertrophic skin occurs due to occupation and skeletal structure. It is painless. It is wider lesion. Paring the top layer exposes the shiny translucent dead skin beneath. xx It is grayish brown hypertrophic raised thick protective phenomenon which occurs commonly in areas of wear and tear like hands and feet. Top roughened layer when peeled off, shiny, translucent, homogenous dead skin can be exposed beneath. xx It is painless; it can get rubbed easily to create a sore. xx As it is a protective phenomenon it is best left alone.

You become successful by helping others to become successful.

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SRB's Manual of Surgery xx Infection, abscess formation and ulceration can occur especially if patient is diabetic. xx Corn may be associated with bursae causing bursitis. xx Corn often recurs after excision.

Treatment xx Excision. xx Local application of salicylic acid preparations or mixture of salicylic acid/lactic acid/collodion may be helpful. Skin softening agents are also tried. xx Eliminating the pressure is very important to prevent recurrence. xx Avoid excision of corn unnecessarily in diabetic (especially with neuropathy) and in ischaemic foot.

Soft Corn It usually occurs between 4th and 5th toes due to friction of bases of adjacent proximal phalanges. Fig. 1.294: Diagram showing differences between corn and callosity.

CORN Types

PLANTAR FASCIITIS (Policeman’s Heel) xx It occurs due to friction or tear of the ossified posterior insertion of the plantar fascia which is common in people who stand or walk for long-time. xx Treatment: Analgesics, rest, steroid injections to the site.

xx Hard corn. xx Soft corn.

INGROWING TOE NAIL (Onychocryptosis) xx It is also called as embedded toe nail. xx It is due to curling of the side of nail inwards, causing it

to form a lateral spike resulting in repeated irritation and infection of overhanging tissues in the nail fold.

Causes xx Tight shoes. xx Improper cutting of nails (very short and convex).

Clinical Features Fig. 1.295: Corn in the plantar aspect of the foot.

Hard Corn xx It is localised area of thickening over a bony projec­tions like heads of metatarsals. xx Histologically it differs from callosity by having severe keratoses with a central core of degenerated cells and cholesterol. xx It presses over the adjacent nerves causing pain. It can get infected causing severe pain and tender­ness with inability to walk. xx It is smaller lesion which is pushed deep into the skin forming a localised palpable painful/tender nodule with a central yellowwhite core of dead cornified skin. xx Corn is common if there is deformity or by wearing tight fitting shoes/foot wears. xx Corn is narrow, deep and painful/tender. xx It is common in females. xx Corn is usually white/gray/yellow coloured, deep seated lesion.

xx xx xx xx

It is common in great toe and is often bilateral. Both medial and lateral sides of the toe can be involved. Recurrent attacks of acute and subacute paronychia occurs. Pain, tenderness, swelling of margins of the toe, often along with granulation tissue and foul smelling discharge.

Treatment xx Regular dressing and packing. xx Antibiotics. Discharge is sent for culture and sensitivity. xx Nails should be cut concavely or straight without leaving

lateral spikes towards soft tissues.

xx Zadik’s or Fowler’s operation: Skin in lateral margin

and root is incised so as to expose the lateral spike and germinal matrix. Infected tissues with pus and germinal matrix of ingrown part of the nail is excised or often entire nail with its root and germinal matrix is excised.

Hand and Foot ONYCHOGRYPHOSIS xx It is curving of nail upwards (Ram’s Horn Nail). xx It occurs due to repeated trauma or fungal infection.

ONYCHOMYCOSIS It is fungal infection of the nail.

ATHLETE’S FOOT xx It is the fungal infection of the skin between the toes— Tinea pedis. xx Fungi enter through cracks; survive due to moisture in between toes. xx Skin is swollen, red, with sticky fluid, macerated with blisters. xx Itching, deep cracks, pain and discharge are common. Fig. 1.296: Zadik‘s or Fowler‘s operation.

Treatment xx Part should be kept dry. Cotton, clean socks should be worn. xx Oral antifungals, antihistaminics and topical antifungals are used. xx Condition is contagious.

HALLUX VALGUS

A

B Figs 1.297A and B: Ingrowing toe nail. Note the granuloma caused by repeated infection and inflammation.

Fig. 1.298: Incision for nail excision. Note the germinal matrix. Removal of nail, entire or partial with adjacent germinal matrix is called as radical nail excision.

xx Here great toe is deviated laterally at first metatarsophalangeal joint. There is outward deviation of great toe with medial deviation of first metatarsal head. xx It may be due to persistent lateral force or occasionally hereditary. xx Condition is often bilateral. xx It is common in females. xx Thick walled bursa (bunion) over medial aspect of the head of the first metatarsal bone is common. xx Undue prominence of head of first metatarsal bone is typical often forming an exostosis at this point. Osteoarthritis of 1st metatarsophalangeal joint can occur. xx Lateral deviation of proximal phalanx over 2nd toe causing crowding of the toes. xx Initially it is painless; but eventually pain and tenderness develops with infection of bunion and splaying of forefoot. xx X-ray shows deviation with often osteoarthritis of the metatarsophalangeal joint.

Fig. 1.299: Hallux valgus deformity.

A positive attitude is like a magnet for positive results.

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SRB's Manual of Surgery Treatment Keller’s operation: Proximal 1/3rd of the proximal phalanx of great toe and medial part of head of 1st metatarsal bone is excised through medial curved incision. Soft tissue interposition is done. Mayo’s procedure: Medial part of base of the proximal phalanx of great toe and head of 1st metatarsal bone is excised—opposite of Keller’s. Simmond’s procedure: Varus osteotomy at the base of 1st metatarsal bone with reinsertion of adductor hallucis tendon is done. McBride procedure: Transfer of adductor hallucis tendon and lateral head of flexor hallucis brevis from proximal phalanx of great toe to the lateral part of head of 1st metatarsal bone. Fig. 1.300: Hallux varus deformity. It is opposite of hallux valgus deformity.

Arthrodesis of metatarsophalangeal joint is done to relieve pain. Excision of bunion, deformity correction, osteotomy, muscle transfers are also done as a combined approach.

L. Arterial Diseases CHAPTER OUTLINE ™™ S urgical Anatomy of Thoracic Outlet ™™ Arteries of Upper Limb ™™ Arteries of Lower Limb ™™ Arterial Diseases ™™ Intermittent Claudication ™™ Rest Pain ™™ Limb Ischaemia ™™ Pregangrene ™™ Gangrene

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Raynaud’s Phenomenon Temporal Arteritis Treatment of Arterial Diseases Subclavian Steal Syndrome Acute Arterial Occlusion Traumatic Acute Arterial Occlusion ™™ Embolism ™™ Reperfusion Injury ™™ Saddle Embolus

™™ D  ifferent Levels of Arterial Obstruction ™™ Other Features of Poor Circulation ™™ Investigations for Arterial Diseases ™™ Diseases of the Arteries ™™ Atherosclerosis ™™ Thromboangiitis Obliterans ™™ Takayasu’s Pulseless Arteritis

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Embolectomy Air/Gas Embolism Therapeutic Embolisation Caisson’s Disease or Decompression Disease Aneurysm Mycotic Aneurysm Abdominal Aneurysm Abdominal Aortic Aneurysm

SURGICAL ANATOMY OF THORACIC OUTLET Thoracic outlet is bounded by manubrium sternum in front, spine posteriorly, and the first rib laterally. At the superior aperture of thorax subclavian vessels, brachial plexus traverse the cervicoaxillary canal to reach the upper limb. Cervicoaxillary canal is divided into proximal Costoclavicular space and distal axilla (divided by first rib). Costoclavicular space is bounded superiorly by clavicle, inferiorly by first rib, anteromedially by the costoclavicular ligament, and posterolaterally by scalenus medius muscle along with long thoracic nerve. Scalenus anticus muscle divides the costoclavicular space into two compartments, the anterior one containing subclavian vein and the posterior one containing subclavian artery and brachial plexus. This posterior compartment is called as Scalene triangle bounded by scalenus anticus anteriorly, scalenus medius posteriorly, and the first rib inferiorly. Cervical rib narrows this triangle and causes compressive features of the C8, T1 nerve roots and subclavian artery. Anything that narrows costo­clavicular space causes Thoracic outlet syndrome.

ARTERIES OF UPPER LIMB Right subclavian artery begins from brachiocephalic trunk (innominate artery) whereas left subclavian artery arises directly from the

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Peripheral Aneurysm Carotid Artery Aneurysm Dissecting Aneurysm Erythromelalgia/Erythralgia Livedo Reticularis Polyarteritis Nodosa Scleroderma/Systemic Sclerosis Acrocyanosis Gangrene Diabetic Foot and Diabetic

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Gangrene Trophic Ulcer Bedsores Frostbite Ainhum Endovascular Surgeries Upper Limb Ischaemia Arterial Substitutes

arch of aorta. From underneath the sternoclavicular joint artery arches over the pleura and apex of lung about 2.5 cm above the clavicle and then reaches the lateral border of first rib to continue as axillary artery. Subclavian artery is divided into three parts by scalenus anterior muscle. Axillary artery is divided into three parts by pectoralis minor muscle. At the lower border of teres major muscle it enters the arm and continues as brachial artery. About 2.5 cm below the crease of the elbow joint, it bifurcates into radial and ulnar arteries which run in the forearm. Ulnar artery forms the superficial palmar arch which is completed by superficial palmar branch of radial artery. Radial artery after passing through the anatomical snuff box enters the dorsum of hand and first intermetacarpal space to form deep palmar arch. It is completed by deep palmar branch of ulnar artery and is 1 cm proximal to superficial palmar arch.

ARTERIES OF LOWER LIMB Abdominal aorta bifurcates at the level of fourth lumbar vertebra (corresponds to the level of the umbilicus in anterior abdominal wall) into two common iliac arteries. Common iliac artery is about 5 cm in length passes downward and laterally; and at the level of lumbosacral intervertebral disc, anterior to sacroiliac joint, it divides into external and internal iliac arteries. Internal iliac artery supplies pelvic organs.

To be calm is the greatest manifestation of the power—Swami Vivekananda.

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SRB's Manual of Surgery External iliac artery continues as common femoral artery at the level of inguinal ligament. About 5 cm below the inguinal ligament common femoral divides into superficial femoral and deep femoral (Profunda femoris) arteries. Deep femoral provides collateral circulation around the knee joint and also communicates above with gluteal vessels to maintain collateral circulation around the gluteal region. Superficial femoral artery at the hiatus in the adductor magnus, continues as popliteal artery up to the inferior angle of the popliteal fossa where it divides into anterior and posterior tibial arteries. Anterior tibial artery supplies anterior compart­ment of leg and ankle, continues as dorsalis pedis artery which forms dorsal arterial arch of the foot. Posterior tibial artery supplies posterior compart­ment of leg and ends as medial and lateral plantar arteries which forms plantar arterial arch of the foot. Posterior tibial artery gives peroneal artery which runs close to fibula supplying calf muscles.

The site of pain depends on site of arterial occlusion. xx The most common site is calf muscles. xx Pain in foot is due to block in lower tibial and plantar vessels. xx Pain in the calf is due to block in femoropopliteal segment. xx Pain in the thigh is due to block in the superficial femoral artery. xx Pain in the buttock is due to block in the common iliac or aortoiliac segment, often associated with impotence and is called as Leriche’s syndrome. Pain commonly develops when the muscles are exer­cising. Cause for pain is accumulation of sub­stance P and metabolites. During exercise increased perfusion and increased opening of collaterals wash the metabolites. Boyd’s classification of claudication Grade I: Patient complains of pain after walking, and distance in which pain develops is called as ‘claudication distance’. If patient continues to walk, due to increased blood flow in muscle and opening of collaterals metabolites causing pain are washed away and pain subsides ™™ Grade II: Pain still persists on continuing walk; but can walk with effort ™™ Grade III: Patient has to take rest to relieve the pain ™™

Claudication Arterial—typically develops after walking for certain distance and resolves rapidly within 5 minutes once walking is stopped ™™ Neurogenic—pain develops in standing or walking and disappears immediately after stopping walk; normal feeling pulses without ischaemic changes are present. It is usually due to narrow lumbar canal (spinal canal stenosis) ™™ Venous—it is rare but definitely occurs. It is observed in chronic pelvic venous obstruction as a mechanical high venous pressure. It is usually due to iliac vein thrombosis. Peripheral pulses ™™

are normal

B

A

Figs 1.301A and B: CT angiogram of aortoiliac segment showing aortoiliac block due to atherosclerosis. Collaterals are also welldeveloped.

ARTERIAL DISEASES xx Stenosis due to trauma, atherosclerosis, emboli. It may be:

In the brain causing transient ischaemic attacks. In the limbs causing claudication and rest pain. In the abdomen causing pain, bloody stool. In the kidney causing haematuria. xx Dilatations are aneurysms. xx Arteritis. xx Small vessel abnormalities.    

INTERMITTENT CLAUDICATION Claudio means “I limp” a Latin word. It is a crampy pain in the muscle seen in the limbs. Due to arterial occlusion, metabolites like lactic acid and substance P accumulate in the muscle and cause pain.

Note:

• •

Beta blockers may aggravate claudication. Claudication is not that common in upper limb but can occur during writing or any upper limb exercise.

REST PAIN xx It is continuous aching in calf or feet and toes or in the region

even at rest depending on site of obstruc­tion. xx It is ‘cry of dying nerves’ due to ischaemia of the somatic nerves. It signifies severe decompensated ischaemia. Pain gets aggravated by elevation and is relieved in dependent position of the limb. xx Pain is more in the distal part like toes and feet. It gets aggra­ vated with movements and pressure. xx Hyperaesthesia is common association with rest pain. xx Rest pain is increased in lying down and elevation of foot; it may be reduced on hanging the foot down. xx Rest pain is worst at night and so patient is sleepless at night. xx Rest pain is apparently reduced by holding the foot with hand, probably due to suppression of transmission of pain sensation.

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SRB's Manual of Surgery Rutherford classification Grade 0 1 2 3 4 5 6

Clinical feature Asymptomatic Mild claudication Moderate claudication Severe claudication Ischaemic rest pain Minor tissue loss Major tissue loss

Limb ischaemia is also classified as: xx Functional ischaemia. xx Critical ischaemia.

Functional Limb Ischaemia Here flow of blood is normal when limbs are at rest; but will not be increased during exercise. It presents as claudication. It is defined as, “Muscle discomfort in the limb reproducibly produced by exercise and relieved by rest within 10 minutes.” Fig. 1.302: Rest pain in a patient suffering from TAO. Holding the foot reduces the pain slightly. Features of arterial stenosis/block in limbs ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Intermittent claudication Rest pain Cold periphery, numbness, paraesthesia Color changes, ulceration, gangrene Altered sensation and decreased function/movements Diminished/absent arterial pulsation Thrill/bruit over the stenosed artery Altered venous filling—normally it is in few seconds; it is delayed in arterial stenosis; it is rapid in AV fistula

Critical Limb Ischaemia It is persistently recurring ischaemic rest pain for 2 weeks, which requires regular analgesics for > 2 weeks or ulceration or gangrene of the foot or toes with an ankle systolic pressure < 50 mmHg or toe systolic pressure < 30 mmHg. Ankle brachial pressure index (ABPI) will be less than 0.3. One should check blood pressure in all 4 limbs. ABPI is checked in supine position; systolic blood pressure in upper and lower extremities (two upper and two lower) is checked and higher value of each extremities is taken; ABPI is calculated. Results—>0.90 is normal; 0.70–0.89 is mild disease; 0.50–0.69 is moderate; 200 metres –– 2b: Poorly compensated—walk only < 200 metres ™™ Stage 3: Rest pain ™™ Stage 4: Gangrene, ischaemic ulcer ™™ ™™

GANGRENE

It is dry, desiccated, mummified tissue caused by gradual slowing of bloodstream. There is a line of demarcation and is localised.

Wet Gangrene It is due to both arterial and venous block along with superadded infection and putrefaction. It spreads proximally and there is no line of demarcation. It spreads faster.

Today’s preparations determine tomorrow’s achievement.

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SRB's Manual of Surgery Organs in which gangrene can develop—appen­dix, bowel, gallbladder, testis, pancreas.

Fig. 1.306: Ischaemic changes in the right leg. Third and fourth toes are gangrenous with line of demarcation. Great and little toes are partly gangrenous. There are ischaemic features in the right foot and leg like hair loss/skin changes/wasting. Features of ischaemia

Fig. 1.303: Gangrene of great and little toes in a patient with vascular compromise. ™™ ™™ ™™

Necrosis: It is microscopic cell death. Sequestrum is dead bone in situ. Slough is dead soft tissue.

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Marked pallor, purple blue cyanosed appearance Thinning of skin Diminished hair Loss of subcutaneous fat Brittle nails, with transverse ridges Ulceration in digits Wasting of muscles Tenderness and temperature (cold)

Line of Demarcation xx It is a line between viable and dying tissue indicated by a band of hyperaemia. It also indicates that disease is getting localised. xx Final separation between healthy and gangrenous tissue occurs by development of a layer of granulation tissue in between. xx It is hyperaesthetic due to exposed nerve endings.

Fig. 1.304: Ischaemic ulcer foot in a diabetic patient.

Fig. 1.307: Clear line of demarcation in gangrenous 4th toe.

Types of Separation xx Separation by aseptic ulceration is seen in dry gangrene. xx Separation by septic ulceration is seen in infected condition and wet gangrene.

DIFFERENT LEVELS OF ARTERIAL OBSTRUCTION A

B

Figs 1.305A and B: Gangrene of all toes at their distal phalanges. All ischaemic features are obvious.

xx Aortoiliac block causes claudication in both buttocks, thighs, and calves; absence of femoral and distal pulses bruit over aortoiliac region. Impotence occurs due to defective perfusion through internal iliac arteries and so into the penis causing erectile dysfunction (Leriche’s syndrome).

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SRB's Manual of Surgery xx Iliac artery obstruction causes claudication in thigh and calf; bruit over iliacs with absence of femoral and distal pulses. xx Femoropopliteal obstruction causes claudication in calf with absence of distal pulses but with palpable femoral. xx Distal obstruction shows absence of ankle pulses with palpable femoral and popliteal pulses.  Paraesthesia over the skin of the foot is due to shunting of blood from the skin to muscles in deeper plane.  Sensation in gangrenous area is absent. But, at the line of demarcation, skin is hyperaesthetic.

OTHER FEATURES OF POOR CIRCULATION xx The affected part is cold with numbness, paraesthesia and colour changes. Observing for colour change is important as, if it is not present one may have to think that numbness could be of neurological origin. On elevation the part blanches, on dependency part becomes purple. Temperature sensation on the ischaemic limb is lost apart from its coldness. xx Ulceration, gangrene, decreased sensation and movements are the features to be checked. xx Delayed capillary filling: Blanched nails or pulp of fingers, on pressure, will show delay in refilling (to turn pink) after release of pressure. xx Delayed venous refilling: Two fingers are placed over the vein. Finger nearest to heart is moved away so as to empty the vein. Distal finger is released to observe the venous refilling. Delay in filling is called Harvey’s sign, signifies ischaemia. Venous filling is increased in AV fistulas. xx Crossed leg test (Fuchsig’s test): Patient is asked to sit with the legs crossed one over the other so that the popliteal fossa of one leg will lie against the knee of other leg. Oscillatory movements of foot can be observed synchronous with the popliteal artery pulsation. This movement is absent with blockage of popliteal artery. xx Disappearing pulse syndrome: Exercise the limb after feeling the pulse. Pulse disappears once patient develops claudication. It is due to vaso­dilatation and increased vascular space occurring as the result of exercise wherein arterial tension cannot be kept adequately and so pulse will disappear (unmasking the arterial obstruction). xx Buerger’s postural test: Patient lying down on his back is asked to raise the leg above. In normal individuals, limb (plantar aspect of foot) remains pink even after raising above 90°. Ischaemic limb, when elevated shows marked pallor and empty veins. The angle in which pallor develops is called as Buerger’s angle of vascular insufficiency. If this angle is < 30°, it indicates severe ischaemia. xx Systolic bruit may be heard over stenosed artery like subclavian artery, femoral artery, carotid artery, iliacs, renal artery. xx Adson’s test (Scalene manoeuvre): In a patient sitting on a stool, the radial pulse is felt. The patient is then asked to take a deep breath (to allow the rib cage to move upwards so as to narrow the cervicoaxillary channel) and turn the face to same side (to contract scalenus anterior muscle so as to narrow the scalene triangle). If the radial pulse disappears or become feeble it signifies cervical rib or scalenus anticus syndrome. xx Elevated arm stress test (EAST), or modified Roos test: With both the arms kept in 90° abduction and external rotation position, patient is asked to make a fist and release repeatedly for 5 minutes. In normal side, patient will continue to do the manoeuvre whereas in diseased (Thoracic outlet syndrome) side patient gets pain and paraesthesia with difficulty in continuing the manoeuvre. Patient drops the arm down to relieve the symp­toms.

xx Costoclavicular compression manoeuvre (Falconer test): Radial pulse becomes absent when patient draws his shoulders backwards and downwards in excessive military position. This is because at this position, subclavian artery is compressed between first rib and clavicle, leading to feeble or absent radial pulse. Halstead manoeuvre another similar test. xx Hyperabduction manoeuvre (Wright test): When affected arm is hyperabducted, radial pulse becomes absent or feeble due to compression of artery by pectoralis minor tendon. xx Allen’s test: It is done to find out the patency of radial and ulnar arteries. Both the arteries are compressed near the wrist and allowed to blanch completely in one minute (In the mean time patient closes and opens the fist several times for further venous outflow). Palm appears pale and white. One of the arteries is released and colour of hand is noted. Normally hand will become pink and flushed in no time; whereas in obstruction, the area will still remain pale. Other artery is also released and looked for changes in hand. Often test has to be repeated to get proper information. xx Abdomen should be examined for the presence of abdominal aortic aneurysms. It presents as pulsatile mass above the umbilicus, vertically placed, smooth, soft, nonmobile, not moving with respi­ration, resonant on percussion. Expansile pulsation is confirmed by placing the patient in knee-elbow position. xx Auscultation for arterial bruit over femoral artery, abdominal aorta, subclavian and carotid arteries is done.

Palpation of Blood Vessels xx Dorsalis pedis artery is felt just lateral to the extensor hallucis longus tendon at the proximal end of first web space, felt against the navicular and middle cuneiform bones. It is absent in 10% cases. xx Posterior tibial artery is felt against the calcaneum just behind the medial malleolus midway between it and tendon Achilles. xx Anterior tibial artery is felt anteriorly in the midway between the two malleoli against the lower end of tibia just above the ankle joint, lateral to extensor hallucis longus tendon. xx Popliteal artery is difficult to feel. It is palpated better in prone position with knee flexed about 40–50°, to relax the popliteal fascia. It is felt in the lower part of the fossa over the flat posterior surface of upper end of tibia. In upper end of the fossa, artery is not felt as there is no bony area in intercondylar region. xx Femoral artery in the groin is felt just below the inguinal ligament midway between anterosuperior iliac spine and pubic symphysis. Often hip has to be flexed for about 10–15° to feel it properly. xx Radial artery is felt at the wrist on the lateral aspect against lower end of the front of radius. xx Ulnar artery is felt at the wrist on the medial aspect against lower end of the front of ulna. xx Brachial artery is felt in front of the elbow just medial to biceps brachii tendon. xx Axillary artery is felt in apex of the axilla against shaft of the humerus. xx Subclavian artery is felt against first rib just above the middle of the clavicle. xx Facial artery is felt against body of mandible at the insertion of masseter. xx Common carotid artery is felt medial to sterno­mastoid muscle at the level of thyroid cartilage against carotid tubercle (Chassaignac tubercle) of transverse process of 6th cervical vertebra (in carotid triangle).

Severely diseased distal aorta in atherosclerosis on arteriography is called as “shaggy aorta”.

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SRB's Manual of Surgery xx Superficial temporal artery is felt just in front of the tragus of the ear against zygomatic bone.

INVESTIGATIONS FOR ARTERIAL DISEASES xx Segmental pressure measurements: Segmental BP is measured at multiple levels (upper and lower thigh, upper calf and ankle); pressure reductions between levels help to localise the occlusion; normally pressures increase as one moves further down the leg (>20 mmHg gradient abnormal); test is inaccurate in calcified artery walls. xx Blood tests: Low Hb delays healing due to poor oxygenation; raised WBC count may be due to infection; raised platelet count may precipitate thrombosis (of arteries and veins both); blood sugar and glycosylated haemoglobin (HbA1C) reflects the diabetic problem; lipid profile; peripheral smear; renal function tests (serum creatinine). xx Doppler to find out the site of block—hand held Doppler can be used (Doppler: Christian Johann Doppler, Austrian physicist).  Duplex scan: It is combination of B mode ultrasound and Doppler study. Difference in transmitted beam of the ultrasound and reflected beam is called as Doppler shift which is assessed and converted into audible signals. It is used to study the site, extent, severity of block, and also about collaterals. Audible sound is heard with normal flow, and sound is important. Turbulence is heard when there is stenosed partially blocked artery. Audible sound will be absent if there is complete block. Using Doppler probe blood pressure at various levels can be assessed. Pulse wave tracing along the artery is also important.

Fig. 1.309: Angiogram showing vessels in both lower limbs; note the significant block on the left side Indications for angiogram ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

TAO Atherosclerosis Raynaud’s phenomenon AV fistulas Haemangiomas Thoracic outlet syndrome (e.g. cervical rib) Aneurysms Neoplastic conditions –– Other angiograms are carotid angiogram, coeliac angio-

gram, superior mesenteric angiogram, coronary angiogram. Seldinger technique (Steps)

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Arterial cannula is passed into the artery, e.g. femoral artery Needle is removed and guidewire is passed through the cannula Cannula is removed Dilator is passed over the guidewire Dilator is removed and arterial catheter (5 French sized) is passed over the guidewire Guidewire is removed –– Femoral artery is used because it can be easily felt and

Fig. 1.308: Hand held Doppler is simpler way to identify and assess the artery.  Arterial diameter, blood flow rate, velocity of flowing blood,

assessment of stenosed segment is properly done using Doppler. xx Angiography:  Angiography is the appropriate investigation for arterial diseases.  Retrograde transfemoral Seldinger (Sweden) angiography: –– It is commonly done angiogram. It is done only when

femorals are felt. If femoral pulsation is not felt then angiogram is done either transbrachially (left brachial artery), or transaortic.

cannulated to pass an arterial catheter.

–– Water soluble iodine dye (Sodium diatrizoate) is injected.

X-rays are taken to see the block, its extent in the affected limb. –– In TAO cork screw appearance is characteristic. Distal run off through collaterals is also important. –– If catheter is passed still proximally angiogram of opposite side is possible. –– Seldinger technique can also be used (to study) to do renal angiogram to detect renal artery stenosis, renal carcinomas, renal anomalies (vascular). But a caution should be remembered that angiogram in limb may precipitate further rapid thrombus formation, worsening ischaemia and precipitating gangrene.

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SRB's Manual of Surgery –– Dye is injected either to an artery or vein. Injecting into a

Complications of retrograde angiogram ™™ ™™ ™™ ™™ ™™ ™™ ™™

Bleeding, hypotension Dissection of the vessel wall, pseudoaneurysm Haematoma formation Embolic blue toe syndrome Thrombosis, AV fistula Infection, osmolarity discomfort Anaphylaxis—4%

 Direct aortic angiogram, practiced earlier, is discouraged at

present because of the risk of aortic dissection and paraplegia due to blockage/spasm of anterior spinal artery.  Digital subtraction angiography (DSA) –– Here vessel (artery) is delineated in a better way by eliminating other tissues through computer system. AV fistulas, haemangiomas, lesion in circle of Willis, vascular tumours, other vascular anomalies are well made out.

xx xx xx xx

xx

xx

vein is technically easier but larger dose of dye is required. Injecting into an artery is technically difficult but small dose of dye is sufficient. –– Advantages: Only vascular system is visualised; other systems are eliminated by computer subtraction. Small lesion, its location and details are better observed with greater clarity. –– Disadvantages: Cost factor and availability. –– Complications: Anaphylaxis, bleeding, thrombosis. CT angiogram/MR angiogram. Ultrasound abdomen to see aneurysm/aorta and its anatomical changes/other vessels in the abdomen/other organs. Treadmill test/ECG/echocradiography to assess cardiac/coronary status. Plethysmography: It measures the blood flow in limbs. Water-filled volume recorder; air-filled volume recorder; mercury in silastic gauze is used after occluding the venous outflow. It is a noninvasive method. Segmental plethysmography using occlusion cuffs of 65 mmHg pressure is placed at thigh, calf and ankle levels and then quantitative measure of pulsation is done. Ankle-brachial pressure index: Normally it is 1. If it is less than 0.9, it means ischaemia is present. If it reaches 0.3 or below then it signifies severe ischaemia with gangrene. Brown’s vasomotor index: Specific nerve of the ischaemic limb is anaesthetised like posterior tibial nerve or ulnar nerve (local anaesthetia or spinal anaesthesia is given to anaesthetise entire limb). If the ischaemic disease is at vasospasm stage (like in TAO), nerve block will relieve the sympathetic vasospasm and skin temperature rises. It is compared to mouth temperature of the patient.

Fig. 1.310: DSA showing total block of right common iliac artery due to thrombosis.

A

B Figs 1.312A and B: Aortic and aortoiliac CT angiogram.

Fig. 1.311: CT angiogram showing abdominal aorta, branches and renal vessels.

It is to assess the degree of vasospasm which is used as a predictor of the efficacy of sympathectomy. (Rise in skin temperature minus rise in mouth temperature) divided by rise in mouth temperature is called as Brown’s vasomotor index. If it is more than 3.5, it is due to vasospasm, and can be relieved by sympathectomy. If less than 3.5, sympathectomy is not beneficial. xx Transcutaneous oximetry: By placing polarographic electrodes over the skin over thigh, leg and foot of oxygen tension (tcPO2) can be measured which is reflection of underlying tissue perfusion. Normal tcPO2 in the foot is 50–60 mmHg. Level less than 40 mmHg shows inadequate wound healing. Level below 10 mmHg suggests critical ischaemia with complete failure of wound healing.

Half of us are blind, few of us feel and we are all deaf.—William Osler

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SRB's Manual of Surgery xx Other tests  Xenon 133 isotope method is used to study muscle blood flow. Xenon 133 after mixing with normal saline is injected IM to study its clearance.  Two electromagnetic electrodes are placed in contact with arterial wall in opposite directions which pick up moving blood force to feed into electronic amplifier. But it is invasive as artery has to be dissected to place electrodes.  Angioscopy to visualize the vessels directly.

Treatment Plan for Arterial Diseases xx Stopping smoking; supervised exercises; regular controlled walk, diet (carbohydrate and lipid free diet); care of limbs. xx Control of hypertension, diabetes; antilipid drugs like atorvastatin 10 mg or pravastatin 40 mg; low dose aspirin 75 mg; clopidogrel 75 mg; vasodilators; ticlopidine; dipyridamole; cilostazole 100 mg are different drugs used. xx Percutaneous transluminal balloon angioplasty (PTA) done mainly to iliac arteries, subclavian arteries, renal artery, carotid and occasionally leg arteries and mesenteric or gastrointestinal arteries. PTA with stenting using expandable stents to the arteries is also often done to get a better result. xx Bypass graft surgeries—aortofemoral; femorofemoral; iliofemoral, etc. Dacron, human umbilical vein (3 mm), saphenous vein; PTFE (Polytetrafluoro ethylene)—are different grafts used. xx Endarterectomy, atherectomy, thrombectomy, profundaplasty, etc.

Risk factors Definitive • Hypercholesterolaemia, and hyperlipidaemia (cholesterol >200 mg%; high LDL (>100 mg%); low HDL ( 30 mmHg for 3 hours or above the mean arterial pressure. Presents with muscle weakness, sensory changes, leg pain which is aggravated by dorsiflexion of toes. xx Other complications are—sepsis, reblock, bleeding and catheterrelated complications.

REPERFUSION INJURY xx It occurs after reestablishment of arterial flow to an ischemic tissue bed which further leads to tissue death causing specifically peripheral muscle infarction. It is due to sudden release of oxygen free radicals which blocks the microcirculation, with release of high levels of potassium (hyperkalaemia) and myoglobin (myoglobinaemia and myoglobinuria). Haemodynamically patient becomes unstable with lactic acidosis, intracellular changes, interstitial oedema and cardiac dysfunction. It is often life-threatening. xx Haimovici triad of revascularisation injury (1960)—(1) Muscle infarction; (2) Myoglobinuria; (3) Acute renal failure. xx Severe ischaemia causes oedema in the muscular compartment with raise in compartment pressure more than the essential capillary perfusion pressure causing acute compartment syndrome. It is common in the anterior compartment of the leg. It is basically in the skeletal muscles deep to deep fascia. Compartment pressure when measured using transducer needles will be more than 40 mmHg or > 30 mmHg for 3 hours or above the mean arterial pressure. Muscle weakness, sensory changes, leg pain which is aggravated by dorsiflexion of toes. xx ‘No re-flow’ phenomenon due to tissue oedema causes capillary perfusion block. Even though compartment syndrome and ‘no reflow’ phenomemenon are separate entities they are always seen together along with reperfusion injury. xx Metabolic acidosis, acute tubular necrosis causing acute renal failure and cardiac arrhythmias may set in and become lifethreatening. xx Features are—toxaemia; oliguria; persistent pain and oedema in the leg with muscular tenderness; raised blood urea and serum creatinine with features of acute ischaemia in the limb. Raised creatinine level (renal failure), creatine kinase (muscle lysis) are typical. xx Treatment:  Mannitol to prevent renal failure; fluid therapy.  Fasciotomy to reduce raised compartment pressure. All four compartments of lower limb should be decompressed surgically. Long vertical lateral deep fasciotomy incision in the calf behind the fibula along the deep fascia and its fibular attachments is a must. Bleeding is common after fasciotomy as patient is heparinised. Infection of the wound can occur. Later, once the patient is stabilised and oedema subsides with healthy wound, secondary suturing or skin grafting is done. If after fasciotomy, patient survives then it is with eventual development of Volkmann’s ischaemic contracture.  Antibiotics and supportive therapy.

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SRB's Manual of Surgery SADDLE EMBOLUS

EMBOLECTOMY

It is an embolus blocking at bifurcation of aorta.

Indications

Causes

xx Acute embolic blockade of artery commonly seen in common femoral, cranial vessels, mesenteric vessels. xx It should be done within 6 hours as after 6 hours irreversible changes occur—Golden hour. xx It is usually done under local anaesthesia under C arm guidance with anaesthetist monitoring the patient. It can be done under spinal or general anaesthesia.

xx Mural thrombus after myocardial infarction. xx Mitral stenosis with atrial fibrillation. xx Aortic aneurysm.

Fig. 1.346: Saddle embolus blocking the bifurcation of abdominal aorta. It causes severe, rapid, dramatic symptoms.

The embolus which blocks at aortic bifurcation is usually large. Fig. 1.347: Embolectomy technique.

Clinical Features xx Features of sudden, rapidly progressive ischaemia in both

lower limbs.

Note: In aortic bifurcation thrombus, there is earlier history of claudication in the buttock often with Leriche’s syndrome. Symptoms are slow and gradual but not dramatic. Collaterals between aorta and iliac arteries have well-formed and so sudden, rapid development of gangrene will not occur.

xx Gangrene of both lower limbs. xx Features of associated infection.

Investigations xx Arterial Doppler, aortic angiogram. xx Ultrasound abdomen.

Methods xx Interventional method is usually employed using Fogarty’s catheter. Good back bleed signifies com­plete­ness of embolectomy. xx Open arteriotomy method is done directly over the artery followed by suturing the artery. Note:

• • • • •

Intraoperative arteriogram is a must to confirm the adequacy of blood flow and completion. Intraoperative thrombolysis as an adjunct to save the limb using urokinase 2,50,000 IU for minutes into distal artery may be beneficial. Prophylactic fasciotomy is needed in delayed cases to prevent reperfusion injury. Postoperative systemic heparin and later oral anticoagulant is given. Treatment for atrial fibrillation, atherosclerotic stenosis and other causes is needed.

Treatment xx Initially, heparin is injected intravenously—10,000 units and

later 5,000 units subcutaneously 8th hourly. xx Embolectomy can be done using Fogarty’s catheter. xx Open arteriotomy and embolectomy can also be tried. xx Antibiotic prophylaxis is given to prevent infection.

Complications ™™ ™™ ™™ ™™ ™™

Bleeding Sepsis Thrombosis Narrowing Incomplete removal

Unless you try to do something beyond what you have already mastered, you will never grow.

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SRB's Manual of Surgery xx Cutaneous: Petechial haemorrhages in the skin. xx Cerebral: Drowsy, restlessness, disoriented, constricted

pupils, pyrexia and coma.

xx Retinal artery emboli is the earliest sign to appear, causing

striae haemorrhages, fluffy exudates confirmed on fundoscopic examination. xx Kidney: Blockage in renal arterioles results in fat droplets in urine. Gurd and Wilson criteria for FES

A

B Figs 1.348A and B: Fogarty’s catheter. It is 80 cm in length with 4 to 7 French size. It is used for embolectomy. Note the inflated balloon at the tip.

After Embolectomy Patient is placed in ICU care. Monitoring with—PTT, thromboplastin time.

FAT EMBOLISM (Ernst Von Bergmann, in 1873) xx 90% of major trauma especially with fractures develop fat

embolism from aggregation of fat globules and chylomicrons derived from bone marrow. Fat globules release fatty acids which act as toxins. xx It is common in fracture long bones, and multiple fractures. It is observed after intramedullary nailing, liposuction, joint reconstruction, parenteral lipid infusion, cardiopulmonary bypass, and pathological fractures. xx Only 5–10% will develop fat embolism syndrome (FES). FES shows respiratory distress (ARDS), and skin manifestations. Approximately 20–30% of the population have a patent foramen ovale; fat emboli pass through the pulmonary circulation causing the systemic manifestations of FES, particularly involving the brain and kidneys. As a result of the occluded cerebral vasculature, patients exhibit encephalopathy, localised cerebral edema. FES has got 20% mortality.

Features xx Pulmonary: Cyanosis, tachypnoea, right heart failure, froth

in mouth and nostrils, fat droplets in sputum, eventually respiratory failure.

Major criteria

Minor criteria

• Symptoms and radiologic evidence of respiratory insufficiency • Cerebral sequelae unrelated to head injury or other conditions • Petechial rash—over upper body, axillae

• Tachycardia (heart rate >110/ min) • Pyrexia (>38.5°C) • Retinal changes or petechiae • Renal dysfunction • Jaundice • Acute drop in hemoglobin level • Sudden thrombocytopaenia • Elevated erythrocyte sedimentation rate • Fat microglobulinaemia

Differential Diagnosis xx Pulmonary embolism. xx Thrombotic thrombocytopenic purpura.

Investigations xx Presence of fat lobules in the blood obtained by pulmonary

capillary wedging is diagnostic. xx Haemoglobin estimation, platelet count and total WBC count. xx Chest X-ray shows snow storm appearance. xx CT chest is useful; CT head is done to rule out causes of intracranial injuries. xx Transesophageal echocardiography (TEE) may be of use in evaluating the intraoperative release of marrow contents into the bloodstream during intramedullary reaming and nailing. xx Bronchoalveolar lavage with staining for fat will show lipid inclusions.

Treatment xx Adequate oxygenation with ventilator support (ICU care). xx Hydration, nutrition, achieving haemodynamic stability,

prevention of DVT, avoiding volume overload with proper fluid therapy. xx Methylprednisolone may be useful; but use of heparin, low molecular dextran and other steroids are controversial even though commonly used. xx Albumin transfusion may be helpful as it binds with fatty acids to reduce the lung injury. xx Early fixation of the fractures; placement of IVC filters will prevent the chances of fat embolism or emboli reaching into the lungs.

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SRB's Manual of Surgery AIR/GAS EMBOLISM

THERAPEUTIC EMBOLISATION

Causes

Indications

xx Through venous access like IV cannula, most common

xx xx xx xx xx

cause. xx During artificial pneumothorax. xx During surgeries of neck and axilla. xx Traumatic opening of major veins sucking air inside, causing embolism. xx During fallopian tube insufflation; laparoscopic surgeries. xx During illegal abortion.

Features It causes respiratory distress, haemoptysis, convulsions, unconsciousness, visual and hearing disturbances, fatigue and numbness, paralysis, haemodynamic instability and coma. ™™

™™

™™ ™™

™™

™™

Amount of air required causing venous air/gas embolism is 15 ml. To precipitate symptoms in venous embolism 100 ml of air required. 100 ml of air at a rate more than 100 ml/second is fatal. When the air enters the right atrium, it gets churned up forming foam which enters the right ventricle and blocks the pulmonary artery. Mill-Wheel murmur (machinery) heard over the precordium through a stethoscope is diagnostic. During open heart surgery/therapeutic pneumothorax, by accidental pulmonary vein puncture or in atrial septal defect (ASD) air may enter left side of the heart (paradoxical air embolism) causing coronary block or cerebral air embolism. Arterial gas embolism is more dangerous and often early fatal. 2 ml of gas/air is fatal in cerebral circulation; and 0.5 ml is fatal in coronary arteries. Through paravertebral veins also air embolism to brain can occur.

Haemangiomas. AV fistulas. Malignancies like renal cell carcinoma, hepatoma. Cerebrovascular problems. To arrest haemorrhage from GIT, urinary and res­piratory tract.  In bleeding duodenal ulcer or gastric ulcer, embo­lisation is

done to occlude gastroduodenal artery or left gastric artery respectively.  It is also useful in bleeding oesophageal varices, secon­daries in liver (mainly due to carcinoids), hepatoma. Materials used for therapeutic embolisation ™™ ™™ ™™ ™™ ™™

Blood clot Gel foam Balloons Quick setting plastics Stainless steel coils

Human dura Plastic microspheres Ethyl alcohol Wool

CAISSON’S DISEASE OR DECOMPRESSION DISEASE It occurs due to rapid decompression from high altitude, aircraft, compressed air chambers, deep sea divers causing bubbling of nitrogen which blocks the small vessels. xx In joints and muscles it causes excruciating pain (bends). xx Spinal cord ischaemia causing neurological deficits. xx Lungs may be affected causing choking with chest pain, tightness and dry cough. xx Treatment  Oxygen therapy.  Recompression and gradual decompression in special chamber.

ANEURYSM

Treatment xx Patient is placed in Trendelenburg left lateral decubitus

position. The Trendelenburg position keeps left ventricular air bubble away from the coronary artery ostia (which are near the aortic valve) so that air bubbles do not enter and occlude the coronary arteries. Left lateral decubitus positioning helps to trap air in the non-dependent segment of the right ventricle (where it is more likely to remain instead of progressing into the pulmonary artery and occluding it). The left lateral decubitus position also prevents the air from passing through a potentially patent foramen ovale (present in as many as 30% of adults) and entering the left ventricle, from which it could then embolise to distal arteries. xx Hyperbaric oxygen is useful in both venous and arterial gas/air embolism as it reduces the ischaemia, reduces the bubble size; in arterial gas embolism it removes the nitrogen from the bubble so that to improve perfusion and oxygenation. xx By passing a needle, the air has to be aspirated from the right ventricle. Often requires life-saving open thoracotomy to aspirate the excess air causing the block.

There is no disease more conducive to clinical humility than aneurysm of the aorta. —William Osler, Circa 1900

It is an abnormal permanent dilatation of localised segment of arterial system. Diameter will be 50% more than expected normal diameter of that artery in aneurysm. Atherosclerosis which is the most common (90%) facilitating cause of aneurysm is due to destruction and loss of stability of tunica media. True aneurysm contains all three layers of artery. False aneurysm contains single layer of fibrous tissue as wall of the sac and it usually occurs after trauma. Types Fusiform—uniform dilatation of entire circumference of arterial wall ™™ Saccular—dilatation of part of circumference of the arterial wall ™™ Dissecting—through a tear in the intima blood dissects between inner and outer part of tunica media of the artery

™™

Food is the unavoidable necessity of existence.

196

SRB's Manual of Surgery  Infective: Syphilis; mycotic; tuberculosis (in lung);

arteritis; acute sepsis.

 Collagen diseases like Marfan‘s syndrome, polyarteritis

nodosa, Ehler-Danos syndrome.

xx Congenital:

 Berry aneurysm; cirsoid aneurysm; congenital AV fistula.

Sites

Fig. 1.349: True and false aneurysms. In true type, all layers are intact. In false type all layers breached with haematoma having a false capsule.

xx xx xx xx xx

Aorta. Femoral. Popliteal. Subclavian. Cerebral, mesenteric, renal, splenic arteries.

The most common is true, fusiform, atherosclerotic, aortic aneurysms.

Berry aneurysms are multiple aneurysms occurring in circle of Willis. Effects and complications of aneurysm Thrombosis and distal ischaemia Release of emboli causing acute arterial occlusion Pressure effects on bone (erosion); skin; veins (oedema); nerves (pain, paraesthesia); stomach (erosion—haematemesis); oesophagus (dysphagia) ™™ Rupture ™™ Infection of aneurysm ™™ ™™ ™™

Clinical Features of Aneurysms xx Swelling at the site which is pulsatile (expansile), smooth, Fig. 1.350: Fusiform and saccular types of aneurysms.

soft, warm, compressible, with thrill on palpation and bruit on auscultation. Swelling reduces in size when pressed proximally. xx Distal oedema due to venous compression. xx Altered sensation due to compression of nerves. xx Erosion into bones, joints, trachea or oesophagus. xx Aneurysm with thrombosis can throw an embolus causing gangrene of toes, digits, extending often proximally also.

Fig. 1.351: Thoracic aortic aneurysm.

Causes xx Acquired:

 Degenerative: Atherosclerosis (most common cause—

90%); mucoid degeneration of intima and media (in South African young Negroes).  Traumatic: Direct; indirect like in post-stenotic dilatation by cervical rib; traumatic AV aneurysmal sac; aneurysm due to irradiation (due to dryness and destruction of vasa vasorum causing weakening).

Fig. 1.352: Chest X-ray showing aortic aneurysm.

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SRB's Manual of Surgery

A

B

C

D

Figs 1.353A to D: Different methods of aneurysm repair. (A) Matas aneurysmorrhaphy for saccular aneurysm; (B) Excision and Dacron grafting; (C) Ligation and exclusion of the aneurysm using autologous vein graft; (D) Excision of aneurysm and bypass using autologous vein graft.

Differential Diagnosis xx Pyogenic abscess: Abscess has to be always con­firmed by xx xx xx xx

aspiration; especially in axilla, popliteal region, groin. Vascular tumours. Pulsating tumours: Sarcomas, pulsating secon­daries. Pseudocyst of pancreas mimics aortic aneurysm. AV fistula.

Investigations xx Doppler study, duplex scan, angiogram, DSA. xx Tests relevant for the cause, like blood sugar, lipid profile,

echocardiography.

Treatment xx Reconstruction of artery using arterial grafts. xx Arterial endoaneurysmorrhaphy—MATAS. It is done

usually for peripheral saccular aneurysm. Matas aneurysmorrhaphy may be restorative or endo-obliterative or reconstructive.

xx Therapeutic embolisation. xx Clipping the vessel under guidance (e.g. cranial aneurysms). xx Older methods which are now not used but popular earlier were— wiring of the aneurysmal sac/wrapping of the aneurysmal sac/ ligatures at different levels (ligation just proximal to aneurysmal sac—Anel’s; ligation proximally proximal to an arterial branch— Hunter’s; ligation just distal to aneurysmal sac—Brasdor’s; ligation distally distal to an arterial branch—Wardrop’s; ligature one proximal and another distal to aneurysmal sac—Antylus’).

xx Common bacteria are gram-positive organisms like Staphylococcus aureus (most common) and Streptococcus. xx Common aetiology is bacterial endocarditis but could be any infective site. xx Common vessels involved are aorta, visceral, head and neck and intracranial. xx Commonly it is saccular, multilobed, with a narrow neck. xx Patient presents with fever, toxaemia and tender pulsatile mass if it is in the periphery. xx Investigations: Leucocytosis. Positive blood culture, MR or CT angiogram are relevant.

Treatment xx Broad-spectrum antibiotics xx Resection of aneurysm; debridement and drainage of the infected aneurysm with adequate blood transfusions. xx Extra-anatomic bypass through uninfected tissue planes to avoid contamination of the graft. xx Long-term antibiotic therapy is necessary. xx It has got 25% mortality. Note:

Microbial arteritis with aneurysm is a different entity is due to bacteraemia occurring in an athero­sclerotic vessel due to Salmonella infection).

ABDOMINAL ANEURYSM xx Abdominal aortic aneurysm is the most common aortic

aneurysm.

xx Splenic artery aneurysm is the 2nd most common type. xx Incidence is 2%. It is more common in males. xx Transverse diameter of aorta in an aneurysm should be

3 cm or more.

MYCOTIC ANEURYSM

xx Common in elderly; common in males (4:1); chance of

xx It is a misnomer. xx It is not due to fungus but due to bacterial infection.

getting aneurysm in genetically related first degree relatives is 10 times more.

When you cease to dream, you cease to live.

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SRB's Manual of Surgery xx Common in smokers (8:1with nonsmokers); in 55% of

patients Chlamydia pneumoniae is identified.

Note:

Smoking is an important factor.

ABDOMINAL AORTIC ANEURYSM (AAA) Causes xx Atherosclerosis (as degenerative process) is the most common

facilitating cause (95%)—aortic wall contains smooth muscle cell matrix, elastin, collagen; elastin (in tunica media) is the main load bearing part with collagen (in adventitia) as safe net in the wall to provide tensile strength preventing aneurysm formation. Elastin in medial layer of aorta is degraded and reduced significantly in infrarenal aorta in relation to collagen, absence or less vasa vasorum in infrarenal aorta and atherosclerotic unstability of the medial wall of aorta cause infrarenal aorta more prone to develop aneurysm. Increased proteolytic activity of aortic medial wall due to increased matrix metalloproteinases (MMP) (derived from aortic smooth muscle cells and macrophages) cause elastin and collagen degradation and increase in diameter of aneurysm. Collagen degradation in adventitia causes rupture. xx Familial aortic aneurysm (associated with 25% of AAA) is more prevalent in females to reduce male-to-female ratio to 2:1. It is related to decrease in type III collagen, α1 antitrypsin and lysyl oxidase. Marfan’s, Ehler Danlos syndromes are related genetically. xx Others: Syphilis, dissection, trauma, collagen diseases, infection, arteritis, cystic medial necrosis, association with Chlamydia pneumoniae (55%). Classification I –– Infrarenal—most common (95%). –– Suprarenal—5%. Isolated suprarenal type is rare; it is usually associated with thoracic and or infrarenal types. ™™ Classification II –– Asymptomatic. –– Symptomatic. –– Symptomatic ruptured. ™™

Asymptomatic Type xx It is found incidentally either on clinical examination or on

angiography or on ultrasound. xx Repair is required if diameter is over 5.5 cm on ultrasound. xx It is identified during routine abdominal palpation or while assessing or operating for some other abdominal conditions.

Symptomatic without Rupture (Clinical features/presentations) xx It presents as back pain, abdominal pain, mass abdomen

which is smooth, soft, nonmobile, not moving with respiration, vertically placed above the umbilical level, pulsatile both in supine as well as knee-elbow position with same

intensity, resonant on percussion. xx Common in males (4:1); common in smokers. xx GIT, urinary, venous symptoms can also occur. xx Hypertension, diabetes, cardiac problems should be looked for and dealt with. xx In infrarenal type upper border is clearly felt. xx Lower limb ischaemia and embolic episodes can occur.

xx Being a retroperitoneal mass back pain is common—may be due to retroperitoneal stretching, nerve irritation or vertebral erosion. xx 5% present as inflammatory aneurysm adherent to ureters, left renal vein, inferior vena cava and duodenum. Expanding aneurysm blocks lymphatics causing inflammation and fibrosis; or it may be due to infection and fibrosis of earlier localised ruptured abdominal aortic aneurysm. Such chronically inflamed aneurysm will not rupture further; but it is always symptomatic with fever and severe pain in abdomen and back. It needs surgical repair through retroperitoneal approach. xx Aortocaval fistula, presents as high output cardiac failure with continuous bruit in abdomen and severe lower limb ischaemia (steal phenomenon). xx Aortoenteric fistula is due to erosion of aneurysm into 4th part of duodenum presenting as GI bleed, malaena, shock. It is treated by duodenal closure, aortic ligation, aneurysmal exclusion with extraanatomic bypass graft with gastrojejunostomy. Contamination is the major threat here. xx Aneurysm in a patient with horseshoe kidney which is anterior to aorta is difficult to manage. Left retroperitoneal approach is needed. EVAR is not possible.

Investigations xx Blood urea, serum creatinine. xx US (most widely used noninvasive test; but neck of the aneu-

rysm, dimensions and relation to renal arteries are difficult to assess), aortogram, DSA, CT scan (most precise). US is an effective screening tool. Screening is done in cardiovascular patients in men (60–85 years), in women (60–85 years); men and women above 50 years with family history; annually in asymptomatic AAA with 4.0–4.5 cm size, with size >4.5 cm once in every 6 months. xx CT angiogram, MR angiogram. xx Blood sugar, lipid profile, other relevant investigations like ECG, echocardiography, cardiac and pulmonary assessment. Note:

X-ray will show eggshell calcification. CT scan is more reliable and precise investigation of choice—gives better information regarding extent on sides/neck, size, dimensions, size and site of the thrombus, calcification, relation of renal arteries, inflammation and fibrosis and adjacent tissues. MRI may be better only in renal failure patients.

Complications of abdominal aortic aneurysm ™™ ™™ ™™ ™™ ™™ ™™ ™™

Rupture, infection Thrombosis, embolism Distal ischaemia/gangrene Aortocaval fistula formation Aortoenteric fistula Erosion of vertebra Spinal cord ischaemia when thrombosis develops

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SRB's Manual of Surgery Treatment Conservative/Medical Treatment xx It is done in low-risk abdominal aortic aneurysm (age below 70 years; active physically without cardiac, respiratory, renal impairment and noninflammatory aneurysm); if aneurysm size is < 5 cm; if growth rate is < 0.5 cm/year. xx It includes risk factor modifications; stopping smoking; control of blood pressure (propranolol), cholesterol; usage of drugs—alpha blockers, elastase inhibitors (NSAID—indomethacin), matrix metalloproteinases (MMP) inhibitor (doxycycline). xx Periodic size measurement of an aneurysm using ultrasound once in 6 months to find out growth rate is essential during conservative treatment.

A

Surgical Treatment xx Indications for surgery  Asymptomatic aneurysm more than 5.5 cm.  Growth rate more than 0.5 cm/year.  Painful, tender aneurysm.  Thrombosed aneurysm, aneurysm with distal emboli. Low-risk abdominal aortic aneurysm—age below 70 years; active physically without cardiac, respiratory, renal impairment and noninflammatory aneurysm. Here surgical mortality is 3 mg%; liver failure status. Here surgical mortality is >10%.

xx Open surgical repair  It is called as endo-aneurysmorrhaphy with intraluminal graft placement (Crawford, 1960). It is done under GA with epidural support. Major challenges during anaesthesia are—blood loss, haemodynamic control, problems during clamping and declamping of aorta, temperature control, renal hypoperfusion, left ventricular strain.  Incision is commonly lengthy midline transperitoneal or supraumbilical transverse. Retroperitoneal approach is used in horseshoe kidney, abdominal wall stoma, inflammatory aneurysm, suprarenal extension, peritoneal dialysis, hostile abdomen. Retroperitoneal approach favors rapid control of proximal aorta but prevents visualisation of abdomen.  After laparotomy, duodenum and small bowel are retracted laterally and above; left renal vein which is in front of aorta is dissected and retracted; occasionally it may require to be ligated and it is safer provided left gonadal and left suprarenal veins are intact. Distal arterial clamps are applied first along common or external and internal iliac arteries on both sides. Proximal aortic clamp is applied at infrarenal level. Aorta is opened longitudinally midline towards right to avoid injury to orifice of inferior mesenteric artery. Atheroma, thrombus is removed until adequate back-bleeding occurs. Lumbar vessels are ligated from the luminal side. Knitted Dacron graft after preclotting or woven Dacron graft or ePTFE tube graft is used. Graft is anastomosed above and below using

Today’s impossibilities are tomorrow’s miracle.

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SRB's Manual of Surgery polypropylene sutures (4 zero). Inferior mesenteric artery can be reimplanted. Clamps are released first below. Colonic and limb perfusion is checked for adequacy. Graft is covered with aneurysmal sac.  Minimal incision aortic surgery (MIAS) is done in thin individual with midline abdominal incision 12 cm in length with its 9 cm part above the umbilicus. Specialised retractors and vascular clamps are used for this. Advantages are less postoperative pain, ileus and incisional hernia. xx Endovascular aneurysm repair (EVAR)  In 1991 Juan Parodi and Julio Palmaz first did EVAR. It is less invasive, less morbid with less mortality rate and shorter hospital stay. It is basically aneurysm exclusion method. It is useful in old age and patients who are not fit for surgery. EVAR is basically a prophylactic procedure. EVAR is indicated if aneurysm is less than 5.5 cm in men and less than 5.0 cm in women. It is usually done in patients after 65 years.  It is endoluminal stent graft placement into the aneurysmal segment of aorta using interventional radiology with Seldinger’s technique approach through femoral artery.  Dacron or ePTFE with integral metallic stent for support and firm attachment is used as stent/endovascular prosthesis.  One aortic and iliac (of one/same side) stent is commonly used together which is passed through same side common femoral. Other iliac is maintained with a separate stent approached through opposite common femoral.  Procedure can cause endoleak, thrombosis, embolism, malposition/displacement of stent, sigmoid ischaemia, renal failure, failure of stent function causing recurrence and infection.

C Graft in place in retroperitoneum Fig. 1.356C

Figs 1.356A to C: Abdominal aortic aneurysm with aortofemoral graft placement (Courtesy: Dr Ashok Shetty, MCH, Cardiothoracic Surgeon, Mangaluru).

Symptomatic Ruptured Aortic Aneurysm  Risk of rupture is 1%, if diameter is within 5.5 cm in size. Risk

increases to 20% once the diameter = 7 cm. It may be anterior rupture (20%) into the free peritoneal cavity causing severe shock and death very early; or posterior rupture (80%) with formation of retroperitoneal haematoma of large size causing severe back pain, hypotension, shock, absence of femoral pulses and with a palpable mass in the abdomen.  Management of Ruptured Aortic Aneurysm –– Immediate diagnosis by ultrasound. –– Resuscitation. –– Massive blood transfusions (10–15 bottles). –– Emergency surgery is the only life-saving pro­cedure in these cases.

Patient has to be shifted to the operation theatre. Abdomen is opened. Vascular clamps or bull dog clamps are applied to the aorta above and below the aneurysm. Adventitia is opened and the clot is removed. Aneurysm is excised and the arterial graft either PTFE (Polytetra­fluoroethylene), knitted dacron graft, or woven dacron graft is placed. The graft is sutu­red to the vessel above and below using monofilament, nonabsorbable suture material, polypropylene 5-zero. Complications of surgery

A ™™

B Aorto bifemoral dacron graft (Woven) with right femoral exposed Figs 1.356A and B

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

MI is the most common cardiac complication in perioperative and in first 2 days of postoperative period Haemorrhage and haemodynamic complications Renal failure—is most common noncardiac complication Colonic ischaemia—10% due to poor IMA circulation Sexual dysfunction Aortoduodenal fistula Aortovenacaval fistula Spinal cord ischaemia—paraplegia Paralytic ileus Distal thromboembolism—blue toe syndrome DVT Graft leak, graft thrombosis, graft failure Anastomotic disruption, pseudoaneurysm formation Prosthetic infection/migration

Arterial Diseases

Fig. 1.357: Infrarenal aortic aneurysm repair. It is the most common site of aortic aneurysm. Adventitia of aorta is opened; aneurysm is excised; graft is sutured above and below; adventitia is wrapped around.

A

B

Figs 1.358A and B: Endovascular aneurysm repair (EVAR). Aortic and one side iliac stent is used as one unit modulus which is passed through same side common femoral artery; opposite side iliac part is inserted as separate modulus through opposite CFA.

PERIPHERAL ANEURYSM

Remember ™™ ™™ ™™ ™™ ™™

™™ ™™

Pulsation of an aneurysm is expansile. Pulsation may be absent if it is thrombosed Abdominal aneurysm of any size which is painful or tender should be operated Abdominal aortic aneurysm of any size causing embolus should be operated Abdominal aortic aneurysm more than 5.5 cm should be operated In ruptured abdominal aortic aneurysm emergency surgery is the only choice operation with rapid resuscitation; immediate opening and repair using graft. Systolic pressure in this patient should be just adequate to maintain the cardiac function but should not be more than 100 mmHg as it will cause more bleeding Anterior rupture is more dangerous than posterior rupture Endoluminal stenting is becoming popular

xx Peripheral aneurysms are less common compared to aneurysms in the cavity. Such surface aneurysms are easily visible and better amenable for clinical examination. But same time it may be mistaken for abscess and inadvertent wrong attempt of incision and drainage can occur leading to disastrous consequences. xx Popliteal type is the most common one. Peripheral aneurysms occur in descending order of frequency in popliteal, femoral, subclavian, axillary and carotid arteries. xx Expansile pulsation which is confirmed using two finger placement with thrill and bruit is typical. Infection, thrombosis make it less pulsatile mimicking an abscess. xx Erosion into adjacent bone and skin, rupture are known to occur. Distal emboli may lead into digital gangrene. xx Pressure on the affected artery proximally reduces the size, and eliminates the thrill/bruit; pressure distal to aneurysm increases the prominence of the aneurysm swelling with bounding pulsation.

A positive thought is a seed of positive result.

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SRB's Manual of Surgery xx X-ray, arterial Doppler, angiogram, echocardiogram are needed. xx Treatment is open repair using arterial graft or endovascular stenting.

Popliteal Aneurysm xx xx xx xx

Is most common (70%). 65% are bilateral. 25% cases are associated with abdominal aortic aneurysm. 75% cause complications in 5 years. Fig. 1.361: Radial artery aneurysm.

Presentations xx Swelling in popliteal region which is smooth, soft, pulsatile,

well-localised, warm, compressible, often with thrill and bruit. It may mimic a pyogenic abscess. xx Thrombosis and emboli from popliteal aneurysm can cause distal gangrene which may spread proximally and may lead to amputation. xx Rupture may cause torrential haemorrhage.

xx Investigations

 Duplex scan, angiogram.  CT scan, MRI.

xx Treatment

 Aneurysmorrhaphy.  Repair with arterial graft using PTFE, Dacron.  Endoluminal stenting.

CAROTID ARTERY ANEURYSM (EXTRACRANIAL) Incidence is less than 4% of peripheral aneurysms. Most common site: Common carotid artery bulb, often extends into the internal carotid artery.

Fig. 1.359: Femoral artery aneurysm with impending rupture— needs emergency surgical intervention. It is rare type.

Fig. 1.362: Carotid aneurysm.

Causes xx xx xx xx

Fig. 1.360: Popliteal aneurysm about to rupture. It is the most common peripheral aneurysm.

Atherosclerosis, trauma. Syphilis, Marfan’s syndrome. Ehler-Danlos syndrome. Congenital.

Clinical Features ™™ 10% bilateral. ™™ Swelling in the neck at the level of the thyroid cartilage, below the angle of mandible. ™™ Pulsatile (expansile pulsation). ™™ Smooth, soft, nontender, horizontally mobile. ™™ Bruit felt. ™™ Neurological features due to embolic episodes (50%). ™™ Hoarseness of voice. ™™ Horner’s syndrome. ™™ Dysphagia. ™™ Swelling extending into the tonsillar bed.

Arterial Diseases Differential Diagnosis

xx It is commonly associated with aortic insufficiency.

Atherosclerosis is not a usual cause for dissecting aneurysm.

xx Carotid body tumour. xx Neurofibroma arising from the vagus. xx Abscess in neck.

I. Classification (DeBakey’s) Type I: Dissection begins in ascending aorta extends into descending thoracic aorta (70%) ™™ Type II: Dissection originates in ascending aorta and extends only up to the origin of the major vessels. It is safer type with less complications ™™ Type III: Dissection begins in the descending thoracic aorta beyond the origin of the left subclavian artery ™™

A

II.  Stanford classification

B Figs 1.363A and B: Basilar artery aneurysm—angiogram (Courtesty: Dr Muralidhar Pai, MCh, Mangaluru).

Complications xx Rupture. xx Thrombosis. xx Hemiplegia.

Proximal—includes DeBakey’s Type I and II Distal—includes DeBakey’s Type III III.  Dissecting aneurysm can be: ™™ Acute ™™ Chronic ™™ Healed dissecting aneurysm which communicates distally again to aorta as double barrelled aorta ™™ ™™

Investigations xx Doppler of neck, carotid angiogram. xx DSA, CT angiogram.

Treatment xx Reconstruction of the artery using vascular graft. xx Ligation of the bulb as a life-saving procedure, but results in hemiplegia. xx Intravascular stents.

DISSECTING ANEURYSM It is a misnomer. It is not an aneurysm, only an aortic dissection. It is the dissection of media of the aorta after splitting through intima creating a channel in the media of the vessel wall.

Causes xx xx xx xx xx

Hypertension (It is associated in 80% of dissecting aneurysms). Cystic medial necrosis. Marfan’s syndrome and collagen diseases. Trauma. Weakening of the elastic layers of the media due to shear forces.

Features xx It is always seen in thoracic aorta, common in ascending

aorta (70%). xx It is uncommon in other parts of aorta or other vessels. xx It can occur in aortic arch or thoracic descending aorta. xx This dissected aortic channel gets lined by endo­thelium, often reopens distally into the aorta causing double-barrelled aorta which, in fact, prevents complications.

Fig. 1.364: Dissecting aneurysm. Complications ™™ ™™

Acute: Rupture into the pericardium or pleura—dangerous type Chronic: Blockage of coronary vessels and major vessels like carotid and subclavian arteries with aortic insufficiency

Clinical Features xx Pain in the chest, back which is excruciating. xx Features of ischaemia due to blockage of different vessels. Investigations ™™ ™™ ™™

Chest X-ray shows mediastinal widening Arterial Doppler Angiogram

Imagination is the highest kite one can fly.

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SRB's Manual of Surgery Treatment Antihypertensives. Surgery: Using Dacron graft reconstruction of aorta has to be done with cardiopulmonary bypass. Indications for surgery ™™ ™™ ™™ ™™

Progressive disease Significant ischaemia Impending rupture Type A aortic dissection

ERYTHROMELALGIA (ERYTHRALGIA) xx It is also called as Mitchell’s disease; an episodic attack precipitated by heat, exertion and stress; common in lower limbs. Primary type is familial and autosomal dominant. Secondary type is seen in gout, erythrocyanosis frigida, polycythaemia, viral infection, mushroom poisoning, drug induced (verapamil, ergots, fluoroquinolines). There is microvascular and neuropathic changes. xx There is severe burning pain in the limbs with redness and sensation of heat. Warmness in the skin; often excoriation or ulceration, flushing, prominent veins, severe hyperesthesia are the usual features. xx Treatment: Mechanical cooling by elevating the limb (Note: Should not place the affected limb in cold water which may flare up the problems); aspirin; pregabalin, gabapentin, IV lignocaine are different drugs used in this condition.

LIVEDO RETICULARIS It is a condition with arteriolar spasm along with obstruction of capillaries by tiny blood clots with dilatation of venules, causing lace like purplish discoloration. Persistent, mottled, reddish-blue dermal streaks that do not blanche is typical. It may be idiopathic or related to vasculitis due to autoimmune conditions along with SLE or drug induced. Condition worsens by cold. Treating the cause; PUVA bath; warming the limb; exercise are different therapies.

POLYARTERITIS NODOSA xx It is a necrotising inflammatory reaction with commonly microscopic polyarteritis and nodule formation, often of small and medium-sized arteries (not capillaries), causing ischaemia of lower and upper limb. xx Visceral arterial (mesenteric) involvement (70%) can cause abdominal pain, GI bleed; mucosal ulceration and perforation of small bowel. Massive hepatic infarction, cholecystitis can develop. xx Renal artery can cause loin pain, haematuria, and renal hypertension. xx Coronary artery also can get involved causing myocardial infarction. xx Disease is common at bifurcation of medium/small sized arteries leading to localised aneurysms. xx It is common in males (3:1); fever, weakness, myalgia, arthralgia are early features. xx Presents with localised small aneurysms, like multiple 5–10 mm nodules, palpable along the course of the artery. xx In late stage presents with myocardial infarction, renal failure, sepsis, GI bled. xx HBsAg is positive in 40% patients of polyarteritis nodosa. xx Angiogram of renal, mesenteric, peripheral arteries will show aneurysms at branching points.

xx Biopsy of tender nodule, tender muscle is useful for diagnosis. xx Treatment is prednisolone 60 mg daily with cytotoxic drugs. xx Prognosis is poor with rapid death in early years.

SCLERODERMA/SYSTEMIC SCLEROSIS xx It is a progressive disease causing fibrosis of skin, GI tract, lungs, heart and kidney. xx It is common in females (4:1) at 4th/5th decade. xx It is considered as vasculitis even though earlier considered as collagen disease. xx Pathology consists of cytotoxic endothelial injury causing interstitial oedema, severe fibroblast proliferation causing fibrosis of affected vessels, and dilatation and proliferation of remaining capillaries as telangiectasis. xx Thin epidermis, thick dermis with more collagen with absence of appendages and rete pegs are typical. xx Lower 2/3rd oesophagus is sclerosed (50%) with increased collagen in submucosa with atrophied mucosa and muscularis. Dysphagia is common. xx Diffuse interstitial fibrosis, thickening of alveolar membrane and pulmonary hypertension occurs. xx Synovial thickening causes arthritis; fibrosis of skeletal muscles; interstitial myocardial fibrosis causes bundle branch block, pericardial effusion. xx Glomerulosclerosis in kidney is common (50%). Renal failure is common. xx Fibrosis of thyroid, periodontal membrane can occur. Malabsorption syndrome is common due to small bowel involvement. xx Involvement of digital arteries present as Raynaud’s phenomenon. xx Calcinosis, Raynaud’s, oesophageal hypomotility, sclerodactyly, and telangiectasia are the presentation of CREST syndrome. xx Investigations—anaemia, raised ESR, elevated IgG, presence of antinuclear antibodies and anticentromere antibodies (in CREST)—are different laboratory findings. Skin and peripheral arterial biopsy is confirmative. xx Treatment—is difficult. Drugs like D pencillamine, colchicines, p amino benzoic acid, vitamin E, dimethyl sulfoxide, ranitidine are tried at various levels. Vasodilators, warming and massaging skin, avoiding detergent soaps, oil and hydrophilic ointment application are used. Steroids, oxygen therapy for irreversible pulmonary fibrosis; haemodialysis for renal failure; digitalis and other drugs for cardiac failure are needed later. xx Death is due to cardiac/pulmonary/renal failure.

ACROCYANOSIS (CRURUM PUELLARUM FRIGIDUM) xx It is persistent, painless cyanosis seen in fingers and often in legs with paraesthesia and chilblains affecting young females. xx It is chronic persistent arteriolar constriction with slow rate of blood flow. xx Trophic changes and ulcerations are not seen. xx Cyanosis which is persisting may aggravate on exposure to cold. xx It may be associated with endocrine dysfunction.

Treatment xx Vasodilators. xx Cervical sympathectomy (effective).

Arterial Diseases Raynaud’s phenomenon

Acrocyanosis

• Episodic

• Persistent

• Painful

• Painless

• Acute arteriolar spasm

• Chronic constriction

• Ischaemic changes are common

• Ischaemic changes are not seen

GANGRENE Fig. 1.366: Dry gangrene—great toe.

If the tips of (the patient’s) fingers are falling off and are black, he will die.

—(Anonymous), circa 2000 BC



It is macroscopic death of tissue in situ (in continuity with adjacent viable tissue) with putrefaction (there will be loss of function also). A It can occur in sites like: ™™ ™™ ™™ ™™ ™™

Limbs Appendix Bowel Testes Gallbladder

Causes xx Secondary to arterial occlusion like athero­sclerosis, emboli,

B

xx Infective: Boil, carbuncle, gas gangrene, Fournier’s

Figs 1.367A and B: Gangrene of foot and leg. Note the line of demarcation. But skip lesion proximally shown signifies more proximal spread of gangrene which may need above knee amputation.

diabetes, TAO, Raynaud’s disease, ergots. gangrene, cancrum oris.

xx Traumatic: Direct, indirect. xx Physical: Burns, scalds, frostbite, chemicals, irradia­tion,

electrical. xx Venous gangrene.

Clinical Features xx Colour changes: Pallor, greyish, purple, brownish black due

to disintegration of haemoglobin to sulphide.

xx Absence of pulse, loss of sensation, loss of function. xx Line of demarcation between viable and dead tissue by a

band of hyperaemia and hyperaesthesia along with development of a layer of granulation tissue.

 In dry gangrene the separation occurs by aseptic ulceration with minimum infection and the gangrene is dry and mummified.   In wet gangrene, separation takes place by septic ulceration. Often demarcation is vague with skip lesions more proximally and so landing with higher level of amputations. Even after amputation skin flap may show die back process, leading to failure of taking up of flap of amputation and so requiring still higher level of amputation. xx Proximal ischaemic features may be present with rest pain, colour changes, hyperaesthesia—pregangrene. Types of gangrene Dry gangrene is due to slow, gradual loss of blood supply to the part causing dry, desiccated, wrinkled, mummified part with proper line of demarcation from the viable adjacent tissues ™™ Wet gangrene is due to infection with putrefaction, causing oedematous, swollen, discoloured part, spreading proximally, with vague line of demar­cation from the adjacent viable tissues ™™

Investigations Fig. 1.365: Gangrene foot with ischaemic ulcer.

xx Hb%, blood sugar. xx Arterial Doppler, angiogram (Seldinger technique). xx US abdomen to find out the status of aorta.

Today well lived makes every yesterday, a dream of happiness and tomorrow, a vision of hope.

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SRB's Manual of Surgery Differences between dry gangrene and wet gangrene Dry gangrene

Wet gangrene (Moist)

Clear line of demarcation is seen

Line of demarcation is vague

Dry, shriveled, mummified

Oedmatous, putrified, discoloured (H2S)

Slow, gradual loss of blood supply

Sudden loss of blood supply

Separation is by aseptic ulceration

Septic ulceration causes separation

Limits to the demarcation

Can extend proximally rapidly

Causes are atherosclerosis, TAO

Emboli, trauma are the causes

Limited amputation is sufficient

Major higher amputation is often needed

can be fitted better and also the move­ments of knee joint are retained. There is no need of external support and limp is absent. xx In above-knee amputation range of movements are less, limp is present, and often requires third (stick) support to walk. Different amputations done are Ray amputation, below-knee amputation (Buerger’s amputation), Gritti-Stokes transgenial amputation, above-knee amputation. Lisfranc’s, Chopart’s, Symes’, Modified Symes’ amputations are not commonly used in ischaemic limb as flaps will not survive.

DIABETIC FOOT AND DIABETIC GANGRENE Fig. 1.368: Ischaemic features of right hand; compare to left side which is normal.

Treatment Limb saving methods: xx Drugs: Antibiotics, vasodilators, pentoxiphylline, praxilene, dipyridamole, small dose of aspirin, ticlopidine. xx Care of feet and toes:  The part has to be kept dry.  Any injury has to be avoided.  Proper footwear is advised (Microcellular rubber footwear, MCR).  Measures for pain relief is taken.  Nutrition supplementation is done.  The limb should not be warmed.  Pressure areas has to be protected.  Localised pus has to be drained. xx Cause is treated. xx Diabetes is controlled. xx Surgeries to improve the limb perfusion: Lumbar sympathectomy, omentoplasty. Profundaplasty, femoropopliteal thrombectomy or endarterectomy, arterial graft bypass are done according to the need. Life-saving procedures: Amputations may have to be done ofen. Level of amputation is decided on skin changes, temperature, line of demarcation, Doppler study. xx Below-knee amputation is a better option as BK prosthesis

Foot is a complex structure with many layers of muscles, ligaments, joints, arches, fat, thick plantar fascia, vascular arches, neurological system which maintains weightbearing, gravity, normal walk, stability and gait (swing and stance phases). Problems in diabetic foot Callosities, ulceration Abscess and cellulitis of foot Osteomyelitis of different bones of foot like metatarsals, cuneiforms, calcaneum ™™ Diabetic gangrene ™™ Arthritis of the joints ™™ ™™ ™™

Meggitt’s classification of diabetic foot ™™ ™™ ™™ ™™ ™™ ™™

Grade 0: Foot symptoms like pain, only Grade 1: Superficial ulcers Grade 2: Deep ulcers Grade 3: Ulcer with bone involvement Grade 4: Forefoot gangrene Grade 5: Full foot gangrene

Pathogenesis of Diabetic Foot/Gangrene xx High glucose level in tissues is a good culture media for

bacteria. So infection is common.

xx Diabetic microangiopathy causes blockade of micro­

circulation leading to hypoxia.

xx Diabetic neuropathy: Due to sensory neuropathy, minor

injuries are not noticed and so infection occurs. Due to motor

Arterial Diseases –– Feet has to be kept clean and dry, especially the toes

neuropathy, dysfunction of muscles, arches of foot and joints occurs. And loss of reflexes of foot occurs causing more prone for trauma and abscess. Due to autonomic neuropathy, skin will be dry, causing defective skin barrier and so more prone for infection. xx Diabetic atherosclerosis itself reduces the blood supply and causes gangrene. Thrombosis can be pre­cipitated by infection causing infective gan­grene. Blockage occurs at plantar, tibial, and dorsalis pedis vessels. xx Increased glycosylated haemoglobin in blood causes defective oxygen dissociation leading to more hypoxia. At tissue level there will be increased glycosylated tissue proteins, which prevents proper oxygen utilisation and so aggravates hypoxia.

and clefts.

–– Hyperkeratosis has to be avoided.

Clinical Features Pain in the foot. Ulceration. Absence of sensation. Absence of pulsations in the foot (Posterior tibial and dorsalis pedis arteries). xx Loss of joint movements. xx Abscess formation. xx Change in temperature and colour when gangrene sets in. xx Patient may succumb to ketoacidosis, septicaemia or myocardial infarction. xx xx xx xx

Fig. 1.369: Diabetic foot with ischaemic ulceration and gangrene.

Investigations xx xx xx xx xx xx xx xx

Blood sugar, urine ketone bodies. Blood urea and serum creatinine. X-ray of part to look for osteomyelitis. Pus for culture and sensitivity. Doppler study of lower limb to assess arterial patency. Angiogram to look for proximal blockage. Ultrasound of abdomen to see the status of abdominal aorta. Glycosylated haemoglobin estimation.

Treatment xx Foot can be saved only if there is good blood supply.

 Antibiotics—decided by pus C/S.  Regular dressing.  Drugs: Vasodilators, pentoxiphylline, dipyridamole, low

dose aspirin.

 Diabetes is controlled by insulin only.  Diet control, control of obesity.  Surgical debridement of wound.  Amputations of the gangrenous area. Level of amputa-

tion has to be decided by skin changes and temperature changes or Doppler study.  Care of feet in diabetic: –– Any injury has to be avoided. –– MCR footwears must be used (Microcellular rubber).

Fig. 1.370: Gangrene of 3rd and 5th toes in a diabetic. Patient already underwent amputation of 4 the toe earlier for gangrene.

TROPHIC ULCER xx Aetiology: Diabetic neuropathy, spinal injury and diseases, other neuropathies. Causes ™™ ™™ ™™ ™™ ™™

Pressure Anaemia Malnutrition Injury Moisture

xx Common Sites: Heel, heads of metatarsals, sacrum, ischium, occipital region. Bedsore is a trophic ulcer. xx Clinical Features: They are deep, punched out, nonmobile ulcers, with bone as its base. xx Investigations: X-ray spine, nerve conduction studies, blood sugar, Hb%. xx Treatment

Don’t wait for your ship to come; swim out to it.

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Nutrition is improved. Anaemia is treated. Diabetes is controlled. Regular dressing is done. Pressure and injuries has to be avoided.

BEDSORES (Decubitus Ulcer) (Pressure Sores) Bedsore is a trophic ulcer with bone as the base. It is nonmobile, deep, punched out ulcer. It is common in Old age Bedridden

Tetanus

Diabetic Paraplegic

Comatose

Patients with orthopaedic and head injuries

Sites of bedsore are occiput, heel, sacrum, ischium, scapula. Factors: Malnutrition, pressure, anaemia, sensory loss, moisture.

Treatment xx Gradual warming is done. Part should be wrapped with cottonwool and rested. Warming is gradually done with 44°C in 30 minutes with warm water. Limb elevation is done to reduce oedema. Intra-arterial vasodilators may help. xx Warm drinks, analgesics, paravertebral injections to sympathetic chain, hyperbaric oxygen are effective. xx If gangrene develops, amputation is needed.

AINHUM Ainhum also known as ‘dactylolysis spontanea’ is a painful constriction of the base of the fifth toe frequently (occasionally other toes also) followed by bilateral spontaneous auto-amputation a few years later. Grooving → pain → constriction deepens → tendon, nerve and vessel involvement → bone gets cut spontaneously without any bleeding (auto-amputation) in many (2–5) years. xx Commonly affects males (can also occur in females). xx Common in blacks, in Negroes. xx History of running barefoot in childhood is common. xx Fifth toe is commonly affected. xx A fissure develops at the interphalangeal joint which becomes a fibrous band, that encircles the digit causing necrosis (Gangrene of little toe). xx Often it can be bilateral.

Fig. 1.371: Large bedsore over the sacrum in a abedridden patient. Note the size and slough on the surface.

Treatment Change of positions is always encouraged. Use of water bed, ripple bed is advised. Moisture has to be avoided. Soaking by urine, sweat, pus, and faeces has to be taken care off. Good nursing, regular dressing, good nutrition are necessary. Antibiotics, blood transfusions are very essential. Excision of dead tissue followed by skin grafting or local rotation flaps may have to be done. xx Rehabilitation. xx xx xx xx xx xx xx

FROSTBITE xx It is due to exposure to cold wind or high altitude. xx It is common in old age during cold spells. xx Damage to vessel wall occurs causing oedema, blistering, gangrene formation. xx Part is painless and waxy. xx Cells get frozen at – 5°C. Initially redness and oedema (1st degree); blister formation (2nd degree); skin necrosis (3rd degree); gangrene (4th degree) develops gradually.

Fig. 1.372: Bilateral Ainhum involving 4th and 5th toes of both feet. Note the constriction ring in the toes. Treatment: It is early “Z” plasty. Amputation is often required later. Most often autoamputation occurs. Note:

Yoruba people of Nigeria named ainhum.

ENDOVASCULAR SURGERIES It is mainly used in peripheral vessels like femoropopliteal, renal, coronary, cerebral vessels.

Types xx Balloon angioplasty: It is useful in short segment stenosis in large vessles like renal vessels, iliofemoral, coronary vessels. It is less effective compared to open surgery. xx Intravascular stenting: Balloon expandable and self-expanding stents are used at stenosed area. xx Endovascular grafts (PTFE, DACRON).

Arterial Diseases xx Endovascular atherectomy. xx Angioscopy: Flexible, small, fibreoptic scopes to visualise vessel wall with sufficient irrigation to avoid opacifi­cation by blood. xx Intravascular ultrasound: To evaluate the vessel wall morphology. Indications ™™ ™™ ™™ ™™ ™™ ™™

Aneurysm for stenting and grafting Aortoiliac constrictive disease Renal artery stenosis Carotid occlusive disease AV fistulas Management of pseudoaneurysm

Complications xx xx xx xx xx

Fig. 1.373: Upper limb ischaemia with gangrene extending proximally towards elbow joint.

Chronic Type

Thrombosis. Rupture. Sepsis. Fluid overload. Air embolism.

UPPER LIMB ISCHAEMIA It is a rare uncommon entity compared to lower limb ischaemia but important because of its difficulty in managing. Higher-level amputations are rare in upper limb ischaemia. Its incidence is rare (5%) due to abundant collateral supply, infrequency of atherosclerosis, decreased metabolic demand and smaller muscle mass. It mostly affects distal small arteries (90%). Symptoms are usually delayed.

Types of Upper Limb Ischaemia xx Acute. xx Chronic.

Acute type Causes: xx Embolism—common: 30% of the peripheral emboli lodge in upper extremity. The most common site is at the bifurcation of brachial artery (40%); next common is at axillary artery (12%). Embolism is due to:  Cardiac origin (70%)—valvular lesions (atrial fibrillation, endocarditis), IHD, paradoxical.  Others—aneurysms, thoracic outlet syndrome, plaque. xx Trauma—most common: Brachial artery injury is seen in 30% of civilian trauma with arterial injuries, blunt injuries, fractures and dislocations, penetrating injuries. xx Iatrogenic. xSymptoms x Post AV fistula ‘Steal syndrome’. of acute ischaemia x™ x Aortic dissection. ™ Pain, pallor, poikilothermia, paraesthesia, paralysis.

Causes: xx Arteritis—aortoarteritis, Takayasu arteritis, giant cell arteritis, connective tissue disease/vasculitis—scleroderma, SLE, RA, PAN, etc. xx Atherosclerosis—most common cause in USA. xx TAO of upper limb. xx Others—fibromuscular dysplasia; postirradiation—lung, breast; occupational injuries; vibration injury, hypothenar hammer syndrome; hypercoagulable states; APLA, polycythemia, cold agglutinins. Symptoms of chronic ischaemia ™™ Upper limb ‘Claudication’. ™™ Weakness and wasting. ™™ Digital ischaemia—ulcer, gangrene in finger tips. ™™ Raynaud’s phenomenon. Signs of chronic ischaemia ™™ Wasting of arm, forearm and hand muscles. ™™ Ischaemic changes in skin; tapering of finger tips. ™™ Drop in systolic pressure >20 mmHg. ™™ Proximal thrill or bruit. ™™ Mass in the neck, thrill and bruit in the neck in supraclavicular region. ™™ Adson test, hyperabduction (Halsted) test, Roos test, Allen`s tests are important.

Raynaud’s Phenomenon xx It is episodic vasospasm. It is common in upper limb. xx Raynaud’s disease: It is primary Raynaud’s phenomenon—no cause could be demonstrated (Idiopathic). xx Raynaud’s syndrome: It is secondary Raynaud’s phenomenon— secondary to a demonstrable lesion like SLE, scleroderma, TAO or atherosclerosis. xx Symptoms: Pain, discolouration, sensation of cold and numbness, pronounced on exposure to cold, and under stress. xx Signs: Cyclical colour changes—Pallor, Cyanosis and Rubor with swelling; seen in fingers, toes, nose, ear lobes and lips. xx Pathology of Raynaud’s phenomenon: Exaggerated vasomotor response to stress; more common in females; no structural changes in the vessels, except in late stages; recurrent attacks can lead to atrophy of skin, subcutaneous tissue and muscles, ischaemic ulcers and gangrene.

He who attempts the absurd can achieve the impossible.

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SRB's Manual of Surgery xx CT scan neck and thorax. xx Blood sugar, lipid profile, cardiac evaluation.

Fig. 1.374: Left upper limb ischaemia with gangrene of three fingers and ischaemic changes in hand, forearm and arm.

Fig. 1.376: Upper limb angiogram showing blocks in subclavian artery.

A Fig. 1.375: Gangrene of left index finger. Patient has undergone cervical sympathectomy.

Investigations in Upper Limb Ischaemia xx Lab tests for vasculitis, hypercoagulable states, and athero-

sclerotic risk factors.

xx X-rays—for cervical rib; clavicular and first rib fractures;

fractures and dislocations in extremity; pulmonary lesions of connective tissue disorders. xx Arterial Doppler study. xx Angiogram (Subclavian angiogram)—CT/MR; conventional.

A

Figs 1.377A and B: (A) Carotid subclavian bypass; (B) Subclavian carotid transposition.

Management of Upper Limb Ischaemia xx Treatment of the cause.

Treatment of Embolus xx Time since the first symptom is very important. xx Clinical assessment of extent of ischaemia, immediate anticoagulation with heparin, Doppler study and angiogram of the arterial system, evaluation for the source of embolus—are the protocols. xx Embolectomy

Arterial Diseases  Brachial embolectomy: Local/regional/general anaesthesia is

used. Longitudinal incision in the arm is used for proximal embolus; Lazy S-shaped incision across the elbow is done for embolus extending into the bifurcation and to expose the branches.

Upper limb ischaemia ™™ ™™ ™™ ™™

Treatment in Trauma

™™

xx General evaluation and resuscitation. xx Control of bleeding in open wound: Pressure bandage/manual compression (DO NOT USE TOURNIQUET). xx Time since the event and clinical assessment of limb perfusion. xx Stabilisation of fractures and dislocations xx Doppler study of arterial system, angiogram if required. xx Arterial repair; bypass graft either venous or synthetic.

Treatment of Chronic Ischaemia xx Medical management  Risk modification—diabetes, hypertension, dyslipidemia, smoking, homocystinaemia, exercise training.  Antiplatelets—aspirin/ticlopidine/clopidogrel.  Anticoagulants—heparin/warfarin.  Xanthines/pentoxiphylline/cilostazol. Cilostazol—suppresses cAMP phosphodiesterase III rise in cAMP levels with antiplatelet, antithrombotic effects; induces vasodilatation; increases plasma HDL cholesterol; decreases plasma triglycerides. xx Catheter based interventions  Atherectomy.  Angioplasty + stenting by conventional or subintimal approach.  Stent grafts.  Cryoplasty. xx Surgery  Endarterectomy.  Bypass surgery.  Sympathectomy, extraperiosteal resection of the cervical rib.

Bypass Surgeries in Upper Limb Ischaemia

™™ ™™ ™™ ™™ ™™

Trauma/cervical rib are the common causes Opposite limb, lower limbs should be examined Cardiovascular system should be examined Neck should be examined Wasting/girth should be checked All relevant clinical methods are equally significant Auscultation over neck/axilla/carotids for bruit are important Doppler; angiogram; nerve conduction studies; CT neck and thorax are essential investigations Arterial repair; therapy for cervical rib; scalenotomy; cervical sympathectomy are the different modalities of treatment Digital amputation may be required

ARTERIAL SUBSTITUTES Ideal arterial substitute is not yet developed. Ideal arterial substitute should be strong, durable for patient’s life, biocompatible, nonthrombogenic, should be resistant for infection, easily available, should have a long-term patency rate, and should have elastic property of normal artery. Features of ideal graft Strong Durable for patient’s life Non-thrombogenic Biocompatible Resistant to infection Flexible Should maintain long-term patency Should have elastic property of normal artery

Should be leak proof on restoration of blood flow Should not chemically or physically degenerate Should not cause any abnormal reaction to surrounding tissues Should not occlude when flexed Should not damage blood contents

xx Conventional bypass  Aorto-subclavian/axillary bypass.  Subclavian: Axillary/brachial bypass.  Brachiodistal bypass. xx Extra-anatomical bypass  Carotid: Subclavian/Axillary bypass.  Subclavian: Subclavian bypass.  Axillary: Axillary bypass. xx Subclavian: Carotid transposition.

Carrel and Guthrie first did venous autograft into arteries of dogs. They did extensive histological study of viable and nonviable grafts. Lexer in 1907 used saphenous vein for axillary artery repair. Murray started to use intraoperative heparin. Enaz Moniz and dos Santos originated technique of arteriography. Gross and his colleagues in 1948 started to use viable arterial allografts. Later it was found that, as of graft is considered tissue viability is not essential for success of graft uptake.

Treatment of Raynaud’s Phenomenon

Classification of Arterial Substitutes

xx Avoiding triggering agents xx Drugs (vasodilators)—calcium channel blockers, angiotensin II receptor blockers, alpha-1 adrenergic blockers, Sildenafil, prostaglandin E1. xx Surgery—sympathectomy.

xx Arterial allograft—not used. xx Arterial autograft—internal mammary artery (common), internal iliac artery. xx Arterial xenograft—bovine carotid artery graft—not used. xx Venous autograft—long saphenous vein (common), small saphenous vein, basilic vein, cephalic vein. xx Venous allograft—umbilical vein graft. xx Prosthetic grafts

Note:

Individual topics about causes of upper limb ischaemia are discussed in different places.

The greatest happiness of life is the conviction, that we are loved.

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SRB's Manual of Surgery  Textile grafts –– Dacron graft—knitted or woven or crimping or velour

types. Dacron is polyethylene terephthalate.

–– Teflon graft—knitted or woven crimping or velour types.

 Non-textile semi-inert polymer graft: –– ePTFE graft—expanded polytetrafluoroethylene graft.

Preclotting the noncoated knitted or woven Dacron graft is done to seal the graft and to prevent leak, and to create a smooth lining at graft—blood interface. This step is not necessary for PTFE or newer grafts.

Complications of Graft xx Neointimal fibrous hyperplasia at suture lines of the graft is due to surgical trauma, PDFG, arterial smooth muscle proliferation. xx Graft infection—incidence is 2%. It is more in lower limb graft

than abdominal graft. Peroperative cephalosporin administration reduces the rate of graft infection. If infection occurs graft should be removed and revascularisation is achieved using a saphenous vein graft. xx Graft failure is rare but can occur. It is due to fiber degeneration, manufacturing defect, diffuse dilatation of graft (is due to expansion of the knit in knitted Dacron). xx Anastomotic false aneurysm (3%) occurs just adjacent to suture line towards host artery. It is tearing of the artery adjacent to suture line due to mismatched graft artery compliance, improper suture placement, and arterial degeneration. There will be partial or total separation of the graft from the host with blood collection in a covering of fibrous capsule. Eventually it will rupture/may cause thrombosis and embolism. Treatment is graft—artery reanastomosis with insertion of additional piece of graft.

M. Vascular Lesions and Hamartoma CHAPTER OUTLINE ™™ Vascular Anomalies ™™ Haemangioma ™™ Vascular Malformations

™™ Cirsoid Aneurysm ™™ Arteriovenous Fistula ™™ Campbell De Morgan Spots

VASCULAR ANOMALIES xx It is a collective term used for haemangioma and vascular malformations. xx Haemangioma is a benign tumour containing hyperplastic endothelium with cellular proliferation with increased mast cells. Growth in tissue culture is observed. It is absent at birth, seen by 1 month in 30%. It usually shows biphasic growth phase with slow involution. 95% of cases achieve spontaneous involution. Fast growing type can cause platelet trapping and thrombocytopenia. Associated skeletal changes are not common but can occur. But bone erosion by the lesion can occur. It is common in girls (3:1). xx Vascular malformations are single layer endothelium lined spaces derived from arterial, capillary, venous or lymphatic system. There is no growth in tissue culture. Raise in mast cells is not seen. 90% cases are seen at birth; only few at later period. It is equal in both sexes (1:1). Quiescent endothelium with vessels showing progressive ectasia is the feature. Intravascular coagulation and mild thrombocytopenia can develop. Skeletal changes and overgrowth are common. Spontaneous involution is not common. xx Disfigurement, tissue destruction, deformity, dysfunction, telangiectasia, skin scarring are common. xx Szilagyi classification—(1) Cavernous haemangioma; (2) Microfistulous AV communications; (3) Macrofistulous communications; (4) Anomalous mature vascular channels. xx Humburg classification—(1) Predominantly arterial/venous/ lymphatic defects with aplasia or obstructive dilatation which is limited or infiltrative; (2) Predominantly AV shunting defects with deep/superficial limited or infiltrating lesions; (3) combined vascular defects—arterial, venous and haemolymphatic which may be limited or infiltrating. xx Diagnosis is made clinically and by radiological imaging— coloured Doppler, DSA, MRI. MRI is better than CT to identify the flow (MR angiogram is ideal). Haemangiomas show intense parenchymal staining; vascular malformations show ecstatic vessels without much parenchyma; AVM shows rapid venous shunting.

™™ Parry-Romberg Disease ™™ Hamartomata

HAEMANGIOMA xx It is the most common tumour in children (in 10% of term

deliveries). xx It shows cellular endothelial hyperplasia with increased

mast cells. xx Onset is few weeks after birth with biphasic growth

showing initial rapid growth with gradual involution over 5–7 years. xx It is benign vascular endothelial tumour, common in girls (3 : 1). xx It is commonly seen in skin and subcutaneous tissue but can occur anywhere in the body like in liver, brain, lungs or other organs. xx It grows rapidly in first year and 70% involutes in 7 years. xx Early proliferative lesion is bright red, irregular; deep lesion is bluish coloured. Involution causes colour fading, softness, shrinkage leaving crepe paper like area. xx Commonly it is central; common in head and neck region (60%). xx Often large haemangiomas may be associated with visceral anomalies. Head and neck haemangioma is associated with ocular and intracranial anomalies; sacral with spinal dysraphism. Multiple cutaneous haemangiomas may be associated with haemangioma of liver causing hepatomegaly, cardiac failure (CCF), anaemia. xx Ulceration, bleeding, airway block and visual disturbances are common complications. xx A definitive even though rare, but important life-threatening complication is platelet trapping and severe thrombocytopenia presenting as ecchymosis, petechiae, intracranial haemorrhage massive GI bleed.

You may be disappointed if you fail, you are doomed if you don’t try.

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SRB's Manual of Surgery xx Raised angiogenic (fibroblastic) growth factor which is

secreted in patient’s urine is useful lab investigation to differentiate it from vascular malformations. Haemangioma classification (old) Capillary –– Strawberry haemangioma ™™ Cavernous haemangioma ™™

Note: Salmon patch and port wine stain are actually capillary vascular malformations even though they were earlier classified under capillary haemangioma.

Capillary Vascular Malformations xx Salmon patch (stork bite):  It is actually capillary vascular malformation also called as naevus simplex; it is very commonly seen in 40% of newborns.  It presents at birth. It commonly occurs in nape of the neck (50%), face, scalp and limbs. It usually involves wide area of skin. It is caused by an area of persistent fetal dermal circulation. With age, it goes for spontaneous regression and disappears completely (usually in one year). Hence masterly inactivity is the treatment.

Fig. 1.379: Port-wine stain (Naevus flammeus).

Capillary Haemangioma xx Strawberry haemangioma:  It may start at birth or child is normal at birth; between

one to three weeks it appears as red mark which rapidly increases in size in 3 months to form strawberry/raspberry haemangioma. It contains immature vasoformative tissues. There will be eventually intravascular thrombosis, fibrosis and mast cell infiltration.

Fig. 1.378: Salmon patch. xx Port-wine stain (Naevus flammeus):  It presents at birth and persists throughout life without any change. Spontaneous regression will not occur. It presents as smooth, flat, reddish blue/intensely purple area; common in head, neck and face; often with maxillary and mandibular dermatomes of 5th cranial nerve. Eventually surface becomes nodular and keratotic.  It persists throughout life. It is less common; seen in 0.3% of all newborns. It is also a capillary vascular malformation.  It is actually a capillary malformation even though considered under haemangioma. It results from defect in maturation of sympathetic innervation of skin causing localised vasodilatation of intradermal capillaries.  It is often associated with Sturge-Weber syndrome, KlippelTrenaunay-Weber syndrome and Proteus syndrome.  It needs treatment—laser (pulsed dye/diode); excision and grafting; cosmetic coverage. Expected result by treatment is not possible many times. Note:

Presently word ‘capillary haemangioma’ is restricted to strawberry type only; salmon patch and port-wine stain are actually classified under vascular malformations.

Fig. 1.380: Strawberry haemangioma.

It is a true capillary haemangioma. It is 20 times more common than port wine stain. It is common in white girls. Male to female ratio is 1 : 3. It is common in head and neck region. It is clinically compressible, warm with bluish surface. Bleeding can occur after minor trauma and also ulceration. It involves skin, subcutaneous tissues and often muscles also.  After one year of age, it slowly begins to disappear, and completely in 7–8 years (70% in 7 years).  It is the most common haemangioma.       

Vascular Lesions and Hamartoma ™™

™™

™™ ™™ ™™ ™™

Haemangioma in periorbital region obstructs the vision in newborn with amblyopia and if it persists for 7 days causes permanent visual damage. Astigmatism also can occur Haemangioma in nasal area in newborn may obstruct nasal airway seriously (as newborn cannot breathe through mouth— obligatory nasal breathing) Skin ulceration may cause haemorrhage Infection can occur which may lead into sepsis, necrosis or rarely septicaemia Systemic steroid for 3 weeks induces involution Usually there is no role for surgery. Surgery is done only for retained tissue after involution

Contd... Maffucci syndrome: Cavernous haemangioma + dyschondro­plasia Proteus syndrome: Naevus flammeus + regional gigantism with lymphaticovenous malformation (asymmetrical hypertrophy) ™™ Osler-Rendu-Weber syndrome: Haemangioma of skin and lip with gastrointestinal tract haemangioma (hereditary haemorrhagic telangiectasia), (autosomal dominant) ™™ ™™

Cavernous Haemangioma xx It is present at birth and consists of a multiple venous

channels. xx Its size increases gradually and may cause problems. xx It often contains feeding vessels which is of surgical

Treatment xx They are treated by wait and watch policy commonly—

allowed for spontaneous regression. xx Pulsed dye laser (diode laser), surgical excision and reconstruc-

tion. Feeding vessels may need to be ligated after wide exposure before achieving complete extirpation. Sclerotherapy/ cryotherapy/CO2 snow therapy cause unpleasant scarring. xx Preoperative embolisation facilitates surgical excision and reduces the operative blood loss. When once embolisation done, surgery should be done as early as possible otherwise recurrence occurs and much more worried formation of enlarged collaterals can occur. xx Materials used are—foam, plastic spheres, stainless/platinum steel coils, ethanol, polyvinyl alcohol foam of 1000 µ meters size, and rapidly polymerizing acrylic. Problems are tissue necrosis, reaction, normal tissue embolisation. Procedure is done with interventional radiology under image intensifier guidance. xx Rapidly growing haemangioma may need systemic/oral and intralesional steroid therapy. xx Antiangiogenic interferon 2a may be useful. xx Life-threatening platelet trapping may be controlled by cyclophosphamide chemotherapy. xx Haemangioma with drug resistant CCF can be treated with radiotherapy.

Uncontrolled growth Functional impairment like vision or hearing Accidental haemorrhage

Associated syndromes Klippel-Trenaunay-Weber syndrome: Naevus flammeus + osteo­ hypertrophy of extremities (soft tissue and bone hypertrophy) + varicose veins of lower limbs. If there is an association of arteriovenous fistula (AV fistula), it is called as Parkes-Weber syndrome ™™ Kasabach Merritt syndrome: Capillary haemangioma + DIC (Disseminated intravascular coagulation) with thrombocytopenia ™™ Sturge-Weber syndrome: Haemangiomas (Naevus flammeus) + hemiplegia and Jacksonian epilepsy (calcified vascular cerebral and meningeal deposits) + glaucoma ™™

Contd...



internal organs. xx Large or multiple cavernous haemangiomas can cause

congestive heart failure (hyperdynamic) due to shunting of large quantity of blood. xx Cavernous haemangioma with dyschondroplasia is called as Maffucci syndrome. xx Cavernous haemangioma is often mixed with lymphatic component also (mixed vascular and lymphatic).

B

A

Figs 1.381A and B: Cavernous haemangioma in (A) tongue and (B) knee.

Clinical Features xx It is smooth, soft, well-localised, warm, fluctuant, compress-

Indications for surgery or intervention ™™ ™™ ™™

importance.

xx Sites: Head, neck, face, limbs, tongue, liver and other

ible, nonpulsatile swelling with bluish surface occurring in skin and subcutaneous tissue (often in mucosa like oral cavity) without any transillumination. xx Compressibility and bluish surface is diagnostic. When swelling is pressed it reduces partially/often completely but when pressure is released it slowly attains its original size and shape. Vascular and lymphatic malformations are compressible. xx It is usually nontender unless it gets infected or undergoes thrombosis or causes haemorrhage.

Differential Diagnosis xx Lymphangioma: It is brilliantly transilluminant unless it is

infected or fibrosed.

xx Lipoma, cold abscess, lymph cyst—clinically it is easier to

differentiate.

When I was young, I observed that nine out of ten things I did were failures. So I did ten times more work. —George Bernard Shaw

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SRB's Manual of Surgery Complications xx xx xx xx xx xx

Haemorrhage. DIC. Thrombosis. Infection, ulceration and septicaemia. Erosion into the adjacent bone. High output cardiac failure.

Investigations xx xx xx xx

Ultrasound, Doppler. Angiogram to find out feeding vessel. Platelet count. MRI/MR angiogram to see feeding vessels and deeper extension.

Fig. 1.383: Laparoscopic view of cavernous haemangioma of liver. It is the most common benign tumour of the liver.

Treatment xx Sclerosant therapy: It is the initial first line of therapy. It

A

causes aseptic thrombosis and fibrosis of the cavernous haemangioma with less vascularity and smaller size. It is directly injected into the lesion. Sodium tetradecyl sulphate/ hypertonic saline are used. Often multiple injections are needed to achieve complete required effect. Later excision of the lesion is done. xx Ligation of feeding artery and often at later stage excision is done once haemangioma shrinks. xx Therapeutic embolisation. xx If small and located in accessible area, excision is the initial therapy. xx Laser ablation—diode pulsed laser is becoming popular because of good control of bleeding. CO2/Nd:YAG laser is also equally effective.

VASCULAR MALFORMATIONS

B Figs 1.382A and B: Cavernous haemangioma in the cheek near angle of the mouth and in the tip of the tongue. Haemangioma tongue is one of the causes of macroglossia.

xx Secondary to defect in development of vascular components, in 8th week of intrauterine period. xx Single layer endothelium lined spaces derived from arterial, capillary, venous or lymphatic system showing ectasia. xx There is no growth in tissue culture. Raise in mast cells is not seen. xx Associated with many syndromes. xx Can be located in skin or in deeper planes. xx Present at birth and grows in proportion to child’s growth. Pale skin which later darkens over the age or faint blue mass is the presentation. xx Spontaneous involution is not common. xx Capillary malformation (CM) type is due to lack of sympathetic control. xx Venous malformation (VM) type is most common vascular malformation which shows hypoplasia, hyperplasia or aplasia of superficial or deeper system. It is seen in subcutaneous plane as faint blue compressible mass with morning pain and stiffness of the area. xx Lymphatic malformation (LM) type can be microcystic (lymphangioma) or macrocystic (cystic hygroma). It can cause lymphoedema,

Vascular Lesions and Hamartoma

xx

xx xx xx

xx

soft tissue and bony hypertrophy, asymmetry (face), macrochelia, macroglossia, macrotia, cellulitis. Low/slow flow malformations can cause skeletal hypoplasia; high/ fast flow malformations can cause hypertrophy. AVM is high flow type. Consumption coagulopathy (DIC) can occur. It is equal in both sexes (1:1). Doppler is commonly used investigation; but MRI (MR angiogram is ideal) with contrast is ideal to identify and to differentiate low and high flow types. Treatment—conservative with compression garments and sclerotherapy. Laser photocoagulation is the choice for superficial malformations; multiple sittings may be needed; complete clearance may not be achieved. Surgical excision can be done. Preoperative embolisation may be needed.

Vin rose patch: It is a congenital intradermal pale pink vascular malformation with dilatation of vessels in subpapillary dermal plexus. It may be associated with haemangiomas; AV malformations in limbs; congenital lymphoedema.

CIRSOID ANEURYSM xx It is actually a rare arteriovenous fistula / malformation of the scalp usually of congenital origin but occasionally can be traumatic. 90% occur in relation to superficial temporal artery but few occur additionally also in relation to occipital arteries. It should be differentiated from the true aneurysm of the superficial temporal artery. Cirsoid means varix. xx It is a rare variant of capillary haemangioma occurring in skin, beneath which abnormal artery communicates with the distended veins. xx Commonly seen in superficial temporal artery and its branches. xx Often the underlying bone gets thinned out due to pressure. xx Occasionally extends into the cranial cavity. xx Ulceration is the eventual problem which will lead to uncontrollable haemorrhage.

Clinical Features Pulsatile swelling in relation to superficial temporal artery, which is warm, compressible, with arteria­lisation of adjacent veins and with bone thinning (due to erosion). It feels like a ‘pulsating bag of worms’.

Investigations xx Doppler study, CT scan. xx Angiogram, X-ray of the part.

Treatment xx Ligation of feeding artery and excision of lesion, often requires preliminary ligation of external carotid artery. xx Intracranial extension requires formal neuro­surgical approach. xx Endovascular therapy is also useful.

ARTERIOVENOUS FISTULA (AVF) It is an abnormal communication between an artery and vein.

Types xx Congenital—is arteriovenous malformation. xx Acquired (Trauma is common cause).

Congenital Arteriovenous Malformation (Fistula)—AVM (AVF) During developmental period AV communications occur. It is high flow type of vascular malformation. It is 30% of all vascular malformation. 90% of AVM contains both arterial and venous components. Shuting of blood with thrill and bruit with hyperdynamic circulation is common.

Sites xx Limbs, either part or whole of the limb is involved. It may

be localised to toes or fingers.

xx Lungs. xx Brain—in circle of Willis. xx Other organs like bowel, liver.

Clinical Features Structural changes in the limb:

xx Limb is lengthened due to increase in blood flow since

developmental period.

xx Limb girth is also increased. xx Limb is warm. xx Continuous thrill and continuous machinery murmur

all over the lesion.

xx Dilated arterialised varicose veins are seen due to

increased blood flow and also due to valvular incompetence.

xx Often there is bone erosion or extension of AVF into the

bone as such. Physiological changes Because of the hyperdynamic circulation, there is increased cardiac output and so often congestive cardiac failure. Complications ™™ ™™ ™™

Haemorrhage Thrombosis Cardiac failure (CCF)

Investigations xx xx xx xx

Angiogram—MR angiogram is ideal. Doppler study. X-ray of the part. ECG, echocardiography.

Treatment xx Conservative—sclerotherapy, compression, avoiding injury. xx Indications for intervention

When stethoscope is applied aneurysm is either silent or a systolic bruit can be heard, but an arteriovenous fistula emits a continuous murmur throughout the systole and diastole. —Charle G Rob

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A

B Fig. 1.384: MR angiogram of AV malformation in cranial cavity.

C

D

Fig. 1.385: MRI picture of AV malformation.

E

A

B

Figs 1.386A and B: Hypertrophic changes due to AV malformation.

Figs 1.387A to E: Congenital arteriovenous malformation involving right upper limb, axillary region and part of right half of neck and face. Note the limb lengthening and widened girth. Limb is warmer. Limb should be measured at each level. Auscultation reveals continuous bruit over the limb. Note the dilated tortuous veins due to hyperdynamic circulation.

Vascular Lesions and Hamartoma  Absolute: Haemorrhage, ischaemia, CCF.  Relative: Pain, functional disability, cosmesis, limb asymmetry.  Emergency: Torrential bleeding usually after trauma (example—

xx Physiological changes: Cardiac failure due to hyper-

Interventions

xx Structural changes:

road traffic accidents).

Pathophysiology dynamic circulation.

 Surgical ligation of feeding vessels and complete excision of

the lesion. Often if lesion is extending into deeper planes it is technically difficult; but with usage of tourniquet, careful meticulous dissection and ligation of all vessels will lead into successful excision of entire lesion.  Therapeutic embolisation/preoperative embolisation hasten the proper surgical excision.  In emergency bleeding, adequate transfusion of blood, tourniquet usage, intraoperative embolisation and then excision of entire lesion is done. Occasionally when extensive AVM is present often involving the entire limb, amputation is the final option left as a life-saving procedure.

Changes at the Level of Fistula Blood flows from high pressure artery to low pressure vein causing diversion of most of the blood. Between the artery and vein, at the site of fistula, dilatation develops with formation of fibrous sac called as aneurysmal sac. This presents as warm, pulsatile, smooth, soft, compressible swelling at the site with continuous thrill and continuous machinery murmur.

Acquired Arteriovenous Fistula (AVF)

A

B

Fig. 1.388: AV fistula.

Figs 1.389A and B: Acquired arteriovenous fistula in the wrist over radial vessels. It should be palpated for compressibility and thrill. It should be auscultated for bruit.

Causes xx Trauma in (most common cause):

Femoral region. Popliteal region. Brachial region. Wrist. Aorta—vena caval. Abdomen. It may be following road traffic accidents, penetrating wounds, cock-fight injury (common in South India). xx After surgical intervention of major vessels. xx Therapeutic: For renal dialysis, AVF is created (Cimino fistula) to achieve arterialisation of veins and also to have hyperdynamic circulation. It is done to have easy and adequate venous access for long time haemodialysis. Common sites are wrist, brachial, and femoral region.      

Fig. 1.390: AV fistula created for treating chronic renal failure has formed an aneurysm. It may rupture to cause severe haemorrhage. Thrombosis or sepsis also can occur in this.

Honesty breeds respect and respect breeds trust.

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SRB's Manual of Surgery Changes Below the Level of the Fistula Because of diversion of arterial blood distal part becomes ischaemic. Because of high pressure arterialisation of veins and valvular incompetence occurs causing varicose veins.

Changes Proximal to the Fistula xx Hyperdynamic circulation causes cardiac failure. Cardiac failure may be very severe in traumatic AVF (often resistant to drug therapy). xx If pressure is applied to the artery proximal to the fistula, swelling will reduce in size, thrill and bruit will disappear, pulse rate and pulse pressure becomes normal. This is called as Nicoladoni’s sign or Branham’s sign.

Investigations xx Doppler, angiogram. xx ECG, echocardiography.

xx In emergency situation, quadruple ligation, i.e. both artery and vein above and below are ligated without touching the fistula and sac. Patient recovers well from cardiac failure. xx Therapeutic embolisation may be tried. Hunter’s ligation should be avoided. It is used as life-saving measure because it invariably causes limb ischaemia and gangrene even though patient recovers from cardiac failure. It is ligation of artery proximally so as to make cardiac function normal. But it invariably steals the blood from the limb leading to gangrene.

CAMPBELL DE MORGAN SPOTS xx It is usually smaller (0.2 to 6 mm) in size, circular, elevated and bright red swelling. xx It is common in trunk. Common in elderly. xx Also called as cherry angiomas. xx Usually it does not require treatment. xx When needed, excision or electrodesiccation or laser removal is done.

Treatment xx Excision of fistula and reconstruction of artery and vein

with graft. Done in early stages—larger vessels. Venous or Dacron graft is used.

PARRY-ROMBERG DISEASE xx xx xx xx

It is hemifacial atrophy of skin, soft tissue and bone. Common in females. It usually begins at twenties. Atrophy of skin, fat, muscle, cartilage and bone causing coupe de sabre deformity. xx It is a self-limiting disease. xx Aesthetic reconstruction is offered when severe deformity develops.

HAMARTOMATA Hamartano means ‘I miss’ (Greek). Or ‘fault’ or ‘misfire’ or ‘error’— (missing the mark in spear throwing). Note: Presently this terminology is not very much in use.

Fig. 1.391: Reconstruction of AV fistula using graft.

xx It is a benign lesion with aberrant differentiation producing a mass of disorganised but mature specialised cells or tissue indigenous to the particular site. xx It is tumour like overgrowth of tissue or tissues proper to that part. xx It may be single lesion or multiple lesions. xx Haemangiomas, lymphangiomas, AV malformations, neural malformations are the examples. Problems with hamartomas ™™ ™™ ™™ ™™ ™™

A

B

Figs 1.392A and B: (A) Quadruple ligation of AV fistula. (B) Hunter’s ligation is ligation of artery proximal to AV fistula. It should not be done as it causes diversion of all blood from periphery leading to gangrene of distal part.

Pressure symptoms locally Bleeding Infection Gigantism Cosmetic problem

Treatment xx Depends on site, type, extent. xx Cryotherapy, ligation of feeding vessels, sclerotherapy, excision or laser therapy.

N. Venous Diseases CHAPTER OUTLINE ™™ Anatomy of Veins of Lower Limb ™™ Physiology of Venous Blood Flow in Lower Limb ™™ Deep Vein Thrombosis ™™ Varicose Veins ™™ Venous Ulcer

™™ Compression Therapy for Varicose Veins ™™ Thrombophlebitis ™™ Klippel-Trenaunay Syndrome ™™ Anticoagulants ™™ Heparin

™™ ™™ ™™ ™™

Oral Anticoagulants Direct Thrombin Inhibitors Antiplatelet Drugs Pulmonary Embolism

ANATOMY OF VEINS OF LOWER LIMB

Fig. 1.393: Anatomy of lower limb veins.

Deep Veins

Fig. 1.394: Bilateral varicosity of great saphenous veins.

xx Tibial, popliteal, femoral veins are called as “veins of conduits” which drain blood into iliac veins and then to IVC. xx Pumping veins: They are venous sinuses existing in the calf muscles which pump blood towards major veins. They are better termed as musculo­venous pumps. They are also called as the peripheral heart.

Superficial Veins xx Long (Great) saphenous vein (LSV / GSV): It begins from the medial part of the dorsal venous arch of the foot runs in front of the medial malleolus ascends up to the posteromedial aspect of the knee joint, and then ascends upwards in the thigh towards the saphenous opening. Saphenous opening lies 3.75 cm below and lateral to the pubic tubercle. It pierces the cribriform fascia to enter the femoral vein. LSV contains 12–20 valves. It is the longest vein in the body. In the lower part of the leg LSV is closely associated with saphenous nerve which can get damaged during surgeries to LSV varicosity. Tributaries of GSV are— posterior arch vein, anterior vein of the leg, anterolateral vein, posteromedial vein and sometimes accessory saphenous vein. xx Short (Small) saphenous vein (SSV): Lateral marginal vein of the foot behind the lateral malleolus continues as SSV ascending upwards along the lateral margin of the tendoachilles. It runs along

Fig. 1.395: Long saphenous vein, anatomy and its tributaries.

The fool is never satisfied while the wise man finds wealth in contentment

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A

B Figs 1.396A and B: Short saphenous vein varicosity.

Fig. 1.397: Long saphenous vein with perforator incompetence with venous ulcer.

the middle of the back of the leg between two heads of the gastrocnemius into the lower part of the popliteal fossa and ends into the popliteal vein. It has got 6–12 valves. Sural nerve runs closely along the SSV which may get injured during surgery. Saphenopopliteal junction is variable, but usually located at popliteal fossa; it can be above or below the actual site. xx Posterior arch vein of Leonardo from medial ankle to the LSV below. xx Anterior arch veins to popliteal veins.

xx Venous valves are abundant in the distal lower extremity and

Note:

Superficial veins have got multiple valves; blood always drains from superficial veins towards deep veins. Inferior vena cava (IVC) and iliac veins do not have valves. Superficial veins of lower limb drains skin and subcutaneous tissues (10% of blood). Veins can accommodate large quantity of blood hence called as capacitance vessels.

Perforator Veins They are the veins which connect superficial to deep veins at various levels. They travel from super­ficial fascia through an opening in the deep fascia before entering the deep veins. The direction of blood flow here is from superficial to deep veins. These per­forators are also guarded by valves so that the blood flow is unidirec­tional, i.e. towards deep veins. Reversal of flow occurs due to incompetence of perforators which will lead to varicose veins. Types ™™ ™™ ™™ ™™ ™™

Ankle perforators (May or Kuster) Lower leg perforators: I, II, III (of Cockett) Gastrocnemius perforators (of Boyd)—below knee Mid-thigh perforators (Dodd) Hunter’s perforator in the thigh

PHYSIOLOGY OF VENOUS BLOOD FLOW IN LOWER LIMB xx Veins are thin-walled vessels with collapsible walls, that

assume an elliptical configuration in collapsed state and circular configuration in the filled state.

the number of valves decreases proximally, with no valves in superior and inferior vena cava.

Venous Return xx Arterial pressure across the capillary increases the pumping action of vein. xx Calf musculovenous pump: During contraction phase of walking, pressure in the calf muscles increases to 200–300 mmHg. This pumps the blood towards the heart. During relaxation phase of walking, pressure in the calf falls and so it allows blood to flow from superficial to deep veins through perforators. Normally while walking, pressure in the superficial system at the level of ankle is 20 mmHg. xx During walking, foot pump mechanism propels blood from plantar veins into the leg. xx Gravity. Note:

Pressure in arteriolar end of the capillary is 32 mmHg; venular end of capillary is 12 mmHg.

Factors responsible for venous return ™™ ™™ ™™ ™™

Negative pressure in thorax Peripheral pump—calf muscles Vis-a-tergo of adjoining muscles Nonrefluxing valves in course of veins

DEEP VEIN THROMBOSIS Deep vein thrombosis (DVT) is called as phlebothrombosis. It is semisolid clot in the vein which has got high tendency to develop pulmonary embolism and sudden death. Common site of beginning of thrombus is soleal veins which later propagate proximally, often getting detached to cause acute massive pulmonary embolism or moderate sized emboli can cause pyramidal/wedge shaped pulmonary infarcts.

Venous Diseases Aetiology: Factors

xx Recent myocardial infarction, heart failure, nephrotic

syndrome. Virchow’s triad ™™ ™™ ™™

xx Thrombosis can occur in individuals who sit with computers

for long time—‘ethrombosis’.

Stasis Hypercoagulability Vein wall injury

Causes xx xx xx xx

Following childbirth. Trauma—to leg, ankle, thigh, pelvis. Muscular violence. Immobility: Bed ridden patients, individuals on long duration air or bus travel (Traveller’s thrombosis). xx Debilitating illness, obesity, immobility, bed rest, pregnancy, puerperium, oral contraceptives, estrogens. xx Postoperative thrombosis (Most common cause): Common after the age of 40 years. Incidence following surgeries is 30%. In 30% of cases both legs are affected. Usually seen after prostate surgery, hip surgery, major abdominal surgeries, gynaecological surgeries, cancer surgeries. Bedridden for more than 3 days in the postoperative period increases the risk of DVT. xx Spontaneous thrombosis is common in visceral neoplasm like carcinoma pancreas or carcinoma stomach. It is often migrating type. xx Thrombus may start in a venous tributary which eventually may extend into the main vein causing DVT. xx Axillary vein thrombosis

Sites a. Pelvic veins—not uncommon; involves internal iliac veins. It is more common in PID (pelvic inflammatory disease) in females. In males prostatic veins may be the site of origin. It is difficult to identify clinically even though rectal or vaginal examination may help. b. Leg veins—very common in veins of soleus muscle in calf; femoral vein/iliofemoral vein thrombosis can occur along with calf veins or independently without calf vein thrombosis which shows adductor canal tenderness. Iliofemoral vein thrombosis is common on left side due to its lengthy course/compression by right iliac artery/often due to presence of web at its entry into IVC. Incidence of bilateral leg DVT is 30% which should be differentiated from bilateral pedal oedema due to other causes like hypoproteinaemia, renal failure and cardiac causes. c. Upper limb veins—not uncommon (Axillary vein thrombosis).

Phlegmasia alba dolens It is DVT of femoral vein (deep femoral vein commonly) causing painful congestion and oedema of leg, with lymphangitis, which further increases the oedema and worsens the situation (white leg).

 It can occur sponta­neously, following compression by cervical

  

   



rib, by various causes of thoracic inlet syndrome, or arm being in the hyperabduction state for prolonged period (e.g. painting the ceiling), after axillary lymph node block dissection, after radiotherapy to axilla, occasionally as a compli­cation of venous cannulation. Upper limb DVT is rare compared to lower limb DVT (5% of all DVT). It may be axillary or subclavian vein or both. But 30% of upper limb DVT can cause pulmonary embolism. Primary upper limb DVT is Paget-Schroetter syndrome, is due to subclavian vein compression that occurs in thoracic outlet syndrome. It may be precipitated by exertion of arms, swimming, exercise, etc. Idiopathic upper limb DVT is rare. Occult underlying malignancy should be thought of. Secondary upper limb DVT is due to CVP line, pacemaker thrombocytosis, malignancy, surgeries, radiotherapy, etc. Unilateral arm, forearm swelling with bluish discolouration, pain, pitting oedema, often with skin blebs are the features. Investigations are—Duplex scan, MR venography (as clavicle obscures proper duplex evaluation), BT, CT, PT, APTT, platelet count estimation. Treatment is similar, with heparin/LMWH/warfarin, thrombolysis using tissue plasminogen activator, elevation of the arm, using compression stockings.

xx Polycythaemia vera, thrombocytosis. xx Deficiencies of antithrombin III, protein C, protein S, factor

V of Leiden, thrombophilia.

Fig. 1.398: Deep vein thrombosis (DVT) in both legs. 30% cases of DVT are bilateral.

Fig. 1.399: Right leg venous gangrene. Note the discolouration, blebs and oedema.

Peace begins with a smile. Beauty is power; smile is its sword.

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SRB's Manual of Surgery Phlegmasia caerulea dolens It is extensive DVT of iliac and pelvic veins causing blue leg with either venous gangrene or areas of infarction. Features of DVT ™™ ™™ ™™ ™™ ™™ ™™

Commonly it is asymptomatic—60% Fever—most common Tense, tender, warm, pale/bluish, shiny swelling calf Positive Homan’s, Mose’s or Neuhof’s signs Inverted champagne bottle sign Features of pulmonary embolism

system. Occlusive and nonocclusive thrombus can be differentiated by this. But as it is invasive one, it is not commonly done at present. MR venogram is under trial at present. Impedance plethysmography is used to measure the rate of venous emptying. Vein occlusion is done using cuff around upper thigh which is confirmed by flat electrical wave pattern. When cuff is released rapid flow of wave is observed in normal; sluggish flow of wave is seen in DVT.

Clinical Features xx Fever—earliest symptom. xx Pain and swelling in the calf and thigh (often). Pain is often

so severe that the patient finds it difficult to flex (or move) the leg. xx Leg is tense, tender, warm, pale or bluish with stretched and shiny skin. xx Positive Homan’s sign: Passive forceful dorsiflexion of the foot with extended knee will cause tender­ness in the calf. xx Mose’s sign: Gentle squeezing of lower part of the calf from side-to-side is painful. Gentleness is very important otherwise it may dislodge a thrombus to form an embolus. xx Neuhof ’s sign: Thickening and deep tenderness elicited while palpating deep in calf muscles. xx Most often, DVT is asymptomatic and presents suddenly with features of pulmonary embolism like chest pain, breathlessness and haemoptysis. xx After applying tourniquet at saphenofemoral junction, patient is made to walk and without removing the tourniquet, limb is elevated—persisting prominent superficial veins will be observed in DVT—Linton’s test. Differential diagnosis for DVT ™™ ™™ ™™ ™™ ™™

Ruptured Baker’s cyst Ruptured plantaris tendon Calf muscle haematoma Cellulitis leg Superficial thrombophlebitis

Investigations xx Venous Doppler. xx Duplex scanning



It shows noncompressible vein which is wider than normal. On compression over calf muscles, it does not show any augmentation of flow. Normal venous sound at the area of femoral vein which disappears during inspiration is conspicuously absent in DVT. xx Venogram  Contrast material is injected into venous system to get detailed

idea of the veins after applying tourniquet into superficial

Fig. 1.400: US showing IVC thrombosis. xx Radioactive I125 fibrinogen study  Sodium iodide 100 mg orally is given to the patient 24 hours before the test to block the thyroid activity. I125 labelled fibrinogen 100 µ curies is injected intravenously. First radioactivity of heart is measured by placing the scintillation counter over precordium. Reading obtained by this is adjusted as 100%. After that legs are elevated using adjustable stands and to prevent venous pooling, scintillation counter is placed over the calf. Counting in the leg is done from below upwards at 5 cm intervals. Procedure is done in preoperative period; on 1st, 3rd and 6th postoperative days. A 20% or more raise in percentage value suggests deep vein thrombosis in leg. I125 labelled fibrinogen is used (earlier I131 labelled fibrinogen was used) because it has got shorter radioaction; its detectability is done with much lighter and mobile apparatus. xx Haemogram with platelet count; D-dimer test/analysis of fibrin degradation products (FDP) are relevant tests used. D-dimer test is measurement of cross-linked degradation products which interprets the plasmin activity on fibrin. Negative D-dimer test is of more value. xx Ventilation—perfusion scanning with mismatched defects; pulmonary artery CT scan with filling defect; pulmonary angiography are the investigations to confirm the pulmonary embolism.

Treatment xx Rest, elevation of limb, bandaging the entire limb with crepe bandage. xx Anticoagulants: Heparin/low molecular weight heparin, warfarin, phenindione. xx For fixed thrombus:  Initially high dose of heparin of 25,000 units/day for 7 days is given. Then later patient is advised to continue warfarin for 3–6 months. Dose is controlled by assessing Activated Partial Thromboplastin Time (APTT). Duration of heparin treatment is usually for 7–10 days. Dose of heparin is often calculated as— 80 units/kg bolus of heparin followed by 15 units/kg of infusion.  Low molecular weight heparin is preferred to heparin.  Warfarin should be started as early as possible (same day of

Venous Diseases heparin therapy). Day one and day two—10 mg each day; day three—5 mg. On day three prothrombin time should be done. Warfarin is given for 3–6 months with regular monitoring, depending on the cause, risk group, and severity of DVT. INR should be maintained between 2.0 to 3.0.  Oral anticoagulants being teratogenic cannot be used during pregnancy. LMWH is the drug of choice used during pregnancy and postpartum period.

xx For free thrombus:

Free thrombus ™™ ™™ ™™

Fibrinolysins Thrombectomy using Fogarty’s catheter In filter

 Fibrinolysins: Streptokinase, 6 lakhs to start with and

later one lakh hourly. It is commonly infused directly into the affected vein through a venous catheter. Urokinase or tissue plasminogen activator may also be used to dissolve thrombus (it should not be given when patient is on heparin).

Fig. 1.401: Palma operation for iliofemoral block. Using opposite saphenous vein femoral vein is connected to other femoral vein.

Fibrinolysins Tissue plasminogen activator—directly into the thrombus through popliteal/femoral vein ™™ Urokinase—1,20,000 to 2,50,000 units/hour; derived from human urine ™™ Reptilase—0.5-1 unit/hour ™™ Streptokinase—2.5 to 6 lakh to start with later one lakh hourly; derived from streptococci ™™

 Venous thrombectomy is done using Fogarty venous balloon

catheter.

Fig. 1.402: Crepe bandages applied to both legs in bilateral varicose veins and DVT.

 Thrombotic emboli is prevented from reaching the heart by

filtering it at IVC level using intracaval filters—Kim ray Greenfield filter, suture sieve plication, stapler plication, vena caval ligation, Mobin Uddin umbrella filter.  Special thrombectomy device of 7–9 French sheath is passed through the thrombosed segment to have partial mechanical thrombectomy and through that thrombolytics (tissue plasminogen activator) are infused. Thrombus can be removed nowadays through balloon angioplasty tube. Open venotomy and thrombectomy also can be done. Modified Well’s criteria for predicting pulmonary embolism (PE)

Points

Clinical symptoms and signs of DVT

3

Alternative diagnosis less likely PE

3

Heart rate >100

1.5

Immobilization more than 3 days or surgery within last 4 weeks

1.5

Previous DVT or PE

1.5

Haemoptysis

1.0

Malignancy in last 6 months

1.0

Score 4 = suggestive of PE.

xx Palma operation: In iliofemoral thrombosis, common femoral vein below the block is commu­nicated to opposite femoral vein through opposite long saphenous vein. xx May-Husni operation: When blockage is in popliteal vein, popliteal vein below the block is anastomo­sed to long saphenous vein (endto-end) so as to bypass the blood across the popliteal block.

Prevention of DVT Categorise the patient as low/moderate and high-risk. Low-risk— young patients undergoing surgery for less than 30 minutes. Moderate-risk—patients above 40 years of age undergoing major surgery. High-risk—one who had existing cardiac diseases, stroke, previous history of DVT, suffering from malignancy ™™ Mechanical methods—elastic compression bandage; elevation; external pneumatic bandage ™™ Pharmacological—low molecular weight heparin—once a day ™™

xx Care has to be taken to see for proper positioning of legs with no pressure on the calf muscles. xx Pressure bandage to the legs has to be applied during major surgeries, laparoscopic surgeries. During postoperative period,

Oral contraceptives increases the risk of DVT by 3–5 times.

225

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SRB's Manual of Surgery elevation, massa­ging, pressure bandage, early ambulation, main­ taining hydration are essential measures. xx Low dose heparin is given in suspected cases, in major surgeries and continued during postopera­tive period till the patient is ambulated. 5,000 units is given subcutaneously 2 hours before surgery. Low molecular weight heparin is preferred drug than heparin as it can be used once a day; it does not require monitoring; it does not cause thrombo-cytopenia (like heparin); and there is lesser risk of bleeding. xx Various measures like graduated static compres­sion, elastic stockings, electrical stimulation of calf muscles, pneumatic compression are used to prevent sluggish flow of blood. xx Dextran 70, intravenously 500 ml during surgery and another 500 ml postoperatively in 24 hours can also be used to prevent DVT. xx Smoking increases the viscosity of blood and so should be stopped. xx Patients on oral contraceptives or oestrogens should stop the drug 6-8 weeks prior to any elective surgery.

Classification I xx Long/great saphenous vein varicosity. xx Short/small saphenous vein varicosity. xx Varicose veins due to perforator incompetence.

Effects and sequelae of DVT Pulmonary embolism—15% Infection; venous gangrene Partial recanalisation, chronic venous hypertension around the ankle region causing venous ulcers—chronic venous insufficiency—CVI ™™ Recurrent DVT—30% ™™ Propagation of thrombus proximally—20–30% ™™ ™™ ™™

VARICOSE VEINS

A

B

C

Figs 1.404A to C: (A) Great saphenous vein varicosity. (B) Small saphenous vein varicosity. (C) Perforator incompetence (blow outs).

Classification II

They are dilated, tortuous, elongated veins in the leg. There is reversal of blood flow through its faulty valves. xx It is permanently elongated, dilated vein/veins with tortuous path causing pathological circulation. xx Risk factors being heredity; female sex; occupation that demands prolonged standing; immobility; raised intra-abdominal pressure like in sports, tight clothing, pregnancy, raised progesterone level and altered estrogen-progesterone ratio, chronic constipation, high heels. xx Prevalence of varicose veins is 35%; severe varicose veins is 10%; chronic venous insufficiency (CVI) is 8%; ulcer is 2%.

xx Thread veins (or dermal flares/telangiectasis/spider veins/Hypen veins are 0.5–1 mm in size): Are small varices in the skin usually around ankle which look like dilated, red or purple network of veins (Venulectasia). Spider naevi/venous flares are common in females. xx Reticular varices (1–3 mm in size): Are slightly larger varices than thread veins located in subcutaneous/subdermal region. xx Varicose veins: They are dilated, tortuous, elongated superficial veins located in the subcutaneous tissue (saphenous compartment) equal or more than 3 mm in diameter measured in standing position. xx Combination of any of the above.

Fig. 1.405: Thread veins are up to 1 mm diameter; reticular veins are 1–3 mm in diameter. Note:

A

B

C

Figs 1.403A to C: Typical varicose vein and with skin changes and venous ulceration.

•

•

Atrophic blanche is localized white atrophic skin surrounded by hyper pigmentation and dilated capillaries. Saphena varix is a large groin varicosity at SFJ which disappears on lying down and imparts an impulse and thrill on coughing.

Venous Diseases Pathogenesis Two theories ™™ ™™

Fig. 1.406: Atrophic blanche.

• •

Small varicose vein is 4 mm in diameter. Corona phlebectatica are blue telangiectasias on the medial aspect of the foot below the malleolus around ankle level. More than 5 such lesions are the best independent predictor of the skin changes.

Classification III Ceap Classification of Lower Limb Varicose Veins (2004) CEAP classification C—Clinical signs (grade 0–6); (A) for asymptomatic or (S) for symptomatic presentation E—Etiological classification: Congenital (Ec), Primary (Ep), Secondary (Es), no venous etiology (En) A—Anatomic distribution: Superficial (As), Deep (Ad) or Perforator (Ap), No venous location identified (An) P—Pathophysiologic dysfunction: Reflux (Pr), Obstructive (Po), Both, or no pathophysiology identified (Pn)

Grading of clinical signs (C) 0—No visible or palpable signs of venous diseases 1—Telangiectases, reticular veins or malleolar flare 2—Varicose veins 3—Oedema without skin changes 4—Skin changes due to venous diseases like pigmentation, eczema or lipodermatosclerosis 4a—pigmentation; 4b—lipodermatosis, atrophia blanche 5—Skin changes as above with healed ulceration 6—Skin changes as above with active ulceration

Anatomical distribution (A) As—superficial system: 1–Telangiectases, reticular veins 2–Great saphenous vein above the knee—ostial and preterminal 3–Great saphenous vein below the knee 4–Small saphenous vein 5–Nonsaphenous—43% Ad—deep system: From 6 to 15 Ap—perforator system: 17–Perforator vein (PV) of the thigh 18–Perforator (PV) of the calf and leg An—no anatomical lesion identified

Fibrin cuff theory White cell trapping theory

Incompetence of venous valves ↓ Stasis of blood ↓ Chronic ambulatory venous hypertension ↓ Defective microcirculation ↓ RBC diffuses into tissue planes ↓ Lysis of RBC’s ↓ Release of haemosiderin ↓ Pigmentation ↓ Dermatitis ↓ Capillary endothelial damage ↓ Prevention of diffusion and exchange of nutrients ↓ Severe anoxia ↓ Chronic venous ulceration (Fibrin cuff theory). xx Inappropriate activation of trapped leucocytes release proteolytic enzymes which cause cell destruction and ulceration—White cell trapping theory. Fibrin deposition, tissue death, scarring occurs together, called as lipodermatosclerosis. xx Secondary valvular failure → venous reflux → venous wall dilatation → effects. Weakening of the venous endothelial wall and valves occur due to raised venous wall tension by—(1) Shearing stress pressures of blood flow, (2) increased matrix metalloproteinases (MMPs) activity on endothelium and smooth muscle cells reducing structural integrity of venous wall with decreased elastin content in the media of the vein, (3) Changes in normal venous constriction and relaxation properties, (4) Recurrent inflammation. xx Venous system in the lower limb is maintained by—(1) Valvular competence, (2) Venous patency, (3) Calf muscle pump which is venous channel/plexus within the soleus muscle. Any change in any of these systems can cause venous insufficiency. xx Chronic venous insufficiency (CVI) is a syndrome resulting from continuous chronic venous hypertension/ambulatory venous hypertension [AVP] (>80 mmHg venous pressure at ankle) in the erect posture either on standing or exercise (in normal people venous pressure in superficial system falls during calf contraction). CVI consists of postural discomfort, varicose veins, oedema, pigmentation, induration, dermatitis, lipodermatosclerosis and ulceration. CVI patients may be having superficial vein incompetence (30%) with or without perforator incompetence or deep vein incompetence (30%) or having previous DVT with complete obliteration or partial recanalisation with incompetence called as post-thrombotic syndrome (30%). xx Varicose vein is a condition of progressive deterioration even often with interventions.

Pulsatile varicose veins in lower limb is seen in Klippel-Trenaunay syndrome.

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SRB's Manual of Surgery  Stretching of deep fascia.  Inheritance (family history) with FOXC2 gene.  Klippel-Trenaunay syndrome, avalvulia, Parkes-weber

syndrome. Here varices are of atypical distribution. xx Secondary varicosities:  Recurrent thrombophlebitis.  Occupational—standing for long hours (traffic police,

guards, sportsman).  Obstruction to venous return like abdominal tumour,

retroperitoneal fibrosis, lymphadeno­pathy, ascites.  Pregnancy (due to progesterone hormone), obesity,

chronic constipation. B

A

Figs 1.407A and B: Lipodermatosclerosis is pigmentation, thickening, and induration of the skin due to venous diseases.

 AV malformations—congenital or acquired.  Iliac vein thrombosis.  Tricuspid valve incompetence.

Clinical Features

Predisposing factors for varicose veins are—age, sex, race, obesity, height, left > right, occupation, family history, erect posture.

Symptoms in varicose veins Dragging pain, postural discomfort Heaviness in the legs ™™ Night time cramps—usually late night ™™ Oedema feet, itching (feature of CVI) ™™ Discolouration/ulceration in the feet/painful walk ™™ ™™

Causes of pain/cramps in varicose veins/venous diseases ™™ ™™ ™™ ™™ ™™ ™™

Fig. 1.408: Typical site of venous ulcer. Note the pigmentation and chronicity.

™™

Increased venous wall tension—chronic venous hypertension Hypoxia of tunica media of the venous wall due to altered function of vasa vasorum Increased capillary pressure Hyperviscosity of red cells—haemorrheological disorders Platelet hyperaggregation Reduction in capillary permeability causing capillary functional disorder Altered cutaneous microcirculation due to leucocyte adhesion and accumulation into the venous wall; release of free radicals cause microvascular lesional disease 

Sites where varicosities can occur ™™ ™™ ™™ ™™

Lower limb Pampiniform plexus of veins Vulva, perineum Sites of portosystemic anastomosis

Oedema in venous diseases ™™ ™™ ™™

Aetiology of Varicose Veins Varicosities are more common in lower limb because of erect posture and long column of blood has to be supported which can lead to weakness and incompe­tency of valves. Incidence is 5% of adult population. xx Primary varicosities due to:  Congenital incompetence or absence of valves.  Weakness or wasting of muscles—defective connective tissue and smooth muscle in the venous wall.

™™ ™™

™™

Can be localised or generalised Localised oedema is due to ankle flare or dilatation of medial marginal vein Cellulitis and lymphangitis association causes oedema Scarring and thickening of dermal and subdermal tissues—lipodermatosclerosis (brawny induration) Ankle becomes narrower due to contraction of skin and subcutaneous tissues but calf remains prominent—champagne bottle appearance Pale atrophic skin with white patches surrounded by dilated capillaries and pigmentation—atrophic blanche

It is more common in females (10 : 1). Often it is familial. Familial varicose veins begin in younger age group, seen bilaterally, involves all veins including deep veins.

Venous Diseases Signs

A Fig. 1.410: Site of saphena varix—in the lower part of groin just below the inguinal ligament.

B Figs 1.409A and B: Thread (2 cm in 1st trimester with features of embolism. Calf and thigh US for leg DVT and MRI for pelvic DVT should be done. Echocardiography should be done to check embolism; chest X-ray with abdominal shield may be needed. LMWH should be given. Warfarin (crosses placenta), rivaroxaban are avoided. TPA crosses the placenta but is used in massive pulmonary embolism with haemodynamic instability as life-saving often along with embolectomy. LMWH is given throughout the pregnancy; stopped peridelivery period; continued postnatal period for 1 month with 75% of earlier dose; later compression stockings and warfarin for 6 months. Compression stockings, hydration, ambulation, left lateral position are preventive measures in pregnancy often along with LMWH if needed/indicated. ACCP guidelines 2012 for VTE therapy: –– Initial phase up to 7 days—UFH/LMWH/Fondaparinux/rivaroxaban; –– Long-term up to 3 months—LMWH/rivaroxaban/dabigatran/VKA with INR 2–3 range (optimum 2.5); –– Extended is beyond 3 moths—VKA/rivaroxaban/dabigatran/LMWH if needed

O. Lymphatics CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™

Surgical Anatomy Lymphangiography Isotope Lymphoscintigraphy Lymphoedema Lymphomas

™™ ™™ ™™ ™™ ™™

Hodgkin’s Lymphoma Non-Hodgkin’s Lymphoma Mantle Cell Lymphoma Malt Lymphomas Burkitt's Lymphoma

SURGICAL ANATOMY Primordial lymphatic system begins to develop during 6th week of development adjacent to jugular vein as lymph sacs. Peripheral lymphatic systems develop from these primordial lymph sacs. Lymphatic system has three components. Terminal lymphatic capillaries, which have high porosity absorb lymph, macromolecules, cells and microbes from tissues into the system; lymphatic vessels which collect and transport lymph; lymph nodes which are interposed in the lymphatic pathway filter lymph and maintain immunity of the body. Lymphatic vessels run adjacent to main blood vessels reaching the major lymphatic channels. Cisterna chyli is formed in the abdomen, continues as thoracic duct (formed at 9th week of gestation) in the thorax which has got initial main course towards right side of the mediastinum; but later towards left side entering the internal jugular vein at its joining point of the subclavian vein. In the periphery, there is hardly any lymphovenous communications. Lymphovenous communications occur at lymph node level; iliac, subclavian and jugular levels. Lymphatics are absent in epidermis, cornea, CNS, cartilage, tendon and muscle. Great lymph ducts are—the thoracic duct—single; right lymph duct—single; subclavian, bronchomediastinal and jugular trunks on both sides. These ducts contain valves to prevent backflow. Cisterna chyli is formed by joining of right and left lumbar lymphatic trunks and intestinal lymphatic duct. Lumbar trunks are short lymph vessels arising from para-aortic lymph glands. It receives lymph from lower limb, pelvis and pelvic viscera, kidney, adrenal and deep lymphatics of abdominal wall. Left lumbar trunk is behind the aorta. Intestinal lymph duct arises from preaortic nodes. It joins the cisterna chyli from front. It receives lymph from stomach, intestines, liver (except most convex surface which drains into right lymph duct), spleen and pancreas. Cisterna chyli is a lymph sac lying in front of the L1 and L2 vertebrae between aorta and crus of the diaphragm. From its upper end it continues as thoracic duct. Thoracic duct passes through the aortic orifice of the diaphragm, runs medial to azygos vein and right of the aorta in posterior mediastinum. In front it is related to oesophagus, diaphragm and pericardium; behind right intercostal arteries, hemiazygos and accessory hemiazygos vein. At the level of 7th thoracic vertebra, it crosses towards left side behind the oesophagus obliquely reaching left side at 5th thoracic vertebral level. It runs upwards between left margin of oesophagus, medial part of left pleura, and behind left subclavian artery. In the neck, it passes in front of vertebral system (vertebral vessels and sympathetic chain) and behind carotid system (Common carotid artery, internal jugular vein, vagus

™™ ™™ ™™ ™™ ™™

Cutaneous T Cell Lymphoma Chylous Ascites Chylothorax Chyluria Sarcoidosis

nerve), crossing scalenus anterior, phrenic nerve, transverse cervical and suprascapular arteries ending as a single vessel at the junction of internal jugular vein and subclavian vein with a valve. Tributaries of thoracic duct are—trunk from lateral intercostal nodes from lower six spaces; efferents from posterior mediastinal nodes, lateral intercostal nodes of upper six spaces, left jugular lymph trunk from head and neck region, left subclavian lymph trunk from left upper limb, left bronchomediastinal trunk from left side of the thorax. Single termination of duct is common (77%); but double/triple/quadruple terminations are known to occur. Occasionally it may end in left subclavian vein, left vertebral vein, right internal jugular vein, right subclavian vein. Thoracic duct is 45 cm in length and 5 mm wide (wider at both ends; narrow in the middle).

Fig. 1.436: Thoracic duct anatomy; cisterna chyli; tributaries of thoracic duct.

In very early oedema, during pinching, there is a resistance that is not present on normal site, owing to thickening of dermis and subcutaneous tissue. —Sidney S Rose

246

SRB's Manual of Surgery mediated immunity, paracortex expansion occurs. Afferent lymph vessels enter the node through the capsule. It enters the marginal sinus, communicates with intranodal sinus, merging as efferent lymph vessels which enter the hilum. Intranodal sinus lining is highly phagocytic containing littoral cells and sinus lining histiocytes. Main artery and veins pass through the hilum to enter the medulla, paracortex and inner part of cortex. Superficial cortex is supplied by direct capsular vessels.

Function of lymphatics

Fig. 1.437: Watershed zones/areas of lymphatic drainage. Vertical sagittal midline; clavicular horizontal line; umbilical line—are used to divide areas into three zones on each side. Above clavicular line drainage occurs to cervical nodes; between clavicular line and umbilical line drainage occurs into axillary nodes; below umbilical line drainage occurs to inguinal lymph nodes. At the level of (lines) drainage can occur to lymph nodes on either side. Right lymph duct is 2.5 cm in length, formed by right jugular, right subclavian and right bronchomediastinal trunks; runs on the scalenus anterior joining the junction of right internal jugular vein and subclavian vein. There are about total 450–600 lymph nodes in the body. Around 200 in the neck; around 100 in the thorax; around 50–60 in the axilla; around 250 in the abdomen and pelvis; around 50 in the groin area.

Most of the intravascular proteins are daily filtered through lymphatics and returned to the circulation again. Macromolecules (albumin, globulin and fibrinogen) and microbes are also filtered at the nodal level as first immune system. From GIT fat is absorbed directly through lymphatics. Lymph shows centripetal flow. Cholesterol, long chain fatty acids, fat soluble vitamins are transferred through lymphatics into cistern chyli directly from GIT bypassing the liver. Transport is mainly due to intrinsic contractility of the lymphatic vessels which contain valves for effective forward flow. To a lesser extent other factors like muscle contraction, arterial pressure, thoracic pressure, respiratory movements play role. 8 litres of lymph is produced daily; once it reaches to lymph nodes it is concentrated to 4 litres which enters the venous circulation. Protein concentration in lymph is very high (25 grams/litre). Note: Lymph drains protein rich fluid; there are no communicating/perforator lymphatics; lymphatics will not regenerate

Lymphatic watersheds of skin Lymph from the dermis and appendages drain into a plexus in deep fascia which in turn drains into respective lymph nodes. There are six watershed areas in the body for lymphatic drainage. One vertical midline divides into right and left. Two horizontal lines on each side divide the area into three zones. First lies above the line of clavicle; second between line of clavicle and line at umbilical level; third below the level of umbilical line. First drains into head and neck lymph nodes; second drains into axillary nodes; third drains into inguinal/ groin nodes. Malignancy drains into their respective nodes depending on the location. Lesion on the line can spread to both territory lymph nodes. In skin and appendageal cancers, deep fascia also should be cleared.

Microanatomy of lymph node Lymph node contains three regions—cortex; paracortex and medulla. Cortex contains mainly follicles. It may be rounded lymphocytic aggregations of primary follicles or lymphocytic aggregation with germinal centres of secondary follicles due to antigenic stimulation. It contains B lymphocytes, macrophages, dendritic reticulum cells. Germinal centre is surrounded by small B lymphocytes. Both cortex and medulla are associated with humoral immunity. Proliferation of germinal centres suggests active humoral immunity with antibody production. Central medulla contains mainly lymphatic sinuses, arteries and veins, plasma cell and B lymphocytes. Paracortex is located in a zone between cortex and medulla. It contains T lymphocytes, related to cell mediated immunity. Post-capillary venules with high endothelial cells and lymphocytes in the wall are typical. In cell

Fig. 1.438: Acute lymphangitis leg. Usually regional lymph nodes are enlarged and tender.

LYMPHANGIOGRAPHY Indications xx Congenital lymphoedema like aplasia, hypoplasia, hyperplasia. xx Lymphomas show reticular pattern. It is also useful to assess the response to treatment. xx Secondaries in lymph nodes, especially iliac and para-aortic lymph nodes.

Lymphatics Technique

LYMPHOEDEMA

Patent blue dye or 1 ml isosulphan blue is injected subcutaneously between toes. Dye is taken up by lymphatics which will be visualised clearly. After making incision, one of the lymphatic vessels is dissected and 30 G needle is passed. Ultra-fluid lipiodol which is an oily contrast medium is injected slowly using pressure pump at a rate of 1 ml in 8 minutes (total quantity is 7 ml). Slowly in 24 hours, it passes through the lymphatics and reaches the iliac and para-aortic lymph nodes. Radiographs taken will help to visualise both lymphatic vessels as well as lymph nodes. Secondaries in lymph nodes causes filling defects. Lymphomas shows enlarged nodes which have foamy or reticular appearance.

It is accumulation of fluid (lymph) in extracellular and extravascular fluid compartment, commonly in subcutaneous tissue. It is primarily due to defective lymphatic drainage. It is increased protein rich interstitial fluid.

Classification Kinmonth classified lymphoedema as:

xx Primary without any identifiable lymphatic disease. xx Secondary is acquired due to definitive cause. Most common

form.

Disadvantages xx xx xx xx

Primary type

Technically difficult. Extravasation of dye can occur. Dye may not reach the required area. Time consuming and invasive procedure.

Lymphangiographic classification of lymphoedema (Browse classification): (Norman Browse) ™™ Congenital hyperplasia (10%): Congenital; common in males; entire leg is involved; one or both sides; with often family history; progressive; involves increased number of lymphatics and lymph nodes associated with chylous ascites, chylothorax and protein losing enteropathy ™™ Distal obliteration (80%): Common in females; starts at puberty; calf and ankle are involved; often bilateral; with often family history; slow progression; aplasia/hypoplasia of lymphatics ™™ Proximal obliteration (10%): Occurs at any age; equal in both sexes; leg and thigh involved; unilateral; rapid progression; proximal aortoiliac nodal block

ISOTOPE LYMPHOSCINTIGRAPHY xx Radioactive technetium labelled sulphide colloid particles, or radioiodinated human albumin are injected into the web space using fine needle. These particles are specifically taken up by lymphatics. xx Using gamma camera, limb and inguinal region is exposed to visualise the lymphatics and inguinal lymph nodes. xx Radioactivity in inguinal nodes is measured at 30 and 60 minutes. Normal uptake is 0.6–1.6%; if it is 2% it suggests rapid abnormal clearance due to oedema as the result of venous disease. xx In 3 hours, it reaches the para-aortic lymph nodes, other abdominal lymph nodes and liver. xx Later thoracic duct also can be visualised. It can be compared to the take up on the other limb.

Advantages xx xx xx xx xx

It is more sensitive. Technically easier and faster compared to lymphangiography. Thoracic duct, other lymph nodes and liver can be visualised. It is the test of choice. It is simple and safe. It has 90% sensitivity; 100% specificity.

It affects commonly females. ™™ It is common in lower limb and left side. It can be: ™™ Familial ™™ Syndromic (Turner’s / Klinefelter’s / Down’s / Klipple Trenauny Weber) It can be: ™™ Lymphoedema —  present at birth— 1/3rd widening of mediastinum at T5–T6 or >10 cm maximum dimension of nodal mass.

Differential diagnosis ™™ ™™ ™™ ™™ ™™ ™™ ™™

Tuberculosis NHL HIV Chronic lymphatic leukaemia Nonspecific lymphadenitis Sarcoidosis Secondaries in lymph nodes

creatinine. Serum alkaline phosphatase and calcium may elevated. xx FNAC of lymph nodes. Not very sensitive; but initially done to rule out secondaries or tuberculosis. xx Excision biopsy of lymph nodes. Full lymph node is excised to retain the architecture of the lymph node. It is important to grade the tumour. It is better to have immunohistochemistry of tumour tissue. As cell mediated immunity is decreased, CD4/ CD 8 ratio will be decreased. CD 15, 30, 45 are very useful. xx Chest X-ray—to look for mediastinal lymph nodes, pleural effusion. xx Ultrasound abdomen—to look for the involvement of liver, spleen, abdominal lymph nodes. xx CT scan of mediastinum/chest, abdomen and pelvis is better, ideal and essential. CT is used ideally to stage the disease. xx MRI and PET scan are very useful to identify extranodal tissue involvement. Gallium scan is less useful. xx Bone marrow biopsy or aspiration to stage the disease and to see the response to treatment. Usually iliac crest biopsy is done under local anaesthesia. It gives the staging. xx Chamberlain’s mediastinoscopy and biopsy of mediastinal lymph node is done if peripheral nodes are not available for biopsy. Laparoscopy and biopsy of different abdominal lymph nodes is also a good option. Lower limb lymphangiography to look for the pelvic and retroperitoneal lymph nodes. It shows reticular pattern in node; it can be used to assess the therapeutic response and prognosis. Lymphoscintigraphy is better and acceptable. It is prognostic tool also. ™™ Staging laparotomy: –– The abdomen is opened. Splenectomy is done mainly to remove the tumour bulk, as spleen is commonly involved and also to avoid irradiation to splenic area which often causes unpleasant pulmonary fibrosis. Biopsies are taken from both lobes of the liver (needle biopsy) from para-aortic, celiac mesenteric, iliac nodes. In females, ovaries are fixed behind the uterus to prevent radiation oophoritis (oophoropexy/ ovarian translocation). ™™

Lymphatics Staging laparotomy is not routinely done now. It is done only if it benefits the patient to have better plan of treatment or better result. –– It is done in stage I/IIA lymphoma (HL) in selected patients. Note: Staging laparotomy, splenectomy (requires for immune function), lymphangiogram, IVU are no longer/very rarely done now for HL. ––

Treatment for HL Treatment strategy for HL Early favourable stage—extended field radiation only Early unfavourable stage—extended radiation plus chemotherapy ™™ Advanced stage—extensive chemotherapy often with local radiation ™™ ™™

Problems in HL Pleural effusion—respiratory discomfort SVC obstruction Spine if involved—not very common but can occur Opportunistic infection—mycobacteria, cytomegalovirus, herpes zoster ™™ Bronchopneumonia, septicaemia ™™ Immunosuppression and its effects ™™ Risk for other malignancies in later life ™™ ™™ ™™ ™™

Unfavourable signs in early HL Large mediastinal mass Extranodal disease Elevated ESR Four or more involved regions Presence of B symptoms Anaemia 75% epithelial pearls Grade II: Moderately differentiated—50–75% epi­thelial pearls Grade III: Poorly differentiated—25–50% epithelial pearls Grade IV: 2 cm is worse

™™

Tumour border—ill-defined border is worse

™™

Associated immunosuppression is worse

™™

Differentiation—poorly differentiated is worse

Perineural involvement has worse prognosis Invasion; depth < 2 mm has got better prognosis; depth more than 16 mm has got worst prognosis ™™ Local recurrence rate is 20%. Recurrence period is 5 years, not beyond ™™ ™™

Finding fault is easier. Finding remedy is the one which is more difficult.

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SRB's Manual of Surgery MARJOLIN’S ULCER (1828) xx It is a well-differentiated squamous cell carcinoma which

occurs in chronic scars like burn scar, scar of venous ulcer. xx As it develops in a scar due to chronic irritation and there

are no lymphatics in scar tissue, it will not spread to lymph nodes. xx As scar is relatively avascular it grows slowly. As scar does not contain nerves, it is painless. xx Once it reaches the normal skin it may behave like any other squamous cell carcinoma, i.e. it will spread to lymph nodes. It occurs in unstable scar of long duration. 

Clinical Features

Fig. 1.526: Note the common site of BCC—in the face above the line drawn between angle of mouth and ear lobule—Onghren‘s line.

xx History of pre-existing venous ulcer or burn scar. xx Indurated, painless, nontender, ulcer with raised and everted

xx Basal cell naevus syndrome (Gorlin syndrome) with BCC;

edge. xx Biopsy from the edge confirms the diagnosis.

xx It is only locally malignant. It does not spread through

medulloblastoma; bifid ribs.

lymphatics nor through the blood. But it erodes deeply into local tissues including cartilages, bones causing extensive local destruction. Hence the name “rodent ulcer”.

Treatment xx Wide excision. xx In case of large ulcer, amputation is required. xx Radiotherapy should not be given as it may turn into poorly

differentiated squamous cell carcinoma. It is a curable malignancy.

Fig. 1.525: Marjolin’s ulcer foot in a pre-existing burns scar. It is a well-differentiated squamous cell carcinoma occurring in an unstable scar of long duration.

BASAL CELL CARCINOMA (Rodent Ulcer) It is a low grade, locally invasive, carcinoma arising from basal layer of skin (or adnexal basal layer of hair follicle) or mucocutaneous junction. It does not arise from mucosa. xx It is the commonest (70%) malignant skin tumour. xx It is more common in white-skinned people than blacks. xx Common in places where exposure to UV light is more (Australia). xx Other causes are—arsenics, coal tar, aromatic hydrocarbons, skin tumour syndromes. xx It is common in males, common in middle-aged and elderly. xx Common site is face—above the line drawn between angle of mouth and ear lobule (90%)—Onghren’s line. xx It is called as tear cancer because it is commonly seen in area where tears roll down. xx Often it can occur in muco-cutaneous junctions.

Types 1. Nodular—common in face. 2. Cystic/nodulocystic. 3. Ulcerative. 4. Multiple, often associated with syndromes and other malignancies. 5. Pigmented BCC—mimics melanoma. 6. Geographical or field fire or forest fire BCC is wide area involvement with central scabbing and peri­pheral active proliferating edge. 7. Basi-squamous—behaves like squamous cell carcinoma which spread into lymph nodes. BCC which has not been treated for long time can turn into Basisquamous carcinoma. Note:

Nodulocystic and noduloulcerative is the commonest form (70–90%).

A

B

Figs 1.527A and B: (A) BCC in perianal region. It is nodular type. Wide excision is required; (B) Nodular BCC in the nose (Common in face).

Skin Tumours

Fig. 1.528: Sebaceous epidermal naevus. It is common in females, often extensive, begins in childhood. It needs surgical excision and skin grafting. It has got 10% chances of turning into BCC.

Clinicopathological Types a. Superficial type—small buds of tumour masses. b. Morpheic type—dense stroma with basal cells and type IV collagen; spreads rapidly; sclerosing BCC. c. Fibroepithelioma type of Pinkus shows elonga­ted cords of basaloid cells with mesh work. It contains outer palisading columnar cells with central polyhedral cells but no prickle cells or kerati­nisation.

A

B Fig. 1.529: BCC lesions in different places (multiple).

Clinical Features xx Ulcer on the face in a middle-aged man which is nontender,

dry, slowly growing, nonmobile, with raised and beaded edge with central scab, often with central depression or umbilication. xx Site of beading signifies the area of active pro­liferating cells. In between beaded areas dormant nonactive cells are present. xx No lymph node or blood spread occurs. Due to large sized tumour cells/tumour cluster, it does not spread through lymphatics. xx BCC can be low risk or high-risk. High-risk BCC ™™ ™™ ™™ ™™ ™™

Size >2 cm Near the eye/nose/ear Ill-defined margins Recurrent tumours Immunosuppressed individuals

C Figs 1.530A to C: Basal cell carcinoma in different locations. Note the nodularity and ulceration. Note the beaded edge.

Differential Diagnosis 1. Squamous cell carcinoma. 2. Melanoma. 3. Keratoacanthoma. 4. Seborrhoeic keratosis. Moles must never be cauterised or curetted.

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NAEVI

Wedge biopsy, X-ray of the part, CT scan.

xx It is a hamartomata of melanocytes due to excessive stimu-

Treatment

xx It may present during birth or appear later in life.

xx It is radiosensitive. If lesion is away from vital structure

Types

lation.

(like away from eyes), then curative radio­therapy can be given. Radiotherapy is not given, once it erodes cartilage or bone. RT is not given to BCC of ear and close to lacrimal canaliculi. xx Surgery: Indications for surgery ™™ ™™ ™™

Rodent ulcer eroding into cartilage or bone BCC close to the eye Recurrent BCC

 Wide excision (1 cm clearance) with skin grafting, primary

suturing or flap (Z plasty, rhomboid flap, rotation flap) is the procedure of choice.  Laser surgery, photodynamic therapy, 5 fluorouracil local application.  Cryosurgery.  MOHS (Microscopically Oriented Histographic Surgery) (Federic E Mohs, American Surgeon) is useful to get a clearance margin and in conditions like BCC close to eyes, nose or ear, to preserve more tissues. MOHS is becoming popular in BCC/dermatofibrosarcoma protuberans/melanoma. Procedure is done by dermatological surgeon along with a histotechnician/ histologist. Under local anaesthesia, a saucerised excision of the primary tumour is done and quadrants of the specimen are mapped with different colours. Specimen is sectioned by histotechnician from margin and depth, and it is stained using eosin and haematoxylin. It is studied by MOHS surgeon or histologist. Residual tumour from relevant mapped area is excised and procedure is repeated until clear margin and clear depth are achieved. Clearance must be complete and proper in BCC otherwise there will be very high chance of recurrence (70%).

Fig. 1.531: Different types of naevi. 1. Hairy mole is a mole with a hair growing on its surface.

TURBAN TUMOUR It is a descriptive term wherein entire scalp looks like a turban because of multiple scalp swellings. It can be due to multiple cylindroma; multiple hidradenomas; subcutaneous neurofibromas; nodular multiple basal cell carcinoma. xx Multiple cylindroma is usually considered disease under this term. Cylindroma is a variant of eccrine spiradenoma (skin adnexal tumor). Multiple firm pinkish nodules in the scalp are the presentation in multiple cylindroma. They are rare, often locally malignant, grows slowly over the span of many years to cover entire scalp with reddish lobulated lesion. xx Hidradenoma is a rare benign sweat gland tumour. Multiple tumours commonly look like a turban in the scalp. They are painless, disfiguring, cosmetically problematic, soft, boggy, non-fluctuant, non-compressible cutaneous swellings; commonly observed in middle age group. xx Multiple sebaceous cysts over the scalp mimic the same. xx Management is initial biopsy to find out the cause; then wide excision with skin grafting.

Fig. 1.532: Hairy naevus. 2. Nonhairy mole. 3. Blue naevus. It is seen in children. It is located deep in the dermis, hence appears blue. It is common in buttock (Mongolian spot), hand, feet. 4. Junctional naevus. It lies centred in the junctional layer (basal layer) of the epidermis as clusters. It is immature, unstable and premalignant. Micro­sco­pically there is proliferation of melanocytes at the epidermal junction. Features of malignant transfor­m ation are—change in the size, colour, bleeding, ulceration, crusting, satellite spots.

Skin Tumours 12. Naevus of Ota is dermal melanocytic hamartoma seen in distribution area of trigeminal nerve (ophthalmic /maxillary). It is seen in oriental and African race adolescent females (thigh) with a hormonal influence. 13. Naevus of Ito is similar lesion occurring in shoulder region. 14. Dysplastic naevus is proliferation of atypical melanocytes from epidermal basal layer having variegated irregular look; it is usually >5 mm in size; can be familial; 10% cases may turn into superficial spreading melanoma. 15. Congenital naevus: It is present since birth. Fig. 1.533: Junctional naevus. 5. Compound naevus. It is combination of intradermal and junctional naevus. Intradermal part is inactive but junctional part is potentially malignant.

Fig. 1.536: Congenital naevus. Note:

• Fig. 1.534: Compound naevus. 6. Juvenile melanoma (Spitz naevus) (It is a misnomer). It appears as junctional like mole before puberty. It is seen in children on face. They present as brownish red nodular lesion which needs always excision. 7. Hutchinson’s freckle. It is seen in elderly with large area of dark pigmentation. In the macular stage it is smooth and brown. In the tumour stage it is dark and irregular. It can turn into melanoma commonly. 8. Halo naevus: Halo of depigmentation around the pigmented naevus. This halo is due to antibody response to melanocytes. Halo naevus is often seen along with vitiligo. Similar halo may develop around a malignant melanoma lesion. 9. Intradermal naevus: Cluster of dermal melanocytes is seen without junctional component. Common in face.

Giant naevus is naevus more than 1% of body surface area or more than 20 cm in size. Giant congenital pigmented naevus (GCPN) often shows dermatomal distribution. Pigment cells spread from epidermis to fat and muscle often. It may turn into melanoma (5% risk). Such melanomas are usually axial; is usually associated with retroperitoneal / intracranial melanosis. Curettage, dermabrasion, laser, excision and SSG are the treatment options.

Fig. 1.537: Giant congenital naevus (Courtesy: Dr MuraliKeshav, MD, Pediatrician, KMC Mangaluru). Fig. 1.535: Intradermal naevus. 10. Spindle cell naevus: It is dense, black pigmented lesion containing spindle cells and atypical melanocytes at dermoepidermal junction; seen in females on high with malignant potential. 11. Naevus spilus: It is hyperpigmented speckles throughout, also called as speckled lentiginous naevus. Malignant potential is rare.

• •

Mongolian spot is a blue brown/grey pigmented macular area which is seen in sacral region during birth and after initial intense pigmentation regresses fully in 7 years. Normal number of melanocytes releasing abnormally higher number of melanin granules is called as freckle/ephilis.

Treatment Excision. Always should be sent for histopathology.

Adversity reveals genius, prosperity conceals it.

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Risk Factors

xx It is a malignant tumour arising from epidermal melanocyte

which is most aggressive cutaneous malignant tumour. xx It is of neural crest (ectodermal) origin. xx It is 20 times more commonly seen in whites than blacks. ™™ ™™ ™™ ™™ ™™ ™™ ™™

Melanoblast: Primitive cell derived from the neural crest. Melanocyte: The cell which synthesises melanin is located in the basal layer (melanocyte : basal cell : : 1 : 10). Melanophores are pigment melanin carriers through dendrites into the epidermis. Melanophages are macrophages having melanin pigment. Melanoblasts and melanocytes contain DOPA oxidase enzyme and synthesise melanin. They show +ve DOPA reaction. Melanophores and melanophages show –ve DOPA reaction. Melanin synthesis is controlled by melanocyte stimulating hormone, ACTH and sex hormones.

DOPA reaction: Tyrosine

DOPA

xx Exposure to sunlight (exposure to UV light; more common in white-skinned—20 times). xx Ethnic factors, socioeconomic status (high society), lifestyle, climate. xx Albinism. xx Xeroderma pigmentosa – RR is 1000 (By Kaposi in 1874): It is an autosomal recessive (Ch 9q) disease with defect in DNA excision repair mechanism causing formation of aberrant nucleotide causing ultraviolet rays’ intolerance, erythema, pigmentation, photophobia, premature skin ageing, multiple malignancies with 60% mortality at the age of 20.

Melanin

                     Tyrosinase Oxidase

Fig. 1.539: Xeroderma pigmentosa with BCC in the nose. Such patients are prone for other skin malignancy like melanoma also. There is defective DNA excision repair.

Fig. 1.538: Large nodular melanoma in the sole. xx xx xx xx

Its incidence is equal in both sexes. Its incidence is increasing over the years. Five per cent of skin cancers are melanomas. It is most common in Queensland, Australia. Auckland, New Zealand.

xx xx xx xx xx

Junctional naevus. Familial dysplastic naevus syndrome. Sporadic dysplastic naevi. 10% risk. Large congenital naevi (larger than 20 cm). Family history of melanoma (10% through chromosomes 1p, 6q, 7 and 9). They often present with multiple primary melanomas; associated with dysplastic naevus. xx History of earlier skin cancers other than melanoma. xx Patients who are on immunosuppressive drugs or after renal transplantation or NHL (RR - 30).

Sites Sites of melanoma ™™ ™™ ™™ ™™ ™™

Head and neck—25% Trunk—25% Lower limb—25% Upper limb—11% Other sites—14%

xx In females, leg is the commonest site. xx In males, the front or back of the trunk. xx In the Bantu tribe, sole is the commonest site.

Other sites: Eyes (iris, ciliary body, choroids), muco­cutaneous junction (anorectal region, genitalia), head and neck (meninges, oropharynx, nasopharynx, paranasal sinuses).

Malignancies which spread from mother to foetus ™™ ™™

Melanoma Lymphosarcoma

Classifications Breslow’s classification (1970): Based on thickness of invasion measured by optical micrometer—most important prognostic indicator until nodal spread I: Less than 0.75 mm II: Between 0.76 to 1.5 mm III: 1.51 mm to 4 mm IV: More than 4 mm

Skin Tumours Relation of Tumour Thickness to Nodal Spread—Based on AJCC Classification Lesion Thin Intermediate Thick

Tumour thickness Nodal spread 4 mm with ulceration M—Metastasis

M0—no blood spread M1a—Skin, subcutaneous tissue, distant node M1b—Lung spread M1c—Other viscera or distant spread and increase in LDH

Node N0 No nodes N1a—one node micrometastasis N1b—one node macrometastasis N2a—2 or 3 nodes micrometastasis N2b—2 or 3 nodes macrometastasis N2c—no nodes but satellite or in transit lesions N3–4 or more nodes; nodes with satellite or in transits Stage 0 – T is N0M0 Stage IA – T1a N0M0; IB – T1b/T2aN0M0 Stage IIA – T2b/T3aN0M0; IIB – T3b/T4aN0M0; IIC – T4bN0M0 Stage IIIA – T1-4aN1a/N2aM0; IIIB – T1-4bN1a/N2aM0, T1-4aN1bN2bM0, T1-4a/bN2cM0; IIIC – T1-4bN1b/N2bM0, any TN3M0 Stage IV – Any T, Any N, M0

xx Relevant other methods depending on site and spread, e.g.

CT scan of head, chest, abdomen, pelvis. xx Urine for melanuria signifies advanced disease. xx Sentinel lymph node biopsy (SLNB). xx Tumour markers—LDH; Melan – A; S 100; tyrosinase; HMB 45 are the tumour markers used. Human melanoma black 45 (HMB 45) is a monoclonal antibody against specific antigen (Pmel 17) present in melanocytic tumours. HMB 45 has got 92% sensitivity. xx MRI of the area; PET scan to detect the spread—in seleted patients only. Tumour markers for melanoma MELAN-A S 100 ™™ HMB 45 (Human Melanoma Black 45.) ™™ LDH ™™ ™™

Treatment Surgery is the main treatment.

For Primary: a. Handley’s wide local excision (WLE) is wide excision with clearance of margin as well as depth. Clearance margin used in olden days is 3–5 cm. Tumour thickness in mm

Wide Local Excision (WLE) margin in cm

2 mm

3 cm

  Present recommendation is— in situ melanoma needs 0.5 cm clearance; melanoma < 1 mm thickness needs 1.0 cm clear-

ance; 1–2 mm thickness needs 1–2 (1.5) cm clearance; 2 cm/3 cm clearance is sufficient for >2.0 mm thickness. Procedure can be done under regional or local anaesthesia. Evidence says that more than 2 cm clearance will not show any additional advantage in treating primary tumour.   Primary closure or SSG or local flaps are used to cover the defect. b. If primary area is wide and deep, then amputation with one joint above is done. c. In fingers and toes, disarticulation is required. d. Melanoma in anal canal may require abdominoperineal resection. e. Enucleation in case of melanoma in eye. f. Melanoma in pregnancy is treated with termination of pregnancy and specific therapy for melanoma. Pregnancy should be postponed for 2 years.

For lymph node secondaries: 1. In a clinically palpable lymph node, FNAC of lymph node is done. In case of spread, then regional block dissection, i.e. ilioinguinal or axillary or neck is done. Once FNAC shows positive lymph node 5-year survival rate reduces to 50%. 2. In a fixed lymph node, only chemotherapy is the treatment because it is inoperable. 3. Lymphatic mapping and sentinel node biopsy (Dr Donald Morton, 1970): Radioactive colloid is injected around primary site and lymphoscintigraphy is done using hand held gamma camera to visualise the micrometastasis in the nodal field. If there are micrometastasis, then regional block dissection (therapeutic LND) is done.   SLN (Sentinel lymph node) can be identified in 95% or more of groin and axillary nodes and in 85% cases of head and neck melanomas. Often both blue dye and technetium sulfur colloid is used together to identify the SLN. SLNB is useful for melanoma with thickness more than 1 mm depth. Less than 1 mm thickness is considered as low-risk for metastases; between 1-4 mm thickness is considered as intermediate-risk for metastases mainly of nodal spread; more than 4 mm thickness will be considered as high-risk for both nodal as well as blood spread. SLNB is the investigation of choice for staging in intermediate thickness melanoma.

Skin Tumours

A

B

A

B

Figs 1.549A and B: Widely excised melanoma specimen from heel. Cut section of widely excised specimen of melanoma from heel shows the depth of the tumour.

Figs 1.552A and B: Melanoma secondaries in groin nodes after block dissection. Black lesions are observed in cut section.

Fig. 1.550: Wide excision and skin grafting done for melanoma.

Fig. 1.553: Disarticulation of lateral two toes for interdigital melanoma.

Fig. 1.551: Wide excision of melanoma from the heel. Note the clearance margin and depth of dissection.

Figs 1.554: Secondaries in inguinal lymph nodes from primary melanoma sole-on table finding. Pigmented nodes are observed.

Creativity begins with thinking different and progress with acting different, thus giving unique results.

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SRB's Manual of Surgery Technique of SLNB Preoperative lymphoscintigraphy is done on the day of surgery for primary tumour. 0.5 mCi Technetium 99 sulphur colloid is injected into the normal dermis within 0.5 cm from the margin of melanoma. Dynamic and static images are taken to identify lymphatic channels, sentinel node (s), interval node (like popliteal node in lower and epitrochlear node in upper limb). After that under general anaesthesia, just before wide local excision (WLE) of the melanoma, 1-5 ml of isosufan blue dye is injected into the dermis similarly. By this, senile lymph node is identified in 99% of patients. SLN is defined as a node which indicates a direct lymphatic drainage pathway from primary; it is the most radioactive node in nodal basin; shows radioactive count 10% more than other nodes; takes blue dye adequately; on table this node will be palpably suspicious of tumour. In melanoma nodal basin usually 2 SLNs are identified (as first echelon nodes in nodal basin). Axillary and inguinal SLNs are easier to identify than head and neck SLNs which are usually located adjacent to spinal accessory nerve. Entire SLN (s) should be removed and sent for histology, immunohistochemistry—S-100 and HMB-45. Interval lymph nodes like popliteal or epitrochlear when involved should be cleared surgically.

Sentinel node biopsy a. Carcinoma breast b. Melanoma c. Carcinoma penis

4. Prophylactic regional block dissection which was previously advocated is now controversial. But still used in many centres. Elective lymph node dissection (ELND) is done when tumour thickness is 1–4 mm. 5. Management in unknown primary (2%) presenting as nodal secondaries is by nodal radical dissection at the region with adjuvant chemotherapy. They have better prognosis than with known primary. Patient should be monitored and evaluated to identify the primary site during every follow up. Once primary is identified it is treated accordingly depending on its location.

For Loco Regional Recurrent Melanoma: xx Local recurrence is one which recurs within 5 cm radius of

the primary tumour in skin or subcutaneous tissues. Risk of local recurrence is 0.2% if primary tumour is less than 0.75 mm; 2% if it is between 0.75–1.5 mm; 6% if it is 1.5–4 mm; 12% if it is more than 4 mm.

 Isolated limb perfusion (Creech et al, New Orleans, 1958) using



cytotoxic agents like Melphalan (M for M), interleukin 2, tumour necrosis factor (TNF). Concentration used here is 15–25 times more than that is used for systemic therapy. Melphalan dose is 10 mg/l perfusion solution in leg (13 mg/l in arm). Melphalan is injected at high temperature of 41°C with a pump and oxygenator through cannulas in femoral artery and vein with a proximal tourniquet in situ. Hyperthermia and oxygenation increase the metabolic activity of tumour cells to make it more vulnerable to melphalan. Procedure controls the local disease well with preserving the functioning limb. Complications like DVT, bleeding, sepsis can occur. It is used in local recurrence or ‘In- transit’ deposits.

  It shows 80% response rate with 15% complete response; but only of short period.  Laser ablation of multiple small cutaneous lesions.  Isolated limb infusion (Thompson, 1993): Vascular catheters are passed and placed across femoral artery and vein through opposite femoral vessels or through arm vessels. The limb is warmed; patient is anaesthetised 2 hours later and also heparinised; papaverine is injected into arterial catheter and tourniquet is applied in the thigh/arm. Melphalan 7.5 mg/l, actinomycin D 75 µg/l in 400 ml saline (10 mg and 100 µg/l in 300 ml NS in upper limb) is infused into the isolated limb for 6 minutes which is pumped around the limb repeatedly for 30 minutes with a hypoxia in limb; drugs are washed out using a Hartmann’s solution; tourniquet is removed and normal circulation is regained with removal of vascular catheters. Protamine is given to reverse heparin action.

For Distant Spread xx Brain, lung and liver are the most common sites; skin, bone, GI are less common sites. But melanoma is one of the commonest tumours to spread to intramural GIT to present as intussusception. xx Distant spread when found or suspected, CT scan of head, chest, abdomen and pelvis are needed. PET scan and tumour markers are very useful.  Chemotherapy and immunotherapy is the main treatment.  Isolated lung or liver metastasis can be resected.  Radiotherapy is useful for bone and brain secondaries. Stereotactic program using gamma knife is better for brain secondaries.

Chemotherapy for Melanoma Indications: a. Secondaries in lungs, liver, bones. b. After surgery for melanoma. Usually it is given intravenously. Drugs are: a. DTIC: Diethyl triamine iminocarboxamide. b. Melphalan (Phenyl alanine mustard) (Melphalan for melanoma). c. Carboplatin, vindesine. d. CVD regime—is cisplatin, vinblastine and dacarbazine.

Immunotherapy/Biological Therapy xx It is done using specific tumour antibodies, BCG, levamisole, Corynebacterium parvum, alpha interferon, interleukins and tumour vaccines is tried with some success rate up to 40% in advanced melanomas. xx Biochemotherapy is combination of CVD with interferon α and interleukin 2. xx Interferon α is a cytokine which is antiangiogenic and stimulator of natural killer NK cells. Dose is 20 mU/m2 IV 3 times a week for 4 weeks then maintenance dose of 10 mU/m2 subcutaneously 3 times a week for one year. Severe myelodepression and fulminant liver necrosis are the toxicity and so often dose is reduced to 3 mU/m2 three times weekly for 2 years. xx GM2 ganglioside based vaccine (stimulates production of IgM antibodies), Melacine (contains melanoma cell lysates) and cancerVax are three vaccines under trial at present. xx Ipilimumab is a monoclonal antibody that boosts the body’s immune response against melanoma cells.

Skin Tumours Endolymphatic Therapy

Prognosis for Melanoma

xx It can be done to control disease in the nodes using radioactive I131 or P32 with ultrafluid lipiodol along with lymphangiography.

xx xx xx xx

Targeted therapy xx Signal transduction inhibitor therapy—Vemurafenib, dabrafenib, and trametinib are signal transduction inhibitors; oncolytic virus therapy; monoclonal antibody therapy—are different targeted therapies. Note:

• •

There is not much role for radiotherapy. Radiotherapy is beneficial only in secondaries in brain and bones.

It is not good since it is a very aggressive tumour. Old age has worse prognosis. Females show better prognosis. Extremity melanoma has better prognosis than head and neck.

Prognostic factors—overall poor

Staging as prognostic factor

• Tumour thickness—very important factor • Nodal spread—once regional nodes are positive, 85% of patients will have occult distant spread. Number of positive nodes is also important • Ulceration—poor • Angiogenesis, vascular invasion—poor • In-transit nodules—poor • Vertical growth—poor prognosis • Metastatic disease—poor • Staging • Mitotic activity

Stage I: >90% prognosis Stage II: 70% Stage III: 35% Stage IV: 5 cm should be biopsied in suspicious of sarcoma

Soft tissue sarcoma

™™

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Features xx Sarcomas are much lesser in incidence compared to carci-

nomas.

xx It occurs in younger age group compared to carcinomas. xx They can arise from bone (osteosarcoma) or from any soft

tissues (soft tissue sarcomas) (Mesenchymal tissue). xx They are much more aggressive compared to carcinomas. xx They are rapidly growing tumours with fleshy appearance. xx They are not encapsulated but often are having pseudocapsule. xx They spread through blood especially to lungs often also to other organs. xx Lymphatic spread is not common with certain exceptions. xx Main method of treatment is surgery, i.e. wide excision, amputation. xx In inoperable cases debulking is the accepted method of treatment. xx Chemotherapy is the adjuvant therapy. xx Commonest sarcoma of bone is osteosarcoma  

 

Note:

Commonest malignancy of bone is secondaries.

™™ M  alignant Peripheral Nerve Sheath Tumour ™™ Kaposi’s Sarcoma

™™ ™™ ™™

xx Commonest soft tissue sarcoma is liposarcoma / malignant

fibrous histiocytoma (MFH – 25%) overall; in the extremities both MFH and liposarcoma; in the retroperitoneum it is liposarcoma. xx Commonest visceral (GIT) sarcoma is leiomyosarcoma. xx In genitourinary system leiomyosarcoma is commonest in adults and rhabdomyosarcoma in paediatric age group; in uterus leiomyosarcoma; in myocardium angiosarcoma; in hand and foot synovial sarcoma; in skin Kaposi’s sarcoma; in head and neck region angiosarcoma.

Sarcomas Incidence of STS

Fig. 1.556: Soft tissue sarcoma foot. Note the vascularity.

In adults xx MFH and liposarcoma—35–45%. xx Rhabdomyosarcoma—10%. xx Leiomyosarcoma—9–15%. xx Synovial sarcoma—7%. xx Malignant peripheral nerve sheath tumour (MPNST)—6%. xx Fibrosarcoma—5%. In children xx Rhabdomyosarcoma, neuroblastoma are common tumours. Aetiology ™™

Fig. 1.557: Osteosarcoma of the upper end of humerus in an adolescent boy.

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Genetic –– von Recklinghausen disease –– Gardner’s syndrome –– Tuberous sclerosis –– Basal cell naevus syndrome –– Li-Fraumeni syndrome Chemicals—PVC, tetrachlorodibenzodioxin, arsenic Viral—HIV in Kaposi’s sarcoma, cytomegalovirus Ionising radiation—malignant fibrous histiocytoma (p53) Lymphangiosarcoma in post-mastectomy lymphoedema— Stewart—Treves syndrome. Osteogenic sarcoma in Paget’s disease of bone/exposure to radium Retinoblastoma associated sarcoma Gorlin’s syndrome Thorotrast, vinyl chloride, arsenic, pesticides

Clinical Features of Soft Tissue Sarcoma xx Painless swelling of short duration with progressive increase

Fig. 1.558: Osteosarcoma upper tibia. Note the size of the tumour and ulceration. It is very vascular.

in size—soft tissue mass. Thirty percent of patients may present as pain during first evaluation. xx Compression of adjacent structures xx Smooth, firm/hard, warm and vascular xx Features of secondaries in lung—cough, haemoptysis and chest pain. Lung is the commonest site of secondary. xx Secondaries in liver as a principal site especially in visceral STS. xx There are no reliable findings to distinguish benign from malignant swellings. xx One has to maintain a high index of suspicion in any soft tissue mass deep-to-deep fascia, any soft tissue mass > 5 cm, any new enlarging or symptomatic soft tissue mass.

B

A

Figs 1.559A and B: X-ray pictures of osteosarcoma in tibia and femur. Note:

• •

Many liposarcomas arise at sites devoid of adipose tissue. Most rhabdomyosarcomas arise in locations that lack voluntary muscle. 40% of soft tissue sarcomas are more than 10 cm in size at the time of presentation; 30% are 5-10 cm and 30% are less than 5 cm.

A

B

Figs 1.560A and B: Soft tissue sarcoma upper chest wall. Note the vascularity and extent.

All things are difficult before they are easy.

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SRB's Manual of Surgery Investigations Preoperative evaluation of STS is done: ™™ ™™ ™™ ™™

To obtain a tissue diagnosis To determine the “exact extent” of the tumour To evaluate metastatic disease Other investigations

Tissue diagnosis xx Incision biopsy is the most reliable method of diagnosis. It provides adequate tissue sample. Incision biopsy for soft tissue sarcoma ™™ ™™

™™ ™™ ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™

™™ ™™

It is the ideal tool to conclude sarcoma histologically Incision should be placed in such a way that it can be included in wide tumor excision at a later period—as biopsy track is always contaminated One should achieve absolute / adequate haemostasis to avoid haematomas as tumours are vascular Proper site of incision biopsy should be decided One should use shortest possible route to tumour while taking incision biopsy; should not violate more than one compartment; should avoid neurovascular bundle. (Injury to vessels and nerves should be avoided) Smallest longitudinal incision is used to provide adequate specimen (Incision should be longitudinal in limbs) Transverse incision is contraindicated in the limbs except over the flexures Minimal tissue disturbance and avoiding raising of flaps are crucial (Flaps should not be undermined) It is better to use cold knife One should avoid crushing/distorting the specimen Frozen section/Imprint specimen can be used to avoid sampling error. Drains are not used routinely in incision biopsy. If used exit near/ close to the wound and not away/distant from the incision biopsy wound. Excise the biopsy tract and drain site enbloc during the definitive procedure. Immunohistochemistry and cytogenetics are possible

Fig. 1.561: Incision for biopsy in STS should be longitudinal so that it can be included in future surgical wide excision. Never place transverse incision for biopsy.

xx Trucut biopsy/core needle biopsy is an acceptable first diagnostic step as it is technically easier, not costly, with fewer complications. But it is not useful in visceral STS. Again if it is inadequate one should not be hesitant to go for incision biopsy at the earliest. It is done using 14 gauge needle; often US / CT guide is used. xx Excision biopsy is done only if the tumor size is < 3 cm which is cutaneous or subcutaneous wherein wide local re-excision is possible. Otherwise excision biopsy should be avoided as it may contaminate the tumour bed and restricts the therapeutic options. Note:

FNAC is of less value in STS. It is significant only if it positive. It is useful in local or distant recurrences in documented sarcoma patients, or to evaluate nodal status if enlarged. CT guided FNAC is useful for retroperitoneal/intra-abdominal sarcomas.

Assessment of the extent of tumour Imaging in STS provides a 3–dimensional extent of the tumour and helps in accurate planning of surgical procedure. But it does not reliably distinguish between a benign and malignant process. It assesses macroscopic and not microscopic extent of the disease. Imaging is essential for metastatic work up. xx MRI is the investigation of choice as it determines the vascularity, relation to vessel and fascial planes (extent and invasion). Advantages of MRI are—imaging of choice in STS, excellent soft tissue delineation, without radiation, multiplanar imaging possible. Images of skip metastases are possible. Disadvantages of MRI are—cost, bone involvement is poorly delineated, claustrophobia, not possible in presence of metal implants and pacemakers. xx CT scan also can be used to see the extent and invasion but not equivalent to MRI. CT scan helps in identifying presence and extent of the soft tissue mass, status of the adjacent structures, with mandatory contrast enhancement isodense masses, vasculature are better delineated. SPECT—3 dimensional reconstruction feasible. Advantages of CT are—easy availability, relatively cost effective, best to demonstrate bony involvement, useful for guided biopsies. Disadvantages of CT are—cross-sectional imaging, ionizing radiation, inferior soft tissue detail. xx US is less sensitive investigation. It is useful in extremity lesions to assess vascular system. It is initial/first investigation done in GI leiomyosarcoma/retroperitoneal sarcoma. It is useful for serial studies, guided trucut biopsy.

Fig. 1.562: MRI of STS leg.

Sarcomas Other Investigations xx Radionuclide scintigraphy (Gallium-67). xx -p-MRS (p-Magnetic Resonance Spectroscopy) and FDG (Fluor2-Deoxy Glucose) PET are done to assess the metabolic activity of tumour. xx Immunohistochemistry and FISH (fluorescence in situ hybridization). xx Tumour markers. xx Haematocrit, peripheral smear, ESR, serum alkaline phosphatase, serum creatinine.

Staging Staging of the soft tissue tumour is done depending on the tumour size, nodal status, metastasis and histological grading of the tumour (GTNM staging). Fig. 1.563: MRI picture of the soft tissue tumour thigh encasing vessels partially and eroding the bone. Patient needed high level, above-knee amputation.

TNM staging of soft tissue sarcoma Grade (G)

Tumour (T)

Gx Cannot be assessed

Tx Cannot be assessed

G1 Well-differentiated

T0 No primary

G2 Moderately differentiated

T1 Size < 5 cm or 5 cm (maximum dimension)

G3 Poorly differentiated

T1a: Superficial T1b: Deep tumour

G4—is now not used

T2 Size > 5 cm

G is assessed by differentiation; mitoses; necrosis through scores

T2a: Superficial T2b: Deep tumour

Fig. 1.564: CT picture of retroperitoneal leiomyosarcoma.

xx X-ray of part is not necessary; it is only used in initial phases to differentiate STS from bony lesion. xx Angiogram is traditionally used to delineate adjacent vasculature. It is upstaged by CECT/MRA. It is not necessary to do regularly in all cases but when there is a need for accurate assessment of vasculature it is ideal. It is used in intra-arterial chemotherapy for unresectable tumours. xx CT abdomen is better in GI/retroperitoneal sarcomas.

Regional lymph nodes (N)

Distant spread (M)

Nx Nodes cannot be assessed

Mx Cannot be assessed

N0 No nodes

M0 No distant spread

N1 Nodes present

M1 Distant spread present

Note: Superficial tumour is outside the superficial fascia. Deep tumour is deep to superficial fascia or any tumour invading the superficial fascia.

AJCC 2010/UICC staging of STS Stage IA—G1, Gx; T1a, T1b; N0; M0. Stage IIB—G1, Gx; T2a, T2b; N0; M0 Stage IIA—G2, G3; T1a, T1b; N0; M0. Stage IIB—G2; T2a, T2b; N0; M0 Stage III—G3, any G; T2a, T2b, any T; N0, N1; M0 Stage IV—Any G; Any T; Any N; M1 Note: Desmoid tumour, Kaposi’s sarcoma and infantile fibrosarcoma are excluded; angiosarcoma, Ewing’s sarcoma, dermatosarcoma protuberans are included.

Evaluation of Metastatic Disease xx Chest X-ray is done to look for secondaries. xx CT chest is ideal to see early lung secondaries. It is done in all deep seated, high grade and tumour more than 5 cm in size. xx US abdomen is sufficient to check liver secondaries. But CT abdomen may be better choice. Often CT pelvis is also added. xx PET scan or Integrated PET scan (with CT) is often useful to identify metastatic diseases.

Grading of sarcomas Low Dermatofibrosarcoma, liposarcoma. here 50% chances of metastases Undetermined—fibrosarcoma, Leiomyosarcoma

Knowledge is fire and it is antidote to fear.

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• • • • •

STS is an aggressive, invasive, destructive growth with high recurrence and distant metastases rate. Tumour shows fish flesh cut appearance. Basis used for classification of STS—STS being highly heterogeneous group of tumour is classified based on adult tissue it resembles; i.e the type of tissue formed rather than from the type of origin. Grade is the single most important factor in staging. It denotes the “biological aggressiveness” of the sarcoma. It predicts the likelihood of metastases. Nodal metastases are rare in STS (3%). It has the poor prognosis. M1 is – Distant metastases.

Differential diagnosis for soft tissue sarcoma ™™ ™™ ™™ ™™

Haematoma Abscess Aneurysm Myositis

FIg. 1.565: Different surgical approaches for STS.

Treatment Principles of treatment xx Surgery is the main treatment modality. Amputation rate

for STS has come down drastically from 50% in 1960 to 5% at present. It is also because of proper adjuvant radiotherapy following function/limb sparing complete excision, application of microvascular surgeries. Neoadjuvant chemotherapy, perioperative/postoperative RT also play a major role.

xx In low grade tumour without any spread—functional/limb sparing complete wide excision is sufficient without any adjuvant therapy. If microscopic margin is positive for tumour then postoperative External Beam RT (EBRT) is given. xx In high grade tumour 4 cm T4 Tumour is of any size involving bone, soft tissues, muscles T4a Tumour invading adjacent structures (e.g. through cortical bone, into the deep (extrinsic) muscles of the tongue, maxillary sinus, or skin of the face) T4b Tumor invades masticator space, pterygoid plates, or skull base and/or encases internal carotid artery Nx Nodes cannot be assessed N0 No lymph node spread N1 Lymph node size < 3 cm, same side N2 Lymph node size 3–6 cm and single (N2a); multiple lymph nodes 3–6 cm size on same side (N2b); bilateral or opposite side nodes up to 6 cm size (N2c) N3 Lymph node spread, more than 6 cm size Stages Stage I – T1,N0,M0. Stage II – T2,N0,M0. Stage III – T3,N0,M0; T1-3,N1,M0. Stage IV – T4,N0,M0; T1,N2-3,M0; T0,N0,M1.

Fig. 3.19: Oral cavity carcinoma with mandibular involvement, with T4 lesion. Features of advanced carcinoma cheek ™™ ™™ ™™ ™™

Involvement of retromolar trigone Extension into the base of skull and pharynx Fixed neck lymph nodes Extension to the opposite side

Problems with oral carcinomas Upper airway obstruction and bronchopneumonia Feeding difficulties and severe malnutrition Immunosuppression Secondary sepsis, uncontrollable bleeding Fixity of secondaries, fungation and disability Psychological trauma When once trismus develops, patient is unable to take adequate food and eventually leads into cancer cachexia. Trismus may develop by tumour infiltration or after RT ™™ Orocutaneous fistula causes salivary dribbling which is distressing ™™ ™™ ™™ ™™ ™™ ™™ ™™

Investigations

Fig. 3.18: Advanced carcinoma cheek with fungation and orocutaneous fistula.

1. Wedge biopsy, usually taken from two sites. Biopsy has to be taken from the edge as it contains active cells; not from the centre as it is the area of necrosis. Malignant squamous cells with epithelial pearls (Keratin pearls) are the histological features.

Fissuring of tongue due to ariboflavinosis is longitudinal and the bottom of fissure is beefy red. —Dimitri Afonsky

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Broder‘s histological grading a. b. c. d.

Treatment may be curative or palliative.

Well-differentiated: > 75% epithelial pearls Moderately differentiated: 50–75% epithelial pearls Poorly differentiated: 25–50% epithelial pearls Very poorly differentiated: < 25% epithelial pearls

Treatment Strategy

Present grading system GX G1 G2 G3

Grade cannot be assessed Well differentiated or low grade Moderately well differentiated or intermediate grade Poorly differentiated or high grade

2. FNAC from lymph nodes. 3. CT scan is used to assess the extent of tumour into mandible, pterygoid region, in patient with trismus, with neck lymph nodes, with carotid involvement by lymph nodes. MRI is very useful in assessing the soft tissues, base of skull, and perineural spread. 4. Orthopantomogram to look for the involvement of mandible—destruction and fracture sites. Symphysis menti and lingual plate are not clearly appreciated. So often OPG may be supported with dental occlusion and intraoral X-rays. 5. Opinion and help of dentist is taken for teeth extraction, dental care, for prosthesis preparation especially for palate, alveolus, dentures.

Fig. 3.20: Orthopantomogram showing secondaries in mandible. Note:

• • •

Surgery. Wide excision, hemimandibulectomy, neck lymph nodes block dissection. ™™ Radiotherapy: Curative or palliative; external or brachytherapy. ™™ Chemotherapy: Intra-arterial, IV or orally. ™™

Open biopsy should be avoided in case of secondaries in lymph nodes as it may aggravate the spread to further level of lymph nodes. Biopsy from the centre is taken only from post-radiotherapy ulcer and ulcerated minor salivary gland tumours. Incidence of second primary lesion is 30% mainly at upper aerodigestive tract.

xx Early growth without bone involvement:

1. Curative radiotherapy using 137Caesium needles or 192 Iridium wires, i.e. brachytherapy. Advantages: i. Surgery is avoided. ii. No surgical mutilation. iii. Parts are retained. iv. As it is a squamous cell carcinoma, primary is radiosensitive—90% cure rate. 2. Other option is wide excision with 1–2 cm clearance. Often, the approach to the tumour is by raising the cheek flap (outside). After the wide excision, the flap is placed back (Patterson operation). 3. Present advanced technology in radio­therapy, facilitates the use of external radiotherapy also. The incidence of dreaded complication like osteoradionecrosis of mandi­ble has been reduced due to better RT methods. xx Growth with mandible involvement: Here along with wide excision of the primary tumour, hemimandi­b ulectomy or segmental resection of the mandible or marginal mandi­bulectomy (using rotary electric saw) is done. xx Operable growth with mandible involvement and mobile lymph nodes on the same side (con­firmed by FNAC): Along with wide excision of the primary, hemimandibulectomy and radical neck lymph node dissection is done (like commando operation). Wide excision of primary lesion, hemimandibulectomy with radical neck node dissection is called as composite resection. xx Operable growth with mandible involvement; mobile lymph nodes on same side and opposite side: Along with wide excision of the tumour, hemi­ mandibulectomy, radical neck lymph node dissection on same side and functional block dissection on opposite side are done, retaining the internal jugular vein, sterno­mastoid, spinal accessory nerve.

Indications for surgery

Advantages

Disadvantages

• • • • • • •

• Pain is controlled • Often curative • Fungation, ulceration, bleeding is prevented

• Mortality (5%) • Morbidity, sepsis, flap necrosis, fibrosis • Cosmetic problem • Loss of anatomy and its function

Early tumour Tumour spreading to mandible bone/alveolus Fungation, haemorrhage due to erosion Recurrence of tumour after RT Multiple sites Soft tissue spread Locally advanced but amenable to surgical resection

Oral Cavity

Fig. 3.21: Patient who has undergone hemimandibulectomy with primary closure. Note the defect.

Fig. 3.22: Hemimandibulectomy, resected specimen (Courtesy: Dr Jagadish Chandra, MDS).

A

B

C Fig. 3.23: Patterson incision to approach carcinoma cheek by raising skin flaps from lower part of face adjacent to lower margin of the mandible.

Figs 3.24A to C: Lip-split incision approach for carcinoma cheek. It gives adequate exposure of the cheek. Lower extension is for neck block dissection.

Aphthous ulcer is rare after the age of 50. —Wilfred Sircus

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Fig. 3.25: Radical neck dissection for secondaries in neck through MacFee incision. Fig. 3.27: Specimen showing primary tumour in cheek with mandible (hemimandibulectomy) and block dissection nodes.

Fig. 3.26: Defect in the cheek after wide excision for carcinoma cheek. Defect needs coverage using PMMF with skin graft inside (Courtesy: Professor Kishore Chandra Prasad, ENT Surgeon and Dr Sampath, ENT Surgeon, Mangaluru). xx Operable primary tumour with mobile lymph nodes on

same side but without mandibular involvement: Wide excision of primary tumour and radical neck lymph node dissection on same side are done. Mandible is not removed. xx Fixed primary tumour or advanced neck lymph node secondaries: Only palliative external radiotherapy is given to palliate pain, fungation and to prevent anticipated torrential haemor­ rhage. xx Pre-operative radiotherapy is often used in fixed lymph nodes to downstage the disease so as to make it operable. xx Post-operative radiotherapy is given in T3 and T4 tumours: N2 and N3 nodal status to reduce the recurrence and to improve the prognosis (in multiple nodes and nodes with extracapsular spread).

Fig. 3.28: Visor approach for oral malignancy. Visor approach for anterior mandible, floor of the mouth and tongue. Here skin over the anterior curved margin of the mandible is incised to approach the floor of the mouth for needed procedure. xx Prophylactic block dissection has become popular in N0

diseases. Reasons are:  Even though clinically, lymph nodes are negative, there may be microscopic involvement of lymph nodes (25–65%).  Clinically detectable disease in lymph nodes of the patient signifies extracapsular spread which has got poor prognosis.  Recurrence rate is less after prophylactic block compared to block dissection with clinically positive nodes because

Oral Cavity xx Role of chemotherapy: Drugs used are metho­trexate, cisplatin, vincristine, bleo-

mycin, adriamycin. Often it is given intra-arterially through external carotid artery using arterial pump or by increasing the height of the drip more than 13 feet, so as to attain a pressure more than systolic pressure. Chemo­therapy can also be given IV or orally—post-operatively.  Initial chemotherapy to downstage the tumour followed by surgery and later again end with chemotherapy.  Chemoradiotherapy is used in unresectable tumours—as consecutive therapies.

Reconstruction after Surgery Flaps used for reconstruction after oral surgery Forehead flap based on superficial temporal artery Deltopectoral flap based on 1, 2 and 3 perforating vessels from internal mammary vessels ™™ Pectoralis major myocutaneous flap (PMMF) based on thoracoacromial artery ™™ Free microvascular flaps may be from radial artery forearm flap ™™ For small defects—tongue flap, buccal flap, palatal mucoperiosteal flap ™™ ™™

Fig. 3.29: Carcinoma cheek operated with radical neck dissection of same side lymph nodes. Reconstruction done using pectoralis major myocutaneous flap.

Split skin graft. Deltopectoral cutaneous flap. Forehead flap, radial artery forearm flap. Pectoralis major myocutaneous flap. Mandible reconstruction by cortical bone graft or rib, fibula or synthetic material like titanium, stainless steel plate. xx Free fibular flap; radial forearm flap, anterolateral thigh flap, tongue flap, cheek advancement flaps are becoming popular. xx xx xx xx xx

Fig. 3.30: Carcinoma cheek, on table wide excision. It requires pectoralis major myocuta­neous flap for reconstruction.

there is no extracapsular spread in the former even if there is microscopic spread of tumour in many cases.  Block dissection is an acceptable surgery as there is negligible mortality and less morbidity.  It is advocated in T3, T4 lesions, carcinoma alveolus or floor of the mouth. xx If growth is extending to upper alveolus: Partial maxillectomy or total maxillectomy may be required.

A

Halitosis is better breath than no breath at all !!!

Fig. 3.31A

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B

Fig. 3.33B

Figs 3.33A and B: Reconstruction of the mandible after segmental mandibulectomy using plate and opposite rib fixation (Courtesy: Jagadish Chandra, MDS).

B Fig. 3.31B

Figs 3.31A and B: Pectoralis major myocutaneous flap to cover the defect in the cheek after wide excision (Courtesy: Professor Kishore Chandra Prasad, ENT Surgeon and Head of the Department and Dr Sampath, ENT Surgeon, KMC, Mangaluru).

Fig. 3.34: Harvesting fibular flap for mandibular reconstruction. (Courtesy: Dr Satish Bhat, MCh, Plastic Surgeon, Mangaluru).

Fig. 3.32: Forehead flap is used after wide excision of carcinoma cheek. It is based on superficial temporal artery—anterior branch.

A Fig. 3.33A

A

B

Figs 3.35A and B: Forehead flap used to cover the defect after wide excision for carcinoma lip or cheek (Courtesy: Professor Kishore Chandra Prasad, ENT Surgeon and Head of the Department and Dr Sampath, ENT Surgeon, KMC, Mangaluru).

Fig. 3.36: Deltopectoral flap used to cover defect after surgical clearance in carcinoma cheek. It is based on 2nd perforator, a branch of internal mammary artery (Bakamjian—1965).

Oral Cavity Approaches to Carcinoma Cheek xx xx xx xx

Transoral/intraoral approach. Lip split incision. Patterson approach. Visor approach for anterior mandible, floor of the mouth and tongue. Here skin over the anterior curved margin of the mandible is incised to approach the floor of the mouth for needed procedure. (Visor is French derived word which means mobile lower part of the helmet which covers the chin). Different mandibular resections

™™ ™™ ™™ ™™ ™™ ™™

Marginal mandibulectomy Segmental resection Partial mandibulectomy Hemimandibulectomy Rim resection of mandible Resection of the anterior mandible through visor approach

Fig. 3.40: Hemimandibulectomy.

Fig. 3.37: Marginal mandibulectomy.

Fig. 3.38: Segmental resection of the mandible (angle of mandible to mental foramen).

Fig. 3.41: Rim resection of mandible done for carcinoma floor of the mouth.

Marginal Mandibulectomy

Fig. 3.39: Partial mandibulectomy is removal of mandible one side from mental foramen to line of coronoid process including coronoid process but leaving condylar process.

xx It is in continuity wide excision of tumour with gingival and adjacent margin of the mandible. xx Superior margin is removed using electric saw after proper marking leaving at least 1 cm of inferior margin. xx It is done in lesion which is close to mandible but not invading. Invasion needs segmental resection. Invasion is invariably through dental root leading into mandibular canal and cancellous bone. xx Mandibular involvement either clinically or radiologically, previous RT, retromolar lesion (as pterygoid clearance is needed here) are the contraindications.

In great attempts, it is glorious even to fail.

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SRB's Manual of Surgery Problems with surgery Mutilation (surgical) Anaesthesia complications Bleeding Infection Flap necrosis Requirement for reconstruction Mortality Morbidity—stiffness; contracture; cosmetic problem; cutaneous anaesthesia; speech and swallowing problems ™™ Problems of neck dissection—hypoglossal, accessory, phrenic nerve injuries; thoracic duct injury, carotid blow out; oedema neck and face ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Problems with radiotherapy ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

When mandible is irradiated, chances of the dreaded problem, osteoradionecrosis is high which requires the removal of mandible Loss of taste sensation and dryness, xerostomia Infection, mucositis, dental diseases Skin excoriation, hair loss Trismus may get aggravated Can itself cause dysphagia, laryngeal oedema Hypothyroidism if neck is irradiated Radiation neuritis causing severe pain Carotid artery atherosclerosis Visual impairment Shoulder and neck dysfunction Soft tissue fibrosis

Fig. 3.43: Mucositis in cheek and lip in a patient who is receiving chemotherapy for carcinoma. Prognostic factors in oral carcinomas ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Stage of the disease – Stage I and II has got 80% 5 years survival – Stage III and IV has got less than 20% 5 years survival rate T3 and T4 lesions has got poor survival rate Carcinoma lip has got best prognosis Carcinoma posterior 1/3rd tongue has got worst prognosis Cheek, floor of the mouth and palate has got intermediate prognosis Perineural invasion and angioinvasion carries poor prognosis Histologically positive nodes decrease the survival rate by 50% Level III and IV, node > 3 cm, bilateral nodes extracapsular nodal spread are poor prognostic factors Grading (differentiation) of the tumour Tumour thickness > 6 mm has got poor prognosis Exophytic tumour is better than infiltrating type

Recurrent carcinoma cheek 90% recur within 11/2 to 2 years of first surgery/therapy. Local recurrence (20%) is more common than regional recurrence (nodal—10%). ™™ It is confirmed by biopsy. ™™ MRI of the area is very useful to assess spread. ™™ Treatment: It is difficult to treat. Wide surgical excision with reconstruction is the initial treatment. Since usually patient had already received RT, repeat RT is contraindicated and chemotherapy with ideal drugs and regimes should be undertaken. Reconstruction is technically difficult in a post- RT field. ™™ ™™

Fig. 3.42: Radiodermatitis after RT to tonsillar growth. Problems with chemotherapy ™™ ™™ ™™ ™™ ™™ ™™

Bone marrow suppression Megaloblastic anaemia GIT symptoms Hepatotoxicity and renal toxicity Alopecia Nausea, vomiting and severe stomatitis

Fig. 3.44: Recurrent carcinoma of cheek.

Oral Cavity LIP xx Lip begins at vermilion border. It has got upper lip, lower lip and oral commissure. SCC is the commonest lip cancer (90%). SCC is common in lower lip; BCC is common in upper lip. Other cancers in lip are spindle cell carcinoma, adenoid squamous carcinoma, malignant melanoma, minor salivary gland tumour. xx Mucous cyst of lip is a common condition. It can occur in upper or lower lip. It is a retention cyst derived from mucous glands of the lip. It presents as bluish, soft, fluctuant often transilluminating well localised swelling. It may resolve on its own. If it does not it should be excised under local anaesthesia. Absorbable suture is used to appose the wound starting from vermilion margin. Usually vertical elliptical incision is used to excise. Sutured wound heals rapidly with very limited scar. xx Macrocheilia is enlargement of lip mass in other than neoplastic conditions. Lymphangioma is the common cause. Haemangioma, inflammatory conditions also can cause macrocheilia. xx Papilloma, lipoma, pyogenic granuloma, keratoacanthoma, minor salivary tumours are other swellings which can occur in lip. xx Cheilitis often associated with stomatitis is common in vitamin deficiency, malnutrition, sepsis, drug induced, RT induced presents as redness, pain, diffuse swelling. In chronic cases, there will be linear ulcers especially at commissure. Actinic cheilitis is a premalignant lesion. Cause is treated. xx Pigmentation of lip occurs in Peutz-Jeghers syndrome (brown), Addison’s disease (black). xx Herpes labialis is formation ulcers in lip due to herpes simplex virus. Repeated multiple ulcers develop in lip. It is contagious by kissing. So kissing should be avoided including children. Touching repeatedly can transfer the virus to eye causing herpes keratitis. xx Cleft lip is a common congenital condition.

A

B Figs 3.47A and B: (A) Haemangioma lip causing macrocheilia; (B) Macrocheilia due to inflammatory cause.

Fig. 3.45: Mucous cyst upper lip. It requires simple excision. It is a retention cyst.

Fig. 3.46: Mucous cyst seen in lower lip. It is bluish, localised, smooth, non-tender, soft, fluctuant swelling, arising as a retention cyst from mucous glands of lip. It needs excision.

Fig. 3.48: Aphthous ulcer lower lip. It is painful, self-limiting ulcer. It can occur in tongue, lip, cheek and other parts of the oral mucosa.

Knowledge is the only treasure that increases on sharing.

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SRB's Manual of Surgery NEOPLASM OF LIP One may…cure cancers of the lip without applying caustics or any similar thing…. Pass a threaded needle through the cancer so the thread held in the left hand can lift and control the cancer without any of its escaping. One can then cut to good flesh with scissors in the right hand; and so cut that a layer of good flesh of the lip remains to serve as a base and foundation for regeneration of flesh in place of the portion amputated, supposing the cancer has not taken root and spread from top to bottom. —Ambroise Paré, 1585

Basal cell carcinomas (BCC) are common in upper lip. Minor salivary gland tumours also often occur in upper lip; pleomorphic adenoma is the usual type. Squamous cell carcinoma is the commonest cancer in the lower lip.

A

CARCINOMA LIP

B Fig. 3.49: Carcinoma lip involving both upper and lower lips.

Figs 3.50A and B: Carcinoma of lip involving extensively.

xx Incidence of carcinoma lip is 15% of head and neck cancers

xx Commonly due to exposure to sunlight (ultraviolet rays).

and 1% of all cancers. xx It may arise from vermilion surface or mucosa part of the lip. xx It is common after 40 years of age. In younger age group even though it is rare, carries poor outcome. xx It is more common in whites; rare in blacks. It is common in Caucasians. xx Khaini, a mixture of tobacco and lime kept under the lip called as khaini chewers are more susceptible for carcinoma lip. xx All’S’s and irradiation are predisposing factors. xx Verrucous carcinoma can occur in lip. It is well differentiated SCC with exophytic, warty, dry surface. It usually will not invade the deeper tissue and lymph node spread is rare. It carries good prognosis. xx It is common in men (15:1). Common in lower lip (90%); upper lip 5–10%. Upper lip is not exposed to direct actinic radiation.

Common in pipe smokers.

xx Initially starts as a red, granular dry lesion which eventu-

ally gets ulcerated and forms an ulceroproliferative lesion. Occasionally it occurs at the angle of mouth. xx It spreads to submental nodes and later to other neck nodes on both sides. xx Usually it is a well-differentiated squamous cell carcinoma. xx Commissure tumours are 2% of all lip cancers but has higher rate of lymph node spread. xx Initially it is well localized. A depth of more than 5 mm will spread to lymph nodes mainly submental and submandibular (level I). xx Painless ulcerative lesion is the most common presentation. Pain develops once necrosis occurs or tumour infiltrates nerve, periosteum of bone underneath. xx Pigmented SCC can occur. It mimics melanoma. xx Anaesthesia of chin can occur if mental nerve is invaded. xx Staging is same as other oral cancers.

Oral Cavity

A

B

C

Figs 3.51A to C: Carcinoma lip—different locations in the lower lip. SCC is most common in lower lip; in upper lip BCC is common. Clinical features of carcinoma lip Non-healing progressive ulcer, painless to begin with Everted edge with indurations Growth moves with the lip Submental, submandibular and upper deep neck nodes may get enlarged. ™™ Tender firm lymph node may be due to infection; hard initially non-tender node is due to carcinoma spread. ™™ In half of the cases lymph nodes are enlarged due to infection or as reactive process ™™ Fungation, bleeding, halitosis ™™ ™™ ™™ ™™

layers keeping vermilion border in proper apposition without causing any microstomia. xx Excision of more than one-third of the lip requires reconstruction using different flaps.

Predisposing Factors xx xx xx xx xx xx xx

Cheilitis—actinic type Solar keratosis. Papilloma. Leukoplakia. Smoking, U-V rays, pipe smokers, reverse smoking. Tobacco chewing, Khaini chewers (tobacco+lime). Agriculturists who are commonly exposed to sunlight get carcinoma lip and is called as countryman’s lip.

Fig. 3.52: Primary repair of lip after wide excision of small tumour One-third of the lip can be sacrificed. Lip is sutured in layers. First layer, muco-muscular layer with absorbable suture. Second layer is skin with non-absorbable monofilament sutures like polypropylene.

Differential Diagnosis Keratoacanthoma. Basal cell carcinoma. BCC occurs only in upper lip. Minor salivary gland tumours. Often carcinoma of lip is an extension from carcinoma of cheek. xx Pyogenic granuloma in early cases only. xx Malignant melanoma in case of pigmented SCC. xx xx xx xx

Diagnosis Wedge biopsy, FNAC of lymph nodes, USG/CT neck.

Treatment xx If lesion is less than 2 cm, then curative radiotherapy, either

brachytherapy or external beam radiotherapy. It gives a good cure. xx If tumour is more than 2 cm, wide excision is done. Excision of lower lip up to one-third can be sutured primarily, in

Fig. 3.53: Lower lip tumour after excision when primary suturing not possible, then upper lip flap based on upper labial artery can be used—Abbe-Estlander flap.

Methods 1. Abbe-Estlander’s rotation flap used for either upper or lower lip lesions (of less than ½ of lip) located at the angle based on labial

Attitude is a small thing that makes a big difference.

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A

4. Nasolabial flap: It is used when defect is more than ½ of lip laterally or defect is in the floor of the mouth. 5. Cheek flap. 6. Free radial artery flap. 7. Abbe flap (switch flap) is used for upper or lower lip lesions at the middle or at the site other than angle based on the labial artery.

B

D

C

E

Figs 3.54A to E: For upper lip tumour when primary repair is not possible, then lower lip flap based on inferior labial artery can be rotated to upper lip—Abbe flap.

Fig. 3.55: It is used for central lip tumours. Angles of the lower part of the defect and upper part of the angles of the mouth are rotated inwards with Burow’s triangles at the site of rotation—Bernard flap.

Fig. 3.56: It is done for lower lip middle tumour which is less than 1/3rd of the lip—‘W’ flap.

Oral Cavity Here at a later 2nd stage base of the flap should be released once flap takes up. 8. ‘W’ flap plasty: It is done for lower lip middle tumour which is less than 1/3rd of the lip. 9. Gillies fan flap: It is a cheek flap usually bilateral but can be unilateral. Incision is full thickness around commissures extending into nasolabial fold and upper lip upto upper lip vermilion border. Flap which is based on labial vessels is advanced towards the defect. Vermilion is reconstructed with tongue mucosal flap which is divided in 3 weeks. 10. Karapandzic flap: It is modified version of the Gillies flap used for lower lip defect with less angulation towards upper lip. Reverse Karapandzic flap is used for upper lip defect. 11. Johansen ‘stepladder’ procedure is used for extensive carcinoma of lower lip. 12. Other regular flaps like forehead flap, deltopectoral flap also can be used.  Lymph nodes are dealt with by radical neck dissec­tion on one side and functional block or supraomohyoid block dissection on other side. For central tumour N0 disease, bilateral elective (prophylactic) supraomohyoid dissection is done. For

A

lateral tumour N0 disease, elective ipsilateral supraomohyoid dissection is done.  Post-operative radiotherapy is given if tumour is large or if lymph nodes are involved.  When mandible is involved, segmental resection is done.

Prognosis xx Prognosis is good, 5 years survival is 70%. xx Lip has best prognosis. xx Nerve involvement, fixation, nodal spread, upper lip or commissure lesions, age less than 40 years—are poor prognostic factors.

TONGUE Anatomy of Tongue Tongue is a muscular organ located in the floor of the mouth.

Parts 1. Tip: Anterior free end lies behind the upper incisor teeth. 2. Root: Attached to the mandible above and hyoid bone below. 3. Body: Dorsal surface is rough due to papillae; and is divided into anterior 2/3rd (oral part) and posterior 1/3rd (pharyngeal part) by sulcus terminalis. Ventral surface is smooth, has a median fold, ‘frenulum linguae’ and deep lingual vein on either side.

B Figs 3.57A and B: Gillies fan flap.

Fig. 3.59: Anatomy of the tongue showing parts and papillae.

Papillae 1. Vallate—large, located in front of sulcus termi­nalis. 2. Fungiform—lies over the tip and margin of the tongue. 3. Filiform—lies over the dorsum of tongue, gives the velvety appearance—commonest. 4. Foliate—over the margin.

Muscles of Tongue

A

B

Figs 3.58A and B: Nasolabial flap used in extensive lower lip defect or over the defect after wide excision of a tumour in the floor of the mouth.

xx Intrinsic muscle: Superior and inferior longitu­dinal, transverse and vertical. xx Extrinsic muscle: Genioglossus, hyoglossus, stylo­glossus, palatoglossus. Blood supply is from lingual artery, a branch of external carotid artery. Venous drainage by deep lingual vein which drains into fascial vein or internal jugular vein.

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SRB's Manual of Surgery Movements of the tongue Forward protrusion—genioglossus—most commonly affected by carcinoma ™™ Backward movement—styloglossus ™™ Elevation of tongue—palatoglossus ™™ Depression of tongue—hyoglossus ™™

Lymphatic Drainage of the Tongue xx Tip of tongue drains into submental lymph nodes. xx Lateral margin drains to submandibular lymph nodes and into upper deep cervical lymph nodes. Many lymphatic vessels pass as subperiosteal lymphatics of mandible. So carcinoma can involve the bone through this route. xx Lymphatics in the midline of tongue freely cross communicate with each other and so spread of malignancy can occur to both side neck lymph nodes. xx Lymphatics from posterior third of tongue drain into phary­ngeal group of lymph nodes, as well as to the upper deep cervical lymph nodes. Early spread to the pharyngeal lymph nodes from carcinoma of posterior third of tongue has a poor prognosis.

Aphthous Ulcer It can be: 1. Minor aphthous ulcer, common in menstruating women as a crop with painful, round, yellow-based ulcer with red margin. It regresses spontaneously in 2 weeks. 2. Major aphthous ulcer, large and deep which often becomes chronic and takes more time to subside with a scar. Chlorhexidine gluconate, local application of triamcinolone acetate, choline salicylate gel are different local applicants used to promote healing. 3. Behcet’s syndrome is genital ulcer, conjunctival ulcer and multiple oral ulcers. Reiter’s syndrome is urethritis, arthritis, periarteritis nodosa, conjunctivitis, and oral ulcers. 4. Herpetiform aphthous ulcer is not due to herpes simplex. They are small, 1–2 mm diameter ulcers in crops which heal by usual drugs mentioned above.

Lymphatic vessels are named as ™™ ™™ ™™ ™™

Apical vessels Central vessels Marginal vessels Basal vessels

Development and Nerve Supply of the Tongue xx Anterior 2/3rd develop from first branchial arch through two lingual swellings and one tuberculum impar. It is supplied by lingual nerve for general sensation and by chorda tympani for taste sensation. xx Posterior 1/3rd develops from third arch from cranial half of hypobranchial eminence. It is supplied by glossopharyngeal nerve for both general and taste sensations. xx Posterior most part develops from the fourth arch. It is supplied by vagus nerve (internal laryngeal nerve). xx Muscles of the tongue are derived from occipital myotomes and are supplied by hypoglossal nerve except palatoglossus, which is supplied by cranial part of accessory nerve.

TONGUE ULCERS Differential diagnosis for tongue ulcers ™™ ™™ ™™ ™™ ™™ ™™

Dental ulcers—painful Aphthous ulcers—painful Ulcers in lichen planus—painless Syphilitic ulcers—painless Tuberculous ulcers—painful Malignant ulcers—painless

Dental Ulcer It is common on sides of tongue due to sharp tooth, denture, and broken tooth. Usually it is acute painful, self-limiting ulcer. Occasionally repeated trauma form an indolent chronic ulcer which mimic carcinoma; it should be excised to rule out carcinoma and to cure the ulcer.

Fig. 3.60: Aphthous ulcer tongue. It is one of the common benign ulcers of the tongue.

Syphilitic Ulcer Extragenital chancre often occurs in tongue in primary syphilis which is painless with shotty, submental and submandibular lymph nodes. In secondary syphilis, multiple shallow snail track ulcers in the margins and undersurface; mucous patches on the tongue and fauces; Hutchinson’s condyloma wart in midline of tongue can occur. In tertiary syphilis, gummatous ulcer occurs in anterior 2/3rd of tongue as a deep punched out painless ulcer as gumma with wash leather slough. Endarteritis is the cause for the punched out look. Interstitial glossitis with loss of papillae causes longitudinally fissured bald lobulated tongue in tertiary syphilis. In carcinoma arising from syphilitic ulcer, RT is questionable as blood supply is precarious due to endarteritis; RT further compromises it leading to tongue necrosis.

Tuberculous Ulcer It is undermined shallow, often multiple, painful ulcer. Ulcer can occur in margins, tip or anterior 2/3rd of tongue. Neck nodes may be involved. Associated tuberculous larynx and lung may be present.

Herpetic Lingual Ulcer It is involvement of lingual nerve presenting as acute neuralgia with vesicles which form multiple superficial painful ulcers.

Other Ulcers Multiple ulcers in smokers due to glossitis (smoker’s ulcer), ulcers due to vasculitis, eosinophilic granuloma. Post-pertussis ulcer in whooping cough occurs on upper part of frenum linguae and under the tip of tongue.

Oral Cavity Macroglossia (Megaloglossia/Pachyglossia) It is a disorder in which the tongue is larger than normal. It is commonly painless, diffuse enlargement of the tongue. Macroglossia is usually caused by an increase in the amount (volume) of tissue on the tongue, rather than by a growth, such as a tumour. It is often seen in haemangioma, lymphangioma, muscular macroglossia (in cretins), acromegaly, Beckwith-Wiedemann syndrome (hypoglycaemia, abdominal wall defects, Wilms’ tumour, macroglossia, adrenal tumour), Down’s syndrome, mucopolysaccharidoses, primary amyloidosis, occasionally plexiform neurofibromatosis. Often it causes functional and cosmetic problems. Causes 1. Lymphangioma—soft, painless enlarged tongue with ulcers— bilateral; prevents closure of lip and jaw. 2. Haemangioma—soft, fluctuant, compressible, bleeding, red/blue lesion i. Both are treated by sclerotherapy (ethona­lamine oleate)/ partial excision ii. Angiogram/MR angiogram is a must in haemangioma iii. Ligation of lingual artery/ECA on both sides may be needed in large lesions Note: – Varicosities of sublingual veins mimic haemangioma. – Often causes unilateral enlargement of tongue. – Pressure on alveolus causes spacing of teeth and incisor deformity. Combination of haemangioma and lymphangioma can occur: 1. Neurofibroma—partial excision is done 2. Tongue muscular hypertrophy: Partial excision is done.

Fig. 3.62: Papilloma of the tongue. It is a premalignant condition. It requires excision biopsy.

Elongation is corrected by wedge resection of anterior part of extra tongue from midline. Vertical thickening is rectified by slice cutting of lateral margins without injuring lingual artery and nerve.

Fig. 3.63: Pyogenic granuloma of tongue under surface.

Fibroepithelial Polyp It is due to repeated trauma at one place may be due to teeth (incisor) forming a thickened submucous scar which gets pulled out like a stalked polyp due to sucking and swallowing mechanism. It commonly enters the gap between the lower incisor teeth.

Granular Cell Myoblastoma Fig. 3.61: Macroglossia.

BENIGN TUMOURS OF TONGUE Benign tumours of the tongue ™™ ™™ ™™ ™™ ™™ ™™

Papilloma Fibroepithelial polyp Haemangioma and lymphangioma Neurofibroma Lipoma Granular cell myoblastoma

It is a benign non-capsulated firm mobile mass in the tongue showing pseudoepithelial hyperplasia of mucosa of tongue with eosinophilic granular cells in deeper plane. It is often mistakenly diagnosed as carcinoma of tongue. It is treated by excision.

TONGUE FISSURE xx Congenital fissures are transverse which run laterally from midline with normal papillae in between. Candida infection can occur on this. xx Syphilitic fissures are deep bald and longitudinal.

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Fig. 3.64: Tongue showing fissuring. Fissuring is one of the presentations of carcinoma tongue.

Fig. 3.66: Congenital fissures of tongue are transverse; syphilitic fissures are longitudinal. Median rhomboid glossitis is persistent tuberculum impar.

Other Glossitis

Fig. 3.65: Horizontal fissures of tongue.

xx Hunter’s glossitis is seen in pernicious anaemia. xx Hairy tongue is overgrowth of filiform papillae with black/brown stain on it due to bacteria, fungi, tobacco or drugs. There are no hairs. It is a misnomer. Cessation of causative agent, mechanical scraping, cleaning are the treatment methods. xx Agranulocytosis glossitis. xx Non-specific glossitis. xx Pellagra glossitis, due to deficiency of nicotinamide (B12). xx Chronic superficial glossitis in malnutrition, iron and vitamin B deficiencies.

GLOSSITIS Median Rhomboid Glossitis xx It is smooth, lobulated, triangular firm patch anterior to foramen caecum of tongue in midline with deeper colour. xx Candida infection can occur in it. xx It mimics carcinoma. Biopsy rules out malignancy. Carcinoma is uncommon in midline.

Glossitis Migrans (Geographic Tongue) xx It begins as benign small red patches with white furred margin which spread and recede in an irregular way to appear as fresh patches. xx White margin contains keratinized epithelium and inflammatory cells over filiform papillae. xx It is often seen in patients with congenital heart diseases and acute gastrointestinal diseases. Etiology is unknown.

Fig. 3.67: Severe superficial glossitis.

Oral Cavity TONGUE TIE xx It is short, thick, fibrous frenum linguae. xx During protrusion lateral margin and tip of the tongue is everted with dorsal mid part heaping. xx It causes speech defect, difficulty in cleaning the inner part of lower teeth. xx It is treated surgically under local anaesthesia (or general in child). Tongue lifted upwards with a stay suture at the tip; fibrous frenum is divided using fine scissor; linear wound is closed longitudinally using fine catgut from the tip of the tongue towards the margin of the floor of the mouth.

Fig. 3.69: Carcinoma tongue—lateral margin but involving extensively.

3. Dorsum—6.5%. 4. Ventral surface—9%. 5. Tip—10%.

Clinical Features

B

A

Figs 3.68A and B: Tongue tie—on table photo.

CARCINOMA TONGUE Incidence is equal in both sexes. Presently its incidence is increasing in females due to increase in number of female smokers.

Aetiology xx xx xx xx

Leukoplakia. Erythroplakia. All ‘S’s (as mentioned in leukoplakia). Premalignant conditions mentioned earlier.

Types Gross 1. Papillary. 2. Ulcerative or ulceroproliferative 60%. 3. Fissure with induration. 4. Lobulated, indurated mass—frozen tongue.

Histologically 1. Squamous cell carcinoma—commonest. 2. Adenocarcinoma, may arise from minor salivary glands or mucous glands. 3. Melanomas. 4. Transitional cell carcinoma and lymphoepithelioma rarely can occur in posterior 1/3rd of tongue.

Sites 1. Lateral margin—commonest—47–50%. 2. Posterior third—20%.

xx Painless ulcer/swelling in the tongue which later may become painful. Pain in the tongue due to infection or ulceration or due to the involvement of lingual nerve (pain is referred to ear). Pain on swallowing, in case of carcinoma of posterior third of tongue. xx Excessive salivation. Saliva is often blood stained. xx Dysphagia either due to fixed tongue or due to the involvement of genioglossus or growth in the posterior third of the tongue. xx Visible ulcer in anterior two-thirds of tongue. Ulcer can bleed on touch; edge, base and surrounding areas are indurated. Often indurated area is much more extensive than the primary tumour (it is also common in carcinoma penis). Edge is everted commonly. Ulcer may cross the midline; may extend into the floor of the mouth/alveolus/mandible. Growth or ulcer in posterior third, is usually not visible. xx Ankyloglossia—involvement of muscles of the tongue. xx Movements of the tongue especially forward protrusion is commonly affected. xx Inability to articulate. xx Foetor (Halitosis). Due to infection and necrosis in the oral cavity. It is due to release of ammonia, butyric acid and mercaptan by tumour cells. xx Change in voice. Occurs in posterior third tumours. Tumour in posterior third area is more aggressive. xx Palpable lymph nodes in the neck which are hard, nodular and get fixed to underlying tissues in advanced stages. xx Features of bronchopneumonia—due to aspiration during lying down/sleeping mainly to lower segment of lung.

Spread of Carcinoma Tongue Local spread: In case of anterior two-thirds of tongue, the spread occurs to genioglossus muscle, floor of the mouth, opposite side and mandible. In case of poste­rior third of tongue it spreads locally to tonsil, side of pharynx, soft palate, epiglottis, larynx and cervical spine.

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Fig. 3.72: Carcinoma tip of tongue. Well-circumscribed raised edge is seen.

Fig. 3.70: Anatomy and lymphatic drainage of tongue.

A

Fig. 3.71: Frozen tongue is feature of carcinoma tongue with ankyloglossia.

Lymphatic spread: From tip of tongue it spreads to submental nodes. From lateral margin it spreads to submandibular lymph nodes and later to deep cervical lymph nodes. Lymphatics in the tongue are freely communicating, and so involvement of bilateral neck lymph nodes is common. From posterior third it spreads to pharyngeal nodes and upper deep cervical lymph nodes.

B Figs 3.73A and B: Carcinoma tongue lateral margin (commonest site).

Oral Cavity Note:

• • • • •

Any tongue lesion more than 4 mm depth has 30% metastasis to lymph nodes. Among oral cancers, carcinoma tongue is more aggressive, rapidly growing tumour with high potential for lymph node spread. Bilateral neck lymph node spread is common due to crossing of lymph vessels in tongue. Clearance of lingual lymph node which is located between tongue and submandibular lymph glands has to be done which may contain micrometastasis. Carcinoma tongue has got highest incidence of nodal spread.

Investigations xx Wedge biopsy. xx FNAC of lymph nodes. xx Indirect and direct laryngoscopy to see posterior third

growth.

xx CT scan to see the extension of posterior third growth, or to

see the status of lymph node secon­daries. MRI is also very useful to assess the extent of primary tumour. xx Chest X-ray to see bronchopneumonia. xx Orthopantomogram.

Fig. 3.74: Wide excision is done in small lateral margin tumour of 1 cm size with 1 cm clearance.

Note:

Staging is same as carcinoma cheek.

Treatment Surgery, radiotherapy, chemotherapy.

Surgery xx Wide excision with 1 cm clearance in margin and depth is done in tumour less than 1 cm in size or in carcinoma in situ. Laser (CO2/ diode) can be used. xx Tumour between 1–2 cm in size, partial glossectomy is done with 2 cm clearance from the margin with removal of 1/3rd of anterior two-thirds of the tongue. xx Tumour larger than 2 cm, hemiglossectomy is done with removal of anterior 2/3rd of tongue on one side up to sulcus terminalis.  Raw area in these procedures can be left alone when area is wide allowing it to granulate and heal by epithelialisation. If area is small like in wide excision it can be closed by primary suturing. Wide raw area can also be covered with PMMF or quilted split-skin-graft. xx Larger primary tumour can be given pre-opera­tive radiotherapy, then later hemiglossectomy is done. xx Same side palpable, mobile lymph nodes are removed by radical neck block dissection. xx Bilateral mobile lymph nodes are dealt with one side radical block and other side modified radical block dissection with essentially retaining internal jugular vein (on opposite side) to maintain the cerebral venous blood flow. Other option is doing same side radical neck dissection and on opposite side supraomohyoid block dissection. xx Wide excision is done when growth is in the tip of the tongue. xx Posterior third growth can be approached by lip split and mandible resection, so as to have total glossectomy—Kocher’s approach. It is not done commonly as it carries significant morbidity and mortality due to difficulty in speech, swallowing, aspiration, sepsis. xx When mandible is involved hemimandibulectomy is done.

Fig. 3.75: Tumour between 1 and 2 cm size is treated by partial glossectomy with 2 cm clearance.

Fig. 3.76: Tumour larger than 2 cm requires hemiglossectomy.

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SRB's Manual of Surgery xx The procedure that involves wide excision or hemi­glossectomy, hemimandibulectomy and radical neck dissection together is called as Commando Operation. xx Reconstruction of tongue and other area after surgery: By deltopectoral flap, forehead flap, pectoralis major muscle flap, skin grafting. xx Prophylactic block dissection is becoming popular at present. Post-operative management ™™ ™™ ™™ ™™ ™™

Control of infection and oedema Regular mouth wash Maintaining the airway Prevention of aspiration Nutrition (through nasogastric tube commonly/TPN often)

Radiotherapy xx In small primary tumour—curative radiotherapy (Brachytherapy using caesium or iridium192 needles). xx Large primary tumour—initial radiotherapy is given to reduce the tumour size so that the resection will be better later. xx Advanced primary as well as secondaries in the neck can be controlled by palliative external radiotherapy. xx Post-operative radiotherapy is given in large tumours to reduce the chances of relapse. xx In case of growths in the posterior third of tongue, radiotherapy is of curative as well as palliative mode. Complications of radiotherapy ™™ ™™ ™™ ™™ ™™

Loss of sensation like taste Trismus and ankyloglossia Infection Pharyngeal and laryngeal oedema Dermatitis and skin infection

Chemotherapy xx Given in post-operative period and also for palliation. xx Price-Hill regimen is commonly used. Drugs are methotrexate, vincristine, adriamycin, bleomycin and mercaptopurine. xx It is either given intra-arterially, as regional chemo­therapy through external carotid artery using arterial pump or through IV. It can also be given orally. Complications of chemotherapy ™™ ™™ ™™ ™™

Megaloblastic anaemia Bone marrow suppression Alopecia Sepsis

xx For melanoma, Melphalan and DTIC are used. xx Anterior chemotherapy (pre-operative) is be­coming popular

to downstage the tumour.

Terminal events Inhalational bronchopneumonia Haemorrhage from erosion of lingual artery. In poste­rior third of the tongue, erosion of internal carotid artery can occur ™™ Cancer cachexia ™™ Asphyxia due to pressure on air passages or due to oedema glottis ™™ ™™

Prognosis Five-year survival for females is 50%, for males is 25%. Nodal prognostic factors ™™ ™™ ™™ ™™ ™™

Positive histology in node reduces the survival Level III and IV has poor prognosis Bilateral/contralateral nodes carry poor prognosis Extracapsular spread/size > 3 cm carry poor survival > 3 in number of nodes involved is poor sign

Prognostic Factors xx xx xx xx xx xx

Size of the tumour > 4 cm caries poor prognosis. Site of tumour (posterior third has got poor prognosis). Tumour crossing the midline. Lymph nodes status. Differentiation. Bone involvement.

CARCINOMA OF POSTERIOR ONETHIRD/BASE OF THE TONGUE xx Lesion may remain asymptomatic for long time. xx Clinically may be missed easily. xx Earlier symptoms are features mimicking sore-throat and throat discomfort. xx Dysphagia and change in voice (hot potato voice) occurs later. xx Referred pain in the ear, bleeding from mouth, visible mass in posterior third of tongue is late local features. xx Induration on palpation in posterior third tongue is diagnostic of the carcinoma. xx As posterior third tongue has got abundant lymphatics which cross communicates on either side, lymph node spread is common (70%). Bilateral nodal spread is common. Massive nodes and involvement of jugulodigastric node are also common. xx Infiltration into the tongue muscles like genioglossus, epiglottis, pre-epiglottic space, tonsillar pillars and hypopharynx are common. xx Carcinoma posterior third of the tongue is often poorly differentiated and so caries poor prognosis. xx Blood spread can occur into bones, liver and lungs in posterior third cancers. xx Palpation under anaesthesia gives better idea about the tumour, its spread and also allows the biopsy. xx Presentation as unknown/occult primary and often with blood spread can occur. xx CT scan/MRI is always needed to plan the staging and therapy. xx T1, T2, N0 and N1 diseases are treated by surgical wide excision or often by total glossectomy using midline mandibulotomy incision (mandible split) with neck dissection on both sides (MRND one side). Post-surgery radiotherapy is needed if it is a poorly differentiated type or nodal status is more than N1. xx Advanced lesions need palliative radiotherapy or chemotherapy. xx T4 lesions are often treated by total glossectomy with laryngectomy and neck dissection but overall outcome is not good. xx In many centres primary curative radiotherapy is used. xx Lymphoepithelioma and transitional cell carcinoma can occur in posterior third tongue (rarely).

Oral Cavity Carcinoma alveolus It is squamous cell carcinoma arising from gums It is common in males It is common in India It is commonly due to tobacco/pan chewing Features and precipitating factors are similar to other oral carcinomas ™™ There will be invariable bone involvement by direct extension ™™ Nodal spread is also common ™™ Wide excision with mandibulectomy and block dissection of neck is the treatment ™™ ™™ ™™ ™™ ™™

Carcinoma floor of the mouth ™™ ™™ ™™ ™™ ™™ ™™ ™™

™™ ™™

It is usually aggressive tumour It is rare in India It is 2nd common site of oral carcinoma (SCC) in western countries It invades hyoglossus, mylohyoid, genioglossus and anterior mandible early Bilateral neck nodes are commonly involved Rim resection of mandible with wide excision of tumour with muscles and soft tissues and bilateral neck dissection is necessary Often visor anterior approach with anterior mandible resection followed by proper reconstruction with bone graft and plates is needed Post-operative radiotherapy and later chemotherapy is used to prevent recurrence Prognosis is poor and also has poor cosmetic results

xx HO’s triangle in supraclavicular fossa (bounded by medial and lateral ends of clavicle and point where neck meets the shoulder) is the site where metastatic nodes commonly exist in nasopharyngeal carcinoma. xx In 50% of cases nodal involvement is bilateral. Often cervical lymphadeno­pathy may be the first presentation. xx Clinical features may be nasal, otogenic, ophthalmoneurogenic (involving most of the cranial nerves with facial pain, squint, diplopia, exophthalmos, and ophthalmop­legia), jugular foramen syndrome (cranial nerves IX, X, XI spread), nodal spread and distant spread to bones, lungs and liver. xx Unilateral serous otitis media may be the only presentation.

Clinical Features xx Epistaxis, nasal speech, post-nasal discharge and nasal obstruction. xx Pain in the ear with unilateral deafness due to compression of Eustachian tube with fluid collection in the middle ear. xx Elevation and immobility of soft palate on the same side. xx Pain in the area of distribution of trigeminal nerve due to direct infiltration of the nerve at foramen lacerum. xx Palpable secondaries in upper deep cervical lymph nodes (70%). Trotter‘s triad ™™ ™™ ™™

Unilateral deafness Immobile elevated soft palate Pain in the distribution of trigeminal nerve

Differential Diagnosis xx Lymphoma. xx Lymphoepithelioma. xx Minor salivary gland tumour.

Investigations xx xx xx xx

Biopsy from the primary site. FNAC from the neck lymph nodes. X-ray of the skull to visualise erosions. CT scan skull.

Histological Type Fig. 3.77: Carcinoma of floor of the mouth. It has got poor prognosis.

NASOPHARYNGEAL CARCINOMA xx Nasopharynx lies above the level of the soft palate which divides it from oropharynx below. xx It is also called as post-nasal space or epipharynx. Eustachian tube opens on its anterolateral wall. Fossa of Rosenmuller is located above and behind the opening of the Eustachian tube as a small depression. xx Nasopharyngeal carcinoma is common in China and Mongolia. In India it is common in North-East region. It is commonly squamous cell carcinoma (85%). Lym-phoma, minor salivary tumours and sarcoma are other malignancies that can occur rarely in nasopharynx. xx It can be of proliferative, ulcerative, and infiltrative types. Commonest site is fossa of Rosen­muller in lateral wall of pharynx. It is three times common in males.

Squamous cell carcinoma.

Treatment xx External irradiation for primary. RT is the main modality of treatment. xx Radical block dissection of cervical lymph nodes. xx In N2a, N2b and N2c contralateral neck dissection is needed. Spinal accessory nerve is never preserved while doing block dissection in nasopharyngeal carcinoma. xx Chemotherapy: Methotrexate, Vincristine. xx Skull base surgeries are useful.

MAXILLARY TUMOURS They are rare. xx Maxillary sinus is the commonest site for malignancy of paranasal sinuses. Ethmoids, frontal and sphenoids are next in order. xx It is common in people working in furniture industries, mustard gas industries, and leather industries. It is common in Bantus in South Africa where snuff with nickel and chromium is commonly used.

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Fig. 3.78: Carcinoma maxillary sinus in a boy. Note the extension into the palate.

Fig. 3.79: An imaginary plane is drawn extending between medial canthus of eye and the angle of mandible and line in this plane is called as Ohngren’s line.

Types xx xx xx xx xx xx

Squamous cell carcinoma 80%. Adenocarcinoma. Transitional cell carcinoma. Salivary gland tumours. Sarcomas and melanoma. Burkitt’s lymphoma.

Behaviour and Presentation xx Initially may be symptomless or may present with epistaxis or features of chronic sinusitis. xx When it spreads to the floor, loosening of the teeth, necrosis, antrooral fistula can occur. xx Extension medially causes nasal block, fungation, nasal discharge, blockage of nasolacrimal duct (epiphora). xx Extension anteriorly causes pain, anaesthesia and swel­ling in the cheek, ulceration and fungation in the skin of cheek. xx Spread above into the orbit causes epiphora, diplopia, proptosis. xx Posterior spread is most dangerous as it is not revealed easily. It causes postnasal discharge, pain, trismus, limitation of temporomandibular joint movement. xx Involvement of upper deep cervical lymph nodes in later stage is common.

Differential Diagnosis Chronic sinusitis.

Classification 1. Ohngren’s classification An imaginary plane is drawn extending between medial canthus of eye and the angle of mandible. Growth situated above this plane is called as suprastructural which has got poor prognosis. Growth below this plane is called as infrastructural and has got better prognosis.

Fig. 3.80: Diagrammatic representation of Lederman’s classification. 2. Lederman’s classification Two horizontal lines are used, one passes through the floor of the orbit, another passes through the floor of the antra. These lines are called as line of Sebileau. xx Suprastructure type: In this type olfactory area of nose, ethmoidal, sphenoid, and frontal sinuses are involved. xx Mesostructural type: This involves maxillary sinus and nasal respiratory part. xx Infrastructural type: This type involves alveolar process. Lederman’s classification is further divided by two vertical lines over medial walls of the orbit to separate ethmoid sinuses and nasal fossa from maxillary sinuses. TNM staging

Staging

• T1 Tumour limited to antral mucosa • T2 Tumour causing bone erosion/ destruction including extension into hard palate or middle meatus of nose. • T3 Tumour invading bone of posterior wall of maxillary sinus/skin of cheek/ medial wall of orbit/infratemporal fossa/pterygoid plates/ethmoid sinuses. • T4 Tumour invading orbital contents beyond the floor or medial wall including orbital apex/cribriform plate/base of skull/nasopharynx/ sphenoid or ethmoidal sinuses

Stage I T1 N0 M0 Stage II T2 N0 M0 Stage III T3 N0 M0, T1/T2/T3 N1 M0 Stage IVA T4 N0 M0, T4 N1 M0 Stage IV B Any T N2 M0, Any T N3 M0 Stage IVC Any T Any N M1

Oral Cavity Diagnosis xx X-ray of the part—pacity of the involved sinus with destruction of bony walls is seen—Water's PNS view. xx CT scan—ideal method. xx Sinus endoscopy for detailed examination of sinus and for biopsy. xx Biopsy is done through nasal/oral or on early stage through Caldwell-Luc operation.

Treatment xx Pre-operative megavoltage radiotherapy is given. After six weeks, total maxillectomy is done. Recons­truction of maxilla along with dental reconstruction is required. xx When lymph nodes are involved radical neck lymph nodes dissection is done. xx Post-operative radiotherapy and chemotherapy is given as an adjuvant therapy. xx Overall prognosis is 30–40%.

B

Fig. 3.81: Incision for Caldwell-Luc operation which is used for taking biopsy from maxillary tumour. Incision is not used for definitive therapy for carcinoma maxilla. Incision also used in benign conditions to approach maxillary sinus. Gingivobuccal mucosa is incised and mucoperiosteum is raised. Bone of canine fossa is cut to reach the maxillary antrum.

C

D Figs 3.82B to D

A Fig. 3.82A

Figs 3.82A to D: Carcinoma maxilla extending into the nose with X-ray and CT pictures. It is a fairly advanced growth.

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Fig. 3.83: Carcinoma maxillary antrum extending outwards on to all walls. An advanced malignancy.

Fig. 3.84: Weber-Ferguson’s incision used for total maxillectomy.

MALIGNANT TUMOURS OF TONSIL xx Carcinoma of tonsil: It is squamous cell carcinoma, similar to carcinoma cheek, but more aggres­sive with poor prognosis. xx Carcinosarcoma of tonsil. xx Lymphoma—NHL type.

Fig. 3.85: Lymphoepithelioma of tonsil.

xx Minor salivary gland tumours are more common in palate. xx In males, in reverse smokers (Churat is rolled tobacco leaf) squamous cell carcinoma is seen in palate due to repeated thermal injury. xx Malignant tumours may spread to periosteum, bone, maxilla, sinus, or nose. xx Salivary gland tumours are commonly malignant and are of adenoid cystic type. Other types also can occur. It presents as a single, solid, smooth swelling with ulcer over the summit. xx Squamous cell carcinoma is ulcerative with raised and everted edge. xx Upper deep cervical lymph nodes are involved in 25% of patients. xx Investigations are edge biopsy, FNAC lymph node and CT scan to see extensions. xx Treatment is wide excision with removal of the underlying palatal bone. Often partial or total maxillectomy (Weber-Ferguson incision) may be required. Myocutaneous flap with dental prosthesis is essential to reconstruct after surgery. Post-operative radiotherapy and neck block dissection are often required.

Fig. 3.86: Minor salivary gland tumour in posterior half of the palate. Note the nodular lesion with ulceration over the summit (Courtesy: Professor Kishore Chandra Prasad, ENT Surgeon and Head of the Department and Dr Sampath, ENT Surgeon, KMC, Mangaluru).

Fig. 3.87: Carcinoma hard palate extending laterally.

Oral Cavity LARYNGEAL TUMOURS Benign xx Epithelial can be papilloma, vocal nodule or vocal polyp. Papilloma is usually single in adult, multiple in children. xx Connective tissue tumours like fibroma, myxoma, angioma.

Indirect laryngoscopy (ILS) or direct laryngoscopy confirms the diagnosis. Childhood papilloma

Adult papilloma

Multiple, of viral origin (Papova)

Single, of neoplastic origin

Can occur in glottic, supra and infraglottic

Glottic only

Not premalignant

Premalignant

Recurrence common

Not common after complete excision

Excision is difficult

Easier removal

Causes more dyspnoea, stridor, cough Hoarseness only

Fig. 3.88: Anatomy of larynx showing supraglottic, glottic and subglottic regions.

May require tracheostomy

Note: Stridor can be inspiratory, expiratory or biphasic.

Treatment xx Endoscopic removal. Application of podophyllum xx Cryosurgery, laser surgery.

MALIGNANT TUMOURS OF LARYNX Aetiology

rich lymphatics in this area. Throat pain, dysphagia, palpable neck nodes and referred pain are common features. Hoarseness of voice, loss of weight, respiratory obstruction, and halitosis are late features. Carcinoma in epiglottis causes bilateral nodal spread. Local spread occurs to vallecula, base of tongue and pyriform fossa. xx Glottic (65%):  It is the commonest type. It begins from upper part or

free edge of vocal cords (mid or anterior) often extending 10 mm below. Lymphatic spread is slow (only 4%) as this area has got least lymphatics. Opposite vocal cord can involve as kiss cancer. Vocal cord mobility is unaffected in early cases. Vocal cord fixation signifies spread to thyroarytenoid which is a poor prognostic sign. It presents very early due to hoarseness of voice. Eventual cord fixation causes stridor. Locally it spreads anteriorly to anterior commissure, posteriorly to vocal process and arytenoids, above to ventricle and false vocal cords, below to subglottis.

xx Smoking, tobacco. xx Alcohol intake. xx Occupational/industrial exposure to chemicals like mustard gas, asbestos, benzopyrones, petroleum products. xx Previous radiation. xx Genetic: Russians develop familial laryngeal cancers. xx Papillomavirus, keratosis, malnutrition.

Incidence xx Squamous cell carcinoma is commonest (95%). xx Common in males (10 : 1). xx Common in 5th/6th decade.

xx Subglottic (2%)

 Is less common involving under-surface of true vocal

cords and subglottic space. It spreads to deep cervical and paratracheal nodes (20%). Upward spread is rather late and so hoarseness is not an early symptom in this type. It can spread through cricothyroid membrane or thyroid gland.

Types xx Ulcerative. xx Proliferative. Note:

Anatomical Types xx Supraglottic (25%):  It arises from infrahyoid part of epiglottis, ventricles, and arytenoids. It spreads to neck lymph nodes early (40%) due to

• •

In Indian subcontinent supraglottic tumours are more common than glottic. Glottic type is common in Western countries. Fixation of cords is due to involvement of thyroarytenoid muscle or cricoarytenoid joint.

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Fig. 3.89: Laryngeal carcinoma, types. Note the typical sites. Glottic is the commonest site. Next is supraglottic. Subglottic is rare.

Clinical features

Investigations

• Hoarseness of voice • Pain and discomfort • Cough, dyspnoea, stridor, dysphagia in late cases • Bloody sputum • Palpable neck nodes, which eventually get fixed

• ILS (Indirect laryngoscopy) • Direct laryngoscopy and biopsy • CT neck—very useful investigation

• Absence of laryngeal crepitus • Common in males—10:1

• Chest X-ray • FNAC of lymph node • Microlaryngoscopy in small lesions to identify and to have proper biopsy • Toluidine blue staining to stain early superficial cancers which facilitate the accurate biopsy • Hopkin’s endoscopy • Flexible, fibreoptic laryngoscopy

T3 Tumour spreads beyond one anatomical region within larynx with cord fixation. T4 Tumour spreads beyond larynx. Nodal staging is similar to any other oral carcinomas.

Treatment xx Supraglottic: Stage I—curative radiotherapy is the choice. In stage II and III total laryngectomy and block dissection of neck nodes. xx Glottic: Radiotherapy is the choice as nodes are commonly not involved. Endoscopic laser surgery or open partial laryngectomy can be done.

Staging Tumour T1 Tumour confined to one anatomical site in larynx with normal cord mobility. T2 Tumour confined to one anatomical region within larynx.

Fig. 3.90: View of larynx as seen through a laryngoscope.

Oral Cavity

Fig. 3.93: Carcinoma larynx—patients underwent total laryngectomy with permanent tracheostomy.

Conservative laryngeal surgery Fig. 3.91: Endoscopic view of vocal cords, pyriform fossa and aryepiglottic fold.

Indications

Advantages

• Early growth without fixation especially glottic type

• Permanent tracheostomy is avoided Voice is retained

Types

Disadvantages

• Cordectomy through laryngofissure–excision of vocal cord after splitting of larynx • Partial frontolateral laryngectomy–excision of vocal cord and anterior commissure • Partial horizontal laryngectomy–excision of supraglottis (epiglottis, aryepiglottic folds, false vocal cords and ventricle)

• Inadequate clearance • Recurrence of the disease

Fig. 3.92: Indirect laryngoscopy to visualise larynx and its parts. xx Subglottic: Total laryngectomy is the treatment of choice with nodal block when needed. xx In advanced stage IV carcinomas surgery and radiotherapy both are not possible. Here chemotherapy is given using cyclophosphamide, cis platin and methotrexate. xx In advanced resectable tumours, induction chemotherapy for 3 cycles with methotrexate and cisplatin 100 m/sq metre BSA (at 0, 22. 43 days) and total laryngectomy is under trial. Concurrent chemotherapy and radiotherapy are also under trial in these cases.

Role of Radiotherapy in Laryngeal Cancer xx In early growth with no impairment in motility curative RT is very useful with 90% cure rate with preservation of voice xx It is commonly used in superficial exophytic lesions, growth in tip of epiglottis and aryepiglottic folds. xx In subglottic extension, fixed growths, and in presence of nodes, radiotherapy is less effective.

Fig. 3.94: Gluck-Sorenson's laryngectomy incision. Extension lines sideward can be used for adding radical neck dissection.

Imagination is the beginning of the creation; you imagine what you desire; you will what you imagine; at last you create what you will.  —George Bernard Shaw

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Khanna and Andrade group classification of trismus (1995)

Indications

Technique

• • • • •

• Entire larynx with hyoid bone, pre-epiglottic space, strap muscles, one or more rings of trachea are removed • Pharyngeal wall is repaired • Lower tracheal stump is sutured to the skin as permanent tracheostomy • Often laryngo-oesophagectomy is done when pharyngeal spread is present. Gastric pull-up is done to maintain GI continuity • Technique may be combined with neck nodal dissection both sides

T3 lesions with cord fixation All T4 lesions Bilateral arytenoids spread Thyroid/cricoid spread Transglottic cancers involving ventricle with fixation of the cord • Posterior commissure disease • Failure of conservative surgery or RT Problems • Mortality of surgery • No speech • Having permanent tracheostomy and its problems

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Group I: Earliest stage without limitation of mouth opening with an interincisal distance of greater than 35 mm. Group II: Patients with an interincisal distance of 26–35 mm. Group III: Moderately advanced cases with an interincisal distance of 15–26 mm. Fibrotic bands are visible at the soft palate, and pterygomandibular raphe and anterior pillars of fauces are present. Group IVA: Trismus is severe, with an interincisal distance of less than 15 mm and extensive fibrosis of all the oral mucosa. Group IVB: Disease is most advanced, with premalignant and malignant changes throughout the mucosa.

xx It is often clinically assessed by placing fingers perpendicularly between two jaws at incisor level. More than 3 fingerbreadth is considered as normal. xx Problems with trismus are—inability to put fingers or spoon into mouth; difficulty in cleaning the mouth; infection; difficulty in assessing the tumour/pathology clinically. During surgery, intubation is difficult and so tracheostomy may be needed in these patients. xx Management—treating the cause; release of soft tissue in case of fibrosis; draining the abscess and antibiotics for infection.

Care after total laryngectomy Speech therapy by pseudoglottis creation, battery operated artificial larynx or Singer-Blom prosthesis or Panje’s prosthesis. Tracheo-oesophageal prosthesis (TOP) is ideal ™™ Social and job rehabilitation ™™ Care of permanent tracheostomy by avoiding immersion in the water, care during bath, shower use and swimming. Shower covers are available for this purpose ™™ Often along with total laryngectomy, total thyroi­dectomy and removal of parathyroid glands are required. Patient then needs supplementation of thyroxine and calcium for life time ™™

TRISMUS xx It is inability to open the mouth adequately. xx Causes are—submucosal fibrosis, carcinoma buccal and gingivobuccal complex, post-radiotherapy sequelae, infection like tetanus, parotitis, dental or peritonsillar abscess. xx In carcinoma, invasion of tumour to pterygoids, buccinator, masseter, temporalis causes trismus.

Fig. 3.95: Trismus due to advanced carcinoma cheek. Patient is on chemotherapy so developed alopecia.

Chapter

4

Salivary Glands (Three weeks after arriving at the anatomy laboratory of Gerhard Blasius in Amsterdam) fortune so favoured me that in the first sheep’s head, which I…was dissecting alone in my room, I found a duct which, so far as I knew, had been described by no one before. —Niels Stensen, 1661

CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Anatomy Saliva Sialography Salivary Calculus and Sialadenitis Sialosis Sialectasis Recurrent Childhood Parotitis Parotid Abscess Parotid Fistula Sjögren’s Syndrome Mikulicz Disease Salivary Neoplasms

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Pleomorphic Adenoma A  denolymphoma Oncocytoma Basal Cell Adenoma Mucoepidermoid Tumour Adenoid Cystic Carcinoma Acinic Cell Tumour Malignant Mixed Tumour Adenocarcinoma of Salivary Glands Squamous Cell Carcinoma of Salivary Glands

ANATOMY Parotid Gland (Para—around, otis—ear) It is the largest of the salivary gland, situated below the acoustic meatus between the ramus of mandible and sternomastoid muscle. The deep cervical fascia splits to form a capsule (parotid capsule) to enclose the gland. The superficial layer is thickened and adherent to the gland. It is deep to parotid fascia, superficial to masseter. So parotid swelling occupies below, behind, in front of the ear lobule, obliterating the normal hollow below the ear lobule. When patient opens the mouth, parotid fascia stretches and swelling may become less pre-eminent but this test is difficult to elicit. When patient clinches his teeth, masseter contracts and parotid becomes more prominent.

™™ S ubmandibular Salivary Gland Tumours ™™ Management of Malignant Salivary Tumours ™™ Minor Salivary Gland Tumours ™™ Parotid Lymphoma ™™ Parotidectomy ™™ F rey’s Syndrome ™™ Facial Nerve Injury

Parts of the Parotid Gland xx Superficial part (80%)—lies over the posterior part of the ramus of mandible. xx Deep part (20%)—lies behind the mandible and medial pterygoid muscle; in relation to mastoid and styloid process.

Accessory Parotid It is prolongation of the gland above the parotid duct (socia parotidis).

Parotid Duct Parotid (Stensen’s) duct is 2-3 mm in diameter, 5 cm in length, emerges from anterior surface of the gland, runs over the surface of the masseter

Both over-salivation and under-salivation are not advised. Only optimum salivation is accepted and ideal.

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Facial Nerve It emerges from the stylomastoid foramen lying between external auditory meatus and mastoid process. It passes around the neck of the condyle of mandible and becomes superficial, later dividing into temporofacial and cervicofacial branches which in turn divides into many branches. Some of these may be interconnected as pes anserinus (goose foot). Branches are – temporal (auricularis anterior and superior part of frontalis), zygomatic (frontalis and orbicularis oculi), upper buccal and lower buccal (buccinator, orbicularis oris, elevators of the lip) mandibular (lower lip muscles) and cervical (platysma). While exiting the skull through stylomastoid foramen (it is accompanied by stylomastoid branch of posterior auricular artery which enters the same foramen), it gives posterior auricular nerve and motor nerves to posterior belly of digastric and stylohyoid. Trunk is initially 1 cm from posteromedial surface (extraglandular) and intraglandular for 1 cm before giving divisions. Gland is often called as parotid sandwich due to transverse of facial nerve.

Blood Supply It is from external carotid artery; and venous drainage is by external jugular vein.

Nerve Supply It is from autonomic nervous system, parasympathetic is secretomotor from auriculo­tem­poral nerve, sympathetic is vasomotor from plexus around the external carotid artery.

Faciovenous Plane of Patey Faciovenous plane of Patey is of surgical importance. Facial nerve is superficial to this plane which contains retromandibular vein and posterior facial vein. External carotid artery dividing into superficial temporal artery and maxillary artery is deeper to venous plane.

Fig. 4.1: Superficial lobe (80%) and deep lobe (20%) are separated by external carotid artery, retromandibular vein and facial nerve from deep to superficial.

Fig. 4.2: Anatomical relations of the parotid gland.

Lymphatic Drainage of Parotid It drains into parotid lymph glands which are partly intra­ glandular and partly extraglandular (preauricular and infraauricular). Mainly intraglandular nodes are involved which later drains into deep cervical lymph glands. Parotid lymph nodes also drain from temple, side of scalp, lateral part of auricle, external acoustic meatus, upper part of cheek, parts of eyelids and orbit. Structures within the parotid gland from deep to superficial External carotid artery, maxillary artery, superficial temporal artery, posterior auricular artery ™™ Retromandibular vein (by maxillary and superficial temporal veins) ™™ Facial nerve with its branches ™™

Great auricular nerve (cutaneous sensory around angle and lower part of the ear lobule) and auriculotemporal nerve which is from mandibular division of trigeminal nerve (secretomotor to parotid gland) are other nerves present in relation to parotid gland.

Fig. 4.3: Pes anserinus.

Salivary Glands

A

Fig. 4.4: Vascular plane of parotid.

B Figs 4.6A and B: Relations of the submandibular salivary gland and its deep lobe.

Fig. 4.5: Anatomical relations of the submandibular salivary gland.

Submandibular Salivary Gland It is a ‘J’ shaped salivary gland situated in the anterior part of the digastric triangle.

xx Lingual nerve and submandibular ganglion are attached to upper pole of the gland. Hypoglossal nerve is deep to the gland. xx Facial artery emerges from under surface of the stylohyoid muscle, enters the gland from posterior and deep surface, reaching its lateral surface crossing the lower border of mandible to enter the face. xx Venous drainage is to anterior facial vein. xx Nerve supply: Branches from the submandibular ganglion. xx Resting salivary flow usually arises from the submandibular salivary gland. Sialorrhoea is increased salivary flow often seen due to drugs, in cerebral palsy, physically handicapped person, children, and psychiatry patients. Intractable sialorrhoea can be corrected by different surgeries to submandibular salivary gland like duct repositioning to excision of the gland. xx Xerostomia is decreased salivary flow. It is seen in post-menopausal women, depression, dehydration, use of antidepressant drugs; anticholinergic drugs, Sjogren’s syndrome, radiotherapy to head and neck region.

Parts

Minor Salivary Glands

xx Superficial part: Lies in submandibular triangle, superficial to mylohyoid and hyoglossus muscles, between the two bellies of digastric muscle. xx Deep part is in the floor of the mouth and deep to the mylohyoid. xx Submandibular (Wharton’s) duct (5 cm), emerges from the anterior end of the deep part of the gland, enters the floor of the mouth, on the summit of papilla beside the frenulum of the tongue.

xx There are around 450 minor salivary glands which are distributed in lips, cheeks, palate and floor of the mouth. Glands also may be present in oropharynx, larynx, trachea and paranasal sinuses. They contribute to 10% of total salivary volume. xx Sublingual glands are minor salivary glands one on each side; located in the anterior aspect of the floor of the mouth in relation to mucosa, mylohyoid muscle, body of the mandible near

How a person masters his fate is more important than what his fate is.

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Ectopic Salivary Glands xx Ectopic salivary gland also called as aberrant salivary gland is nothing but ectopic lobe of the juxtaposed salivary gland. It is commonly seen in relation to submandibular salivary gland. xx Commonest ectopic salivary tissue is Stafne bone cyst (Edward C Stafne, Dental Surgeon, Mayo Clinic). It is invagination of the juxtaposed submandibular salivary gland into the mandible bone on its lingual aspect. xx X-ray shows radiolucent area due to the cyst below the angle of the mandible, lower to inferior dental vessels and nerve.

A

SALIVA xx 1500 ml of saliva is secreted per day. pH of resting saliva is less, 7.0; active saliva is 8.0. xx Saliva contains lingual lipase secreted from tongue glands, α amylase from salivary glands. xx Saliva contains mucin, glycoproteins, immunoglobulin IgA, lysozyme, lactoferrin which binds iron, proline rich proteins that protect enamel and bind toxic tannins. xx Parotid saliva is 20% of total secretion of saliva per day and is serous and watery; submandibular is 70% and is mucous and moderately viscous; sublingual is 5% and is mucous and viscous. Minor salivary and other oral glands—5%. xx Saliva facilitates swallowing, keeps mouth moist, serves as solvent for taste buds, facilitates speech, keeps oral cavity rinsed and clean, antibacterial, and neutralizes gastric acid content in regurgitation to relieve heartburn.

SIALOGRAPHY Indications

B Figs 4.8A and B: Submandibular gland sialogram pictures (Courtesy: Professor Kishore Chandra Prasad, ENT Surgeon and HOD, KMC, Mangaluru; Dr Sampath, MS ENT, KMC, Mangaluru). Dye used is lipiodol or sodium diatrizoate (Hypaque). 24-gauge cannula is passed into either Stensen’s duct or Wharton’s duct and one ml of the dye is injected into the duct and X-ray is taken. Findings ™™ ™™ ™™ ™™ ™™

Narrowing (Stricture) Grape-like cluster appearance (Sialectasis) Dilatations Communications (Fistulas) Mass lesions

1. Salivary fistulas. 2. 3. 4. 5.

Sialectasis. Congenital conditions. Extraglandular masses. Parotid duct stones.

Precautions xx Sialography should never be performed in acute inflammation. xx Only one ml of dye should be injected, if more dye is injec­ted it causes extravasation and chemical sialadenitis.

SALIVARY CALCULUS AND SIALADENITIS xx 80% submandibular. xx 80% radio-opaque. xx It is commonly calcium phosphate and calcium carbonate

stones. xx Calculi are more common in submandibular gland, because

Fig. 4.7: Sialogram X-ray done to visualise the ductal pattern in parotid.

the gland secretion is viscous, contains more calcium and also, its drainage is nondependent, causing stasis. xx Secretion from parotid is serous, contains less calcium and so stones are not common. xx Stone is single in 75% of cases. xx Incidence of stone in sublingual gland is 1%.

Salivary Glands Salivary calculi Submandibular gland ™™ 80% common ™™ 80% radio-opaque ™™ Seen in plain X-ray (intraoral) ™™ Sialogram is not needed

Parotid gland 20% incidence (Rare) ™™ Radiolucent ™™ Not seen in plain X-ray ™™ Identified by sialogram ™™

Calculi are common in submandibular salivary gland, because: ™™ Viscous nature and mucin content ™™ Calcium content ™™ Nondependent drainage ™™ Stasis ™™ Hooking of nerve by submandibular duct

Fig. 4.10: Stone in the submandibular salivary gland as seen in X-ray (Courtesy: Dr Jagdish, Mangaluru).

Presentation Acute Sialadenitis—Features

Chronic Sialadenitis—Features

xx Pain, swelling, tenderness is seen in submandibular region

and floor of the mouth. xx Dysphagia, trismus, fever. xx Double chin appearance due to spreading of oedema downwards. xx Duct is inflamed and swollen. Causes for submandibular sialadenitis

Types of sialadenitis

• Bacterial—more common. It is usually due to obstruction and stasis

• Acute –– Bacterial—occurs following submandibular salivary ductal obstruction (Wharton’s) or in parotid gland. In parotid, suppuration can occur leading into parotid abscess –– Viral—common in parotid

• Trauma over duct causing oedema/stricture and stasis • Viral—mumps—rare (Paramyxovirus)

• Chronic—common after partial obstruction of submandibular gland duct or due to stones in submandibular gland or hilum proximal to the level of crossing of the lingual nerve over the duct

xx Pain is more during mastication due to stimulation (Salivary

colic which can be induced by meals, lemon juice, etc.). Salivary colic is pain induced by obstruction to the outflow of saliva may be ductal stone. During salivation size of the swelling will decrease again 2 hours after meal/stimulation. xx Salivary secretion is more during mastication causing increase in gland size. xx Firm/rubbery tender swelling is palpable bidigitally. xx When stone is in the duct, it is palpable in the floor of the mouth as a tender swelling with features of inflammation in the duct. Pus exudes through the duct orifice. (Irritation of the lingual nerve, which is in very close proximity to submandibular salivary duct, causes referred pain to tongue—lingual colic). xx In submandibular salivary gland, often the stones are mul­ti­ple, with chronic inflammation of gland (sialadenitis). xx Often acute on chronic sialadenitis can occur. xx Kuttner tumour is chronic sclerosing sialadenitis of submandibular salivary gland.

Differential Diagnosis xx Submandibular lymphadenitis. xx Salivary neoplasm.

Investigations xx Intraoral X-ray (dental occlusion films) to see radio-opaque

stones (80%).

xx FNAC of the gland to rule out other pathology. xx Total count and ESR in acute phase. xx USG will demonstrate stone with posterior acoustic shadow. Note:

Radiological demonstration of stone/stones is called as sialolithiasis.

Treatment Fig. 4.9: Submandibular sialadenitis in a young boy who required excision of gland

xx If the stone is in the duct, removal of the stone is done

intraorally, by making an incision in the duct. Incised duct is

Diagnosis means finding the cause of the disorder, not just giving its name.—Sydney Walker

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Fig. 4.11: Stone in the duct of submandibular salivary gland (Wharton’s duct). Fig. 4.14: Incision for removal of the submandibular salivary gland.

Fig. 4.12: Excised specimen of submandibular salivary gland with stone in the gland.

Fig. 4.13: X-ray (OPG) showing left sided submandibular salivary stone.

not sutured as it may result in stricture. Laying open allows free drainage of saliva. Procedure is usually done under local anaesthesia. xx If stone is in the gland, excision of submandibular gland is done—sialadenectomy. It is always done under general anaesthesia.

Fig. 4.15: Incision for excision of submandibular salivary gland. It should be 2–4 cm below the margin of the mandible to avoid injury to marginal mandibular nerve.

Approach is from submandibular region (outside). An incision is made on the skin in submandibular region, about 5–8 cm length, parallel to and 2–4 cm below the mandible. Incision is deepened through the deep fascia until the gland is visualised without raising the flaps (so as to avoid injury to marginal mandibular nerve, branch of facial nerve). Facial artery is ligated twice. Lingual nerve and hypoglossal nerves are taken care of. Mylohyoid is retracted so as to remove the deep portion of the gland. Drain is placed after removal of the gland. Antibiotic coverage is a must. Facial artery lies in the groove on the deeper aspect of the gland; often embeds in the gland or runs around the gland with a variable course and so artery has to be ligated twice above anteriorly and below posteriorly. Marginal mandibular nerve is in subplatysmal plane in neck, so incision should be deepened across the deep fascia without raising subplatysmal plane to avoid injury to this nerve.

Salivary Glands Complications of Surgery xx Haemorrhage. xx Infection. xx Injury to marginal mandibular nerve, lingual nerve, hypoglossal nerve. xx Injury to nerve to mylohyoid causing anaesthesia over submental skin. Note:

• •

Stone in parotid duct can be removed by opening the duct longitudinally. Stone in the gland or in collecting duct is treated by parotidectomy.

Indications for submandibular salivary gland excision

Steps in submandibular salivary gland excision

• Chronic sialadenitis • Submandibular salivary tumours

• Anaesthesia—general

Pathway of secretomotor fibres of the submandibular and sublingual salivary glands Superior salivary nucleus ↓ Preganglionic fibres ↓ Facial nerve, Chorda tympani nerve ↓ Lingual nerve ↓ Submandibular ganglion— post-ganglionic fibres ↓ Submandibular and sublingual salivary glands

• Position—neck extension with chin to opposite side • Incision—2–4 cm (3 cm) below and parallel to the margin of the mandible 5–8 cm in length (6 cm) • Mobilisation of the gland– intracapsular in sialade- nitis; extracapsular in tumours with ligation of anterior facial vein • Facial artery ligation proximally and distally as artery is in the gland or in the groove posteriorly • Dissection of deeper lobe from mylohyoid muscle • Identification of lingual and hypoglossal nerves • Duct identification and ligation • Wound closure with a suction drain

Rule of 2 in submandibular salivary gland 2 parts divided by mylohyoid muscle 2 conditions affect it—tumour and stone 2 superficial nerves—cervical and mandibular branch of facial nerves ™™ 2 deep nerves—lingual and hypoglossal nerves ™™ Incision—2–4 cm below the mandible ™™ Ligate facial artery at 2 places ™™ ™™ ™™

SIALOSIS xx It is enlargement of the salivary gland due to fatty infiltration, as a result of various metabolic causes like diabetes, acromegaly, obesity, liver disease, alcoholism, bulimia, idiopathic, drug induced (sympathomimetics, carbimazole, thiouracil).

xx It is diffuse, bilateral, non-inflammatory, non-neoplastic asymptomatic swelling of the salivary gland mostly of parotids with fatty infiltration and acinar cell hypertrophy. xx Clinical features: Bilateral diffuse enlargement of parotids, which is smooth, firm, non-tender. xx Treatment: The cause is treated.

SIALECTASIS xx It is an aseptic dilatation of salivary ductules causing grape-like (cluster-like) dilatations. xx It is a disease of unknown aetiology with destruction of parenchyma of gland accompanied by stenosis and cyst formation in the ductules. xx It is common in parotids; often bilateral. xx Presents as a smooth, soft, fluctuant, nontransillu­minating swelling which increases in size during mastication. It is tender initially. It lasts for many days with a long symptom-free period of the disease. xx Sialogram is diagnostic (grape or cluster-like dilata­tions). xx Treatment is conservative (nonsurgical).

RECURRENT CHILDHOOD PAROTITIS It is a recurrent, rapid enlargement of one or both parotids with fever and malaise in children of age group between 3 and 6 years without any known aetiology. Recurrent episodes with a quiescent period in between are typical. Sialogram shows snowstorm punctate sialectasis. Low dose antibiotics for long period may be required. Occasionally patient may need total conservative parotidectomy especially if it occurs late in adolescent period.

PAROTID ABSCESS (SUPPURATIVE PAROTITIS) xx It is a result of an acute bacterial sialadenitis of the parotid

gland. xx It is an ascending bacterial parotitis, due to reduced

salivary flow, dehydration, starvation, sepsis, after major surgery, radiotherapy for oral malignancies and poor oral hygiene. xx Parotid fascia is densely thick and tough and so parotid abscess does not show any fluctuation until very late stage. xx Causative organism are Staphylococcus aureus (commonest), Streptococcus viridans and often others like gram-negative and anaerobic organisms. Causes of acute parotitis (Differential diagnosis of suppurative parotitis) ™™ ™™ ™™ ™™ ™™ ™™ ™™

Viral—Mumps, Coxsackie virus A and B, parainfluenza 1 and 3, Echo and lymphocytic choriomeningitis Bacterial—Staphylococcus aureus Allergic HIV infection Radiotherapy, postoperative period Specific infections like syphilis Sjogren’s syndrome often causes bilateral parotitis

By perseverance the snail reached the ark.—Charles Haddon Spurgeon

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SRB's Manual of Surgery Skin is incised in front of the tragus vertically and then parotid sheath (pyogenic membrane) is opened horizontally. Pus is drained using sinus forceps and sent for C/S. Antibiotics are continued (Blair’s incision).

Fig. 4.16: Parotid abscess

Clinical Features xx Pyrexia, malaise, pain and trismus. xx Red, tender, warm, well-localised, firm swelling is seen in

the parotid region (brawny induration). xx Tender lymph nodes are palpable in the neck. xx Features of bacteraemia are present in severe cases. xx Pus or cloudy turbid saliva may be expressed from the parotid duct opening.

sium permanganate solutions, nutrition. Often patient with parotid infection needs admission and treatment.

PAROTID FISTULA

tivity.

formation of pus.

Types

xx U/S of the parotid region. xx Pus collected from duct orifice is sent for culture and sensixx Needle aspiration from the abscess is done to confirm the Note:

•

xx Proper hydration, mouth wash using povidone iodine/potas-

xx Parotid fistula may arise from parotid gland or duct or ductules. It may open inside the mouth as internal fistula; or open outside onto the skin as external fistula. Fistula from the duct has profuse discharge. Fistula from the gland often shows only minimal discharge. xx Incidence of salivary fistula is 0.2–3%.

Investigations

•

Fig. 4.17: Blair’s incision used to drain the parotid abscess.

In suppurative parotitis patient may develop severe laryngeal or pharyngeal oedema and may require steroids, tracheostomy and critical care. Sialogram is contraindicated in acute phase, as it will cause retrograde infection leading into bacteraemia.

Complications of suppurative parotitis and parotid abscess ™™ ™™ ™™

Septicaemia Severe trismus Rupture into the external auditory canal

1. Duct fistula forms after superficial parotidectomy. It is profuse and often persisting. So duct should be ligated using nonabsorbable suture as far as possible, anteriorly to allow normal saliva drainage from deep lobe. If common duct is ligated deep lobe atrophies without causing any fistula. 2. Gland fistula occurs from the raw surface after superficial parotidectomy. It is mild and symptom subsides in a month with anticholinergic drugs. Jacobsom tympanic neurectomy completely stops the secretion from the fistula in this type.

Causes After superficial parotidectomy. After drainage of parotid abscess, ruptured abscess. After biopsy. Trauma. Recurrence of malignant tumour.

drainage is done under G/A.

xx xx xx xx xx

Areas where one should not wait for the abscess to form

Clinical Features

Treatment xx Antibiotics are started depending on culture report. xx When it is severely tender and localised, incision and

™™ ™™ ™™ ™™

Parotid Breast Ischiorectal fossa Thigh

xx Discharging fistula in the parotid region of the face, and discharge is more during eating. xx Tenderness and induration. xx Trismus.

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Salivary Glands ™™ ™™ ™™ ™™ ™™

Fistula due to ductal disruption leaks profusely and invariably needs surgery to close it Submandibular gland fistula commonly closes spontaneously, rarely if not requires complete removal of the gland Anticholinergics, irradiation, denervation of the gland, duct ligation are done to reduce saliva production Excision of fistula, repair of the duct, diversion of the duct into the mouth are other options In severe intractable cases, removal of the gland/total conservative parotidectomy is needed

SJÖGREN’S SYNDROME It is an autoimmune disease causing progressive destruction of salivary and lacrimal glands, leading to keratoconjunctivitis sicca (dry eyes), and xerostomia (dry mouth). Fig. 4.18: Parotid fistula with discharging saliva and pus.

Diagnosis xx Sialography to find out the origin of the fistula whether from parotid gland or duct or ductules. xx Fistulogram or CT fistulogram. xx Discharge study. xx MRI.

Treatment Anticholinergics—hyoscine bromide (probanthine). Radiotherapy. Often exploration of fistula is required. Repair or reinsertion of the duct into the mucosa. Newman Seabrock’s operation—a probe is passed into the parotid duct through the opening in the mouth. Another probe is passed through the fistula. Duct and fistula are dissected over the probe. After removal of the fistula track severed duct ends are identified; and ends are trimmed. Probes are removed. A tantalum wire is passed into the duct across the severed ends and duct is sutured over it using 4 zero vicryl. Tantalum stent is removed after 3 weeks. xx If still persists, auriculotemporal nerve which supplies secretomotor component of parotid is cut. xx If there is stenosis at the orifice of the Stenson’s duct, papillotomy at the orifice may help. xx Total conservative parotidectomy is done in failed cases. xx xx xx xx xx

Remember about salivary fistula Commonly from the parotid It can be internal draining into the mouth or can be external draining outside ™™ It is acquired commonly but rarely can be congenital ™™ It can be due to surgery, trauma or due to sepsis ™™ Fistula arising from the gland parenchyma drains through suture line but usually closes sponta­neously. Leakage will be more during meals. Saliva is confirmed by its high amylase content compared to seroma/serous fluid ™™ ™™

Types 1. Primary. 2. Secondary.

Primary Sjögren’s Syndrome (Primary Glandular Sicca Syndrome) xx xx xx xx xx

Severe dry mouth. Severe dry eyes. Widespread dysfunction of exocrine glands. Incidence of developing lymphomas is high. There is no association of connective tissue disorders. Primary extra-glandular sicca syndrome

™™ ™™ ™™

Dry mouth, dry eyes Hyperglobulinaemic purpura, vasculitis Raynaud’s phenomenon or B cell lymphoma

\

Secondary Sjögren’s Syndrome xx Dry mouth. xx Dry eyes. xx With association of connective tissue disorders like:  Primary biliary cirrhosis (near 100%).  SLE (30%).  Rheumatoid arthritis (RA) (15%). xx Female to male ratio is 10 : 1.

Clinical Features xx It is common in middle aged females who present with dry eyes, dry mouth, enlarged parotids and enlarged lacrimal glands. xx Often they are tender. xx Superadded infections of the mouth, Candida albicans is common.

Investigations 1. Autoantibody estimation—rheumatoid factor, antinuclear factor, salivary duct antibody. 2. Sialography. 3. Estimation of salivary flow.

Tumours of ectopic salivary glands are of low grade malignancy (cylindroma) may ultimately metastasize to regional lymph nodes, the viscera and the skeleton.  —Kenneth Harrison

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SRB's Manual of Surgery 4. Slit lamp test of eyes. 5. Schirmer test—to detect lack of lacrimal secretion. 6. FNAC of parotids and lacrimal glands. 7. 99Technetium pertechnetate scan for gland function.

2. Carcinomas –– Mucoepidermoid carcinoma—most common malignancy. –– Acinic cell carcinoma—1%. –– Adenoid cystic carcinoma—very aggressive—10%; common minor salivary glands. –– Adenocarcinoma. –– Squamous cell carcinoma—2%. –– Carcinoma in ex pleomorphic adenoma. –– Undifferentiated carcinoma.

Treatment: It is conservative. xx Artificial tears. xx Artificial saliva. xx Frequent drinking of water. xx Treat the cause.

MIKULICZ DISEASE xx It is a clinical variant of Sjögren’s syndrome. xx It is an autoimmune disorder of salivary and lacrimal glands, resulting in infiltration of the glands with round cells. xx It may be due to or associated with sarcoidosis, Sjögren’s syndrome, leukaemia, lymphoma.

Note:

Carcinoma can be: Low grade (acinic cell; adenoid cystic; low grade mucoepidermoid) or High grade (adenocarcinoma; squamous cell carcinoma; high grade mucoepidermoid) mesenchymal.

• •

Triad Symmetrical and progressive enlargement of all salivary glands Narrowing of palpebral fissures due to enlarge­ment of the lacrimal glands ™™ Parchment-like dryness of the mouth ™™ ™™

SALIVARY NEOPLASMS Aetiology xx Genetic—loss of alleles of chromosomes in 12q, 8q, 17q.

Eskimos are more prone for salivary neoplasm.

xx Infective—mumps, Epstein-Barr virus, chronic sialadenitis

may be the cause; but not proved emphatically. Recurrent inflammation can cause duct dysplasia and carcinoma. xx Radiation—it is more common in survivors of atomic bomb explosion; mucoepidermoid carcinoma is more in these patients. xx Smoking—adenolymphoma of Warthin’s shows 40% risk in smokers. xx Sex—benign tumours and many malignancies are common in females; Warthin’s and some malignancies are common in males. xx Environment and diet—Arctic-Eskimos show dietary deficiency of vitamin A and develop salivary tumour. Industrial agents like nickel, cadmium, hair dyes, silica, preservatives may increase the risk of salivary tumours.

Classification (WHO) a. Epithelial (90%): 1. Adenomas –– Pleomorphic adenoma. –– Monomorphic adenomas. »» Adenolymphoma (Warthin’s tumour). »» Oncocytoma (oxyphil adenoma) seen in elderly; seen in parotid gland. »» Basal cell adenoma—it is a rare benign tumour.

Fig. 4.19: Parotid enlargement in a boy of 11-year-old.

b. Nonepithelial: xx Haemangioma—commonly seen in infants, usually in parotids. Spontaneous regression is common. Most common benign salivary gland tumour in paediatric age group. xx Lymphangioma. xx Neurofibromas and neurilemmomas. c. Malignant lymphomas—NHL type: xx Common in parotids. xx Common with HIV, Sjögren’s syndrome (44 times more chances than normal people). d. Secondary tumours from head and neck region; bronchus and skin. e. Lymphoepithelial tumours:  Benign—it is 5% of all benign salivary tumours (Godwin’s tumour). It is common in females; can be bilateral. Benign lymphoepithelial lesion (BLEL) is of unknown etiology characterized by replacement of salivary parenchyma with lymphoid tissue. It may be diffuse/focal/capsulated/unencapsulated. It may be associated with Mikulicz’s disease or Sj ö gren’s syndrome.  Malignant—it is rare tumour occurs in parotid and submandibular glands (ESKIMOMA).

Salivary Glands xx Even though it is capsulated, tumour may come out as

A

B Figs 4.20A and B: Neoplasm of parotid gland (Malignant).

Incidence

pseudopods and may extend beyond the main limit of the tumour tissue. xx When disease occurs in parotid, commonly it involves superficial lobe or superficial and deep lobe together. xx But sometimes only deep lobe is involved and then it presents as swelling in the lateral wall of the pharynx, soft palate and posterior pillar of the fauces. There may not be any visible swelling in the preauricular region. It is called as ‘dumbbell tumour’. This tumour is in relation to styloid process, mandible, stylohyoid, styloglossus, stylopharyngeus muscles.

Clinical Features

xx Eighty per cent salivary neoplasms are in the paro­tids of

which 80% are benign; 80% of these are pleomorphic adenomas; 80% occur in superficial lobe. xx Fifteen per cent of salivary tumours are in the submandibular salivary gland, of which 50% are benign. 95% of these are pleomorphic adenomas. xx Ten per cent of salivary neoplasms are in the minor salivary glands—palate, lips, cheeks, and sublingual glands. Of these only 10% are benign. Note:

• • • • •

Parotid tumours are common but only 20% are malignant. Submandibular tumours are uncommon but 50% of them are malignant. Minor salivary gland tumours (other than sublingual glands) are rare and 90% of them are malignant. Sublingual salivary tumours are very rare but almost all sublingual salivary tumours are malignant. Incidence of malignancy in salivary glands is inversely related to size of the gland; in parotid it is 15%; in submandibular it is 50%; in sublingual it is 85%.

PLEOMORPHIC ADENOMA (Mixed Salivary Tumour)

Clinical features of parotid tumour Swelling, pain, ulceration, dysphagia (if deep lobe is involved) Raised ear lobule Cannot be moved above the zygomatic bone—curtain sign Deviation of uvula and pharyngeal wall towards midline in case of deep lobe tumour ™™ Facial nerve, masseter, skin, lymph node and bone involvement eventually occurs in case of malignancy ™™ ™™ ™™ ™™

80% common. Common in females (3:1). Occurs in any age group. But common in 4th and 5th decade Usually unilateral. Present as a single painless, smooth, firm lobulated, mobile swelling in front of the parotid with positive curtain sign (As the deep fascia is attached above to the zygomatic bone, it acts as a curtain, not allowing the parotid swelling to move above that level. Any swelling superficial to the deep fascia will move above the zygomatic bone). xx Obliteration of retromandibular groove is common. xx xx xx xx xx

xx Commonest of the salivary gland tumour in adult. xx It is 80% common. xx More common in parotids (80%). 10% in submandibular

salivary gland; 0.5% in sublingual salivary gland.

xx It is mesenchymal, myoepithelial and duct reserve cell

origin. xx Grossly it contains cartilages, cystic spaces, solid tissues. xx Microscopically it is biphasic in nature with epithelial and

stromal components. Benign tumours will usually not show necrosis. Histologically it shows: ™™ ™™ ™™ ™™

Epithelial cells Myoepithelial cells Mucoid material with myxomatous changes Cartilages/pseudocartilages

Fig. 4.21: Pleomorphic adenoma showing curtain sign.

Remember that the faith to move a mountain always carries a pick. — Anonymous

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Fig. 4.22: Deep lobe tumour of parotid is examined per orally.

Fig. 4.24: Parotid tumour showing typical raise in earlobe pleomorphic adenoma.

Pain in salivary tumours Benign tumours are usually painless Sudden onset of pain denotes malignant transformation Pain is dull boring at primary site or referred to ear through auriculotemporal nerve ™™ Pain is due to: – Capsular distension by tumour – Obstruction to free flow of saliva – Nerve infiltration – Inflammation like in Warthin’s – Tumour necrosis ™™ ™™ ™™

Fig. 4.23: Typical parotid swelling with ear lobe raised. Facial nerve should be tested by clenching the teeth. xx The ear lobule is lifted. xx When deep lobe is involved, swelling is commonly located

in the lateral wall of pharynx, posterior pillar and over the soft palate—10%. Deep lobe tumour passes through Patey’s stylomandibular tunnel pushing tonsils, pharynx, soft palate often without any visible swelling or only small swelling when only deep lobe tumour is present; it also presents as dysphagia. Bidigital palpation of parotid is significant in such occasion with one finger inside mouth. xx Facial nerve is not involved. Long-standing pleomorphic adenoma may turn into carcinoma (carcinoma in ex pleomorphic adenoma). Its features are: ™™ Recent increase in size ™™ Pain and nodularity ™™ Involvement of skin, ulceration ™™ Involvement of masseter ™™ Involvement of facial nerve—lower facial nerve palsy—(Difficulty in closing eyelid, difficulty in blowing and clenching teeth) ™™ Involvement of neck lymph node ™™ Restriction of jaw movements

Complications xx Recurrence—5–50%. xx Malignancy.

 3–5% in early tumours.  10% in long duration (15 or more years) tumours.

Investigations xx FNAC is very important and diagnostic. xx CT scan to know the status of deep lobe, local extension

and spread.

xx MRI is better method. Note:

Incision biopsy of parotid tumour is contraindicated as chances of seedling and recurrence are high and also there is a chance of injuring the facial nerve, and chance of developing parotid fistula while doing the biopsy.

Open biopsy is contraindicated in parotid tumours due to: ™™ ™™ ™™

Chance of injury to facial nerve Seedling and high chance of recurrence Chance of parotid fistula formation

Salivary Glands

Fig. 4.25: CT picture of pleomorphic adenoma.

Treatment xx Surgery—first line treatment. xx If only superficial lobe is involved, then superficial parot-

B Fig. 4.26B

Figs 4.26A and B: Recurrent parotid tumour which has attained large size. Note facial nerve is intact. Duct orifice should be inspected using retractor. without any capsule. Expression of MUC1/DF3 in the tumour is marker to predict recurrence.

idectomy is done wherein parotid superficial to facial nerve is removed. xx If both lobes are involved, then total conservative parotidectomy is done by retaining facial nerve.

ADENOLYMPHOMA (Warthin’s Tumour, Papillary Cystadenoma Lymphomatosum)

Note:

• • • • • •

Enucleation is avoided as it causes high recurrence due to extension of tumour outside as pseudopods across the capsule. Incomplete excision, 10% of tumours which are highly cellular are other causes for recurrence. RT is given after surgery eventhough it is benign controversial; a debate. Inexplicable metastasis can occur even though it is benign. Tumour may implant due to spillage while surgical removal into retained residual parotid (deep lobe in superficial parotidectomy). Recurrence after parotidectomy in pleomorphic adenoma is 5%. It is due to spillage, improper technique, inadequate margin, retained pseudopods, multicentricity. Recurrent tumour is multinodular

xx It is a misnomer. It is not malignant, it is not lymphoma. xx It is a benign tumour that occurs only in parotid, usually in

the lower pole. xx It is said to be due to trapping of jugular lymph sacs in

parotid during developmental period. xx It composed of double layer of columnar epithelium, with

papillary projections into cystic spaces with lymphoid tissues in the stroma. xx It usually involves only superficial lobe of parotid gland. It may also be multicentric. xx Smoking (40%/8 times more risk than nonsmokers) and radiation exposure may be the cause.

Clinical Features xx It presents as a slow growing, smooth, soft, cystic, fluctuant xx xx xx xx xx

swelling, in the lower pole, often bilateral and is nontender. It is common in males—4:1. Common in smokers. Common in old people – 60 years. Its incidence is 10%. Common in Whites. It is 2nd most common benign tumour. It is often bilateral—10%.

Investigations xx Adenolymphoma produces a “hot spot” in

A Fig. 4.26A

99

Technetium pertechnetate scan—it is diagnostic (Due to high mitochondrial content).

Nothing comes from without; all things come from within.

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SRB's Manual of Surgery xx FNAC.

Adenolymphoma does not turn into malignancy. But occasionally it can simultaneously be associated with pleomorphic adenoma, carcinoma or lymphoma of parotid.

BASAL CELL ADENOMA xx It is rare, benign, now classified under monomorphic adenoma containing isomorphic basaloid cells with basal layer and basement membrane. xx It is common in minor salivary glands; in major salivary glands it is multicentric. xx Grossly it looks like lymph node. xx Microscopy—isomorphic basaloid cells with solid/trabecular/ tubular/membranous pattern. xx Canalicular adenoma is its variant with bilayered ribbons of columnar cells separated by vascular stroma.

MUCOEPIDERMOID TUMOUR

Fig. 4.27: Warthin’s tumour. It is seen in parotid gland usually in superficial lobe, in lower pole.

xx It is the commonest malignant tumour in parotid. xx It is 2nd common malignant tumour in submandibular and sublingual salivary glands. xx It is commonest malignant tumour of parotid in childhood. xx Incidence is 9% of salivary tumours; 20% of malignant salivary tumours. xx It occurs both in major as well as minor salivary glands. Parotid is the commonest site; palate is the commonest minor salivary gland site (In the palate adenoid cystic carcinoma is common). xx Radiation is the commonest etiological factor. xx Gross—unencapsulated solid tumour with cystic spaces. xx Microscopy—biphasic with mucin secreting (+ve for PAS, – ve for diastase) low grade and epidermoid with high grade; clear cell with intermediate type. xx It is slowly progressive, often attains a large size and spreads to neck lymph nodes. xx It contains malignant epidermoid and mucous secreting cells.

Types

Fig. 4.28: Warthins tumour of parotids. It is common in males; often bilateral; common in elderly.

xx Low grade—mucous cells mainly—spreads to regional nodes. xx Intermediate—clear cell variety xx High grade—epidermoid cells mainly—spreads to regional nodes and also shows high propensity for distant spread. Facial nerve involvement is late in mucoepidermoid carcinoma of parotid.

Treatment Superficial parotidectomy.

ONCOCYTOMA (Oxyphil Adenoma) It is 8 mm invasion carries 5-year survival < 50%.

ADENOID CYSTIC CARCINOMA (10% of Salivary Tumours) xx It is most common tumour in submandibular and sublingual salivary glands. 50% of cases occur in minor salivary glands—palate. xx It is also called as cylidromatous carcinoma. xx It is 2nd most common malignant salivary tumour; but it is rare in parotid (2% of parotid tumours, 15% of malignant parotid tumours. xx It is common in females (3:2). Common in 5th and 6th decades. xx It is slow growing but highly malignant with remarkable capacity for recurrence. But it is classified under low grade malignancy. xx Microscopy: Cribriform, tubular, and solid are 3 types. Cribriform type shows cells in nests separated by round or oval spaces— ‘Swiss-cheese’ pattern. Myo and duct epithelial cells with lace like pattern are also seen. It invades periosteum and bone medulla early and spreads extensively. xx It has got high affinity for perineural spread (both axially and circumferentially; antegrade and retrograde fashion) along mandibular and maxillary divisions of trigeminal (common) nerve and facial nerve. It infiltrates nerve more proximally for long distance. Tumour may reach Gasserian trigeminal ganglion, pterygopalatine ganglion and cavernous sinus. xx Blood spread can occur to lungs, bones and liver. Lung secondaries may remain dormant for many years and so is not a contraindication for surgery of primary tumour. Blood spread can occur decades after removal of primary tumour. xx Radical parotidectomy/wide or radical excision of submandibular and sublingual glands with neck nodal dissection and postoperative RT is the treatment of choice. xx Positive margin, perineural spread, solid type on microscopy carry poor prognosis. Lung metastasis will not affect the prognosis. xx Local recurrence is common. 5-year survival is 70%. xx Regional nodal spread can occur but rare.

ACINIC CELL TUMOUR xx It is a rare, slow growing tumour that occurs almost always in parotid and is composed of cells alike serous acini. xx It is more common in women. It occurs in adult and elderly. xx It is 3% of salivary tumours; 90% occurs in parotid. xx Microscopically, it can be microcystic (commonest), papillary, follicular, medullary etc. xx It can involve facial nerve or neck lymph nodes. xx Clinically, it is of variable consistency with soft and cystic areas. xx It is low grade malignant tumour.

MALIGNANT MIXED TUMOUR (MMT) xx It is 10% of salivary malignancy in incidence with epithelial and mesenchymal elements. xx It carries worst prognosis.

ADENOCARCINOMA OF SALIVARY GLANDS xx It is 3% of parotid and 10% of submandibular and minor salivary gland tumours. xx It is equal in both sexes. xx It is common in children xx It can be tubular, papillary and undifferentiated. xx 20% involve facial nerve clinically. xx Undifferentiated type is aggressive.

SQUAMOUS CELL CARCINOMA OF SALIVARY GLANDS xx xx xx xx xx xx xx xx xx xx

It is rare in salivary glands. In salivary glands, parotid is the common site. It is almost never seen in minor salivary glands. It is classified as high grade tumour. It is common in men (3:1). It occurs in 6th or 7th decade. It is aggressive nonencapsulated tumour arising from ductal system. It grows rapidly causing pain, facial palsy, skin fixity, ulceration. It spreads commonly to neck nodes. It carries poor prognosis. Radical parotidectomy and RT is the treatment of choice.

SUBMANDIBULAR SALIVARY GLAND TUMOURS Benign tumours:

xx They are commonly pleomorphic adenomas, are smooth, firm or hard, bidigitally palpable, without involving adjacent muscles or hypoglossal nerve or mandible bone. xx Diagnosis is by FNAC, Orthopantomogram (OPG) and CT scan. xx Excision of both superficial and deep lobes of the gland is done.

Malignant tumours of submandibular salivary gland:

xx They are hard, nodular, often get fixed to skin, muscles, hypoglossal nerve and mandible. xx Diagnosis is by FNAC of primary tumour and of lymph nodes when involved, CT scan and OPG.

It’s your imagination that can take you anywhere.

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SRB's Manual of Surgery xx Treatment:  Wide excision, with removal of adjacent muscle, soft tissues and mandible.  If lymph nodes are involved, block dissection of neck (Classical neck dissection) is done.

General features of malignant salivary tumours Fixation Resorption of adjacent bone Pain and anaesthesia in the skin and mucosa Muscle paralysis Skin involvement and nodularity Involvement of jaw and masticatory muscle Nerve involvement (facial nerve in parotid or hypoglossal nerve in submandibular salivary gland) ™™ Blood spread when occurs, commonly to lungs ™™ Mandibular branch of 5th cranial nerve may be involved when tumour tracks along the auriculotemporal nerve to the base of the skull causing severe pain in the distribution area ™™ ™™ ™™ ™™ ™™ ™™ ™™

MANAGEMENT OF MALIGNANT SALIVARY TUMOURS TNM Staging of Malignant Salivary Tumours (AJCC, 7th Edition, 2010, Clinical Staging) T—Tumour Tx —Tumour cannot be assessed. T0 —No evidence of primary tumour. T1 —Tumour < 2cm without extraparenchymal spread. T2 —Tumour 2–4 cm, without extraparenchymal extension T3 —Tumour >4 cm. —or with extraparenchymal spread. —but no facial nerve spread. T4 —Spread to facial nerve, skin, mandible, ear canal —T4a. —or spread to base of skull, pterygoid plates, encased external carotid artery – T4b.

A

Staging

B Figs 4.30A and B: Submandibular salivary gland tumour both external as well as intraoral look.

Stage I Stage II Stage III Stage IVA Stage IVB Stage IVC

– – – – – –

T1N0M0 T2N0M0 T3N0/N1Mo T4aN2N1N0M0 T4b any NM0; any T N3M0 Any T any N M1

Note: 

Pathological TNM staging is also present which differs from clinical in many points. Example—T3 is tumor of size 4-6 cm; T4 is size > 6 cm.

N—Lymph node Nx — Nodes not assessed. N0 — Regional nodes not involved. N1 — Single ipsilateral node < 3 cm. N2a — Single ipsilateral node 3–6 cm. N2b — Multiple ipsilateral nodes < 6 cm. N2c — Bilateral or contralateral nodes < 6 cm. N3 — Single node spread > 6 cm. M—Metastases M0 — No blood spread. M1 — Blood spread present.

Specific Investigations Fig. 4.31: Submandibular salivary gland tumour which is malignant. Patient underwent wide excision.

xx FNAC.  FNAC also confirms possibility of (35% of patients) lymphoma/inflammatory masses.

Salivary Glands  But FNAC may cause haematoma leading to difficulty in

Fig. 4.32: Submandibular salivary gland tumour in old female.

surgical dissection. Sampling problem, difficulty in finding histological type.  Conservative approach for benign tumours in high risk surgical candidates may be thought of. xx CT scan  It is to see the deep lobe of the parotid: the involvement of bone, extension into the base of the skull; relation of tumour to internal carotid artery, styloid process, deep lobe tumour, parapharyngeal space extension. Neck nodes are better assessed. Bony changes in the foramina, erosions and sclerotic margins in fissures or canals, enlarged diameter of canal and fissure are the CT features of perineural spread. xx MRI  It is very useful to find out perineural spread, bone marrow involvement, skull bones, internal architecture and intracranial extensions, recurrent tumours. Replacement of perineural fat with tumour, contrast (gadolinium) enhancement, increased size of the nerve are features of perineural spread. xx Other  OPG.  Blood grouping and cross-matching; required amount of

blood is kept ready.

 FNAC of lymph node.  MRI shows better soft tissue definition than CT scan.

Note:

Sialogram is not useful in assessment of tumour.

Treatment In Parotid xx Surgery Indications for surgery T1, T2, T3 tumours of low grade—total conservative parotidectomy ™™ T4 tumours, high grade tumours, SCC—radical parotidectomy It includes facial nerve sacrifice, may involve resection of skin, mandibular ramus, masseter muscle, infratemporal fossa dissection, subtotal petrosectomy. ™™

A

Note: In T1 low grade, superficial parotidectomy is often practiced; but not ideal.

a. Radical parotidectomy is done which includes removal of both lobes of parotid, soft tissues, part of the mandible with facial nerve.  It is done in high grade malignant tumours and squamous cell carcinoma. Indications for facial nerve sacrifice Preoperative weakness/paralysis of nerve Intraoperative evidence of gross invasion even in presence of normal preoperative function ™™ Tumours transgressing through facial nerve from superficial to deep lobe ™™ Nerve stump is checked for frozen section for negative margins, if positive mastoidectomy and nerve dissection in temporal bone is needed ™™ ™™

B Figs 4.33A and B: CT scan pictures of salivary tumours.  FNAC allows preoperative counselling regarding nature of

tumour, likely extent of resection (conservative/radical), management of facial nerve (high grade adenoid cystic), and likelihood of neck dissection (high grade).

 Facial nerve is reconstructed using greater auricular nerve, or

sural nerve. All branches except buccal branch are repaired using cable graft. Nerve graft is not a contraindication for future RT.

In time of test, family is best.

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SRB's Manual of Surgery  Often lateral tarsorrhaphy or temporal sling recons­truction

is done. b. Total conservative parotidectomy is becoming popular in many parotid malignancies. Complications of surgery ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Haemorrhage Infection, flap necrosis Fistula Frey’s syndrome Facial nerve palsy Facial numbness Numbness in ear lobule due to injury to great auricular nerve Sialocele

xx Postoperative radiotherapy It is quite useful to reduce the chances of relapse. Usually, external radio­therapy is given. It is given in all carcinomas, but more useful in adenoid cystic and squamous cell carci­nomas.

A

Indications for radiotherapy T3, T4 tumours ™™ High grade tumours ™™ Perineural spread ™™ Adenoid cystic carcinomas ™™ Deep lobe tumour ™™ Vascular involvement ™™ Close clearance margin ™™ Multiple neck nodes involvement ™™ Recurrent malignant tumours ™™ Recurrent pleomorphic adenoma ™™ Spillage after surgery for pleomorphic adenoma ™™ Residual/refractory tumours/nerve involvement ™™ Inadequate clearance margin Note: – It is given in 3–6 weeks after surgery. Dose is 50–70 Gy; 1.5–2.0 Gy in 5–8 weeks – RT is delayed for 6 weeks if nerve grafting is done – Neuron beam therapy is used Complications ™™ Xerostomia ™™ Osteoradionecrosis of temporal bone/mandible ™™ Skin ulcers, mucositis ™™ Fibrosis of optical apparatus, brainstem injury ™™ Trismus due to fibrosis of masseter, pterygoids and TM joint ™™ Otitis media, localized hair loss ™™

xx Chemotherapy It is also given. Drugs given here depends on tumour type. Intraarterial chemotherapy is beneficial. But overall efficacy of chemotherapy is very less compared to RT. 5 FU, cisplatin, doxorubicin, epirubicin, cetuximab are used. xx Preoperative radiotherapy It is given in large tumours to reduce the size and make it better operable, i.e. to down stage the disease. xx If lymph nodes are involved, which is confirmed by FNAC, radical neck dissection is done. It is also done in N0 with high-grade tumour or T3/T4 tumours.

In Submandibular Salivary Gland Wide excision is done, with removal of mandible, and soft tissues around—extraglandular excision. If lymph nodes are involved, then block dissection of the neck is done.

B Figs 4.34A and B: Recurrent parotid tumour right side. Note the scar of previous surgery. It was adenoid cystic carcinoma. Recurrence has occurred after 6 years. Patient underwent radical parotidectomy. Neck nodes were involved in this patient even though it is rare in adenoid cystic carcinoma. Patient needs radiotherapy and chemotherapy.

MINOR SALIVARY GLAND TUMOURS xx It is 10% of salivary tumours. xx It is common in — palate (40%)

— lip — cheek — sublingual glands xx Palate is the commonest site. xx 10% are benign—commonly pleomorphic adenomas. xx 90% are malignant—commonly adenoid cystic carcinomas. xx They present as swelling with ulcer over the summit. xx If it is malignant, then extension into the palate, maxilla, pterygoids can occur often with involvement of the lymph node.

Differential Diagnosis Squamous cell carcinoma of oral cavity.

Investigations 1. Incision biopsy. 2. CT scan. 3. X-ray maxilla. 4. FNAC of lymph node.

Salivary Glands region, it usually re-epithelialise if once left open to allow it to granulate. If bony palate is infiltrated then that part of palate bone is removed to get a clearance; area is reconstructed by moulds, synthetic materials.

xx Reconstruction by dental plates, skin grafting, or flaps are done. xx Lymph node block dissection of the neck is done if involved. xx Excision with primary closure is done for benign tumours.

B

A

Figs 4.35A and B: Minor salivary gland tumour in the palate. Palate is the common site of minor salivary gland tumour.

Points to be remembered ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Salivary gland tumours are usually benign in an adult It is rare in children but when it occurs, it is commonly malignant Clinical and FNAC are diagnostic methods Open biopsy is contraindicated Sialogram is not useful in salivary tumours CT scan or MRI are often needed Nerve should be preserved in benign lesions Nerve can be sacrificed to achieve clearance in malignancies

PAROTID LYMPHOMA xx Parotid lymphoma can occur from the lymph nodes in the

gland or from parotid parenchyma. xx It can occur in HIV patients; lymphoepithelial diseases and

in Sjögren’s syndrome. A

xx Common in elderly. xx Disease may be confined to parotid gland or may involve

other nodes in neck, mediastinum.

xx When it is confined to parotid total parotidectomy with

radiotherapy and later chemotherapy is the treatment. xx When many other nodes are involved chemotherapy is the

choice therapy. Note:

Lymphoma occasionally can occur in other salivary glands also (10% of all salivary lymphomas).

PAROTIDECTOMY Types

B Figs 4.36A and B: Minor salivary gland tumour of hard palate. It is excised with 1 cm margin; area is allowed to granulate and epithelialise.

Treatment xx Wide excision often with palatal excision or maxillec­tomy

is done—for malignancy.

xx If the tumour is less than 1 cm in size excision biopsy is

done with 1 cm clearance margin. If the tumour is more than 1 cm in size, initially incision biopsy is done and then wide excision is done. Even in larger defect in hard palate

1. Superficial parotidectomy: It is the removal of superficial lobe of the parotid (superficial to facial nerve). Done in case of benign diseases of super­ficial lobe of the parotid. 2. Total conservative parotidectomy: It is done in benign diseases of parotid involving either only deep lobe or both superficial and deep lobes. Here both lobes are removed with preservation of facial nerve. Here initially superficial parotidectomy is done and facial nerve and its branches are retracted gently and deep lobe is removed. 3. Radical parotidectomy: Both lobes of parotid are removed along with facial nerve, fat, fascia, muscles (masseter, pterygoids and buccinator), lymph nodes. It is done in case of carcinoma parotid. Later facial nerve reconstruction is done using great auricular nerve graft.   Conservative surgeries are becoming popular for malignancy but they are not universally accepted. 4. Suprafacial parotidectomy is done in lower pole parotid tumours wherein all branches of the facial nerve need not be dissected.

You will soon break the bow if you keep it always stretched.

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Lazy ‘S’ incision—modified Blair's/Sistrunk's approach and raising the skin flaps Mobilisation of the gland Flap is reflected in front just up to anterior margin of the parotid; never beyond. After identification of sternocleidomastoid great auricular nerve is identified and can be sacrificed. Posterior belly of digastric is identified. Location of stylomastoid branch of posterior auricular artery is anterior to facial nerve trunk which enters the stylomastoid foramen. Thrust the mosquito haemostat 5 mm in front of facial nerve; open the blades for 5 mm; lift the blades for 5 mm. One should worry about the nerve but not small bleeding. Identification of facial nerve trunk. Dissection of the gland off the facial nerve using bipolar cautery. Removal of parotid—superficial/both. Distilled water (hypertonic) irrigation to kill spilled tumour cells. Haemostasis and closure with a suction drain.

Fig. 4.38: ‘S’ shaped incision for parotidectomy.

Fig. 4.39: On table exposure of facial nerve branches after superficial parotidectomy for a benign tumour.

Fig. 4.37: Incision for parotidectomy. Typical lazy ‘S’.

A

B Figs 4.40A and B

Salivary Glands

C

D Figs 4.40C and D

Figs 4.40A to D: Steps in parotidectomy and demonstration of facial nerve. Note the placement of drain after surgery (Courtesy: Professor Kishore Chandra Prasad, ENT, Mangaluru; Dr Sampath, MS, ENT, Mangaluru).

Identification of facial nerve ™™ ™™ ™™ ™™ ™™ ™™

Facial nerve is 1 cm deep and below the tip of the inferior portion of the cartilaginous canal—Conley’s point By nerve stimulator It is inferomedial to tragal point Deep to digastric muscle and tympanic plate Nerve is just lateral to the styloid process Tracing branch from distal to proximal (Hamilton-Bailey technique)

Complications of parotidectomy ™™ ™™ ™™ ™™ ™™ ™™ ™™

Facial nerve injury Haemorrhage Salivary fistulas Infection—Flap necrosis is common Frey’s syndrome Sialocele Numbness over the face and ear—due to injury to great auricular nerve. Female patients find difficult to wear ear rings. Spontaneous recovery may occur in 1½ to 2 years.

FREY’S SYNDROME (Auriculotemporal Syndrome, Gustatory Sweating); (Lucie Frey—Polish Surgeon—1932) xx Occurs in 10% of cases. xx It is due to injury to the auriculotemporal nerve, wherein postganglionic parasympathetic fibres from the otic ganglion become united to sympathetic nerves from the superior cervical ganglion (Pseudos­ynapsis). There is inappropriate regeneration of the damaged parasympathetic autonomic nerve fibres to the overlying skin. xx Auriculotemporal nerve has got two branches. Auricular branch supplies external acoustic meatus, surface of tympanic membrane,

Fig. 4.41: Parasympathetic and sympathetic supply of the parotid gland. Otic ganglion located just below the foramen ovale close to mandibular nerve relays the parasympathetic supply from glossopharyngeal nerve through tympanic branch, tympanic plexus in middle ear and then lesser superficial petrosal nerve. Postganglionic fibres run in auriculotemporal nerve along with unrelayed sympathetic fibres from middle meningeal plexus. skin of auricle above external acoustic meatus. Temporal branch supplies hairy skin of the temple. Sweating and hyperaesthesia occurs in this area of skin.

Causes xx Surgeries or accidental injuries to the parotid. xx Surgeries or accidental injuries to temporoman­dibular joint.

You may say you KNOW, but by your actions it is KNOWN.

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SRB's Manual of Surgery Clinical Features xx Flushing, sweating, erythema, pain and hyperaesthesia in the skin over the face innervated by the auriculotemporal nerve, whenever salivation is stimulated (i.e. during mastication). xx Condition causes real inconvenience to the patient. xx Involved skin is painted with iodine and dried. Dry starch applied over this area will become blue due to more sweat in the area in Frey’s syndrome—Minor's Starch iodine test.

Surgeries for facial nerve palsy

Treatment

Static – Suspension surgeries using temporal fascia – Correction of medial canthus – Lateral tarsorrhaphy—to prevent exposure keratitis due to widened palpebral fissure – Upper lid weights ™™ Dynamic – Muscle transfer—temporal to masseter – Free muscle graft. Gracilis muscle neurovascular transfer – Cross-facial nerve transplant from opposite facial nerve to injured facial nerve using sural nerve – Nerve grafts ™™

xx Initially conservative and reassurance. Most often they recover without any active treatment in 6 months. Antiperspirants, anticholinergics like scopolamine 3%, glycopyrrolate 1%, methyl sulfate, radiation 50 Gy are used. xx Occasionally (10%) they require surgical division of the tympanic branch of the glossopharyngeal nerve below the round window of middle ear [i.e. intra­tympanic parasympathetic (Jacobsen nerve) neurectomy]. xx Dermal/fat graft; avulsion of auriculotemporal nerve; interposition of temporal fascia, fascia lata, sternomastoid muscle, acellular human dermal collagen; alcohol injection—are all tried. Note:

Incidence is higher with a flap elevation superficial to platysma. Elevation of thick flap or insertion of fat flap under skin during surgery may reduce the chance of Frey’s syndrome.

Treatment of Frey’s syndrome ™™ ™™ ™™ ™™ ™™

xx Suspension of angle of mouth to zygomatic bone using temporal fascia sling. xx Lateral tarsorrhaphy—to prevent corneal ulcera­tion. xx Medial canthus reconstruction—to reduce epi­phora. xx Cross-facial nerve transplantation from opposite side using its insignificant branches. xx Dynamic neurovascular muscle graft. xx Upper lid gold weights to protect cornea.

Reassurance Jacobsen neurectomy (tympanic) Injection of botulinum toxin to the affected skin Antiperspirants like aluminium chloride Syndrome can be prevented on table by placing muscle (sternomastoid) or fascial (temporalis) flaps or artificial membranes over parotid bed, under the skin

The House-Brackmann score It is a score used in facial nerve palsy to grade the degree of damage. It is done by measuring the upward movement of the middle portion of the eyebrow top and the outward movement of the angle of the mouth. Each reference point scores 1 point for each 0.25 cm movement, up to a maximum of 1 cm. The scores are then added together, to give a number out of 8. It is a measure of the range of intentional movement of the patient’s facial muscles. Even though it is a subjective scale, overall reliability is good and is the most commonly used. Electroneuronography is the other method used. Remember ™™

FACIAL NERVE INJURY (Lower Motor Nerve Lesion, Surgically Related) Causes xx xx xx xx

Trauma Surgery—parotidectomy, drainage of parotid abscess Compression of facial nerve—Bell’s palsy. Incidence of temporary/transient facial nerve palsy after parotidectomy is 30%. Recovery occurs usually in 12 weeks. xx It is due to transection of trunk or branches or excessive traction or over use of nerve stimulator.

Clinical Features xx xx xx xx xx xx xx

Inability to close the eyelid. Difficulty in blowing and clenching. Drooping of the angle of the mouth. Obliteration of nasolabial fold. Loss of forehead wrinkles. Wide palpebral fissure. Epiphora.

Treatment xx Nerve grafting using greater auricular nerve, sural nerve, lateral cutaneous nerve of thigh or hypoglossal nerve.

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Taste sensation and general sensation (lingual nerve) should be checked. Patient is not allowed to speak but asked to write in a paper. Taste material is instilled on the surface of the diseased side first and then normal side. Prior to each instillation patient should wash his mouth with warm water. Usually four substances are used. After 10 seconds patient should identify the substance and write. Facial nerve serves 3 tastes—salt (rock salt) on the tip of tongue; sweet using syrup on the tip of the tongue; sour using lemon juice on the lateral aspect of the tongue. Bitter taste is mediated by glossopharyngeal nerve and is tested using quinine on posterior third of the tongue. Secretomotor fibres of parotid: Secretomotor preganglionic fibres from inferior salivary nucleus → glossopharyngeal nerve → tympanic branch → tympanic plexus → lesser superficial petrosal nerve → otic ganglion → post-ganglionic fibres → auriculotemporal nerve, branch of mandibular division of trigeminal nerve → parotid gland. Secretomotor fibres of submandibular salivary gland: Preganglionic fibres from superior salivary nucleus → facial nerve → chorda tympani nerve → lingual nerve → Langley’s submandibular ganglion → postganglionic fibres → sub-mandibular and sublingual salivary glands. Parotid gland is serous. Submandibular gland is mixed (major is mucous). Sublingual is mucous. Minor salivary glands are mucous except von Eber’s glands which empty into the circumvallate papillae and glands in the tongue tip. 70% of total saliva is from submandibular salivary gland. 25% of saliva is from parotids. 10% of total salivary volume is from minor salivary glands. Normal salivary secretion per day is 1500 ml. It is hypotonic fluid with pH 7.0. It contains α-amylase.

Salivary Glands Note:

A

B Figs 4.42A and B: Features of post-parotidectomy facial nerve palsy.

Accessory parotid tumour—Accessory parotid tumour is very rare tumour arising from accessory parotid usually above the parotid duct level in front of the masseter muscle. It can be benign or malignant. Pleomorphic adenoma is common. Tumour behaves like tumour from main parotid gland. Incidence is 1% of all parotid tumours. 30% of them are malignant. It is located in a line at central 1/3rd of the line joining the middle of the tragus to a point between the ala of the nose and vermilion border of upper lip. FNAC confirms the diagnosis. CT scan confirms the anatomical location. Main parotid gland is usually normal. Surgery is the treatment. Standard parotidectomy incision or direct cheek approach can be used. But direct cheek approach can cause higher incidence of buccal and zygomatic branches of facial nerve injuries (40%). Standard parotidectomy approach has got less chance of nerve branch injuries. Lymph node spread in the neck is dealt with radical dissection. Excision cures the benign disease.

Heerfordt’s syndrome is sarcoidosis of parotid swelling; anterior uveitis; facial palsy and fever.

Have equal love for all, and experience a life of equanimity.

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Chapter

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Neck CHAPTER OUTLINE ™™ A  natomy of Lymphatics of Head and Neck ™™ Thoracic Outlet Syndrome ™™ Cervical Rib ™™ Branchial Cyst ™™ Branchial Fistula ™™ Pharyngeal Pouch

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Laryngocoele Cystic Hygroma Ludwig’s Angina Parapharyngeal Abscess Retropharyngeal Abscess Subhyoid Bursitis Carotid Body Tumour

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Torticollis Sternomastoid Tumour Tuberculous Lymphadenitis Cold Abscess Secondaries in Neck Lymph Nodes Chemotherapy for Head and Neck Cancers

ANATOMY OF LYMPHATICS OF HEAD AND NECK Waldeyer’s Lymphatic Ring (Inner) It consists of adenoids above, lingual tonsil below and two palatine tonsils and tubal tonsils laterally one on each side.

Outer Circular Chain of Nodes (Outer Waldeyer’s Ring) Occipital, postauricular, preauricular, parotid, facial, submandibular, submental, superficial cervical and anterior cervical. Facial nodes are: a. Superficial  Upper—infraorbital.  Middle—buccinator.  Lower—supramandibular. b. Deep groups—in relation to pterygoids. Submandibular lymph nodes drain xx The side of the nose. xx The cheek. xx Angle of the mouth. xx Entire upper lip. xx Outer part of the lower lip. xx The gums. xx Side of the tongue.

Submental lymph nodes: Drain from the central part of the lower lip, floor of the mouth and apex of the tongue.

Fig. 5.1: Inner and outer Waldeyer‘s ring anatomy.

Superficial cervical nodes: They lie on outer surface of the sternomastoid around the external jugular vein. They drain the parotid region and lower part of the ear. Deep cervical lymph nodes: Upper deep cervical lymph nodes—jugulodigastric nodes Below the digastric and in front of IJV. Lower deep cervical lymph nodes—jugulo-omohyoid nodes—Above the omohyoid and behind the IJV. They drain the ipsilateral half of head and neck, finally form a jugular lymph trunk from lower deep cervical nodes to join thoracic duct on the left side, and the junction of right subclavian and right jugular vein on right side.

Neck Rule of 7 in the neck 7 days—inflammation 7 months—neoplasm 7 years—congenital defect Note: The Rule of 7 provides a probable diagnosis of the neck mass based on the average duration of the patient’s symptoms ™™ ™™ ™™

Rule of 80 in the neck ™™ ™™ ™™ ™™ ™™

80% of nonthyroid neck masses are neoplastic 80% of neoplastic neck masses are seen in males 80% of neoplastic neck masses are malignant 80% of malignant neck masses are metastatic 80% of metastatic neck masses are from primary sites above the clavicle

THORACIC OUTLET SYNDROME (TOS) It is syndrome complex due to neurovascular bundle compression in the thoracic outlet. Fig. 5.3: Lymphatic drainage of the neck.

Thoracic outlet has got two main spaces: xx Scalene triangle is bound by scalenus anterior, scalenus medius and first rib. It contains subclavian artery and brachial plexus. xx Costoclavicular space is bound by clavicle, first rib, costo­clavicular ligament and scalenus medius. It con­tains subclavian artery and vein and brachial plexus.

Causes xx xx xx xx xx xx xx xx xx xx

Cervical rib. Long C7 transverse process. Anomalous insertion of scalene muscles. Scalene muscle hypertrophy. Scalene minimus. Abnormal bands and ligaments. Fracture clavicle or first rib. Exostosis. Tumours in the region. Brachial plexus trauma and diseases.

A

B Fig. 5.2: Triangles of the neck.

Figs 5.4A and B

Do not worry and hurry so much rather walk this earth lightly and leave your mark.—Dr Saroj Kanna

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X-ray neck and cervical spine. Doppler. Subclavian angiogram, CT angiogram, CT neck. Nerve conduction studies, electromyography.

Treatment xx Conservative—if nerve velocity is > 60 m/second xx Surgical—if nerve velocity is < 60 m/second Conservative treatment for TOS ™™ ™™ ™™ ™™

C

Exercises—neck stretching, postural and breathing exercises Drugs—analgesics, muscle relaxants, antidepres­sants Avoid weight lifting Physiotherapy

Fig. 5.4C

Figs 5.4A to C: Lymph node enlargement due to various causes is the commonest clinical finding in the neck. Nonspecific lymphadenitis, tuberculosis, secondaries and lymphoma are common conditions: (A) Tuberculosis; (B) Secondaries in lymph node; (C) Lymphoma.

Differential Diagnosis of TOS ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Carpal tunnel syndrome Cervical spondylosis Spinal canal tumours Shoulder myositis Angina Raynaud‘s disease Spinal stenosis Ulnar nerve compression, epicondylitis

Clinical Features Neurological symptoms xx Paraesthesia. xx Pain in shoulder, arm, forearm and fingers. xx Occipital headache as referred pain from tight scalene muscles. xx Weakness in forearm, hand. Vascular symptoms xx Claudication, ischaemic ulcers, gangrene. Signs xx Scalene muscle tenderness. xx Pulsatile swelling in supraclavicular region with thrill and bruit (25%). xx Bony mass above clavicle. xx Adson’s test (+ve). xx Roos test (+ve). xx Elevated arm stress test (+ve). xx Costoclavicular compression reveals feeble/absence of manoeuvre. radial pulse due to compresxx Hyperabduction manoeuvre. sion of the subclavian artery. xx Poor capillary refilling. xx Absence or feeble pulse. (Please refer Chapter on Arterial Diseases for details of tests).

Surgical treatment of TOS Transaxillary (ROOS)—mainly for first rib excision and also cervical rib ™™ Supraclavicular approach for cervical rib and soft tissue excision, scalenotomy, neurolysis, arterial reconstruction ™™ Cervical sympathectomy may be needed ™™

CERVICAL RIB Definition xx It is an extension of costal element (anterior part) of trans-

verse process of C7 vertebra more than 2.5 cm (normal).

xx Syndrome caused by it is called as cervical rib syndrome,

thoracic-inlet syndrome, thoracic-outlet syndrome, scalene syndrome. xx It is 0.46% common; common in females; more frequent on right side. xx It can be unilateral or bilateral (50%) can be asymptomatic or symptomatic.

Types (Refer Fig. 5.5) 1. Complete bony: Cervical rib is radio-opaque, anteriorly ends over the first rib or manubrium. 2. Combined: Partly bony partly fibrous. 3. Complete fibrous: Cannot be demonstrated radio­logically. 4. Partial bony: With free end expanding as bony mass, which is felt in the neck.

}

Fig. 5.5: Cervical rib types.

Neck Note:

7 types of cervical ribs are identified. Type III is the commonest which is a band extending from C7 vertebra to scalene tubercle of 1st rib elevating the neurovascular bundle upwards causing compression. 

Pathology xx Cervical rib narrows the scalene triangle (bounded by scalenus anterior, scalenus medius and first thoracic rib below). Compression of subclavian artery; C8 and T1 nerve roots due to cervical rib. ↓ Angulation of subclavian artery occurs. ↓ Causes constriction of artery at the site where artery crosses the cervical rib. ↓ ‘Eddie’s current’ created in the blood flow causes sudden release of pressure distal to the narrowing. ↓ Poststenotic dilatation → Venturi phenomenon. (due to vessel wall ischaemia)↓ Stasis of blood occur. ↓ Thrombosis → Embolus. ↓ ↓ Features of ischaemia in the hand and forearm. Later digital gangrene occurs.

 





thoracic outlet syndrome develops pain, fatigue, paraesthesia of forearm with tingling and numbness of fingers which gradually progresses. Patient will not be able to continue the test for 5 minutes. This test can also differentiate thoracic outlet syndrome from cervical disc prolapse disease. Adson’s test: The hand is raised above after feeling the radial pulse. The patient is asked to take a deep breath and turn the head to the same side. Any change in pulse, i.e. either becoming feeble or absent, is noted. Modified Adson’s test is same as Adson’s, but neck is turned towards the opposite side. Costoclavicular compression manoeuvre (Falconer test): While palpating the radial pulse of the patient, he is asked to move his shoulder backwards and downwards (exaggerated military position) which may cause absence/feeble radial pulse and a bruit may be heard while auscultating the supraclavicular region—military attitude test. This is due to compression of subclavian artery between clavicle and first rib. Similary Halstead manoeuvre is done by 45° abduction and extension of arm with downward pushing of the shoulder with neck turned opposite side to cause radial pulse feebly palpable. Hyperabduction manoeuvre (Wright’s test): While palpating the radial pulse, arm on the diseased side is passively hyperabducted causing feeble or absence of radial pulse. This is due to compression of artery by pectoralis minor tendon (pectoralis minor syndrome). An axillary bruit may be heard on auscultation. Allen’s test: It is used in hand to find out the patency of radial and ulnar arteries. Both radial and ulnar arteries of the patient is felt and pressed firmly at the wrist. Patient clinches his hand

xx Rarely thrombus may extend proximally into the subclavian artery causing vertebrobasilar insufficiency. xx Compression of C8 and T1 causes tingling and numbness along its distribution, i.e. in the little finger, medial side of hand and forearm. xx Paget-Schroeter syndrome is subclavian vein compression by cervical rib. It is rare.

Clinical Features Majority of patients are asymptomatic—(80%).

1. Vascular manifestations:  Pain is due to ischaemia in the muscle. It is more during work,

exercise, and is relieved by rest.  Upper limb claudication usually is observed in forearm and arm

more obvious after usage of limb. Pain (dull pain) in posterior triangle of neck may be due to presence rib mass. Ischaemic pain in the digits and hand may be present.  Vasomotor changes with cyanosis, cold fingers, excessive sweating may be observed.  Roos test: The patient raises his arms to 90° of abduction at shoulder with the arms fully externally rotated and the elbows at 90° of flexion. Their hands are kept in this position for up to 3 minutes. The test is positive if the patient is unable to hold the arms up for 3 minutes, or if the patient feels pain, heaviness or paraesthesia in the shoulder, arm or hand.  Elevated arm stress test (EAST): Both shoulders (arms) are abducted to 90° with arms fully externally rotated and the elbows braced backwards. Patient will open and close (clench and unclinch) the hands rapidly for 5 minutes. Normal individual can do this without any discomfort and pain. Patient with

Fig. 5.6: Allen’s test done upper limb ischaemia to look for perfusion of hand.

Fig. 5.7: Adson’s test—after palpating radial pulse, elbow with stretched hand is slightly raised; neck is turned to same side; deep breath is taken; feeble or pulse becoming absent may be obvious in positive Adson's.

Nothing dies quicker than a new idea in a closed mind.

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A

Fig. 5.9: Upper limb ischaemia showing ischaemic ulcers and gangrene of finger tips.  Card test for interossei muscle weakness, Froment’s sign/test

B

to detect weakness in adductor pollicis are positive. Wasting may be due to neurological cause also.

3. Features in the neck:

 Hard, fixed, bony mass in the supraclavicular region.  Palpable thrill above the clavicle in the subcla­vian artery.  Bruit on auscultation.

Note:

• •

Most common presentation is neurological. Most problematic presentation is vascular which requires surgery.

Differential Diagnosis ™™

C Figs 5.8A to C: Anatomy of cervical rib and its relation to subclavian artery and vein and brachial plexus. Note the Eddie’s current, poststenotic dilatation due to arterial compres­sion by cervical rib. X-ray shows left-sided complete cervical rib. firmly (often repeated clinching) and holds it tightly. After 1 minute clinch is released to open the palm of the hand which looks pale. Pressure on radial artery in the wrist is released to see area of distribution of the radial artery. Normally, it becomes flushed with pink color. If there is block in radial artery, the area will remain white. Test is repeated again. This time pressure on the ulnar artery is released to check the patency of ulnar artery. Area will be pale and blanched after releasing in case of ulnar artery block. Otherwise it becomes pink after release in normal individual.  Wasting of thenar, hypothenar and forearm muscles.  Often digital gangrene, ischaemic ulcers in digits, oedema of fingers and hand are observed.  Limb is colder and paler than the opposite side.

2. Neurological features is due to compression of T1 and C8 causing tingling and numbness in the little finger, medial side of hand and forearm.  Pain, on the medial side, weakness on the medial side of hand

and anaesthesia may be evident.

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Cervical spondylosis—to differentiate, X-ray neck—lateral view should be taken Carpal tunnel syndrome Tumours or swellings compressing over the vessel or nerves in the neck Other causes of digital gangrene like atherosclerosis, Raynaud’s syndrome, collagen diseases, diabetes mellitus, and embolism Syringomyelia, motor neuron disease Pancoast tumour.

Investigations xx Chest X-ray PA view and lateral view including neck—only (radioopaque) bony rib can be identified. xx Nerve conduction studies to confirm neurological compression and also to rule out carpal tunnel syndrome or cervical spondylosis. xx Arterial Doppler of subclavian artery and of the upper limb. xx Subclavian angiogram, electromyogram. xx Other relevant investigations like blood sugar, lipid profile, cardiac assessment. xx CT scan neck and thorax and CT angiogram of subclavian artery are ideal investigations. MRI of neck is useful.

Treatment Note:

For conservative treatment refer TOS above.

Neck Surgical xx In symptomatic cervical rib without arterial compres­sion (subclavian artery), along with scalenotomy (cutting scalenus anterior muscle), extraperiosteal resection of cervical rib and often resection of first rib is done to increase the thoracoaxillary channel and so as to reduce arterial compression. xx In symptomatic cervical rib with significant sub­clavian artery compression along with scaleno­tomy, extraperiosteal resection of cervical rib, resection of first rib, subclavian artery reconstruc­tion with or without a graft is done. xx Along with scalenotomy, extraperiosteal resection of cervical rib, resection of first rib, reconstruction of subclavian artery, cervical sympathectomy is also done to improve the circulation to the ischaemic upper limb. xx Amputation of the gangrenous toe. xx In pectoralis minor syndrome, pectoralis minor tendon is released from its insertion to coracoid process.

tuant, often transilluminant with a sensation of ‘Half-filled double hot water bottle’. xx It is equal in both sexes. Even though congenital, it is seen in late adolescents and early 3rd decade. xx In 3% cases, it is bilateral; it can be familial also. xx Usually painless unless it is infected. xx It contains cholesterol crystals which is from the lining of mucous membrane which contains sebaceous gland. Cheesy toothpaste like material is typical xx Histologically, it is lined by squamous epithelium. Occasionally it contains ciliated columnar epithelium. Cyst wall shows plenty of lymphoid tissue. xx It may get infected to form an abscess. xx FNAC shows cholesterol crystals. xx MRI allows for finer resolution during preoperative planning.

Approaches Supraclavicular approach—mainly when there is need for vascular reconstruction ™™ Transaxillary approach—through axillary crease, rib is approached and removed ™™ Thoracotomy approach ™™

BRANCHIAL CYST xx It arises from the remnants of second branchial cleft.

Normally, 2nd, 3rd, 4th clefts disappear to form a smooth neck. Persistent 2nd cleft is called as cervical sinus (of His) which eventually gets sequestered to form branchial cyst. xx Epithelial infusion within lymph node may be the other cause as branchial cyst contains lymphoid tissues in their wall. xx Six branchial arches with five pharyngeal pouches (endoderm lining) inside and five pharyngeal clefts (ectoderm lining) outside are present.

Features

A

B

Figs 5.11A and B: (A) Branchial cyst—both sides; (B) Positions of branchial cyst and fistula.

Complications xx Recurrent infection. xx Rupture may cause acquired branchial fistula at upper third

of sternocleidomastoid muscle.

xx Swelling in the neck beneath the anterior border of upper

third of the sternomastoid muscle. It is smooth, soft, fluc-

Differential Diagnosis xx Cold abscess, lipoma neck. xx Lymph cyst. xx Chronic lymphadenitis.

Treatment Excision under GA. Cyst is in relation to carotids, hypoglossal nerve, glossopharyngeal nerve, spinal accessory nerve, posterior belly of digastric and pharyngeal wall. Medially it is close to the posterior pillar of tonsils. During dissection, all these structures should be taken care of. Note:

A

•

B

Figs 5.10A and B: Branchial cyst. It is only occasionally transilluminant.

•

Sclerotherapy with OK-432 (picibanil) has been effective, often done under US guidance. In fish, branchial clefts develop into gills.

Everything big starts with something little.

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SRB's Manual of Surgery Complications of Surgery xx Injury to major structures. xx Infection. xx Recurrence/fistula formation due to incomplete removal

of the track. Cholesterol crystals are seen in: ™™ ™™ ™™

Branchial cyst Dentigerous cyst Hydrocele

B

BRANCHIAL FISTULA xx Branchial fistula is commonly a congenital lesion. It is due to persistent precervical sinus between 2nd branchial cleft and 5th branchial cleft having opening in the skin at lower 1/3rd of neck on the inner margin of sternocleidomastoid muscle, often ends as a sinus just proximal to the posterior pillar of fauces behind tonsil which is also the site of inner opening when presents as fistula. Fistula runs between the structures related to 2nd and 3rd branchial arches (2nd arch artery is ECA, nerve is facial; 3rd arch artery is ICA, nerve glossopharyngeal). From external opening at skin below, it runs in subcutaneous plane to pierce deep fascia at level of thyroid cartilage; to travel between ECA and ICA; behind posterior digastric belly and stylohyoid; outer to IJV, stylopharyngeus, hypoglossal and glossopharyngeal nerves; perforates superior constrictor to reach the internal opening. xx Occasionally acquired branchial fistula can occur due to rupture of or after drainage of infected branchial cyst or incomplete excision of the cyst track. This type of fistula is located outside at skin at the level of upper third of sternomastoid muscle.

Features xx It is a persistent second branchial cleft with a communication outside to the exterior. It is commonly a congenital fistula. Occasionally, the condition is secondary to incised, infected branchial cyst. xx Often it is bilateral (30%). xx External orifice of the fistula is situated in the lower third of the neck near the anterior border of the sternomastoid muscle.

A

Fig. 5.12B

Figs 5.12A and B: Branchial fistula in two different patients. Note the location and discharge (Courtesy: Professor Kishore Chandra Prasad, ENT Surgeon and Head of the Department and Dr Sampath, ENT Surgeon, KMC, Mangaluru) xx Internal orifice is located on the anterior aspect of the posterior pillar of the fauces, just behind the tonsils. xx Sometimes fistula ends internally as blind end. xx Track is lined by ciliated columnar epithelium with patches of lymphoid tissues beneath it, causing recurrent inflammation. xx It usually presents at birth. It is common in children and early adolescent period. Equal in both sexes. xx External orifice is very small with a dimple which becomes more prominent on dysphagia with tuck in appearance. xx Discharge is mucoid or mucopurulent. xx Investigations: Discharge study, fistulogram, MR/CT fistulogram.

Treatment Always surgery: xx Under general anaesthesia, methylene blue is injected into the track. Probe is passed into the fistulous track. Through circumferential/elliptical incision around the fistula opening, entire length of the track is dissected until the internal orifice. Care should be taken to safeguard carotids, jugular vein, hypoglossal nerve, glossopharyngeal nerve and spinal accessory nerve. Entire track should be excised.

A Fig. 5.12A

Fig. 5.13A

Neck

B Fig. 5.13B

Figs 5.13A and B: Branchial fistula is usually operated using two transverse parallel incisions with step ladder dissection (Courtesy: Dr Ganesh Pai, MCh) xx Step ladder dissection is done using two parallel incisions one below at lower part another above at upper part of the neck, will make dissection easier and complete.

PHARYNGEAL POUCH (ZENKER'S) xx It is a protrusion of mucosa through Killian’s dehiscence, a weak area of the posterior pharyngeal wall between thyropharyngeus (oblique fibres) and cricopharyngeus (transverse fibres) of the inferior constrictor muscle of the pharynx. xx Thyropharyngeus is supplied by pharyngeal plexus from cranial accessory nerve. Cricopharyngeus is supplied by external laryngeal nerve. xx Pharyngeal pouch is a pulsion diverticulum. It starts in the midline of posterior pharyngeal wall. Once it expands and reaches the vertebra, it deviates towards left side of the neck because of resistance of vertebra. xx Imperfect relaxation of the cricopharyngeus increases the pressure in the pharynx, mainly during swallowing which leads to protrusion of mucosa through the Killian’s dehiscence causing pharyngeal pouch. xx The protrusion is usually towards left. Stages Small diverticulum pointing towards vertebra. It is asymptomatic and incidentally diagnosed by barium meal X-ray. Foreign body sensation in pharynx may be present. ™™ Large, globular diverticulum with vertical mouth/opening causing regurgitation, violent cough, dysphagia, respiratory infection. Regurgitation is more after meals and while turning the neck.

Fig. 5.14: Pharyngeal pouch (Zenker’s diverticulum).

Problems in pharyngeal pouch ™™ ™™ ™™ ™™ ™™

Progressive dysphagia Respiratory problems like pneumonia, and lung abscess Abscess in the neck due to infection in the pouch Weight loss and cachexia Carcinoma may develop in the pouch rarely

Differential Diagnosis xx xx xx xx xx

Branchial cyst. Cold abscess in the neck. Lymph cyst. Haemangioma neck. Other causes of dysphagia like carcinoma, webs and stricture.

™™

xx Large pouch which is visible in the neck as a globular swelling often tender, smooth and soft. Swelling is below the level of the thyroid cartilage and behind sternocleidomastoid muscle and can be emptied on pressure. Opening of the pouch is not vertical but horizontal. They present with dysphagia, features of respiratory infection like pneumonia and lung abscess, weight loss and cachexia. Pouch may itself get infected and may form an abscess. Often the pouch may descend downward and enter the superior mediastinum. Gurgling sound in the neck is observed.

Clinical Features xx Pain, dysphagia, recurrent respiratory infection, swelling in the neck on the left side which is smooth, soft and tender. xx Regurgitation during night while turning neck, smooth, soft, tender swelling in the posterior triangle of the left side of the neck; typical gurgling noise while swallowing—are typical features. It is common in males. xx Swelling is deep to sternocleidomastoid muscle below the level of thyroid cartilage; initially soft and emptying; impulse on coughing may be evident unless opening of the pouch is blocked due to recurrent inflammation. xx Halitosis from decayed food in the pouch is not uncommon. Dyspnoea and change in voice can also occur.

There is only one degree difference between hot water and steam.

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Endoscopic minimally invasive technique

xx xx xx xx

xx Dohlman’s approach – Pouch is excised using double lipped endoscopy. Cautery or laser is used. It is quicker procedure with shorter duration of anaesthesia; with faster recovery. xx Stapling of the diverticula.

Barium swallow—lateral view shows pharyngeal pouch. Chest X-ray shows pneumonia. CT neck is very useful. Indirect laryngoscopy may show pooling of saliva in pyriform fossa.

Note:

Friedrich Albert von Zenker (1851) was a German physician and pathologist. Zenker’s pharyngeal pouch; Zenker’s muscle degeneration; Zenker’s peroneal nerve paralysis.

LARYNGOCELE xx It is a unilateral narrow necked, air-containing diverticulum resulting from herniation of laryngeal mucosa. xx It occurs in professional trumpet players, glass blowers and in people with chronic cough. xx Laryngocoele is an abnormal dilatation of the appendage of the laryngeal ventricle of Morgagni forming an airsac lined with pseudostratified ciliated, columnar epithelium (air-filled dilated saccule). Laryngeal ventricle of Morgagni is an elliptical recess between false and true vocal cords. Anterosuperior blind pouch of it is called as appendage of the ventricle which normally communicates with the laryngeal ventricle through a normal stalk. xx It can be congenital or acquired (common). It may be often associated with laryngeal carcinoma. Fig. 5.15: Barium study showing pharyngeal pouch. Note:

Oesophagoscopy should be gentle or avoided as scope may enter the friable pharyngeal pouch and can cause perforation and life threatening mediastinitis.

Treatment

Types a. External: It is situated in the anterior third of the laryngeal ventricle, between the false cords and thyroid cartilage, herniates through the thyrohyoid membrane where it is pierced by superior laryngeal nerve (25%). b. Internal: Confined within the larynx, presents as a distention of false cords (30%). c. Combined (45%).

Antibiotics and nutritional support initially.

Surgery Indications for surgery ™™

Progressive symptoms; recurrent aspirations; persistent dysphagia.

xx Diverticulectomy with cricopharyngeal myotomy: It is done in large lesion. After general anaesthesia, oesophagoscope is passed and pouch is packed with acriflavine gauze. Nasogastric tube is passed under vision through the oesophagus. Oblique or horizontal incision in the neck is made; sternocleidomastoid muscle is cut; diverticula is excised; oesophagopharyngeal wall is closed after doing cricopharyngeal myotomy (Circular muscle fibers are cut at posterior midline without opening the mucosa) is done to relieve the spasm; drain is placed in the neck; nasogastric tube is kept in situ for 7 days. xx Inversion or diverticulopxey are other procedures. Complications of surgery ™™ ™™ ™™ ™™ ™™

Infection, either mediastinitis or lung infection (Pneumonia or lung abscess) Pharyngeal fistula Abscess in the neck Oesophageal stenosis and recurrence Recurrent laryngeal nerve palsy.

Fig. 5.16: Laryngocele.

Clinical Features xx Swelling in the neck in relation to larynx, adjacent to thyrohyoid membrane which is smooth, soft, resonant and is more prominent while blowing, coughing and Valsalva manoeuvre. xx It moves upwords during swallowing with expansile impulse on coughing. xx Infection is quite common in the sac of laryngocele, leading to the blockade of opening of the sac causing an abscess. xx Pus often may be discharged into the pharynx repeatedly. xx Hoarseness and cough, sudden dyspnoea is often evident.

Neck Diagnosis Clinical features, X-ray neck, laryngoscopy, CT scan.

Treatment External laryngocoele: Excision through neck incision. Neck of the sac should be ligated. Thyrohyoid membrane is repaired using 3 zero nonabsorbable polypropylenes sutures. Internal laryngocoele: Marsupialisation, with the help of laryngoscope. Complications of surgery for laryngocele

A

™™ ™™ ™™ ™™ ™™

Laryngeal oedema causing airway obstruction Subcutaneous emphysema Laryngocutaneous fistula Injury to superior / internal laryngeal nerve Recurrence

CYSTIC HYGROMA (Cavernous Lymphangioma) xx It is a cystic swelling due to sequestration of a portion of

B

jugular lymph sac from the lymphatic system, during the developmental period in utero. xx Present at birth and so may cause obstructed labour. Occasionally present in early infancy. xx Lymphatics fail to communicate to venous system; abnormal budding of lymphatics is seen. xx Often it is associated with Turner’s, Down’s, Klinefelter syndromes and trisomy 18 and 13. xx It is also called as hydrocoele of the neck. xx Cyst will not communicate with normal lymphatics and so existing lymph gets absorbed and cyst will be filled with clear watery mucous derived from endothelial lining of the cyst wall. Cyst even though is subcutaneous; it commonly extends into deeper planes across many anatomical planes and barriers. Cyst is multilocular. Often extension may occur across two or more lymphatic regions; example—involvement of both neck and axilla. xx Lymphangioma circumscripta (5 cm) and lymphangioma ab agne (reticulate pattern) are different variants. For detail refer chapter ‘Swelling’. Sites

C Figs 5.17A to C: Typical laryngocoele in the neck which becomes prominent after blowing. X-rays (AP and lateral) show radiolucent air in the neck. xx If large, causes obstruction to larynx. xx Sudden compression and asphyxia can occur when it is infected. xx Bryce sign: In combined laryngocele, neck mass when compressed from outside will cause hissing sound of air escaping into the larynx.

1. Posterior triangle of the neck—75%—most common site. Eventually may extend upwards in the neck 2. Axilla—20% 3. Cheek 4. Tongue—lymphangiogenetic macroglossia 5. Groin 6. Mediastinum 7. Often multiple sites

Pathology xx It contains aggregation of cysts looking like soap bubbles. Cysts have mosaic appearance with larger cysts near the surface and

One-third of congenital torticollis is due to sternomastoid tumour and two-third due to abnormal position in utero which recovers spontaneously in a few weeks. — Kenneth F Hulbert

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SRB's Manual of Surgery xx When it causes respiratory obstruction, aspiration and tracheostomy is done. xx Under proper antibiotics coverage, drainage of abscess is done. Later sac is excised. xx Preoperative injection of sclerosants (OK–432, PICIBANIL recently used) and later once fibrosis develops excision of entire aggregation of cysts. In olden days injecting boiling water into the cyst as a sclerosant used to be popular. OK– 432 is an inactive strain of group A Streptococcus pyogenes. Pure ethanol, interferon α 2a, doxyclycline are other sclerosants often used. Complications ™™ ™™ ™™ ™™ ™™

Fig. 5.18: Cystic hygroma in newborn baby. smaller cysts in the deeper planes. Each cyst contains clear lymph with endothelial lining. Fluid does not coagulate.

Clinical Features xx Swelling is present at birth in the posterior triangle of neck causing obstructed labour. xx Swelling is smooth, soft, fluctuant (cystic), partially compres­sible, brilliantly transilluminant. It is not reducible completely. xx During crying swelling often increases in size. xx Disfigurement of face of the child which is more worrying factor for the parents.

Respiratory distress Infection → Abscess → Septicaemia Surgery itself may cause torrential haemorrhage Chylous fistula, chylothorax Recurrence of cyst – 15%

LUDWIG’S ANGINA xx It is an inflammatory oedema of submandibular region and floor of the mouth, commonly due to streptococcal infection. xx It causes diffuse swelling and brawny oedema of the submandibular region. It is common in severely ill and in advanced malignancy, causing trismus, laryngeal oedema. Extension of infection into parapharyn­geal space may lead to dreaded internal jugular vein thrombosis. xx As the infection is deep to the deep fascia in a closed fascial plane, it spreads very fast causing dangerous complications. Precipitating factors ™™ ™™ ™™ ™™ ™™ ™™

Caries teeth Oral or other malignancy Submandibular salivary infection/calculi Chemotherapy Chronic diseases like diabetes mellitus Cachexia of any cause

™™

Brawny oedema/diffuse swelling of submandibular and submental region Intraoral oedema in floor of the mouth Putrid halitosis Severe toxicity Dyspnoea, dysphagia May cause laryngeal oedema, septicaemia, extension of sepsis into other spaces in the neck

Special features

™™ ™™ ™™ ™™ ™™

Fig. 5.19: Cystic hygroma. xx Swelling may rapidly increase in size causing respiratory obstruction—dangerous sign. xx It may get infected forming an abscess which is a tender, warm, soft swelling. It may cause septicaemia which may be life threatening. xx Rupture with lymph ooze can occur.

Treatment xx Aspiration of the contents. Later once the sac or capsule gets thickened by fibrous tissue, it is excised. xx Care should be taken to have meticulous dissection across all planes including deeper muscular one to clear entire cyst wall; otherwise recurrence will occur.

Fig. 5.20: Typical Ludwing’s angina.

Neck Clinical Features xx xx xx xx

Fever, toxicity, diffuse swelling, dysphagia, dyspnoea, trismus. Intraoral oedema is common. Brawny swelling in submandibular region. Putrid halitosis, drooling of saliva, earache.

Treatment xx Antibiotics, IV fluids. xx Decompression of the submandibular region is done, by

making a deep incision extending into the deep fascia and also cutting both the mylohyoid muscles. Either it is left open and delayed suturing is done (better option) or it is loosely sutured.

xx Erosion into the internal carotid artery causing torrential bleeding. xx Septicaemia.

Treatment xx Under G/A, drainage is done by making incision (deep incision) between angle of the mandible and hyoid bone. Early drainage is needed. xx Antibiotics are given. xx Causative pathology should be addressed.

RETROPHARYNGEAL ABSCESS Surgical Anatomy The wall of the pharynx has got 5 layers. Mucosa, submucosa, pharyngobasilar fascia, muscular layer (contains 3 constrictors and stylo, salpingo, palato­pharyngeus muscles) and buccopharyngeal fascia covers outer part of constrictors and extends over buccinator. Buccopharyngeal fascia is adherent to prevertebral fascia posteriorly in the midline. Retropharyngeal lymph nodes are located between buccopharyngeal fascia and prevertebral fascia in paramedian (eccentric) position (not midline).

Types xx Acute. xx Chronic.

Fig. 5.21: Incision for draining Ludwig’s angina.

Complications Laryngeal oedema and respiratory distress, may require tracheostomy ™™ Septicaemia ™™ Extension of infection into parapharyngeal space ™™

PARAPHARYNGEAL ABSCESS xx It is infection of pharyngomaxillary space. xx This is a cone-shaped space; base is formed by the base of skull; apex is formed by the greater cornu of hyoid bone; medial wall by the superior constrictor; lateral wall is formed by the lateral pterygoid, angle of mandible and below by submandibular salivary gland. xx Usually, infection arises from the tonsils, after tonsillectomy and from the submandibular space.

Clinical Features xx It causes diffuse swelling in the upper neck, trismus, fever, toxicity. xx Swelling lies behind the posterior pillar with oedema of soft palate.

Complications xx Thrombosis of internal jugular vein.

Fig. 5.22: Note acute and chronic retropharyngeal abscess. Normal anatomy is also shown. Acute is eccentric and is due to suppuration of retropharyngeal lymph nodes. Chronic is central, midline and is due to tuberculosis of the cervical vertebra.

It is better to aim at good things and miss it , than to aim at a bad thing and hit it.

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Investigations

xx It is infection and suppuration of retropharyngeal lymph nodes due to staphylococci or streptococci organisms. xx Commonly from tonsils or pharynx. xx Common in infants and children.

X-ray spine, chest X-ray, ESR, MRI of cervical spine are essential investigations.

Clinical Features

xx Antitubercular drugs. xx Drainage of the abscess should be done through neck approach (never intraoral approach). xx Decompression of the vertebra and stabilisation is also often required.

xx It presents as lateral (paramedian, eccentric) smooth, tender swelling in the pharynx with dysphagia, dyspnoea, cough, toxic features and neck rigidity. xx Diagnosis is obvious on proper clinical examination.

Treatment xx Antibiotics intravenously. xx Drainage is done usually through per oral incision under careful general anaesthesia. Only occasionally drainage may be done through a neck incision. Pus should be sent for culture.

Chronic Retropharyngeal Abscess

Treatment

SUBHYOID BURSITIS (Retrohyoid Bursa/Boyer’s Bursa) xx Subhyoid bursa is space between posterior surface of the body of hyoid bone and thyrohyoid membrane. It lessens friction between these two structures during swallowing. xx Due to constant friction inflammatory fluid collects in the bursa leading to bursitis, which presents like a horizontally placed midline swelling between lower part of the hyoid bone and thyrohyoid membrane. \

xx It is invariably due to tuberculosis of cervical spine. xx Abscess is in the midline behind the prevertebral fascia. xx There is destruction of the body of the vertebra due to tuberculosis.

Clinical Features xx It is midline swelling in the posterior pharyngeal wall, which is smooth and nontender. xx Features of tuberculosis of cervical spine will be observed. xx Often abscess may point in the neck in relation to sternomastoid. xx Neurological manifestations may occur in severe disease.

Fig. 5.24: Sagittal and front view showing location and relation of subhyoid bursa.

Features xx Smooth, soft, cystic, fluctuant, nontransilluminating swelling which moves upwards with deglutition but not while protruding the tongue out. xx It should be differentiated from thyroglossal cyst and prelaryngeal lymph nodes. xx It contains turbid fluid often may get infected to make the swelling tender or to form an abscess. xx Treatment: Excision under general anaesthesia.

CAROTID BODY TUMOUR (Potato Tumour, Chemodectoma, Nonchromaffin Paraganglioma) Fig. 5.23: X-ray neck showing retropharyngeal abscess with tuberculosis lesion involving the C2 cervical spine (Courtesy: Dr Navin Chandra Shetty, MD, Radiologist, Professor and Head, Department of Radiodiagnosis, KMC, Mangaluru).

xx It arises from the carotid body, which is located at the bifurcation of the common carotid artery. xx Carotid is derived from neural crest which is essential for adaptation in fluctuation in the O2, CO2 and pH.

Neck xx Carotid body tumour can be sporadic (75%); familial (20%, common in young, can be multiple); or hyperplastic (5%) which is associated with the chronic hypoxia seen in high altitude (5,000 feet from sea level), COPD, cyanotic heart disease. xx The tumour is situated in the adventitia of the artery. xx They are benign or locally malignant tumours (10%), but in 20% cases spread can occur to the regional lymph nodes and lungs. xx Blood supply to the tumour is from ascending pharyngeal artery and external carotid artery. Tumour does not secrete epinephrine or any endocrine substances. Blood supply comes through Meyer’s ligament on the posteromedial wall of the carotid at bifurcation. xx Pathologically, it is well-encapsulated, hard creamy yellowish tumour with dense fibrous tissue. Carotid body tumour cells are not hormonally active. xx Histologically cells are arranged in a classical pseudoalveolar pattern known as cell ball – Zellballen. It contains type I chief cells with catecholamine granules and type II sustentacular cells without granules.

xx Swelling (75%) in the carotid region of the neck which is smooth, firm, pulsatile (transmitted pulsation—due to pulsatile carotid vessel overlying its surface) and moves only side to side but not in vertical direction (Fontaine sign). xx It can often compress over oesophagus and larynx. xx Headache, neck pain (35%), dysphagia, and syncope are other presentations. xx 10% may present with cranial nerve palsy (hypoglossal, glossopharyngeal, recurrent laryngeal or spinal accessory) or sympathetic chain; so present as pain, tongue deviation towards same side while protruding, dysphagia, unilateral vocal cord palsy, hoarseness of voice, drooping shoulder and Horner’s syndrome. xx Features of transient ischaemic attacks due to com­pression over the carotids, “carotid body syncope.” xx Thrill may be felt and bruit may be heard. xx It is located at the level of hyoid bone deep to anterior edge of the sternomastoid muscle in anterior triangle, vertically placed, round, firm ‘potato’ like swelling. xx Often tumour may extend into the cranial cavity along the internal carotid artery as dumbbell tumour. Sites where dumbbell tumours are seen ™™ ™™ ™™

Parotid tumour Spinal cord tumour Carotid body tumour

™™ ™™ ™™

Type I: Localised, easily resectable (26%) Type II: Adherent, partially surrounding the carotids (46%) Type III: Adherent, encased carotids completely (27%)

Shamblin classification of carotid body tumor

Investigations Fig. 5.25: Carotid body tumour—note the site and location. Splaying of the carotid is common. Carotid body ™™ ™™ ™™ ™™

™™ ™™

Normal carotid body is 3–5 mm sized, 15 mg weight, flat brownish nodule in the adventitious of common carotid artery It consists of chief cells (contains catecholamine granules) and supportive cells Its nerve supply is from Hering nerve, a branch Glossopharyngeal nerve These chemoreceptors are sensitive to changes in pH and temperature in the body especially in hypoxia, help in autoregulation of respiration and circulation Carotid body hyperplasia can occur in people residing in high altitudes who are exposed to chronic hypoxia Other chemoreceptors in the body are—aortic bodies in the arch of aorta; glomus jugular in the bulb of the internal jugular vein; glomus intravagale in relation to ganglion nodosum of the vagus nerve and others like pulmonary (near pulmonary artery) and myocardial (near coronary artery origin) receptors

xx Doppler. xx Angiogram to see the ‘tumour blush’—DSA. Widening/splaying of the carotid artery with tumour blush in an angiogram is called as Lyre sign. xx CT scan, MRI, MR angiography. xx MIBG scan in useful in multiple familial and functioning tumours (they are smaller in size); in nonfunctioning tumours pentetreotide scan using radiolabeled somatostatin analogue is used. No FNAC, No trucut biopsy, No partial excision.

Differential Diagnosis xx xx xx xx

Carotid artery aneurysm. Soft tissue tumour (Sarcoma). Lymph node enlargement. Neurofibroma of the vagus nerve presents as swelling in the carotid triangle in the region of thyroid as vertically placed, oval, hard swelling. On palpation of the swelling, patient often develops bradycardia and dry cough. It does not move with deglutition and has only transverse mobility. As the tumour lies behind the carotid it can stretch the carotid in front causing transmitted pulsation.

Clinical Features (0.5%—Incidence)

Treatment

xx Usually unilateral; 5% bilateral. xx More common in middle age. Common in females.

xx If it is small, then it can be excised easily as the tumour is situated in the adventitia.

Happiness is a direction not a destination.

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SRB's Manual of Surgery xx When it is large, as commonly observed, complete excision has to be done followed by placing a vascular graft. xx During resection a temporary shunt (diversion of blood) is placed between common carotid below and internal carotid above to safeguard cerebral perfusion; external carotid artery is ligated. Venous or prosthetic graft is placed between common carotid and internal carotid arteries. xx Carotid body tumour is not radiosensitive (contro­versial).

Features xx xx xx xx xx

Restricted neck movements. Chin pointing towards opposite side. Squint. Features relevant of the causes. Treatment: The cause is treated.

Complications of the Surgery xx Bleeding. xx Blockage of common carotid artery, leading to contralateral side hemiplegia (3%). This can be prevented by stenting the common carotid artery towards internal carotid artery and is done during surgical excision of the tumour. xx Cranial nerve injury X and XI (40%). Injury to vagus causes hoarseness of voice; injury to superior laryngeal nerve alters the pitch of voice. Cystic swellings in the neck ™™ ™™ ™™ ™™ ™™ ™™ ™™

Cold abscess Cystic hygroma Branchial cyst Thyroglossal cyst Laryngocoele Pharyngeal pouch Subhyoid bursa

TORTICOLLIS (Wry Neck) It is turning of the neck to one side with chin pointing towards opposite side.

Fig. 5.27: Torticollis (right-sided) with chin towards opposite side.

STERNOMASTOID TUMOUR It is due to birth injury to the sternomastoid muscle. It is a misnomer. It is not a tumour.

Causes xx Sternomastoid tumour. xx Trauma—spinal injury, disc prolapse, spondy­losis. xx Inflammatory: Lymphadenitis either tuberculous or suppurative; tuberculosis of cervical spine. xx Spasmodic—due to spasm of sternomastoid muscle of same side or spasm of posterior cervical muscles of opposite side. xx Reflex. xx Rheumatic—after exposure to cold/draught. xx Burns—causing contracture. xx Ocular causes. xx Compensatory due to scoliosis.

Fig. 5.28: Sternomastoid tumour—typical location.

Pathogenesis

Fig. 5.26: Boy having right-sided torticollis.

xx During child birth, injury to the sternomastoid muscle causes haematoma in the muscle which gets organised to form sternomastoid tumour. xx Common in breech delivery.

Neck Features xx It is seen in infants of 3–4 weeks age. xx Swelling of about 2 cm size, in the sternomastoid muscle which is smooth, hard, nontender and adherent to the muscle—in the middle part. xx Chin pointing towards opposite side. Head to­wards same side (Scoliosis capitis). xx In later age groups it causes hemifacial atrophy due to less blood supply as a result of compression of the external carotid artery by sternomastoid tumour and due to kinking by position of neck. Distance between the outer canthus of eye to angle of mouth is reduced, with less arched eyebrow, flat or less filled cheek and flat nose compared to opposite side. xx Compensatory cervical scoliosis. xx Compensatory squint. xx Differential diagnosis: Other causes for torticollis.

Treatment xx Division of the lower end of the sternomastoid muscle or excision of the muscle. Both sternal and clavicular heads of sternocleidomastoid muscle should be divided under general anaesthesia using horizontal incision. One should not injure IJV, carotid, vagus, spinal accessory nerve. Additional all fibrous bands are also cut. Usually over correction is done. Physiotherapy exercise and toricollis harness is used for 6–12 months. xx Exercise and active stimulation of muscles in early cases. Differential diagnosis for neck lymph node enlargement • Tuberculous lymphadenitis • HIV infection • Chronic lymphatic leukaemia • Infectious mononucleosis • Actinomycosis • Toxoplasmosis

• Secondaries in lymph nodes • Lymphomas • Nonspecific lymphadenitis • Sarcoidosis • Brucellosis

Fig. 5.29: Lymphoma neck involving both sides. Lymphomas are smooth, nontender, firm/India rubber consistency.

Fig. 5.30: Swelling in the neck well-localised. Note the scar of previous biopsy/excision. It could be lymph node enlargement due to lymphoma or tuberculosis.

TUBERCULOUS LYMPHADENITIS Causative organism: Mycobacterium tuberculosis (not M. bovis).

Site xx Common in neck lymph nodes. xx Common in upper deep cervical (jugulodigastric—54%)

lymph nodes. xx Next common is posterior triangle lymph nodes (22%). xx Disease can also occur in other lymph nodes like, axillary lymph nodes, para-aortic lymph nodes, mesenteric lymph nodes, inguinal lymph nodes. xx Disease may be associated with HIV infection, lymphomas.

A Fig. 5.31A

Direction is a matter of fact; ideas are matter of opinion.

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SRB's Manual of Surgery its surface; from here infection spreads into jugulodigastric nodes (anterior triangle nodes) then to other nodes. Infection reach lymph node first into subcapsular space/sinus then to lymph node cortex which contains plenty of lymph follicles. Matting is due to periadenitis involving subcapsular sinus/space of lymph node. In children infection to neck node can come from either tonsils or adenoids or both. When it occurs from adenoids, lymph nodes in posterior triangle are involved through retropharyngeal lymphatics. xx It may be associated with pulmonary tuberculosis or renal tuberculosis. Through blood infection reaches medullary cords of lymph node and so medulla of lymph node. xx Rarely spread can occur from tuberculous lesion of the apex of lung through suprapleural Sibson’s fascia/membrane to supraclavicular nodes.

B

Stages of tuberculous lymphadenitis 1. 2. 3. 4. 5.

Stage of infection, and lymphadenitis Stage of periadenitis with matting Stage of caseating necrosis and cold abscess formation Stage of formation of collar stud abscess Stage of formation of sinus which discharges yellowish caseating material

xx Often fibrosis and calcification can occur with or without treatment.

Gross Pathology xx Firm, matted, lymph node, with cut section showing yellowish caseating material.

C Figs 5.31B and C

Figs 5.31A to C: Cold abscess due to caseating tuberculous lymph­ adenitis in neck. Collar stud abscess in the neck. Tuberculous sinus formation after drainage.

Mode of Infection xx Usually through the tonsils, occasionally through blood from lungs. Tonsillar infection shows multiple tubercles on

Fig. 5.32: Tuberculous lymphadenitis—cut section of the specimen. Note the yellowish caseating material with periadenitis (matting). Caseating type is more common than hyperplastic type.

Fig. 5.33: Stages of tuberculous lymphadenitis (Hogarth’s Rake).

Neck Types   1. Hyperplastic

  2. Caseating

 a. 20% common

——

a. 80% common

 b. Discrete, firm or hard

——

b. Matted due to periadenitis

 c. Occurs in the cortex of lymph node

——

c. Involves medulla with periadenitis

 d. Host immunity is good

——

d. Body resistance is not adequate

 e. Drugs act better

——

e. Drugs do not reach in proper concentration and may not be effective

 f. Drug resistance is uncommon

——

f. Drug resistance is common

 g. No cold abscess or sinus formation

——

g. Cold abscess or sinus are common

 h. Blood spread

——

h. Spread from tonsils

Microscopic Features

Differential Diagnosis

xx Epithelioid cells with caseating material are seen along with Langhans type of giant cells.

1. 2. 3. 4. 5. 6. 7.

Clinical types Acute type: Seen in infants and early childhood below 5 years Hyperplastic type: Lymphoid hyperplasia is typical; it is seen in patients with good resistance; hard discrete mobile lymph nodes; 15–20% common ™™ Caseating type: 75–80% common; matted nodes often with cold abscess; poor body resistance; seen in young adults ™™ Atrophic type: Rare type; seen in elderly; small lymph nodes but caseating type with atrophied nodes ™™ ™™

Nonspecific lymphadenitis. Lymphomas, and chronic lymphatic leukaemia. Secondaries in the neck. Branchial cyst mimics cold abscess. Lymph cyst mimics cold abscess. HIV with lymph node involvement. When there is discharging sinus—actinomycosis. Cold abscess

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Clinical Features xx Swelling in the neck which is firm, matted. xx Cold abscess is soft, smooth, nontender, fluctuant, without involvement of the skin. It is not warm. xx As a result of increased pressure, cold abscess ruptures out of the deep fascia to form collar stud abscess which is adherent to the overlying skin. xx Once collar stud abscess bursts open, discharging sinus is formed. It can be multiple, wide open mouth, often undermined, nonmobile with bluish color around the edge. It is usually not indurated. xx Tonsils may be studded with tubercles and so clinically should always be examined. xx Associated pulmonary tuberculosis should also be looked for. In 20% cases of tuberculous lymphadenitis, there may be associated pulmonary tuberculosis or it may be a primary focus. xx Cervical spine is examined for tuber­culosis. xx Axillary nodes, when involved, is due to retrograde lymphatic spread from neck nodes or blood spread. xx Inguinal lymph nodes are involved occasionally through blood. xx Bluish hyperpigmented involved overlying skin is called as scrofuloderma. xx Tuberculous pus with caseating cheesy creamy material is infective as it contains multiplying organisms. xx Atypical mycobacterial tuberculosis can occur occasionally. Such disease may be resistant to drug therapy. xx Sinus may persist due to—fibrosis, calcification, secondary infection, inadequate reach of drug to maintain optimum concentration in caseation.

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Deep-to-deep fascia No evidence of signs of inflammation Not warm, nontender, smooth, soft and fluctuant, non-transilluminating Not adherent to skin (skin is free); no redness Contains cheesy caseating material It is seen in caseating tuberculous lymphadenitis due to caseation necrosis It may form collar stud abscess and later sinus FNAC, AFB, culture are useful investigations Differential diagnosis are branchial cyst, lymph cyst Treated by –– Antituberculous drugs –– ‘Zig-zag’ aspiration by wide bore needle in nondependent area to prevent sinus formation –– Drainage using nondependent incision; later closure of the wound without placing a drain

Investigations xx Haematocrit, ESR, peripheral smear. xx FNAC of lymph node and smear for AFB and culture. FNAC is very useful but not as superior as open node biopsy. False negative, false positive results and altering the node architecture, and so eventual need of open biopsy are the problems. Epithelioid cells (modified histiocytes/macrophages) are diagnostic. Langhans giant cells, lymphocytes, plasma cells are other features. xx Open biopsy when FNAC is inconclusive. Open biopsy is more reliable for tuberculosis (and also in lymphoma; but it is contraindicated in node secondaries); entire node ideally two nodes if possible has to be taken intact; one in formalin for pathology, other in normal saline for microbiology (AFB).

It takes 5 years to learn when to operate, and 20 years to learn when not to.

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SRB's Manual of Surgery xx HIV test (ELISA and western blot). xx Löwenstein–Jensen media is used for culture which takes 6 weeks to give result; so selenite media is often used which shows growth in 5 days. xx Mantoux test may be useful; but not very reliable. xx Chest X-ray to look for pulmonary tuberculosis. xx Polymerase chain reaction (PCR) is very useful method.

1. There is no local response to drugs or 2. When sinus persists. It is done by raising skin flaps and removing all caseating material and lymph nodes. Care is taken not to injure major structures. xx Excision of the sinus track is often essential when sinus develops.

Treatment xx Drugs Antitubercular drugs has to be started: xx Rifampicin 450 mg OD on empty stomach. It is bactericidal. It discolours urine red. It is also hepatotoxic. xx INH: 300 mg OD. It is bactericidal. It causes into­lerance of GIT, Neuritis, Hepatitis (INH). xx Ethambutol 800 mg OD. It is bacteriostatic. It causes GIT intolerance, retrobulbar neuritis (green colour blindness). xx Pyrazinamide 1500 mg OD (or 750 mg BD). It is bactericidal. It is hepatotoxic, also causes hyper­uricaemia and increases psychosis. Duration of treatment is usually 6–9 months. xx Aspiration When there is cold abscess, initially it is aspirated. [Wide bore needle is introduced into the cold abscess in a nondependent site along a “Z” track (in zig-zag pathway) so as to prevent sinus formation].

Fig. 5.35: Tuberculous sinus excision with excision of diseased lymph nodes.

COLD ABSCESS Cold abscess is common in neck. It can also occur in groin, intercostal space, loin or any site where tuberculous caseating material with cheesy content can get collected and localised.

Sites of Origin A

B

Cold abscess may originate from tuberculosis of spine (thoracic or cervical spines), lymph node, internal organs, bone, etc.

In the Neck xx Tuberculous lymphadenitis is common cause. Here cold

abscess is commonly seen in anterior triangle.

xx Tuberculosis of cervical spine is also an important cause.

Commonly here cold abscess occurs in posterior triangle. Caseating material from the cervical spine collects in front of the vertebra behind the prevertebral fascia which eventually ruptures either anteriorly or posteriorly. C Figs 5.34A to C: Typical cold abscess in the neck in which pus is aspirated. Pus should be sent for cytology (for epithelioid cells), staining (Ziehl-Neelsen—AFB) and culture. xx Incision and drainage If it recurs, then it should be drained. Drainage is done through a nondependent incision. After draining the caseating material, wound is closed without placing a drain. xx Surgical removal Surgical removal of tubercular lymph nodes are indicated, when

 Anterior rupture allows passage of caseating material below

and behind the prevertebral fascia reaching superior mediastinum; laterally behind the prevertebral fascia and carotid sheath to form cold abscess in posterior triangle; in midline upper part, protruding forwards from behind the prevertebral fascia in midline presenting as chronic retropharyngeal abscess; in midline lower part protrudes into oesophagus; caseation runs along the axillary sheath and neurovascular plane to reach axilla and arm to cause cold abscess in axilla and arm/cubital fossa.  Posterior rupture occurs towards spinal canal facilitating the passage of caseation along the cervical nerves towards posterior triangle and brachial plexus and so axilla and arm.

Neck Treatment xx xx xx xx

Antituberculous drugs. Nondependent aspiration or drainage of the cold abscess. Excision of the diseased neck nodes. Immobilization of cervical spine by plaster jacket/collar for 4 months. Cervical spine fusion by open surgical method, if diseased spine is unstable.

SECONDARIES IN NECK LYMPH NODES Levels in Neck Nodes (Memorial Sloan— Kettering Cancer Centre Levelling of Neck Nodes)

Fig. 5.36: Tuberculous cold abscess and sinus in the neck.

Features xx It is common in young but can occur in any age group. Equal incidence in both sexes. xx Swelling in the neck, which is smooth, nontender, soft, fluctuant, nontransilluminating, with restricted mobility but is not adherent to skin. xx Neck pain, neck rigidity, restricted movements of cervical spine in case of cervical spine tuberculosis. With every change of position and often when patient is seated he supports his head with his hands and forearm—Rust’s sign (Jan N Rust, Surgeon, Poland). xx Evening fever, loss of weight and appetite, anaemia. xx Features of systemic disease, if present like of pulmonary tuberculosis—cough, haemoptysis. xx Matted lymph nodes adjacent to cold abscess may be palpable. xx Oral cavity, tonsils, chest should be examined. xx Raised ESR, positive Mantoux test, anaemia, lymphocytosis, chest X-ray may show pulmonary tuberculosis, aspiration of cold abscess (FNAC) to see microscopically epithelioid cells. Acid-fast bacilli may be identified from the aspirated fluid using Ziehl-Neelsen stain. xx X-ray neck in case of cervical spine tuberculosis to identify reduced joint space, vertebral destruction, soft tissue shadow. xx MRI of cervical spine, US/CT scan neck are needed to confirm the anatomical location, number of lesions.

Level I—Submental (Ia) and submandibular (Ib) lymph nodes. Level II—Lymph nodes in upper deep cervical region. (It extends from base of skull to hyoid bone and from lateral margin of sternohyoid to posterior margin of sternomastoid muscle). Level IIa is below and in front of the line of the spinal accessory nerve in the upper part; IIb is above and posterior. Level III—Lymph nodes in middle cervical region (from hyoid bone to omohyoid muscle or cricothyroid membrane). Level IV—Lymph nodes in lower cervical region (from omohyoid muscle/cricothyroid membrane to clavicle). Level V—Lymph nodes in posterior triangle including supraclavicular region from posterior border of sternocleidomastoid muscle to anterior border of trapezius muscle. Level Va is above the line of spinal accessory nerve in the lower part; Vb is below. Level VI—Lymph nodes in the midline neck—pretracheal and prelaryngeal from hyoid bone above to suprasternal notch below, medial border of carotid sheath on either side. Level VII—Lymph nodes in the mediastinum. inferior to suprasternal notch to innominate artery below. Note:

•

•

Level II and V are now subdivided into Level IIa/Level IIb and Level Va/ Level Vb; depending whether these nodes are above the level (Level IIb/Level Va) of the spinal accessory nerve or below (Level IIa/Level Vb). Level I node from oral cavity, lip, salivary gland, skin; level II node from oral cavity, oropharynx, nasopharynx, salivary gland; level III node from oral cavity, oropharynx, hypopharynx, larynx, thyroid; level IV node from oropharynx, hypopharynx, larynx, thyroid, cervical oesophagus; level V node from nasopharynx, scalp, GIT, breast, lungs.

Sequelae of Cold Abscess xx Secondary infection of the cold abscess making it tender. xx Formation of collar stud abscess, once pressure increases inside the cold abscess which will give way through the deep fascia to reach the subcutaneous plane to get adherent to skin. xx Sinus formation. xx Spread of disease to multiple lymph nodes and other organs.

Differential Diagnosis xx Branchial cyst and other cystic swellings in neck. xx Secondaries in neck lymph nodes. xx Secondaries in cervical spine.

Fig. 5.37: Levels of neck nodes.

Happiness is when what you think, what you say, and what you do are in harmony —Mahatma Gandhi. 

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SRB's Manual of Surgery Common sites of primary ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Oral cavity, tongue, tonsils Salivary glands Pharynx—nasopharynx Larynx Oesophagus Lungs GIT Thyroid

• • • •

Soft palate, retromolar region, nasopharynx, hypopharynx posterior and lateral oropharynx can involve retropharyngeal nodes. Nasopharyngeal carcinoma spreads to level II-V, retro and parapharyngeal nodes. 15% of secondaries are from infraclavicular primaries—lung, pancreas, oesophagus, stomach, breast, ovaries, testis, prostate. Nodal spread below the lower border of cricoid (level IV and V; Lower) carries poor prognosis compared to nodes above cricoid (Upper).

Branchiogenic Carcinoma

xx It is commonly from squamous cell carcinoma, but can also

be from adenocarcinoma or melanoma. xx Squamous cell carcinoma is mainly from oral cavity, pharynx.

It is a primary squamous cell carcinoma which is uncommon, arising from remnants of branchial cleft or arch. It is a differential diagnosis for secondaries in neck. It is common in men. It is common near the area of carotid bifurcation. Histologically it contains malignant squamous cells with lymphoid tissues around. It spreads to lymph nodes and can infiltrate into adjacent soft tissues. Treatment: Wide excision.

Features of Secondaries in Neck xx Common in adult/elderly male (Male to female ratio is 4:1),

A

B

C

D

presents as painless rapidly increasing localised swelling in the neck. xx Nodular surface and hard in consistency, often fixed when it is advanced. Fungation, ulceration, haemorrhage can occur in advanced disease. xx Secondaries from papillary carcinoma of thyroid can be soft, cystic with brownish black fluid.

Figs 5.38A to D: Typical secondaries in the neck. Note the different levels involved in different patients. Note the skin involvement and sinus formation in few photos. xx Adenocarcinoma is usually from GIT, commonly involving

left supraclavicular lymph nodes. xx Breast, lungs, abdominal viscera are other areas where

primary may cause secondaries in neck which should be examined when suspected. Note:

• • •

• • •

20% of metastatic squamous cell carcinoma is from aerodigestive tract. Source of primary from head and neck region usually have frequency like this—nasopharynx, tonsil, base of tongue, thyroid, larynx, floor of the mouth, cheek, palate, pyriform fossa. Non-head and neck source of primary are bronchus, oesophagus, breast, stomach. Histologically it is SCC (80%) or non-SCC. In non-SCC it may be poorly differentiated carcinoma (10-15%), adenocarcinoma (5-10%) or others like melanoma, poorly differentiated neoplasm (5%). In poorly differentiated neoplasm immunohistochemistry/immunoperoxidase staining, electron microscopy and chromosome analysis are needed to rule out lymphoma, neuroendocrine tumours, undifferentiated sarcomas. 3 years after treatment of one primary, if recurrence occur it is called as new primary in aerodigestive tract. Lower lip, tongue, soft palate and supraglottis can cause bilateral secondaries in neck.

A

B

Figs. 5.39A and B: (A) Typical secondaries in the neck—well localized, hard swelling which is fixed to the sternocleidomastoid muscle; (B) Secondaries in the neck nodes from laryngeal carcinoma. xx Secondaries can infiltrate into carotids, sterno­mas­toid,

posterior vertebral muscles, spinal accessory nerve (shrugging of shoulder is affected), hypo­glossal nerve (tongue will deviate towards the same side), cervical sympathetic chain (Horner’s syndrome). xx Secondaries spread into adjacent soft tissues and also to the skin causing fungation and ulceration. Often because of tumour necrosis, softer area develops in the hard node. Skin fold prominence due to infiltration of the platysma is typical. xx In advanced cases tumour may infiltrate into the major vessels like carotids, or branches of external carotid artery causing torrential haemorrhage. xx Dysphagia, dyspnoea, haemoptysis, hoarseness of voice, ear pain, deafness are other features depen­ding on the primary site.

Neck Types of Secondaries in the Neck 1. Secondaries in the Neck with Known Primary xx Here secondaries are present and primary has been identified clinically in the oral cavity, pharynx, larynx, thyroid or other areas. xx Biopsy from the primary and FNAC from the secondaries are done. xx Primary is treated accordingly either by curative radiotherapy or by surgery (wide excision). xx Secondaries, when mobile are treated by radical lymph node block dissection in the neck.

2. Secondaries in the Neck with Clinically Unidentified Primary

Fig. 5. 40: Fungating secondaries in the neck—terminal illness. ™™ ™™ ™™ ™™ ™™ ™™ ™™

Hoarseness—carcinoma larynx, thyroid Dysphagia—carcinoma posterior 1/3rd of the tongue, pharynx, oesophagus Haemoptysis, cough, dyspnoea—carcinoma lung Ear pain, deafness—nasopharyngeal carcinoma Spinal accessory nerve—shrugging of shoulder is difficult Hypoglossal nerve—tongue deviates to same side with wasting Sympathetic chain—Horner’s syndrome with miosis, anhidrosis, upper eyelid droop (pseudoptosis), enophthalmos, loss of spinociliary reflex

xx Hard neck lymph nodes are the secondaries, but primary has not been identified clinically. xx FNAC of the neck node is done and secondaries is confirmed. Then search for the primary is done by various investigations. They are: a. Panendoscopy  Nasopharyngoscopy.  Direct laryngoscopy.  Oesophagoscopy.  Bronchoscopy—if needed only. b. Blind biopsies are taken from fossa of Rosenmüller, lateral wall of pharynx, pyriform fossa, tonsillar bed, base of tongue, subglottic region (larynx). It is called as surveill­ance biopsy and is done to reveal unknown primary in 15% of cases of secondaries in neck. If this surveillance biopsy is negative, then ipsilateral tonsillectomy may be needed. Presently bilateral tonsillectomy is recommended. c. FNAC of thyroid and suspected areas. d. CT scan.

Once the biopsy confirms the primary, it is treated either by surgery or by curative radiotherapy. Secondaries in the neck is treated by radical neck dissection.

3. Secondaries in the Neck with an Occult Primary A

B Figs 5.41A and B: Advanced secondary carcinoma neck with ulceration and fungation.

It is biopsy (FNAC) proven cancer of the neck node, which even after a complete clinical and radiological workup (that includes physical examination, CT scan, oesophgoscopy, laryngoscopy, bronchoscopy and multiple surveillance biopsies) reveals or yields no primary demonstrable lesion. Occult primary sites which can cause secondaries in neck ™™ ™™ ™™ ™™ ™™ ™™ ™™

Fig. 5.42: Secondaries in neck with nodules and ulceration. Note the deviation of tongue towards same side due to hypoglossal nerve involvement.

Fossa of Rosenmüller Lateral wall of pharynx Posterior third of the tongue Thyroid Paranasal sinuses Bronchus Oesophagus

Histologically secondaries in neck with occult primary may be of squamous cell carcinoma or of nonsquamous cell carcinoma, i.e. adenocarcinoma/poorly differentiated tumours (lymphoma/sarcoma/ melanoma). In upper and midcervical region 80% are due to squamous cell carcinomas. In lower cervical and supraclavicular region 40% can be adenocarcinomas. Common sites of primary here (for adenocarcinoma) are thyroid, breast, gastrointestinal tract, salivary glands, lungs, prostate and kidney.

Example isn’t the best way to teach, it’s the only way.

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SRB's Manual of Surgery xx Here secondaries in the neck lymph nodes are confirmed by FNAC, but primary has not been revealed clinically and by any available investigations. xx When all the investigations mentioned above are done, do not show any evidence of primary, only then it is called as occult primary. xx Primary tumor is not identified at the time when definitive therapy has started. xx 70% of occult nodes occur in jugulodigastric group. xx Differential diagnosis for secondary with occult primary is lymphoma and primary branchiogenic carcinoma. xx Reasons for primary lesion being occult—too small a primary to detect; possibility of immunological spontaneous regression of primary and inability of the present diagnostic tools to detect the primary. xx FNAC is the tool to confirm the occult secondary. If FNAC is inconclusive, only then open biopsy (incision/excision) is done to confirm. Open biopsy helps in high suspects of lymphomas or poorly differentiated carcinomas. It facilitates tissue study, immunohistochemistry, and special stains. Many studies prove that risk of seedling, survival and prognosis will not alter by open biopsy. But at present it is proposed only when FNAC fails or special methods are mandatory to type the disease. After open biopsy, frozen section confirmation and immediate neck dissection has to be done. xx Immunoperoxidase staining can be done in FNAC specimen or formalin fixed paraffin tissue using monoclonal or polyclonal antibodies. Immunoperoxidase is the most commonly used tool. It is mainly useful in lymphomas/neuroendocrine tumours. Electron microscopy is superior to immunohistochemistry as ultrastructure details can be assessed. But it is costly. Chromosomal analysis for tumour specific genes is used in B, T and germ cell lymphomas. xx Initially the secondaries in the neck are treated by radical neck dissection, then regular follow-up is done (at three monthly intervals) until the primary reveals. xx Once primary is revealed it is confirmed by biopsy and treated accordingly, either by curative radio­therapy or by wide excision depending on location of revealed primary. xx This type is usually less aggressive and has got better prognosis.

Fig. 5.43: Diagrammatic representation of neck lymph node staging in secondaries.

Nodal staging in secondaries Nx—nodes cannot be assessed N0—no nodal metastasis N1—single node same side 110/min

Ectopic. Pulsus paradoxus. Wide pulse pressure. Multiple extrasystoles. Paroxysmal atrial tachycardia. Paroxysmal atrial fibrillation. Persistent atrial fibrillation (not responsive to digoxin).

3. Myopathy xx Weakness of proximal muscles occurs, i.e. the front thigh muscles, arm muscles. xx Weakness is more when muscle contracts isomet­rically either while getting down steps, or lifting a full bucket. xx Often when it is severe it resembles myasthenia gravis. Once hyperthyroidism is controlled, recovery occurs.

4. Pretibial Myxoedema It is a misnomer. Pretibial myxoedema is often a feature of primary thyrotoxicosis:

xx Is usually bilateral, symmetrical, shiny, red thickened dry skin with coarse hair in the feet and ankles. xx In severe cases skin of entire leg below the knee with involvement of foot and ankle can occur. xx It is due to deposition of myxomatous tissues (mucin-like deposits) in skin and subcutaneous plane. Glycosaminoglycans (hyaluronic acid) deposition occurs. xx It might or might not regress completely after treatment for toxicity. xx It is associated with exophthalmos with high levels of thyroid stimulating antibodies. xx Skin becomes cyanotic when cold. Skin changes in toxicosis are called as thyroid dermopathy. They include—pretibial myxoedema, pruritus, palmar erythema, hair thinning, Dupuytren’s contracture (fascial).

5. Thyroid Acropachy Thyroid acropachy is clubbing of fingers and toes in primary thyrotoxicosis. Hypertrophic pulmonary osteoarthropathy can develop.

6. Others xx Thrill is felt in the upper pole of the thyroid and also bruit on auscultation. It is because in upper pole, superior thyroid artery enters the gland superficially and so thrill and bruit can easily be felt. In lower pole inferior thyroid artery enters the gland from deeper plane and so thrill cannot be felt. xx Hepatosplenomegaly.

TOXIC NODULE xx Is a solitary overactive nodule. xx There is an autonomous hypertrophy and hyper­plasia of a

part of the gland where there is a nodule. [It is not due to thyroid stimulating antibody (Ts Ab)]. xx Here high levels of circulating thyroid hormones suppress TSH secretion and so, normal thyroid tissue surrounding the nodule is itself suppressed and inactive. xx Once patient becomes euthyroid by drugs, surgery (hemithyroidectomy) or radioactive iodine therapy I131 in a therapeutic dose of 5 m curie is given orally. xx Because normal gland is inactive, radioactive iodine affects only the autonomous nodule, allowing the normal gland to remain intact which later gets activated and functions normally. xx Drugs are used initially, only for a temporary period to make the patient euthyroid.

Investigations for Thyrotoxicosis xx Thyroid function tests Serum T3 and T4 levels are very high. TSH is very low or undetectable. Sometimes, only T3 level is increased and is called as T3 toxicosis. Here in T3 toxicosis, free T3 estimation is important. Free T3, free T4 estimation is done as total T3 and total T4 levels will vary depending on the amount of thyroid binding globulin (TBG). TBG will be raised in pregnancy, cirrhosis, hyperestrogenism. It decreases in conditions with high androgen level, hypoproteinaemia, acromegaly. Free T3 and free T4 are measured using radioimmunoassay. Normal free T3 is 3.0–9.0 pmol/L; free T4 is 8–26 nmol/L. Type of disease

T4

T3

TSH

Conventional hyperthyroidism

Increased

Increased

Undetectable

T3 hyperthyroidism

→

Increased

Undetectable

Subclinical hyperthyroidism

→

→

Undetectable

You don’t drown by falling in the water; you drown by staying there —Edwin Louis Cole

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SRB's Manual of Surgery xx Radioisotope study  Radioisotope study by I131 (Diagnostic dose -5 microcurie is used) shows more uptake, i.e. hot nodules or hot areas. This is very useful in auto­nomous solitary toxic nodule.  I131 causes more irradiation and its half-life is 8 days. So intravenous 99mTc is used for diagnostic purpose. 99m technetium has become isotope of choice for diagnosis as it is cheap, less radiation, scanning is done 20 minutes after IV injection of 99m Tc (half-life is 6 hours). Drawback of technetium is that it concentrates in carcinoma, so forms hot nodule (means hot nodule need not be benign in Tc scanning). Warm nodule in Tc scan may appear as cold nodule in RAI scan and so is called as discordant nodule which suggests malignancy. If radioactive iodine is used for diagnosis, then I123 is better as it has got short half-life (13 hours).  Autonomous toxic nodule is absolute indication for radioisotope scan in toxic thyroid showing hot nodule. Graves disease shows diffuse overactivity (uniform); hypofunctioning cold nodule in Graves disease could be malignant. In secondary thyrotoxicosis internodular tissues are overactive (heterogeneous activity). Non-hyperthyroid toxicosis shows increased uptake in non-thyroid areas of toxicity like struma ovarii in pelvis. xx TRH estimation. xx ECG—to look for cardiac involvement; if required opinion

from cardiologists is taken and cardiac problems are managed. xx Total count and neutrophil count are very essential base-line investigations before starting antithyroid drugs (as it may cause agranulocytosis). xx Thyroid antibodies estimation—antithyroglobulin antibody, TSH receptor antibody, antithyroid peroxidase (anti-TPO) antibody.

1. ANTITHYROID DRUGS Indications for antithyroid drugs: ™™ Toxicity in pregnant women—Propylthiouracil is preferred ™™ Toxicity in children and young adults ™™ Before thyroidectomy, to make the patient euthyroid ™™ Soon after starting radioactive I131 therapy for 6 to 12 weeks (Effects of radiotherapy start only in 6 to 12 weeks)

a. Carbimazole:  Is the commonest drug used.  Dose is 5–10 mg, exactly 8th hourly (as T1/2 of carbimazole

is 8 hours). Each tablet is 5 mg.

 Usually given for 12–18 months.  Peak plasma level should be maintained in optimum concentra-

tion to have a proper benefit.

 Often tri-iodothyronine 20 microgram 4 times daily or

Thyroxine 0.1 mg daily are given in combination with antithyroid drugs, to prevent iatrogenic thyroid insufficiency or to prevent the increase in size of goitre.  It acts by blocking thyroid hormone synthesis. Carbimazole also suppresses the autoimmune process in thyroid in Grave’s disease.  Carbimazole causes fever, rashes, arthralgia, myalgia, neuritis, lymph node enlargement, liver cell dysfunction, psychosis, agranulocytosis.

b. Methimazole:  Methimazole is more potent and longer-acting than propylthi-

ouracil  Once a day dose; 20 – 40 mg.  Methimazole is not used in 1st trimester pregnancy as it may

cause cloacal and scalp abnormalities.

c. Propyl thiouracil:  It acts by blocking thyroid hormone synthesis as well as by

blocking peripheral conversion of T4 to T3.

Treatment for Thyrotoxicosis Medical ™™ Relief of symptoms: –– Beta blockers-propranolol, nadolol, metoprolol - Control cardiovascular and hyperadrenergic manifestations. Bronchial Asthma, heart Block, Cardiac failure are contraindications. –– Calcium channel blockers (e.g. verapamil and diltiazem) can be used –– Oral rehydration ™™ Antithyroid pharmacotherapy. It prevents the– –– Release of hormones: Lugol’s iodine (potassium iodide and iodine) 10 drops – 3 times day –– Production of thyroxine : Methimazole – long-acting, 20–40 mg OD; more potent; but not used in pregnancy; Tapazole 5 or 10 mg tablets. Carbimazole 20 mg three times a day up to 120 mg. Propyl thiouracil (PTU) 100 mg three times a day, used in pregnancy; 50 mg tablets –– Action of thyroxine on end organs: Propranolol – 40 mg tid up to 120–160 mg; PTU –– Production of antibodies: Steroids, methimazole, carbimazole; Levels of TSH R Ab fall and permanent cure may occur in 50% of patients in Grave’s Radioactive iodine therapy Thyroidectomy

 It also decreases the thyroid autoantibody levels.  It can be given for hyperthyroidism in children and in preg-

nancy, lactation.

 Dose is 200 mg 8th hourly.  Propylthiouracil is reserved for use in thyroid storm, first

trimester of pregnancy, and methimazole allergy or intolerance.

 PTU causes dose unrelated hepatoxicity; agranulocytosis;

antineutrophilic cytoplasmic antibody in 20% of patients after long-term usage.

Note:

• • • • • • • •

Dose of antithyroid drug are titrated every 4 weeks until thyroid functions (TSH and FT4) normalize. Toxic multinodular goiter and toxic adenoma will not go into remission. Reduction of thyroid hormones occurs in 2–8 weeks In Graves, once patient is rendered euthyroid options include use of ATD for 12–18 weeks or definitive treatment with RAI or surgery. After cessation of therapy, close follow up for 3–6 months is required to detect relapse. 40% experience recurrence in 1 year in Grave’s; in such situation RAI or surgery has to be considered. Antithyroid drugs are continued during and after surgery, for 7–10 days. It has to be given after starting radioactive iodine therapy for 6 weeks to 12 weeks. Response to treatment and possibility of relapse in primary thyrotoxicosis can be assessed by studying HLA status and TsAb level.

Thyroid d. Propranolol:

Complications of antithyroid drugs

xx It is a beta blocker, which is used as an antithyroid drug. xx Dose is 40 mg tid. xx It reduces the cardiac problems and also blocks the peripheral conversion of T4 to T3, as it is the T3 which is the principle active agent in periphery. xx Contraindications are bronchial asthma, heart block, cardiac failure. xx Long-acting nadolol 160 mg OD can also be used.

Note:



– –

e. Lugol’s iodine (5% iodine + 10% potassium iodide):



It decreases the vascularity of the gland and makes it more firm and easier to handle during surgery. Dose is 10–30 drops/day (minims) for 10 days prior to surgery. Potassium iodide tablets 60 mg tid also can be given instead of Lugol’s iodine. But its use at present is disqualified. (One minim = one drop. One ml = 16 drops).

Note:

•

Lugol’s iodine prevents the release of hormone from the gland – thyroid constipation. After 2 weeks, effect of Lugol’s iodine is lost causing thyroid escape from iodine control.

f. Block and replacement therapy:

It is giving high dose of carbimazole to inhibit T3 and T4 production completely with a maintenance dose of 0.1 mg of L thyroxine. It reduces the iatrogenic thyroid insufficiency.

g. High dose of glucocorticoids.

It impair peripheral conversion of T4 to T3 and also lowers serum TSH level; hence can be used in severe resistant/refractory cases.

Advantages of Antithyroid Drugs xx Avoids surgery and its complications. xx Avoids radioiodine therapy. xx Clinical improvement occurs in 2 weeks. Biochemical

improvement occurs in 6 weeks.

™™ ™™ ™™ ™™ ™™

Allergic reactions Agranulocytosis Severe hepatitis more often with PTU Polyarthritis Lupus vasculitis

They are dose-related in methimazole but not so in PTU. Patients with agranulocytosis usually present with fever and pharyngitis. – After the drug is stopped, granulocyte counts usually start to rise within several days but may not normalize for 10–14 days. – Granulocyte colony-stimulating factor (G-CSF) appears to accelerate recovery in patients with a bone marrow aspiration showing a granulocyte-to-erythrocyte ratio of 1:2 or greater than 0.5.

Other Drugs Which are Effective (But not Commonly Used) xx Potassium perchlorate inhibits iodide transport. xx Iopanoic acid 1 gram/day is used in severe unresponsive cases. It inhibits peripheral conversion of T4 to T3. xx Lithium carbonate 300 mg 6th hourly. xx Guanethidine 40 mg orally 6th hourly. xx Reserpine 5 mg IM. xx Dexamethasone 2 mg orally 6th hourly. It inhibits peripheral conversion of T4 to T3. It is used in thyroid storm. xx 2 mg IV propranolol in thyroid storm. xx Cholestyramine - Decreases reabsorption of thyroid hormones from the enterohepatic circulation; used orally at the rate of 4g four times daily, in combination with methimazole or PTU.

2. SURGERY

 Remission is confirmed by TsAb assessment, which will

be low.

 Permanent remission rate is very less in adults and is

20% in children.

Indications ™™

Disadvantages

™™

xx Prolonged course of treatment for 18 months, and in spite

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of this, cannot predict the remission or relapse. Relapse rate is 40%. Large gland/severe disease/abnormal TSH receptor antibodies (TSH-RAbs) are likely to lead into high recurrence. xx Size of swelling may not regress. xx It may lead to agranulocytosis and thrombocytopenia, liver damage, hair loss (except propranolol). Sore throat is the earliest presentation of agranulo­cytosis. If it is so, drug is stopped, total count is done. If it is less, agranulocytosis is confirmed. High doses of injection benzyl penicillin 10–20 lac, 6th hourly, IV is started to prevent infection. If required, blood transfusion is done. Patient usually recovers by this. To control toxicity, Tab. Propranolol 40 mg tid is started. Rarely they need bone marrow transplantation.

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Failure of drug treatment in primary thyrotoxicosis in young patients Autonomous toxic nodule Nodular toxic goitre When malignancy cannot be ruled out Graves disease in children, Graves with nodules Need for antithyroid drugs for more than 2 years Large goitre, substernal/intrathoracic goitre Pressure symptoms, Graves ophthalmopathy Amiodarone-induced thyrotoxicosis.

xx It is now observed that total thyroidectomy may be a better

option in Graves disease to achieve lowest relapse rate and successful stabilisation of thyroid ophthalmopathy as it clears the antigenic focus in thyroid completely. xx Surgery done is subtotal thyroidectomy—Both lobes with isthmus are removed and a tissue equivalent to pulp of finger is retained at lower pole of the gland on both sides (5–8 grams).

Dissatisfaction and discouragement are not caused by the absence of things but the absence of vision.

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SRB's Manual of Surgery xx In autonomous nodule, hemithyroidectomy is done. Here

Radioactive iodine therapy (RAIT)

entire lateral lobe with whole of isthmus is removed.

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Advantages xx Rapid and high cure rate. xx Problems of radioiodine therapy are avoided. xx Surgery provides tissue for biopsy, removes the occult

malignant foci. xx Surgery is better option for ophthalmopathy due to thyrotoxicosis. xx It is the option for women planning for child. xx Coexisting parathyroid carcinoma can be removed. xx For intrathoracic retrosternal toxic thyroid, surgery is the choice. Antithyroid drugs and also radioactive iodine may increase the goitre size. Patient should be made euthyroid before doing sur­gery. (It should be confirmed by repeated estima­tion of serum T3, T4 and TSH levels).

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Disadvantages xx Recurrent thyrotoxicosis (5%). xx Thyroid insufficiency (20–45%). It is revealed in 6 months

to 2 years and is confirmed by estimating T3, T4 and TSH levels. Hypothyroidism is better than recurrent thyrotoxicosis. It is treated by tab. L-thyroxine 0.1 mg daily (OD) for life-long—usually given in morning. xx Complications of thyroid surgery itself.

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3. RADIOIODINE THERAPY ™™

Indications ™™ ™™ ™™

Primary thyrotoxicosis In autonomous toxic nodule In recurrent thyrotoxicosis

xx Radioiodine destroys the cells and causes the complete

ablation of thyroid gland.

xx Usual dose is 5 to 10 millicurie, or 160 microcurie/gm of

thyroid.

xx Patient is made euthyroid using antithyroid drugs; drug is

discontinued for 5 days; I131 300–600 MBq is given orally; antithyroid drugs are started after 7 days and are continued for 8 weeks. In 30% of patients, additional 2 or 3 doses may be required. xx It takes 3 months to get full response and so until then, the patient has to take antithyroid drugs. Often additional one or two doses of radioiodine are required to have complete ablation. Eventually they go for hypothyroidism and so require main­tenance dose of L-thyroxine 0.1 mg daily. xx To give therapeutic dose, patient should be admitted and isolated for 7 days (Half-life) to prevent irradiation. It is given orally soon after getting from the manufacturer without much delay to have optimal efficacy.

Preferred therapy for hyperthyroidism as it avoids surgery, prolonged drug therapy with >90% cure rate; but proper follow up is needed and facilities should be available (not much centers are having) Administered orally as a single dose in capsule or liquid form 131I (Sodium iodide-131) Causes fibrosis and destruction of the thyroid over weeks to many months causing hypothyroidism It is effective, safe, and does not require hospitalization Given orally as a single dose in a capsule or liquid form - I131 is given (6 to 8 milliCuries) Very few adverse effects as no other tissue absorbs RAI But the effect is less rapid than drugs or thyroidectomy Goal is to make the patient hypothyroid Not recommended with patients of severe ophthalmopathy Not advisable in chronic smokers Pregnancy, breastfeeding, and recent lactation are contraindications A gland-specific dosage based on the estimated weight of the gland and the 24-hour uptake is used. The dose of I131 administered is 75–200 µCi/g of estimated thyroid tissue divided by the percent of 123I uptake in 24 hours No evidence indicates that radioactive iodine therapy for hyperthyroidism causes the development of thyroid carcinoma or results in increased mortality for any other form of cancer, including leukemia Radioactive iodine should be avoided in children younger than 5 years. In children 5 to 10 years old, 131 I therapy is acceptable if the calculated activity of administered131 I is less than 10 mCi. In children older than 10 years of age, radioactive iodine therapy is acceptable if the activity is greater than 150 µCi/g of thyroid tissue Radioactive iodine should never be administered to pregnant women, because it can cross the placenta and ablate the fetus’s thyroid, resulting in hypothyroidism

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Risk of hyperparathyroidism may be there after RAI therapy Similarly, breastfeeding is a contraindication, as the radioisotope is secreted in breast milk. Women will continue to receive increased radiation to the breast from radioactive iodine for few months after ceasing lactation ™™ It is standard practice to check for pregnancy before starting radioactive iodine therapy and to recommend to the patient not become pregnant for at least 6–12 months after the treatment. No excess fetal malformations or increased miscarriage rates have been found in women previously treated with radioactive iodine for hyperthyroidism. ™™ ™™

TOXIC THYROID IN PREGNANCY xx Radioiodine therapy is absolutely contraindicated in pregnancy (High-risk to foetus). xx Antithyroid drugs can be administered carefully. xx But, the problem here is that both TSH and antithyroid drugs cross the placental barrier and baby born may be hypothyroid and goitrous. xx Propylthiouracil is preferred in pregnancy. xx Subtotal/total thyroidectomy can be done in second trimester.

Thyroid TOXIC THYROID IN CHILDREN xx Radioiodine therapy is absolutely contraindicated in children. xx Recurrence rate is also very high after surgery. xx So proposed treatment is initially antithyroid drugs are given until adolescent period and then subtotal thyroidectomy is done.

Note:

• • •

THYROCARDIAC Severe cardiac damage (partly or wholly) resulting from hyperthyroi­ dism, usually secondary type, requires proper opinion from cardiologists and treatment with propranolol. Subtotal thyroidectomy is the treatment.

IN A PATIENT WITH THYROTOXICOSIS, WITH RECENT ONSET OF PROPTOSIS xx Early thyroi­dectomy has to be avoided, because early surgery may precipitate malignant exophthalmos. Here the patient has to be treated initially with antithyroid drugs and if required with steroids, until the proptosis has remained static for six months. Then subtotal thyroidectomy is done. xx Since half-life of L-thyroxine is 7 days, propranolol and antithyroid drugs have to be continued for 7 days after thyroidectomy. xx T3 Thyrotoxicosis should be suspected if the clinical picture is suggestive of toxicosis, but routine tests for thyroid function are within normal range.

RADIOACTIVE IODINE It is used both as a diagnostic as well as a therapeutic agent. 1. I131—is used for radioactive iodine therapy (β-rays are used). 2. I123—is used for diagnostic studies (γ-rays are used). For diagnostic purpose I123 is given orally in empty stomach on previous day (dose—5 micro curie; T1/2 (half-life) of I123 is 13 hours and so it is suitable for diagnostic purpose). Patient should not take L-thyroxine for 6 weeks prior to radioisotope study.

Presently I131 is also becoming popular as a diagnostic tool. For treating malignancy β-rays are more used than γ-rays. Technetium 99 scan is used for diagnostic purpose at present as it is effective and faster (in 20 minutes). IV administration is used. Radioisotope study is done to look for secondaries by doing whole body scanning (total body scinti­graphy). For diagnostic radioactive study Technetium 99 pertechnetate can also be used.

Therapeutic Uses 1. In primary thyrotoxicosis. 2. In autonomous toxic nodule, it is useful as remaining gland still will function adequately after radiotherapy (As during radio­therapy radioisotope will not be taken up by this retained normal gland as it is suppressed in the presence of toxic nodule which will function later adequately). 3. In follicular carcinoma of thyroid, after total thyroidectomy, if there are secondaries elsewhere in the body, as in bones or lungs, then radioiodine therapy is given. I131 is given as its half-life is 8 days. Patient should be isolated for this period and careful disposal of urine has to be done during this period. It is given orally in a dose of 5 millicuries (160 microcurie/g of thyroid).

Problems in Radioactive Iodine Therapy xx xx xx xx

Permanent thyroid failure with hypothyroidism. Effects will be seen only after 3 months. Ophthalmopathy and dermopathy will be worsened. It may induce hyperparathyroidism.

Dose of radioactive iodine Diagnostic • For thyroid-5-50 microcurie • For whole body iodine scan 5–10 millicurie in 72 hours

Note:

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If the patient is on T3 (60 µg/day) medication, the drug is stopped 10 days before radioisotope scan. Injection TRH, if given, radioisotope scan can be done in 24 hours.

xx Thyroid treats this I123 similar to inorganic I127. This I123 enters the thyroid from the circulation and gets incorporated into T3, T4 and later released into circulation as protein bound iodide (PBI). Normal value of PBI is 8 mgm%. xx Using Gieger Muller’s gamma ray counter, scanning of thyroid gland is done to visualize the gland. xx Hot area suggests more uptake, xx Warm area suggests normal uptake, xx Cold area suggests no uptake. I123 radioisotope can be safely used in children and pregnancy for diagnostic purpose only (5 micro­curie) as the dose is low. Indications for diagnostic radioactive iodine study Doubtful toxicity Ectopic thyroid Autonomous toxic nodule After total thyroidectomy, to look for secondaries in follicular carcinoma thyroid ™™ Retrosternal thyroid ™™ ™™ ™™ ™™

Therapeutic • Residual thyroid ablation—50 mCi • Bone secondaries from FCT— 100–120 mCi • Lung secondaries from FCT— 180 mCi

Contraindications for Radioactive Iodine Therapy xx Pregnancy/females desiring to have pregnancy within 1 year/ lactating mothers. xx Children, lactating women. Radioactive isotopes used in thyroid Isotopes

Route of administration

Half-life

Type of rays

I123

Oral

13 hr

γ rays

I125

Oral

60 days

γ rays

131

Oral

8 days

β, γ rays

132

I

Oral

2.3 hr

Tc 99 scan*

IV

6 hr

I

* Used mainly for malignancy in thyroid itself. It is sensitive, convenient, low radiation exposure, inexpensive, with good images but nonspecific and not used for therapy. Lithium is also used as isotope for diagnosis in thyroid diseases. Technetium is better to identify nonfunctioning secondaries.

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SRB's Manual of Surgery Note High dose of retinoic acid will make I131 to concen­trate in tumour cells (70 mg/daily for 2 weeks) ™™ Fertility should be avoided for 1 year after I131 therapy ™™ Avoid contrast CT in thyroid diseases as much as possible because I131 study in later period will be difficult ™™ MRI is ideal when radioiodine therapy is needed ™™

THYROID NEOPLASMS A. Benign Follicular adenoma can be – Colloid (do not have potential for microinvasion; commonest type); Fetal (microfollicular – has potential for microinvasion); Embryonal (atypical – has potential for microinvasion); Hurthle cell/oxyphil or oncocytic (has potential for microinvasion); hyalinising trabecular adenoma. Note:

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All adenomas are invariably follicular. Colloid adenoma is the commonest. The existence of papillary adenoma is doubtful; it is invariably a low-grade papillary carcinoma.

B. Malignant (Dunhill classification). a. Differentiated—80% 1. Papillary carcinoma (60%). 2. Follicular carcinoma (17%). 3. Papillofollicular carcinoma behaves like papillary carcinoma of thyroid. 4. Hurthle cell carcinoma behaves like folli­cular carcinoma. b. Undifferentiated—20% Anaplastic carcinoma (13%) c. Medullary carcinoma (6%) d. Malignant lymphoma (4%) e. Secondaries in thyroid (rare)—from colon, kidney, melanoma, breast.

Incidence and Spread xx Annual incidence of thyroid cancers is 3.7 per 1,00,000

population. It is common in females (3:1).

xx Papillary carcinoma mainly spreads through lymphatics;

follicular through blood; anaplastic through lymphatics and blood.

Aetiology of Thyroid Malignancy xx Radiation either external or radioiodine can cause papillary carcinoma thyroid. There is increased incidence of thyroid carcinoma among children following exposure to ionising radiation after the Chernobyl nuclear disaster in Ukraine in 1986; in children in Marshall island after atomic bomb testing.  Earlier irradiation was practised to head and neck region to treat benign conditions like tonsillitis, adenoids, thymus enlargement, acne vulgaris, haeman­giomas during first two decades of life. As a consequence papillary carcinoma of thyroid became common in these individuals. Radiotherapy received in adolescent period for Hodgkin’s lymphoma may predispose to papillary carcinoma. xx Pre-existing multinodular goitre. It turns into follicular carcinoma of thyroid.

xx Medullary carcinoma thyroid is often familial. xx Hashimoto’s thyroiditis may predispose to NHL/papillary carcinoma of thyroid. xx Familial. xx Elevated TSH is observed in papillary carcinoma of thyroid. xx Genetic—Cowden syndrome is differentiated thyroid carcinoma, carcinoma breast, multiple hamartomas. It is due to germ cell mutation of PTEN tumour suppressor gene. Oncogenes—C myc, C erb, C fos, Ras are associated thyroid neoplasms.

DIFFERENTIATED THYROID CARCINOMA (DTC) xx DTC is a spectrum of disease derived from follicular cells. Both papillary and follicular carcinomas are grouped under this. 90% of thyroid malignancies are differentiated one. Papillary (PTC), follicular (FTC) and Hurthle cell carcinomas are DTCs. Insular variety is poorly DTC having intermediate position between DTC and anaplastic; it can cause bone and lung spread; it is common in younger age group; p53 and p21 are negative; with 40% 10-year survival. xx AGES (Mayo Clinic, Hay); AMES (Lahey clinic); MACIS; Sloan Kettering scoring – are different scoring systems used for DTCs. Sloan Kettering scoring includes low, intermediate and high-risk groups. First three scoring systems have low- and high-risk groups. xx Papillary spreads through nodes; follicular through blood. FCT causes pulsatile vascular secondaries. xx Incidence of thyrotoxicosis in DTCs is 2%. xx Galectin – 3, RET/PTC rearrangements, CD44, leukocyte common antigen (LCA), cytokeratin are the probable tumour markers under evaluation. For indeterminate, FNAC molecular markers are used to identify RAS and BRAF mutations. xx TNM staging for DTCs are –  Tumour - T0 – no evidence of primary tumour; T1 - < 2 cm – (T1a < 1 cm; t1b 1–2 cm). T2- 2–4 cm. T3 - > 4 cm limited to thyroid or only minimally extrathyroid extension (to sternothyroid or soft tissue). T4a – invasion to subcutaneous tissue, larynx, trachea, oesophagus and recurrent laryngeal nerve; T4b – invasion to prevertebral fascia, carotid encasement or involvement of mediastinal vessels.  Regional nodes (central/lateral neck compartment/superior mediastinal) – Nx – regional nodes cannot be assessed. N0 – no nodes. N1a – spread to level VI (pre/paratracheal, prelaryngeal). N1b – neck nodal spread same or opposite or both sides or superior mediastinal nodes.  Metastases – Mx – metastases cannot be assessed. M0 – no distant spread. M1 – distant spread present.  Note: Age is included in staging which is an important factor. Postoperative AJCC staging for DTCs for predicting risk of death Age less than 45 years Stage I – Ant T, any N, M0; Stage II – any T, any N, M1. Age after 45 years Stage I – T1, N0, M0; Stage II – T2, N0, M0; Stage III – T3, N0, M0 or T1, N1a, N0; T2, N1a, M0; T3, N1a, M0 Stage IVA – T4a, N0, M0; T4a, N1a, M0; T1, N1b, M0; T2, N1b, M0; T3,N1b,M0; T4a, N1b, M0 Stage IVB – T4b, any N; M0 Stage IVC – Any T, any N, M1.

Thyroid American thyroid association for predicting the risk of recurrence Low risk—90% of patients ™™ T1–2 N0 M0 and absence of aggressive histology or vascular invasion ™™ Microscopic tumour clearance ™™ No spread to node/blood ™™ No capsular/vascular invasion ™™ Extrathyroid I131 uptake is not found ™™ 25-year mortality is 2% Intermediate risk ™™ T3 or tumour with aggressive histology or vascular invasion ™™ Microscopic perithyroid invasion ™™ Vascular invasion High-risk ™™ T4 or any T, N1 or M1 ™™ Incomplete tumour removal ™™ Macroscopic invasion ™™ Distant spread ™™ Extrathyroid bed I131 uptake present ™™ 25 years mortality is 46%

European Consensus Report defined three risk categories for DTC Very low risk Unifocal T1 (1 cm) or T2 N0 M0 or multifocal T1 N0 M0 High risk Any T3 and T4 or any T, N1, or any M1

Investigations xx US neck is essential investigation. It shows the nature, size, margin, echogenicity, vascularity, nodal status, invasion through thyroid capsule. Lymph node may show loss of hilus, round shape, hypoechogenicity, cystic changes and calcification, with increased peripheral vascularity. xx FNAC of the nodule (US-guided is ideal); it is very useful in PTC; but not much useful in FCT. FNAC of the lymph node is useful; thyroglobulin estimation of the lymph node aspirate is very useful. xx Functional status should be checked – T3, T4, TSH. TSH may be raised in PTC. xx MRI of neck if needed only; CT is not done as iodine contrast is not used; if needed, should be done as non-contrast CT.

Treatment xx Total thyroidectomy with either prophylactic (in T3 and T4 of T staging) or therapeutic (when involved sonologically or FNAC or frozen section [of node] wise) central cervical (compartment) node dissection (CCND). Prelaryngeal, pre and paratracheal, nodes above the level of innominate vein and up to carotids and hyoid bone are removed often may be with thymus (compartment). CCND provides accurate staging; treats micrometastases (90% in

PTC in central nodes) which may be often the cause for recurrence or persistence of disease; central nodes being primary nodes are commonly involved. It also provides accurate RAI dosing; lowers the postoperative serum thyroglobulin level which facilitates the accurate TG monitoring during follow up. Reoperation of CCND is technically difficult after total thyroidectomy as a separate sitting. But there is no oncological survival benefit and increased chances of postoperative hypoparathyroidism and recurrent laryngeal nerve injury. Lateral cervical node dissection (LCND. Nodes -IIA, III, IV and VB) is done only when it shows the evidence of involvement (by FNAC or US); there is no role for prophylactic LCND. xx Only hemithyroidectomy is done if tumour is 1 cm, extracapsular thyroid invasion or locoregional extension, high-risk group, unfavorable histological subtype (follicular, diffuse sclerosing, or tall cell-variant papillary cancer), multifocal disease; BRAF positive tumor in the specimen. Criteria for RAI are - TSH should be >30 mU/ml. L-Thyroxine replacement is stopped 3–4 weeks before radioiodine treatment; OR - in time being switch over to T3 80 mg/day and RAI in 7 days; OR - When L-thyroxine withdrawal is not advisable, TSH stimulation was achieved using Recombinant Human Thyrotropin (rhTSH) (0.9 mg IM one dose – 2 consecutive days; after 24 hours RAI given). Dose of I131 – usually – 3700 MBq (100 mCi); for metastases, it is 200 mCi. xx Suppression hormone therapy using high dose L thyroxine – dose is to make TSH level 50% of MTC patients. CEA >30 mg/ml indicates incurability by surgery; CEA >100 mg/ml suggests extensive nodal spread; raising CEA with stable calcitonin indicates dedifferentiation and poor prognosis. xx CT neck, chest, abdomen should be needed for metastatic work up. CT abdomen is also done for pheochromocytoma. xx Urinary metanephrine, VMA, (24 hours) should be done in suspected pheochromocytoma. xx Serum, calcium and parathormone (PTH) estimation for hyperparathyroidism. xx 111-Indium octreotide scanning is useful in detecting MCT (70% sensitivity). It is also useful in postoperative follow up to find out residual or metastatic disease. xx Genetic testing for ret mutations.

Treatment Surgery is the main therapeutic modality.

xx Total thyroidectomy with bilateral central node dissection and ipsilateral lateral neck dissection if primary tumour is > 1 cm or central nodes are positive. Positivity of central nodes is 81%. xx Opposite lateral neck node dissection is done if US neck shows opposite nodes or extensive ipsilateral neck nodes when present or bilateral primary tumours (multifocal/ bilateral).

Everything has its beauty but not everyone sees it.

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SRB's Manual of Surgery xx Thyroxine replacement/maintenance therapy 100ug morning before food daily, is needed. xx No role of suppressive hormone therapy or radioactive iodine therapy. xx External beam radiotherapy for residual tumour disease. xx Somatostatin/octreotide for diarrhoea. xx Adriamycin is the drug used as chemotherapy with limited results. xx If there is associated phaeochromocytoma, it should be treated surgically by adrenalectomy first and later only total thyroidectomy is done. xx All family members of the patient should be evaluated for serum calcitonin and if it is high they should undergo prophylactic total thyroidectomy (Can also be assessed by genetic evaluation). If there is positive RET proto-oncogene in MCT with MEN II A and familial MCT types, prophylactic total thyroidectomy is done at the age of 5 years. In positive RET proto-oncogene in MCT with MEN II B, prophylactic total thyroidectomy is done at the age of one year. xx MCT with associated parathyroid hyperplasia (30%) in MEN IIA, total thyroidectomy with central nodal dissection with total parathyroidectomy and autotransplantation of half of gland in sternomastoid or nondominant forearm brachioradialis muscle is done.

Other therapies xx External RT; Somatostatin analogues; Imatinib mesylate tyrosine kinase inhibitor; Chemotherapy–less success– adriamycin, capacetabine, 5 FU, irinotecan; newer targeted therapies.

Prognosis xx Sporadic MCT and MCT with MEN syndrome II are aggressive. xx Familial MCT not associated with MEN II syndrome has got better prognosis. xx Presence of nodal disease carries poor prognosis. xx Survival is overall good -10 years – 85%; depends on type, familial nature, association for MEN syndrome; status at the time of presentation – size, nodal status, distant spread. xx Incidence of recurrence is 50% in MCT.

Follow-up xx Serum calcitonin and CEA level. xx Imaging as needed – USG/CT neck and mediastinum. xx Recurrence in the neck should be treated with resurgery – exploration and disease clearance. External beam RT may be useful also. xx PET scan; MIBG scan are also useful. xx Follow-up for late onset pheochromocytoma or hyperparathyroidism should regularly be assessed annually.

Calcitonin xx It is a polypeptide of 32 amino acids. It is derived from ultimobranchial body. It is secreted from C cells of thyroid (parafollicular cells). xx It lowers the plasma calcium and phosphorus levels. It blocks the PTH-induced bone resorption. Calcium from the circulation is shunted into the bone. It increases the excretion of calcium, phosphorus, sodium and potassium. It rapidly lowers the serum calcium. xx Normally, it is less than 0.08 ng/L (undetectable).

xx It is increased in medullary carcinoma of thyroid. It is very good tumour marker for MCT. It confirms the relapse/metastases/ residual disease. Increased levels in family members confirm the genetic relation and such relatives should undergo prophylactic total thyroidectomy. xx Calcitonin level will further increase after injection of calcium 2 mg/kg or pentagastrin 0.5 µg/kg. xx In disease-free individual, after therapy for MCT calcitonin level decreases. xx Calcitonin as a therapeutic agent is used in hypercalcemia, Paget‘s disease, bone pain of neoplastic diseases, menopausal osteoporosis. Calcitonin (pork), 4 units/kg is given SC or IM three times a week. xx Salmon calcitonin SC/IM/nasal spray—50–400 units can be given three times a week or daily depending on need.

MALIGNANT LYMPHOMA xx It is NHL type. Occurs in a pre-existing Hashimoto’s thyroiditis (Not proved well). xx FNAC is useful to diagnose the condition (Often trucut biopsy). xx Chemotherapy and radiotherapy is the main treatment. xx Rarely total thyroidectomy is done to enhance the results.

HASHIMOTO’S THYROIDITIS (Struma Lymphomatosa) xx Also called as diffuse non-goitrous thyroiditis. xx It is an autoimmune thyroiditis—common in women (15 times more common). xx There is hyperplasia initially, then fibrosis, even­tually infiltration with plasma cells and lympho­cytic cells. xx Askanazy cells are typical (like Hurthle cells). xx The river Struma arises in Bulgaria and flows into Aegean Sea. Struma means goitre. Banks of this river are endemic area for goitre.

Features xx Painful, diffuse, enlargement of usually both lobes of thyroid which is firm, rubbery, tender and smooth (occa­sionally one lobe is involved). xx Initially they present with toxic features, but later, they manifest with features of hypothyroidism. Hyperplasia → Hyperthyroid—Hashitoxicosis → Euthyroid. Fibrosis → Hypothyroid. xx There may be hepatosplenomegaly, xx It is often associated with other autoimmune diseases. xx In 85% cases significant rise in the thyroid antibodies (microsomal, thyroglobulin, or colloid antibodies) is observed. xx Common in perimenopausal females. xx It can predispose to papillary carcinoma of thyroid. xx Often condition may be associated with or may predispose to malignant lymphoma. It is, at present, not well-proved.

Investigations FNAC, T3, T4, TSH. Thyroid antibodies assay. Usually ESR is very high (over 90 mm/hour).

Thyroid Treatment

Recent rapid increase in thyroid swelling is due to:

xx L-thyroxine therapy. xx Steroid therapy often is helpful. xx If goitre is large and causing discomfort, then subtotal thyroidectomy is done.

DE-QUERVAIN’S SUBACUTE GRANULOMATOUS THYROIDITIS It is due to viral aetiology either mumps or coxsackie viruses causing inflammatory response with infilt­ration of lymphocytes, neutrophils, multinucleated giant cells.

Previous MNG undergoing malignant transformation Haemorrhage into a nodule ™™ Anaplastic carcinoma of thyroid ™™ ™™

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Remember ™™ ™™ ™™ ™™

Features xx Painful diffuse, swelling in thyroid which is tender xx Commonly seen in females. xx Initially there is transient hyperthyroidism with high T3 and T4 but poor radioiodine uptake. xx FNAC is useful. xx It is usually a self-limiting disease. xx Prednisolone 20 mg for 7 days helps.

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RIEDEL’S THYROIDITIS (0.5% Common) xx A very rare benign entity wherein thyroid tissue is replaced by fibrous tissue which interestingly infiltrates the capsule into surrounding muscles, paratracheal tissues, carotid sheath. xx (‘Woody Thyroiditis’, ‘Ligneous Thyroiditis’). xx It is often associated with retroperitoneal and mediastinal fibrosis and sclerosing cholangitis. xx There is both intrathyroidal as well as extrathyroidal fibrosis. xx It also encroaches parathyroids and recurrent laryngeal nerves. xx It may be unilateral or bilateral.

Features xx Swelling with irregular surface, stony hard consistency, stridor, with positive Berry’s sign (absence/impalpable carotid pulsation); small goitre; common in males. xx Differential diagnosis: Anaplastic carcinoma of thyroid. xx Investigations:  T3, T4 may be low due to hypothyroidism.  Radioisotope scan will not show any uptake.  FNAC to rule out carcinoma.

Occasions wherein thyroid swelling may not move upwards with deglutition Anaplastic carcinoma thyroid—often Carcinoma thyroid with extensive local infiltration into soft tissues, trachea/larynx and posterior muscles ™™ Intrathoracic retrosternal extension with infiltration/impaction ™™ Riedel’s thyroiditis with encasement of trachea ™™ Massive thyroid wherein upward movement is difficult to observe and appreciate ™™ ™™

Narrowing of trachea is seen in: ™™ ™™ ™™ ™™

Scabbard trachea in longstanding MNG Retrosternal goitre Carcinoma of thyroid Riedel’s thyroiditis

THYROID INCIDENTALOMA

Treatment Isthmectomy is done to relieve compression on the airway. They require L-thyroxine replacement later, as hypothyroidism is common. xx High dose of steroid often used. xx Thyroidectomy is not necessary. Causes of dyspnoea/stridor in thyroid diseases ™™ ™™ ™™ ™™

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Goitre is enlargement of the thyroid gland Solitary nodule is single palpable nodule on clinical or sonological examination without palpable rest of the gland Dominant nodule is single nodule with palpable enlargement of the remaining thyroid gland Thyroid swelling is confirmed by its movement with deglutition due to attachment of enclosed pretracheal fascia to inferior constrictor muscle which is attached to trachea and cricoid cartilage and so moves with deglutition Berry’s ligament is condensed vascularised pretracheal fascia postero-supero-medially. It is important as it is close to recurrent laryngeal nerve Any thyroid swelling can be malignant unless proved otherwise Ultrasound neck, FNAC, estimation of T3, T4, TSH are essential investigations CT scan neck is needed in large goitre and fixed or malignant thyroid Radioisotope study I123 is done only in selected cases like borderline toxicity, ectopic thyroid, retrosternal goitre and after thyroidectomy in follicular carcinoma thyroid to see secondaries during follow-up period Normal thyroid gland is usually not palpable A rare entity called as black thyroid shows lipofuscin deposition in thyroid in a patient who is on longstanding tetracycline therapy which may interfere with thyroid function

Carcinoma thyroid infiltrating recurrent laryngeal nerve/trachea Large, long-standing goitre causing tracheomalacia Retrosternal goitre Congestive cardiac failure in thyrotoxicosis

Thyroid incidentaloma is defined as an unsuspected, asymptomatic thyroid lesion that is discovered on an imaging study or during an operation unrelated to the thyroid gland. Thyroid incidentalomas are most commonly detected on ultrasound, followed in frequency by CT scan and MRI, carotid duplex scanning and PET scan. The incidence of carcinoma in incidentaloma is not insignificant. As these imaging methods are done for some other purpose as “non-thyroid “imaging modality, a thorough specific sonographic evaluation of the thyroid gland should be performed in all thyroid incidentalomas. A sonographically confirmed thyroid nodule should be managed like any other clinically identified thyroid nodule/disease.

You never get the second chance to make the first impression.

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SRB's Manual of Surgery THYROIDECTOMY Types 1. Hemithyroidectomy: Along with removal of one lobe, entire isthmus is removed. It is done in benign diseases of only one lobe. It is also done in follicular neoplasm involving only one lobe. Solitary toxic or nontoxic nodule, thyroid cyst are other indications. 2. Subtotal thyroidectomy commonly done in toxic thyroid either primary or secondary and also often for nontoxic multinodular goitre. Here about 8 grams, or a tissue, size of pulp of finger is retained on lower pole, on both sides and rest of the thyroid gland is removed. It is also done in MNG. 3. Partial thyroidectomy (By Thomas) is removal of the gland in front of trachea after mobilisation. It is done in nontoxic multinodular goitre. Its role is controversial. 4. Near total thyroidectomy: Here both lobes except the lower pole (one or other sides) which is very close to recurrent laryngeal nerve and parathyroid is removed (To retain blood supply to parathyroids). It is done in case of papillary carcinoma of thyroid. Here less than 2 grams of thyroid tissue is left behind near its lower pole on one side usually opposite side of the diseased, occasionally on both sides. 5. Total thyroidectomy: Entire gland is removed. It is done in case of follicular carcinoma of thyroid, medullary carcinoma of thyroid. 6. Hartley Dunhill operation is removal of one entire lateral lobe with isthmus and partial/subtotal removal of opposite lateral lobe. It is done in non-toxic multinodular goitre. 4 grams of tissue is left behind only on one side.

 Strap muscles are retracted; in large goitre they are often

divided in upper part to retain their nerve supply ansa cervicalis. Often anterior jugular veins need to be ligated using 3 zero vicryl.  Pretracheal fascia is opened vertically to expose thyroid gland. Short stout middle thyroid vein which enters the IJV is ligated immediately (first vessel to ligate; it is vein without accompanying artery) using vicryl or silk and divided. Avulsion of this vein from its junction to IJV will cause bleeding. Gland is mobilised medially using peanut dissection and bipolar cautery.  Superior pedicle is dissected; artery and vein are individually ligated and divided. In olden days mass ligation close to gland at superior pole was the practice. Chances of injuring external laryngeal nerve and AV fistula may happen in mass ligation. It is also always better to identify external laryngeal nerve entering the cricothyroid. Dissection is done in an avascular plane between cricothyroid and gland.  Parathyroids both superior and inferior are identified. They are 6 × 4 × 2 mm in size weighing 50 mg with yellowish brown/ orange brown colour. Superior (parathyroid IV) and inferior (parathyroid III) glands are identified and dissected. Both

Preoperative preparation ™™ ™™ ™™

™™ ™™ ™™ ™™ ™™

Blood grouping and cross matching. Keep the required blood ready Indirect laryngoscopy. Patient is asked to tell’ E’ to check the abduction of vocal cord Videostroboscopy – it is special method to visualize the vocal cord vibration. 70 degree rigid strobolaryngoscope is used with mounted microphone. Flexible laryngostroboscope also can be used. Patient in sitting position, videostroboscope is passed to visualize vocal cords and patient is asked to tell eeee to examine vocal cord vibration as a slow motion. Serum calcium estimation T3, T4, TSH Thyroid antibodies ECG and cardiac fitness especially in toxic goitre Lugol’s iodine 10 days prior to surgery to make gland firm and less vascular.

Fig. 6.52: Note the incision for thyroid surgery.

Procedure xx Position:  Under general anaesthesia patient is put in supine position with neck hyperextended by placing a sand bag under shoulder— with table tilt of 15 degree head up to reduce venous congestion (Rose position). xx Incision:  Horizontal crease incision is done, two-finger breadth above the sternal notch, from one sterno­mastoid to the other (Kocher’s thyroid incision) (Posterior margin of sternomastoid). xx Procedure:  Skin and platysma are incised (Subplatysmal plane)—upper flap raised up to thyroid cartilage, lower flap up to sterno­ clavicular joint. Deep fascia is opened vertically in the midline.

Fig. 6.53: Hemithyroidectomy: Entire one lateral lobe and entire isthmus are removed retaining entire opposite lateral lobe. It is done in solitary nodule/toxic or nontoxic adenoma in one lobe.

Thyroid

Fig. 6.54: Subtotal thyroidectomy—it is done in toxic/nontoxic multinodular goitre. Most of the gland except lower pole (4-8 gram) on both sides is removed.

Fig. 6.57: Total thyroidectomy is done for follicular carcinoma and medullary carcinoma of thyroid.

Fig. 6.55: Partial thyroidectomy—it is done in nontoxic nodular goitre if there is adequate normal gland posteriorly. Tissue in the tracheooesophageal groove is retained. Isthmus and gland with nodules in front is removed. It is not commonly done now.

Fig. 6.58: Hartley Dunhill procedure: Here one entire lateral lobe, isthmus, and most part of the opposite lateral lobe except small quantity of tissue in the lower pole/tracheo-oesophageal groove— subtotal/partial/one gram is retained.

Fig. 6.56: Near total thyroidectomy is done in papillary carcinoma of thyroid. Here most of the gland except small tissue of 1 g on lower aspect of one side usually is retained to safeguard recurrent laryngeal nerve and parathyroid gland.

Fig. 6.59: Skin flaps raised in thyroidectomy. Thyroid covered with pretracheal fascia is seen.

Do not waste one moment in regret, for to think feelingly of mistakes of the past is to re-infect yourself.

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Fig. 6.60: Total thyroidectomy specimen done for follicular carcinoma of thyroid.

Fig. 6.61: Typical thyroidectomy postoperative scar.

Fig. 6.62: Note the relation of recurrent laryngeal nerve.

glands receive their blood supply from inferior thyroid artery and through an anastomotic branch. Superior parathyroid is above and behind the junction of RLN and inferior thyroid artery; inferior parathyroid is below and in front of this junction.  Recurrent laryngeal nerve should be identified with careful dissection through its entire course. Riddle’s triangle is between inferior thyroid artery above, carotid artery laterally trachea medially. From this area nerve runs upwards to enter the larynx at greater cornu of thyroid cartilage. Many branches of nerve and the variations should be remembered while dissecting here. One should not use monopolar cautery here; only bipolar cautery should be used carefully. Nerve usually crosses the inferior thyroid artery from deeper aspect; but variations are common. Posterior extension of lateral thyroid lobes close to Berry’s ligament is called as Zuckerkandl tubercle which is seen in 40% of cases. Nerve runs upwards in a fissure between Zuckerkandl tubercle and trachea or main thyroid gland. Nonrecurrent laryngeal nerve (0.5%) is occasionally seen in right side due to failure of development of 4th aortic arch; it directly arises from vagus enters the larynx at the level of inferior horn of thyroid cartilage. Recurrent laryngeal nerve is in close contact with suspensory ligament of Berry.  Inferior thyroid artery which is a branch of thyrocervical trunk ascends upwards reaching gland at its lower pole after turning towards midline behind the carotid artery. Here ligation is done at capsular level by identifying every small branch entering the gland (capsular ligation of inferior thyroid artery). This retains the blood supply of parathyroids which is very important. In olden days, ligation of inferior thyroid artery was done away from the gland often in continuation using absorbable suture material, is now no longer in practice.  Mobilized gland is removed. Critical points of recurrent laryngeal nerve injury are—at the entry of inferior thyroid artery and crossing the nerve, at suspensory ligament of Berry, at lower pole of the gland. Thyroid steal: In thyrotoxicosis, patient is taken to operation theatre daily for few days before doing surgery, so as to reduce the anxiety of the patient. MIVAI—Minimally Invasive Video-Assisted Thyroidec­tomy is becoming popular for small nodules and gland without thyroiditis. But it is costly.

Fig. 6.63: Position of the patient for thyroid surgery. Head end elevated, sand bag under the shoulder.

Thyroid

Fig. 6.64: Patient under anaesthesia with proper position for thyroidectomy surgery.

Fig. 6.66: Kocher’s thyroid incision for thyroidectomy.

Fig. 6.65: Position of neck in thyroid surgery.

Fig. 6.67: Suction drain kept after thyroidectomy.

Complications of Thyroidectomy 1. Haemorrhage:

May be due to slipping of ligatures either of superior thyroid artery or other pedicles or small veins. It causes tachycardia, hypotension, breathless­ness and compression over the trachea may cause severe stridor, respiratory obstruction due to tension haematoma under strap muscles. As a first aid, immediate release of sutures including that of deep fascia has to be done and pressure over the trachea is released. Then patient is shifted to operation theatre and under general anaesthesia exploration is done and bleeders are ligated. Blood transfusion may be required.

2. Respiratory obstruction:

It may be due to haematoma (if it is so, the haematoma has to be evacuated), or due to laryngeal oedema, or due to tracheomalacia or bilateral RLN palsy (emergency endotracheal intubation is done along with steroid injections). Often emergency tracheostomy may be required as a life-saving procedure. Laryngeal oedema is the commonest cause may be due to haematoma with tension along with intubation injury and surgical trauma. In such situation even though haematoma should be evacuated immediately to avoid further compression, airway obstruction will not be relieved due to laryngeal oedema and so endotracheal intubation is also needed immediately; in difficult situation if it is impossible to intubate, a needle

tracheostomy using 12-gauge needle (2.3 mm diameter) is done temporarily.

3. Recurrent laryngeal nerve palsy:

It can be transient or permanent. Transient is 3% common. They usually recover in 3 weeks to 3 months. Often they require steroid supplement and speech therapy. Permanent paralysis is rare. It presents with hoarseness of voice, aphonia, aspiration, ineffective cough. Unilateral injury can be well compensated. It is advisable to do routine postoperative ILS on 5th postoperative day. Later ILS is done in 4 weeks and 12 weeks.

4. Hypoparathyroidism:

It is rare 0.5% common. Mostly it is temporary due to vascular spasm of para­thyroid glands, occurs in 2nd-5th postoperative day. Present with weakness, +ve Chvostek’s sign, carpopedal spasm, convulsions. Serum calcium estimation is done and then 10 ml of 10% calcium gluconate is given IV 8th hourly. Later supple­mented by oral calcium carbonate 500 mg 8th hourly. After 3–6 weeks, patient is admitted, drug is stopped and serum calcium level is repeated.   Note:

   Earliest symptom of hypocalcaemia is muscle weakness.

5. Thyroid crisis/thyroid storm/thyrotoxic crisis It is a rare but severe life-threatening complication of hyperthyroidism with acute hypermetabolic state induced by release of excessive thyroid hormones. Crisis can be due to surgical or medical causes.

Everyone should be quick to listen and slow to speak.

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Nerve injuries

Other complications

Hypoparathyroidism • Temporary hypoparathyroidism • Temporary hypocalcaemia without hypoparathyroidism (hungry bone syndrome) • Permanent hypoparathyroidism • Spurious hypoparathyroidism (total calcium is less but ionized calcium is normal) Thyroid crisis Hypothyroidism/thyroid failure/myxoedema

• External laryngeal nerve injury – pitch of the voice is lost • Recurrent laryngeal nerve injury Vascular complications • Haemorrhage – primary and reactionary • Haematoma formation • Compromised tracheo-oesophageal blood supply

• • • •

Intraoperative

Immediate postoperative

Late postoperative

• Haemorrhage • Nerve injuries

• • • • •

• • • • •

Haematoma Laryngeal oedema Respiratory obstruction – stridor Hypoparathyroidism RLN injury and its problems

Causes xx It occurs in a thyrotoxic patient inadequately prepared for thyroidectomy or thyrotoxic patient presents with crisis following an unrelated operation or stress. xx Other causes are – infection, trauma, pre-eclampsia, diabetic ketoacidosis, emergency surgery, stress, drugs like anticholinergics or antiadrenergic or NSAIDs or chemotherapy, diabetes mellitus.

Features xx They present 12–24 hours after surgery; but on table also, it can occur occasionally. xx Hyperpyrexia (> 41°C), severe dehydration, circulatory collapse, hypotension, palpitations, tachycardia, tachypnoea, hyperventilation, cardiac arrhythmias, cardiac failure. xx GI symptoms like vomiting, diarrhoea, jaundice. xx Restlessness, irritability, delirium, tremor, convulsions and coma can occur. xx Bailey’s symptom complex of thyroid storm are – insomnia, anorexia, diarrhoea, vomiting, sweating, emotional instability, fever, tachycardia, aggravated toxic features, multiorgan dysfunction.

Fig. 6.68: Note the location of parathyroid glands.

Respiratory obstruction Skin flap necrosis – rare Infection Discharge and sinus formation • Wound granuloma • Keloid formation

Hypothyroidism Recurrent nodule Recurrent toxicity Wound infection Granuloma/keloid

xx Burch-Wartofsky score (1993) is used to identify or predict the thyroid storm using different parameters – score of below 25 excludes storm; score 25–45 suggests impending storm; more than 45 means thyroid storm. xx Death may ensure suddenly. xx Differentia diagnoses are—malignant hyperpyrexia, septic shock, anxious status, cardiac disorders. xx Investigations – Raised T3, T4, suppressed TSH, raised serum calcium, ECG and echocardiography shows changes, raised total count, altered liver function tests, arterial blood gas (ABG) shows changes; altered electrolytes.

Treatment xx Supportive measures – rehydration by proper fluid therapy, tepid sponging, cooling blankets, antipyretics like paracetamol IV infusion, glucocorticoids (Hydrocortisone 500 mg IV or dexamethasone injections), IV dextrose infusion as there is more metabolic demand, correction of electrolytes, treating cardiac arrhythmias, ICU care with ventilator support. Central line, CVP monitor, nasogastric tube, urinary catheter should be placed. xx Antiadrenergic drugs – Propranolol 80 mg orally or through nasogastric tube 6th hourly, or IV propranolol 1 mg IV in 10 minutes followed by 2 mg in 10 minutes as per need. When propranolol is contraindicated in asthma, heart block and failure, cardioselective beta blockers like atenolol, metoprolol can be used; esmolol IV loading dose as 500 ugm/kg followed by 100 ug/kg minute infusion is also effective. Reserpine 500 ug/kg loading dose, then 5 ug/kg/minute; heart rate should be 0.02 in primary HPT.

Treatment Indications for parathyroidectomy ™™ ™™ ™™ ™™ ™™ ™™ ™™

Fig. 7.2: Plain X-ray skull. Note the characteristic salt-pepper appearance of the skull bone.

A

B

Figs 7.3A and B: X-ray of humerus bone and hand bones showing bone features—brown tumour—osteitis fibrosa cystica.

expensive, it is used in parathyroid re-explora­tion. It is often combined with single photon emission computerised tomography (SPECT). xx Urinary cAMP level increases in 90% cases. xx Angiography, venous sampling, USG-guided biopsy are other methods.

Differential Diagnosis xx Secondaries in the bone—due to secretion of PTH related polypeptide by tumour. Actual PTH is suppressed. xx Multiple myeloma. xx Vitamin D intoxication. xx Sarcoidosis.

Severe symptoms Young age group Markedly reduced bone density Serum calcium more than 11 mg% Urinary calculi Neuromuscular presentations Urinary calcium more than 400 mg /24 hours

xx Surgical removal of the glands and implantation of frag-

ments of the gland in forearm muscle mass (brachioradialis) or neck (sternomastoid). Marker stitch is placed at the transplantation site. 1/3rd of one gland or 100 mg of parathyroid gland is autotransplanted—subtotal parathyroidectomy. xx If it is carcinoma, additional hemithyroidectomy with postoperative radiotherapy is required. xx Adenoma when occurs in one gland with normal other glands, removal of that gland with adenoma may be sufficient. xx When all four glands are diseased, transcervical thymectomy is also added along with total parathy­roidectomy to reduce persistent and recurrent disease. xx In familial and MEN syndromes, total parathyroidectomy is better. xx If it is mediastinal parathyroid adenoma, after proper localisation thoracoscopic removal may be sufficient. xx Nonsurgical care like good hydration, regular exercise, avoiding immobilisation, daily calcium and vitamin D intake is done in patients who have recovered from acute crisis. Estrogens reduce the calcium level and maintain bone density. Raloxifene, a selective estrogen receptor modulator is also reduces the serum calcium level. Biphosphonates mainly alendronate improves the bone mineral density (BMD) in primary HPT but without altering the levels of PTH or calcium. Cinacalcet, a calcimimetic drug activate calcium receptor and reduces the levels of PTH and calcium but not increasing the BMD. Calcitonin, mithramycin are other drugs used. Mithramycin is used once a week but is hepatotoxic and causes thrombocytopenia. But medical treatment for primary HPT is less effective and not popular.

Parathyroids and Adrenals Problems in parathyroidectomy ™™ ™™ ™™ ™™ ™™ ™™ ™™

Permanent hypoparathyroidism Persistent hyperparathyroidism—5% Recurrent hyperparathyroidism—hypercal­caemia recurs 12 months after first parathyroid surgery Recurrent laryngeal nerve injury—1% Often needs additional thyroidectomy Variations in positions of the gland especially lower-may be in mediastinum Sudden drop in calcium level after surgery due to increased absorption of calcium by bones—hungry bone syndrome

PARATHYROIDECTOMY

Parathyroid may be confirmed by frozen section biopsy or on table aspiration of parathyroid tissue which is analysed for PTH assay which will be more than 1500 pg/ml (confirms that removed tissue is parathyroid). Total parathyroidectomy is done for parathyroid hyperplasia by removing all four glands and one-third of one gland is autotransplanted into the forearm muscle (brachioradialis) or sternocleidomastoid muscle with marker stitch. Gland to be transplanted is sliced into 1 mm pieces and around 18 pieces are embedded in decided muscle with a marker stitch or clip. If in postoperative period patient still presents with features of primary HPT; transplanted area is re-explored and further reduction in parathyroid tissue is done. Wound is closed with proper haemostasis.

Indications in Primary HPT

Complications

xx Symptomatic HPT xx Asymptomatic HPT with—Criteria (2002) for surgical intervention are:  Raise in serum calcium level more than 1 mg/dl of upper limit of the normal calcium range;  24 hour urinary calcium if more than 400 mg; creatinine clearance when reduced more than 30%;  Bone density greater than 2.5 standard deviations below peak bone mass in lumbar spine/hip/lower end of radius;  Age below 50 years;  When medical therapy is not possible.

xx Haemorrhage, recurrent laryngeal nerve palsy, hypocalcaemia and hungry bone syndrome are known to occur. xx Persistent HPT (serum calcium does not normalise immediately after surgery leading to total failure) or Recurrent HPT (serum calcium after surgery becomes normal but in 6-12 months, it again increases) may be a problem. xx Hypoparathyroidism with severe hypocalcaemia is a problem when all glands are removed (3½) with bilateral neck exploration. 10 ampoules of calcium gluconate is diluted with one liter of normal saline and given as continuous infusion at a rate of 30 ml/ hour—initial method of management. Hypomagnesemia should also be corrected. xx Migration or inability to identify the transplanted parathyroid is often a problem in autotransplantation of parathyroid. xx Hungry bone syndrome  It occurs usually in patients with preoperative hyperthyroidism. They have increased bone breakdown in their hyperthyroid state. When a patient’s thyroid hormone level drops acutely after surgery, stimulus to break down bone is removed. The bones are now “hungry” for calcium, remove calcium from the plasma rapidly.  It usually occurs after parathyroidectomy; thyroidectomy for toxic thyroid; prostate cancer patients on estrogen therapy. Sudden cessation of existing increased bone breakdown makes bones to absorb calcium, magnesium and phosphorus rapidly. Calcium levels in blood prior to operation cannot predict hungry bone syndrome.  Hypocalcaemia, hypophosphataemia, hypomagnesemia and hyperkalaemia are four typical features in these patients. Estimation and correction of all these four factors is essential. ECG changes can occur. Hyperkalaemia should be treated judicially. Magnesium infusion is needed. There is an unusually high need for calcium, with a low calcium excretion in the urine.  Bone-specific alkaline phosphatase (ALP) continues to rise in the first few weeks indicating increased bone reconstruction.  Supplementation of vitamin D and elemental calcium is needed during discharge for 6 months.  Postoperatively they need calcitriol (gradually increased to 16 mg in 1 month, then gradually reduced) with 2 gm calcium supplement.  Monitoring is done by evaluating serum calcium, albumin, magnesium, phosphorus and bone specific alkaline phosphatase. xx Injury to recurrent laryngeal nerve, oesophagus can occur.

Indications in Secondary HPT Here indication for removal of all four glands with auto-transplantation of parathyroid is only in severe cases or with renal osteodystrophy.

Preoperative Preparation Vocal cords should be assessed by preoperative indirect laryngoscopy. High calcium levels preoperatively may require treatment with hydration; diuresis; steroids (prednisolone 20 mg TID for 5 days before surgery); 100 mmol phosphate infusion in 6 hours; 200 units calcitonin subcutaneous injection for 5 days twice daily before surgery; diphosphanate—etiodronate disodium 7.5 mg/kg daily as slow IV infusion for 3 days; mithramycin 25 µg/kg as single dose.

Anaesthesia and Position General anaesthesia is used with neck hyperextension by placing rolled sheet under the shoulder blades. Head is placed on the head ring; head end of the table is raised to semi-erect position (SemiFowler position).

Incision and Dissection It is same as for thyroidectomy. Flaps are raised in similar way. Strap muscles are separated after opening the deep fascia in the midline. Thyroid gland is mobilised to identify the parathyroid adenoma. Parathyroid having adenoma is mobilised which is close to recurrent laryngeal nerve. End artery of the parathyroid is identified and ligated. Adenoma is separated from adjacent thyroid tissue using gauze dissection. Either on table venous sampling for PTH assay is done or venous sample from cubital vein is done for PTH assay.

The fact which Addison has published seem to lead to the conclusion that these little organ are essential to life. —Charles Edward Brown-Sequard

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SRB's Manual of Surgery Effects of Surgery xx Among neuromuscular symptoms of primary HPT, proximal muscle weakness responds better than respiratory muscle weakness by parathyroidectomy. xx Among psychiatric illnesses, depression and spatial learning and processing improve well by surgery. xx Bone mineral density in hip and lumbar spine becomes better. xx Nephrocalcinosis is improved by surgery; but hypertension and renal excretion will not improve much. xx Half life of PTH is 4 minutes. On table serial PTH assays are done at several intervals—before dissection of the gland, during dissection and after dissection. 50% reduction in PTH level from baseline in post-removal sample is a 96% predictor of complete removal. xx Operative failure rate is 1.5 to 6%. Intraoperative PTH assay improves the success rate very much (76–94%). Cure rate is defined as normocalcaemia in 6 months postoperative period. xx Radio-guided parathyroidectomy using intravenous injection of 20 mCi of 99mTc sestamibi 2 hours before surgery is not routinely practiced but may be useful for removal of adenoma appropriately. Hand-held quantitative gamma counter is used intraoperatively on the neck over all parathyroid tissues.

Surgical Approaches Classic approach (Traditional approach) It is under general anaesthesia exploring bilateral neck to remove parathyroid tissue which is confirmed by frozen section biopsy. It shows 95% cure rate with 2% complication rate.

anterior border of the sternocleidomastoid and over the incision is also used. Post-operative serum calcium and PTH level should be assessed until 7th day.

Median Sternotomy (3%) Extension Median sternotomy is often needed when parathyroid is in anterior mediastinum along with thymus. Often parathyroids may be 5, 6 or 7 in numbers instead of four.

Video-assisted Parathyroidectomy (Paolo Miccoli) It is done in localised single adenoma using multiple ports on one side with intermittent CO2 insufflation and suction irrigation. 1.5 cm incision 1 cm above the sternal notch helps in tactile assessment and dissection. Strap muscles are retracted laterally and thyroid is retracted medially. Conversion rate is 11%; RLN palsy is 2%.

Endoscopic Parathyroidectomy Entire parathyroidectomy is done using laparoscopy. It is first used (1994) for a mediastinal parathyroid adenoma. In 1996, it was used for neck parathyroid hyperplasia by Gagner for removing 3½ glands. Now technique is limited to single adenoma to remove tumour and gland. Low pressure insufflations with 5 mm four trocars are used. Placement of trocars is dependent on the need of the operating surgeon. Many place trocars on one side only; but few prefer to place working trocars on opposite side.

Remedial Parathyroidectomy It is done for persistent HPT (serum calcium is not normalised immediately after surgery leading to total failure) or recurrent HPT (serum calcium after surgery becomes normal but in 6–12 months, it again increases). It is done through lateral approach (Feind) between anterior margin of sternocleidomastoid and strap muscles so that scar tissues are avoided from initial dissection. On table localisation methods, on table PTH assay are needed. Medial sternotomy often may be needed to explore the mediastinum for complete removal of the gland. Parathyroids in such situations may be embedded in the tissue of thyroid or thymus. So removal of these glands also may be a need in such situations.

Subtotal Parathyroidectomy It is indicated in hyperplasia or secondary HPT wherein 3½ glands are removed, retaining ½ of one gland. Fig. 7.4: On table look of parathyroid adenoma of inferior parathyroid gland (left sided).

Minimally Invasive Parathyroidectomy (MIP) It is done in case of single adenoma of parathyroid under regional cervical block anaesthesia usually in ambulatory set up. It is actually unilateral parathyroidectomy with removal of adenoma and involved entire that particular one parathyroid gland using limited neck exploration (small incision of 2–4 cm). Procedure is not useful in multiple adenomas or hyperplasia. Preoperative localisation with sestamibi combined with SPECT is a must. Intraoperative PTH assay is a must to confirm drop in PTH level to required level. Cervical block is given by infiltrating the xylocaine (1%) with adrenaline along posterior and deep to sternocleidomastoid muscle and also along the neck incision. Direct field block along the

Total Parathyroidectomy with Parathyroid Autotransplantation It is done alternatively in hyperplasia wherein all four glands are removed; ⅓ or ½ of one gland is transplanted into sternocleidomastoid or brachioradialis muscle with a marker. Disease control will not occur, if more part of the gland is transplanted. It is removing all four glands and ½ or ⅓ of one gland is autotransplanted into the forearm muscle (brachioradialis) or sternocleidomastoid muscle with marker stitch. Transplanting gland is sliced into 1 mm pieces and around 18 pieces are embedded in decided muscle with a marker stitch or clip. If postoperatively patient still presents with features of primary HPT; transplanted area is re-explored and further reduction in parathyroid tissue is done. Migration or inability to identify the transplanted parathyroid is often a problem in autotransplantation of parathyroid.

Parathyroids and Adrenals MEN SYNDROME (MEA SYNDROME) xx Commonly inherited as an autosomal dominant. xx Cells involved has got common features of apud cells

(Apudomas). Note:

• •

APUD—Amine Precursor Uptake Decarboxy­lation. MEN—Multiple Endocrine Neoplasia; MEA—Multiple Endocrine Adenomatosis.

Types xx Type—I: Parathyroid hyperplasia or adenomas; pituitary

tumour; pancreatic tumour [Endocrine—Insulinoma, gastrinoma, glucagonoma, vipoma]. It is also called as Werner’s syndrome. Here the defect is in chromosome 11. xx Type—II: Also called as Sipple’s disease. 1. IIa includes medullary carcinoma of thyroid + phaeochromocytoma + parathyroid hyper­plasia (50%). Here the defect is in chromosome 10. 2. IIb includes medullary carcinoma of thyroid + phaeochromocytoma mucosal neuromas in lips and eyelids with bumpy-lumpy lesions, with marfanoid face, megacolon. Evaluation and management of MEN syndrome: Family history; biochemical screening with parathormone, serum calcium, prolactin, growth hormone, blood sugar, insulin, proinsulin, pancreatic polypeptide, glucagons, gastrin levels, calcitonin, urinary catecholamines estimation; genetic screening from isolated DNA from peripheral blood white cells for ret proto oncogene. Specific surgical treatment of conditions is needed.

APUDOMAS APUD (Amine Precursor Uptake Decarboxylation) cells are cells having specific cytochemical characteristics. They are:  High amine content.  Capacity of amine precursor uptake.  Property of decarboxylation of these precursors to form amines. xx Initially it is thought that APUD cells are derived from neural crest cells (Pearse) but now found to be from endoderm. Cells share similarities in structure, properties, histological, histochemical, immunocytochemical and electron microscopic appearance. Neuron specific enolase enzyme is specific for these cells. xx These cells have got capacity to synthesize peptides which has got different modes of action. They are: 1. Endocrine action where peptides get secreted into circulation to have distant target actions. 2. Paracrine action where peptides get secreted locally to have action at local sites. 3. Neurocrine action where peptides act as neurotransmitter at neuronal synapses. 4. Neuroendocrine action where peptides stimulate release of peptide product of the neuron into the circulation.

xx Tumours arising from these cells are grouped as Apudomas.

Many of parathyroid tumours, pancreatic tumours are under this group. Their presentations are commonly due to increased secretions of these neuroendocrine hormones. Commonly presentation is like syndromes. Insulinoma, glucagonoma, gastrinoma, VIPoma are different examples. Tumours are entopic type, if they secret hormones normal to the tissue like insulinoma/glucagonoma. They are ectopic type if they produce hormones which are not normal to the tissue of origin like gastrinoma/VIPoma. xx APUDOMAS are commonly associated with MEN syndrome (commonly type I). Radioimmunoassay, MRI abdomen, CT neck are useful investigations. xx Treatment is of individual diagnosed components of the condition.

HYPOPARATHYROIDISM xx Hypoparathyroidism is defined as a PTH level < 10 pg/ml; normal values range between 10 and 65 pg/ml; was considered permanent when it lasted for more than 6 months. xx Permanent hypoparathyroidism would be defined as requirement of therapeutic vitamin D and/or calcium replacement at 6 months or fasting albumin-corrected serum calcium below 8.0 mg/dl.

Types Temporary

More common (2–50%) average 10%

Usually lasts for 2 months maximum up to 6 months. Decrease in calcium; increase in phosphorous

Permanent

Less common (0.4–13%) average 1%

Permanent— continues beyond 6 months. Decrease in calcium; increase in phosphorous

Hungry bone syndrome

Common (5–13%)

Severe, rapid begins in immediate postoperative period. Decrease in calcium; decrease in phosphorous

xx Inadequate production of PTH leads to hypocalcemia. Hypoparathyroidism and the resulting hypocalcemia may be permanent or transient. The rate of permanent hypopara­thyroidism is 0.4–13%. xx Causes are—direct trauma to the parathyroid glands, devascularization of the glands, or removal of the glands during surgery like-thyroidectomy and parathyroidectomy. xx The rate of temporary hypocalcemia is reportedly 2–50%. The cause of transient hypocalcemia after surgery is due to temporary hypoparathyroidism caused by reversible ischaemia to the parathyroid glands, hypothermia to the glands, or release of endothelin-1. Endothelin-1 is an acute-phase reactant which suppresses PTH production. Other hypothesis is—calcitonin release and hungrybone syndrome. Calcitonin is produced by the thyroid C cells which inhibits bone breakdown while stimulating renal excretion of calcium (opposite of PTH).

Great man is the one who treats the little in a great way.

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SRB's Manual of Surgery xx An effective method of evaluation of parathyroid function is to assess ionized calcium (or total calcium and albumin) levels in the perioperative period. A normal postoperative PTH level can accurately predict normocalcemia after thyroid surgery. Immediate postoperative PTH level if 100 g weight are more likely to

be malignant.

Fig. 7.5: Anatomy of adrenal gland.

ADRENAL CORTICAL TUMOURS xx Are usually adenomas. xx Any tumour measuring 6 cm or more are likely to be malignant, or have high risk of turning into malignancy. So requires surgical resection. xx Adenocarcinoma is the commonest adrenal cortical malignancy (1%). It is very aggressive tumour. xx Cortical tumours may be functioning or nonfunc­tioning. xx Functioning tumours secrete mineralocorticoids, glucocortic­oids or sex hormones or combinations of these. xx Investigations:  Ultrasound abdomen.  CT scan, hormone evaluation.

xx Treatment:  Adrenalectomy.

Incidentalomas (3–5%) xx Incidentalomas are adrenal tumours incidentally identified either through U/S; CT scan; MRI; or any other methods done for other reasons. xx Whether incidentaloma is hormonally active; whether it is potentially malignant has to be assessed.

xx Cytologic criteria alone are not diagnostic but should find

capsular infiltration and vascular invasion.

xx Often presents with no symptoms or only vague symptoms. xx May present with mass effect and compression of adjacent

structures. xx Increased secretion of one or more steroid hormones can occur. xx Diagnosis is by hormone evaluation, CT/MRI; MR angiog-

raphy to identify IVC tumour thrombus. xx Secondaries occur commonly in lungs. So HRCT of lungs

is usually done.

xx McFalane staging: Stage I—tumour 5 cm; Stage III—tumour with local invasion; Stage IV— distant spread. In stage I and II, 5 year survival is 25%; in stage III and IV, 5-year survival is 5%. xx Treatment is en block adrenalectomy; adjacent organs like kidney, spleen may be removed if needed; removal of tumour thrombus from vena cava if present; chemotherapy using mitotane—Op-DDD (choice) with cis platin, etoposide and doxorubicin. Adjuvant radiotherapy may be used to prevent recurrence (little role).  Recurrence is treated by debulking and chemotherapy.  Laparoscopic adrenalectomy is not advisable in adrenocortical carcinoma. xx Prognostic factors—tumour size > 12 cm; high mitotic activity > 6 mitoses/ high power field; intratumour haemorrhage.

Laughter is the music of the soul.

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SRB's Manual of Surgery Secondaries in adrenal gland ™™ ™™ ™™ ™™ ™™ ™™

Common entity Commonly from breast, lungs, kidney, melanoma 1/3rd of above primaries show secondaries in adrenal gland Commonly bilateral In unilateral secondaries, adrenalectomy can be done Bilateral secondaries are treated by chemotherapy depending on type of primary

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Posterior lumbotomy Anterior transabdominal Abdominothoracic Laparoscopic Retroperitoneoscopic

Approches for adrenals (surgical)

xx Negative urinary free cortisol and Low dose dexamethasone suppression test rules out Cushing’s syndrome. xx Measurement of corticotropin (ACTH): if low—corticotropin independent Cushing’s syndrome; if high—corticotropin dependent Cushing’s disease. xx Localising methods/imaging: Adrenal—CT scan/MRI abdomen; Iodocholesterol scan. Pituitary—MRI pituitary. It can be incidentaloma in pituitary. Inferior petrosal sinus sampling of blood for ACTH shows central to peripheral ratio of ACTH >3.

Treatment Medical Metapyrone; ketaconazole; aminoglutethamide; mitotane.

Surgical

CUSHING’S SYNDROME

For pituitary disease

xx Results from lengthy and inappropriate exposure to excessive glucocorticoids; iatrogenic administration of steroids (commonest cause); endogenous Cushing can also occur. xx More common in women.

xx Trans-sphenoidal microsurgery. xx Pituitary irradiation—conventional fractionated therapy; Sterotactic radiosurgery. xx Bilateral adrenalectomy.

Corticotropin (ACTH) Dependent—80%

xx Unilateral adrenalectomy in adenoma, carcinoma. xx Bilateral adrenalectomy in macronodular adrenal hyperplasia and primary pigmented nodular adrenal disease.

For adrenal disease xx ACTH secreting pituitary adenoma. xx Ectopic ACTH secreting tumour.

Corticotrophin Independent—20% xx xx xx xx

Adenoma. Carcinoma. Macronodular adrenal hyperplasia. Primary pigmented nodular adrenal disease.

CONN’S SYNDROME (Jerome Conn, 1954) It is primary hyperaldosteronism with excessive secretion of aldosterone from the adrenal gland associated with suppression of plasma renin activity. Aldosterone secretion is related to angiotensin I and II and plasma rennin with angiotensin converting enzyme.

Features

Causes

xx xx xx xx xx

xx Aldosterone producing adrenocortical adenoma (Aldosteronoma)— 65%; xx Idiopathic hyperaldosteronism—30%.

Centripetal obesity; redistribution of fat centrally. Moonface; fullness of supraclavicular pad of fat. Buffalo hump; proximal muscle wasting. “Lemon on toothstick appearance”. Skin changes.

Diagnosis xx Loss of normal diurnal or circadian rhythm of serum cortisol. Values more than 4 fold the upper limit of normal is diagnostic. xx 24 hour urinary free cortisol is elevated > 90% of Cushing’s syndrome. xx Low dose dexamethasone suppression test: Dexamethasone is a potent glucocorticoid that suppresses adrenal production of corticosteroids in normal persons but not in persons with Cushing’s syndrome. 1 mg of dexamethasone is injected; normal— 10 mcg/dl. xx Late night salivary cortisol—Cortisol concentration in saliva correlates with free plasma cortisol; it is independent of salivary flow rate; it shows high sensitivity and specificity.

Features xx Hypertension; hypokalaemia. xx Hypernatremia or normal sodium; metabolic alkalosis xx In primary hyperaldosteronism—hypertension of early onset which is difficult to control and is with hypokalaemia.

Diagnosis xx Hypokalemia; increase in urinary potassium excretion. xx Elevated plasma aldosterone concentration (PAC); suppressed plasma renin activity (PRA); PAC: PRA > 30; it is confirmed by suppression test by oral or IV salt loading. xx Localising tests—CECT abdomen; Selective adrenal venous sampling—Gold standard to differentiate between unilateral versus bilateral aldosterone hypersecretion.

Parathyroids and Adrenals Treatment xx Adenoma—unilateral adrenalectomy. xx Idiopathic hyperaldosteronism—medical treatment with spiranolactone.

VIRILISING SYNDROME OR ADRENOGENITAL SYNDROME xx Virilising tumours/syndromes. Such tumours are excised.  In female: Virilism, ambiguous external genitalia, clitoral enlargement.  In male: Precocious puberty, premature fusion of epiphysis, short stature. xx Congenital adrenal hyperplasia (adrenogenital syndrome) is— enzyme 21 hydroxylase deficiency; autosomal recessive. It is treated by—replacement of deficient steroids. Adrenal hyperplasia does not require surgical intervention but the genital manifestations of excess androgen production, particularly in women, may require specialised surgery.

NEUROBLASTOMA xx Commonest childhood abdominal tumour. xx It is a tumour of adrenal medulla. xx An aggressive malignant tumour in childhood usually below

the age of 5 years. xx Incidence is equal in both sexes. xx A reddish-grey tumour gets invaded early into kidney,

pancreas and adjacent tissues. It can also cause distant spread to liver, bones (skull), orbit. It can occur anywhere in sympathetic chain but common in adrenal gland (40%).

Types 1. Pepper type is right side adrenal neuroblastoma with liver secondaries. Common in infants.

2. Hutchinson’s type is left side adrenal neuroblastoma with secondaries in orbit and skull. Common in late childhood. Secondaries in the skull mimics spicular osteogenic sarcomas.

Risk Groups xx Low risk groups—Stage I disease; Stage II disease with single

N myc value; Stage II with favourable Shimada histology. xx Intermediate risk groups—Stage III without N myc ampli-

fication; Stage III with favourable Shimada’s histology.

xx High-risk groups—all patients with N myc amplification;

stage IV neuroblastoma.

Pathology xx Gross—tumour with vascularity, necrosis, haemor­rhage and

often calcifications.

xx Histologically it contains uniform round cells with hyper-

chromatic speckled nucleus with Homer-Wright rosettes with central fibrillar core. PAS stain is negative and NSE stain is positive. Often histochemistry is needed to differentiate from other tumours. xx Shimada’s histological classification:  Stroma rich tumour: Presence of Schwannian spindle cell stroma.  Stroma poor tumour: Absence of Schwannian spindle cell stroma.

Clinical Features xx Child presents as a huge mass per abdomen, in the loin

which is non-mobile. Not moving with respiration. Knobby (nodular) surface, crosses the midline. xx Dancing eye syndrome and opsomyoclonus. xx Racoon’s eye sign is infraorbital ecchymosis due to secondaries in retroorbital region.

A

Fig. 7.6: Left-sided adrenal neuroblastoma with secondaries in orbit. Note scar of left-sided adrenalectomy.

B

Figs 7.7A and B: Typical secondaries in skull and orbit with primary in adrenal gland. Such patients carry poor prognosis. Racoon’s eye sign is infraorbital ecchymosis due to secondaries in retro-orbital region. Dancing eye syndrome and opsomyoclonus are other eye features. CT picture of the same patient shows obvious secondaries.

There is no service than doing something for someone who will never find it out!

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SRB's Manual of Surgery xx Hypertension, fever, weight loss, anaemia, flushing (due to

catecholamine release) and sweating. xx Diarrhoea, hypokalaemia due to release of Vasoactive Intestinal Polypeptide (VIP). Other hormones like ACTH are also released. Staging of neuroblastoma ™™ ™™ ™™

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Stage I: Localised tumour with gross complete excision. Same side representative nodes are negative on microscopy Stage II A: Localised tumour with incomplete gross excision. Same side representative nodes are negative on microscopy Stage II B: Localised tumour with or without complete gross excision. Same side nonadherent representative nodes are positive but contralateral nodes are (may be enlarged) negative on microscopy Stage III: Unresectable unilateral tumour infiltrating across midline/ localised tumour with opposite side node spread/bilateral nodal spread/midline tumour with bilateral infiltration Stage IV: Any primary tumour with spread to distant nodes, bone, bone marrow, liver, skin and other organs Stage IV S: Localised primary tumour (stage I, IIA, IIB) with spread to skin, liver or bone marrow—limited to infants younger than one year

Differential Diagnosis Wilm’s tumour, which is mobile, with smooth surface, moves with respiration, does not cross the midline.

Diagnosis xx Ultrasound, CT to assess the mass and secondaries in liver.

MRI is better than CT.

xx Plain X-ray abdomen shows stippled calcification. xx Urinary VMA and Homovanillic acid (HVA) esti­mation in

90% cases. xx MIBG scan. xx Bone marrow biopsy may be positive in 60% cases. Iliac

bone both sides under GA.

xx PET scan is done if MIBG is not beneficial.

Treatment xx xx xx xx

Adrenalectomy (Complete surgical excision). In inoperable cases, debulking is beneficial. Postsurgical radiotherapy and folic acid supplements are useful. Chemotherapy is useful adjuvant. Drugs used are carboplatin, doxorubicin, cyclophosphamide and etoposide. xx Rarely spontaneous regression of tumour is known to occur. xx Low risk groups are treated by surgery. Intermediate risk groups are treated by surgery and multidrug chemotherapy. High risk groups are treated by high dose multidrug chemotherapy and later surgery. xx Other treatment modalities—retinoids (fenretinide), immunotherapy (GD2), radionuclide targeted therapy, angiogenesis/ tyrosine kinase/aurora kinase inhibitorsare on trial. Bone marrow or stem cell transplantation are newer methods used.

Prognosis xx It depends on staging of the neuroblastoma—1, 2A, 2B, 3, 4, 4S. xx Low risk has got 3 years survival—90%; intermediate risk—70% and high risk group has got 30%.

xx Factors are—age of the child; stage of the disease; Shimada’s histology; N myc amplification status (more means high risk); DNA ploidy; neurotrophin receptor Trk A (increased favourable); neutrophin receptor Trk B (increased unfavourable).

PHaEOCHROMOCYTOMA xx It is a tumour arising from chromaffin cells, com­monly

from the adrenal medulla but occasionally can arise from extraadrenal chromaffin tissues (Organ of Zuckerkandl). The organ of Zuckerkandl (Emil Zuckerkandl, Professor of Anatomy, Vienna, 1901) comprises a mass of chromaffin cells derived from neural crest located along the aorta beginning above cranial to the superior mesenteric artery or renal arteries and extending below to the level of the aortic bifurcation; highest concentration is seen at the origin of inferior mesenteric artery. xx It is catecholamine secreting tumours that arise from chromaffin cells of sympathetic origin derived from neural crest representing a potentially curable form of hypertension. xx Incidence is 0.005–0.1% of general population; 0.1–0.2% of adult hypertensive population. xx It is a soft, brownish grey pink tumour, mainly secretes noradrenaline or other catecholamines. xx It may also secrete calcitonin, ACTH, VIP (vasoactive intestinal polypeptide), PTH-related polypeptide. xx Prevalence of phaeochromocytoma is 0.05%. In patients with hypertension it is up to 0.6%. 4% of incidentalomas are phaeochromocytoma. xx Often it is difficult to differentiate between benign and malignant types. Necrosis, haemorrhage, high ki-67 positive cells, size of the tumour, increased phaeochromocytoma of adrenal gland scale score (PASS), capsular invasion and vascular invasion, nuclear DNA ploidy and increased neuron specific enolase (NSE) level are possible features of malignant phaeochromocytoma. xx Currently mutations in at least six distinct genes predispose to phaeochromocytomas—RET, NF1, VHL, SDHB, SDHC, SDHD. xx Extra-adrenal pheochromocytoma—10% common; occurs in organ of Zuckerkandl, urinary bladder, paravertebral or para-aortic area, thorax, neck. It secretes norepinephrine rather than epinephrine because they lack the enzyme PNMT. xx Commonly benign (90%). Tumour is: ™™ 10% malignant ™™ 10% extra-adrenal ™™ 10% bilateral ™™ 10% familial ™™ 10% childhood ™™ 10% multiple ™™ 10% not associated with hypertension ™™ 10% calcified

Clinical Features xx Clinical manifestations are due to increased secretion of

epinephrine and norepinephrine.

Parathyroids and Adrenals xx Commonest presentation is severe headache. xx Palpitation, dyspnoea, weakness, pallor, blurred vision and

other symptoms of sympathetic over­activity. xx They may present as persistent or paroxysmal hypertension

xx xx

(90%). xx As an abdominal mass which is nonmobile, smooth, does

not move with respiration, crossing the midline, palpation may cause fluctuation in BP. xx It may precipitate hypertensive encephalopathy, cardiac arrhythmias or cerebral haemorrhage. xx Panic attacks and sudden death are known to occur. xx It may be associated with MEN-IIa or MEN-IIb syndromes which includes medullary carcinoma of thyroid and mucosal neuromas. xx It may be associated with familial multiple neuro­ fibromatosis with cafe au lait spots in the skin (von Recklinghausen’s disease). Or with von Hippel-Lindau syndrome (cystic lesion of pancreas, non-functioning islet cell tumour, phaeochromo­cytoma), RCC, CNS and retinal haemangioblastoma. xx Familial paraganglioma syndrome may be an association with carotid body and extra-adrenal paraganglioma. Differential diagnosis ™™ ™™ ™™ ™™

Hyperthyroidism Anxiety status Cardiac conditions Carcinoids (functioning)

Investigations xx VMA excretion in urine in 24 hours will be >7 mg/24 hr in

xx xx xx xx

propranolol. Then during surgery, sodium nitroprusside IV infusion is used. Adequate fluid therapy to have volume expansion is essential. Careful anaesthetic management with a good postoperative care is very essential. In case of bilateral presentation, opposite side can be operated in later period. Intraoperative hypovolemia and postoperative hypotension is a demanding situation for anaesthetist to manage. Handling of adrenal tumour on table must be careful and gentle. Adrenal vein should be ligated first. CVP, arterial lines should be present for monitoring. Rupture and spillage of tumour should be prevented.

Note:

• • • •

Laparoscopic adrenalectomy is becoming popular. It is choice of approach for benign functioning or non-functioning adrenal tumours that are less than 6 cm in size. It is contraindicated in malignant tumours and tumour more than 6 cm. Recent trends are—cortical sparing adrenalectomy; thoracoscopic transdiaphragmatic approach; Robotic-assisted laparoscopic adrenalectomy. Specimen should be sent for bichromate staining which stains the specimen brown. Metyrosine is indicated in pheochromocytoma who are awaiting for surgery or when surgery is contraindicated or in refractory to phenoxybenzamine therapy. Metyrosine inhibits tyrosine hydroxylase thus reducing the catecholamine biosynthesis.

Remember ™™ ™™ ™™ ™™

pheochromocytoma. xx U/S abdomen, IVU, CT scan. xx MRI is preferred to CT as contrast used for CT scan can

precipitate paroxysms.

™™ ™™

xx Measurement of plasma-free metanephrines is the recom-

mended test of choice for excluding or confirming diagnosis of phaeochromocytoma. xx Urinary normetadrenaline or other catecholamines estimation. xx Arteriography. xx Iodine labelled metaiodo-benzylguanidine (I, MIBG). MIBG is useful to find out extra-adrenal involvement—SPECT scan is very useful. I131 MIBG scan is safe, noninvasive with 100% sensitivity and 95% specificity. xx Measurement of plasma free metanephrine and normetanephrine has the highest sensitivity and specificity and appears to be the best initial test for screening patients with pheochromocytoma.

Treatment Adrenalectomy xx Before surgery, BP is controlled initially by α-blocking agent, phenoxybenzamine or doxazosin; then by β-blocking agent,

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Pheochromocytoma is rarely malignant in MEN II Pheochromocytoma under 40 years of age suspect MEN 2A, VHL Beta-blocker is given only after patient is fully alpha blocked with phenoxybenzamine (20–60 mg/day) or doxazocin Alpha-blocker is given 4 weeks prior to surgery to control hypertension and beta-blocker is given one week before surgery to control tachycardia and arrhythmias Tumours, those secrete dopamine exclusively has got high malignant chances 5-year survival for malignant pheochromocytoma is 50%. It needs additional chemotherapy using vincristine, dacarbazine and cyclophosphamide. Pheochromocytoma in pregnancy has got 50% maternal mortality Vaginal delivery is contraindicated in pregnancy with pheochromocytoma Adrenal vein should be ligated first Avoid breach in the capsule of tumour during surgery Careful handling and haemodynamic monitoring is a must Sodium nitroprusside may be required on table to control the hypertension—10 µg/kg/minute

Malignant pheochromocytoma is 10% common. It is more common in extra-adrenal site. It commonly spreads to lymph nodes, bone and liver. Adrenalectomy in early tumour and debulking in advanced cases with α-blockers, mitotane and I131MIBG therapy and combination chemotherapy are the therapeutic choices. Overall prognosis is not good with 5-year survival being 5 cm in size)—common in Africa. Microscopy: 1. Intracanalicular—large and soft—mainly cellular. Stroma with distorted duct.

xx Normal cyclical hormonal effects on glands and stroma get exaggerated by aberration causing generalised enlargement. Its diseased status is cyclical mastalgia with nodularity also called as fibrocystadenosis.

Involution age group (40–55 years): xx Lobular involution with microcysts, fibrosis, adenosis, apocrine metaplasia and eventual aberrations as macrocysts and cystic disease of breast. Macrocyst is an aberration of normal involution (ANI). Sclerosing adenosis is also a type of aberration. xx Ductal involution may cause ductal dilatation and nipple discharge as aberration. Later disease status develops with periductal mastitis, bacterial infection, nonlactational breast abscess and mammary duct fistula. Periductal fibrosis may cause partial nipple retraction. xx Epithelial changes leads into epithelial hyperplasia and atypia.

Fig. 8.9: Fibroadenoma, on table look—well-capsulated neoplasm. It is part of ANDI.

Breast 2. Pericanalicular—small and hard—mainly fibrous. Stroma with normal duct.

Clinical Features xx It presents as a painless swelling in one of the quadrants,

which is smooth, firm, nontender, well-localised and moves freely within the breast tissue (mouse in the breast). xx Axillary lymph nodes are not enlarged.

Investigations xx Mammography (well-localised smooth regular shadow). It

may show popcorn calcification on mammography.

xx FNAC. xx Ultrasound (to confirm solid nature).

A

B Figs 8.12A and B: Multiple fibroadenomas.

Fig. 8.10: US picture showing fibroadenoma left breast.

Treatment Excision through a circumareolar incision (Webster’s) or submammary incision (Gaillard Thomas incision) is done under general anaesthesia.

Fibroadenoma which is small (2 cm Size of giant gastric ulcer is >3 cm ™™ Size of giant fibroadenoma is >5 cm ™™ Diameter of transverse colon in toxic megacolon is >6 cm ™™ Size of giant naevus is >20 cm ™™ ™™

Fig. 8.11: Large fibroadenoma left breast in a 14-year-old female.

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SRB's Manual of Surgery Microscopic changes Stromal fibrosis Microcyst formation ™™ Glandular proliferation (Adenosis) ™™ Hyperplasia (Epitheliosis)—in ducts and acini ™™ Papillomatosis—within the ducts, often with apocrine metaplasia ™™ ™™

xx It is an estrogen dependent condition. One of the cysts may

A

B Figs 8.13A and B: Subareolar and submammary incision to excise benign lesions of the breast.

get enlarged to become a clinically palpable, well-localised swelling—bluedome cyst of Bloodgood. It is fluctuant, transilluminant, nontender, often tensely cystic swelling (macrocyst) with thin bluish capsule. It should be aspirated initially. Surgical excision is done if it persists or recurs even after two aspirations; if it is blood stained; if there is residual lump after aspiration. xx When diffuse small, multiple cysts are the main component, it is called as Schimmelbusch’s disease. xx It is the most common breast disease. xx It is common in upper and outer quadrant. xx It is an exaggerated response of breast stroma and epithelium to hormones and growth factors. xx It is rare in nulliparous/ovulating/OCP taking women.

Classification xx Nonproliferative—moderate hyperplasia of ductal luminal

cells—no life time risk for cancer.

xx Proliferative without atypia (severe hyperplasia). xx Proliferative with atypia (Atypical ductal/lobular hyper-

plasia)—is risk factor for breast cancer—often mimics in situ carcinoma. RR is 4.5.

Fig. 8.14: Diagram showing circumareolar and submammary (Gaillard Thomas) incisions.

FIBROCYSTADENOSIS (FIBROCYSTIC DISEASE OF THE BREAST/MAMMARY DYSPLASIA/CYCLICAL MASTALGIA WITH NODULARITY) xx It is due to Aberration of Normal Development and Involu-

tion (ANDI) of breast causing changes in the breast. xx It is presently called as cyclical mastalgia with nodularity.

Usual hyperplasia is presence of 3 or more layers of proliferating epithelial cells without atypia above the basement membrane in a lobular or ductal unit. It can be mild, moderate or florid. It is seen in 20% of biopsies. Risk of developing cancer is 1.5 times. Observation of such patient is the advice. Atypical ductal hyperplasia (ADH) is defined as a lesion that has got some but not all features of DCIS; a lesion that has all features of DCIS but less than 2 mm in size; lesion with all features of DCIS but involving less than 2 duct spaces. Its incidence is 30% of all mammographies and 5% of benign breast disease biopsies. Risk of developing cancer is 5 times the normal women of that age. Atypical lobular hyperplasia (ALH) is LCIS with half of the acini of lobular unit is involved. Developing invasive carcinoma in 10 years is 20%.

Stages I—Stromal proliferation or hyperplasia. II—Adenosis (increased glands). III—Cyst formation.

Breast Pathophysiology of fibrocystadenosis ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

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Drugs are:  Oil of evening primrose used in moderate pain—drug of

Oestrogen predominance over progesterone is considered causative Serum levels of oestrogen > Luteal phase is shortened Progesterone level decreased to 1/3rd normal Corpus luteum deficiency/anovulation in 70% Patients with premenstrual tension syndrome more likely to develop fibrocystadenosis Prolactin levels are increased in 1/3rd of women with fibrocystadenosis. It is probably due to oestrogen dominance on pituitary Thyroid in suboptimal levels sensitize mammary epithelium to prolactin stimulation Methylexanthiones derived from increased intake of coffee, tea, cold drinks, chocolate is associated with development of fibrocystadenosis Oestrogens stimulate proliferation of connective and epithelial tissues Fibrocystadenosis entails simultaneous progressive and regressive change

Clinical Features xx Presentation is during menstruating age group as a bilateral,

painful, diffuse, granular, tender, swelling which is better felt with palpating fingers (poorly felt with palm). xx Common in upper outer quadrant. xx Pain and tenderness are more just prior to menstrua­­tion (cyclical mastalgia). xx It subsides during pregnancy, lactation and after menopause. xx Discharge from the nipple when present will be serous or occasionally greenish. xx Occasionally shotty enlargement of axillary lymph nodes can occur (20%). xx Not fixed to skin, muscle or chest wall.

 

  

  

II. Surgery:

xx Subcutaneous mastectomy with prosthesis place­ment—only in severe, persistent disease. xx Excision of the cyst or localised excision of the diseased tissue. Indications for surgery ™™ ™™ ™™ ™™ ™™

•

xx FNAC (Epitheliosis, when florid is undoubtedly prema-

lignant).

Treatment I. Conservative line of management is preferred. 1. Reassurance, avoid caffeine, chocolate, salt. 2. Medical (Drugs) –– Goal: -- To stop progression. -- To relieve pain. -- To reverse changes. -- To soften breast tissue. –– Indicated when: -- Fibroadenosis is not increasing in size. -- No nipple discharge especially blood. -- No psychological effect.

Intractable pain Florid epitheliosis—on FNAC Bloodgood cyst Persistent bloody discharge Psychological reason

Note:

Investigations xx Ultrasound. xx Mammography.

choice. It contains gamolenic acid which reverses saturated to unsaturated fatty acids. 1000–3000 mg/day for 4–6 months— but costly. It also contains 7% of linolenic acid and 72% of linoleic acid. Gamolenic acid—120 mg/day. Danazol—interferes with FSH and LH (gonadotrophin releasing hormone inhibitor); most effective drug; but second drug of choice; used in severe cases; 200 mg/day; very effective but causes acne, hirsutism, weight gain and amenorrhoea. It is teratogenic and so cannot be used if patient is planning for pregnancy. Bromocriptine—lowers prolactin—2.5 mg/day for 3 months. Tamoxifen—10 mg BD is an antiestrogenic drug. LHRH agonist (Goserelin) is reserved for refractory cases. It shows 96–99% success. But it causes reversible postmenopausal symptoms. Vitamin E and B6 are tried. NSAIDs—oral and topical. Diuretics even though used by many—not effective.

•

Subcutaneous mastectomy is removal of entire breast with retaining skin over the breast, areola and nipple. It is done through a submammary Gaillard Thomas incision. Adequate skin flap containing subcutaneous fat is raised which maintains the blood supply of the flap and prevents flap necrosis. After haemostasis drain is placed. Breast implant can be placed in subcutaneous/submuscular plane either immediately or as delayed reconstruction. Indications for subcutaneous mastectomy are—fibrocystadenosis with epitheliosis, sclerosing adenosis, persistent nodules, gynaecomastia and DCIS. Macrocysts (>1 cm) is an advanced form of fibrocystic disease; occurs in women in their forties and pericystic fibrosis develops later making cyst harder.

SCLEROSING ADENOSIS xx It is a benign proliferative condition of terminal duct lobular units with increased number of acini. xx It occurs in 30–50 years of age group. xx It may be diffuse or focal. xx Multiple, small, firm, nodules with fibrous tissue and tiny cysts are common pathology. xx Recurring pain alike cyclical mastalgia and often breast mass (20% cases) is the presentation.

Gratitude, joy, love, passion, excitement, enthusiasm, hope, goal, satisfaction, humility, contentment – are different needs of happy life but difficult to acquire.

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SRB's Manual of Surgery xx Tender breast often with palpable tender firm mass may be felt with granular surface. xx It contains proliferative terminal ductules and acini with proliferation of stroma often with deposition of calcium. Number of acini per terminal duct is increased more than double the number of normal lobule. There is lobular enlargement, fibrous stromal proliferation and distortion. xx Complex type is with papilloma and epithelial hyperplasia often with fibroadenoma. Radial scar is a variant of this. xx Condition mimics carcinoma clinically, radiologically and histologically. xx It is at present included in ANDI. xx Sclerosing adenosis can co-exists with both or either invasive and in situ carcinoma breast. xx Mammography may show distortion, asymmetrical density, amorphous calcifications mimicking carcinoma breast. xx MRI is better investigation with guided trucut or stereotactic or vacuum assisted biopsy. xx It is considered as an independent risk factor for developing breast cancer with 1.5–2 higher risk. But it is not a precancerous condition. xx Treatment: Like ANDI. Regular follow is needed.

xx Cells show hypercellularity and pleomorphism. xx It may be a variant of intracanalicular fibroade­noma of

breast (Giant type).

Clinical Features xx They occur in premenopausal women (30–50 years). xx It is usually unilateral, grows rapidly to attain a large size

with bosselated surface.

xx Swelling is smooth, nontender, soft, fluctuant with necrosis

of skin over the summit due to pressure.

PHYLLOIDES TUMOUR (CYSTOSARCOMA PHYLLOIDES/SEROCYSTIC DISEASE OF BRODIE) xx They are not simply giant fibroadenoma. xx They show a wide spectrum of activity, varying from almost

a benign condition (85%) to a locally aggressive and sometimes metastatic tumour (15%). xx Depending on mitotic index and degree of pleomorphism they are graded as low grade to high grade tumours. xx When malignant (sarcoma) spreads to lungs or bone. xx Phylloides tumour is the most commonly occurring nonepithelial neoplasm of the breast, although it represents only about 1% of tumors in the breast. It can also often be fibroepithelial. xx They can be benign, borderline or malignant. Gross: Large capsulated area with cystic spaces and cut surface shows soft, brownish, cystic areas.

Fig. 8.16: Phylloides tumour of left breast (Cystosarcoma phylloides of left breast).

Fig. 8.17: Operated specimen of cystosarcoma phylloides. xx Skin over the breast is stretched, red and with dilated veins Fig. 8.15: Cystosarcoma phylloides of right breast. Note the dilated veins. Tumour occupies the entire breast.

Microscopy: xx It contains cystic spaces with leaf like projections, hence

the name (Phylloides—Greek—leaf-like).

over it. Tumour is warmer, not fixed to skin or deeper muscles or chest wall. Nipple retraction is absent. Lymph nodes are usually not involved. These are the differentiating features from carcinoma. xx Tumour grows rapidly; undergoes necrosis at various places; causes cystic areas. xx Recurrence is common.

Breast Cyclical xx xx xx xx xx

Pain related to menstrual cycles. Usually seen in ANDI like fibrocystadenosis. Present in women of menstruating age group. Pain is more during menstruation. It is bilateral, diffuse with “heavy feeling”.

Treatment: xx xx xx xx xx xx xx xx xx

A

Evening primrose oil 325 mg BD. Gamolenic acid 120 mg BD. Danazol (100–200 mg BD)—antigonadotrophin agent. Bromocriptine (2.5 mg BD)—prolactin inhibitor. Tamoxifen (20 mg daily). GnRH analogue 3.6 mg injection depot-monthly. Testosterone undecanoate 40 mg BD. Vitamin B6, B12. Analgesics.

Noncyclical xx Other causes of breast pain are periductal mastitis, malignancy, cervical root pain, musculoskeletal pain, previous surgery, Tietze’s syndrome, idiopathic, Mondor’s syndrome. xx It is unilateral, chronic, burning or dragging in nature, occurs both in pre- and postmenopausal age group. xx 5% of breast cancers present as pain during first presentation.

Treatment:

B Figs 8.18A and B: Recurrent cystosarcoma phylloides.

Investigations xx xx xx xx

Ultrasound. FNAC, core biopsy Mammography. Chest X-ray CT chest in malignancy to see secondaries.

Treatment xx Excision or subcutaneous mastectomy is done. xx If malignant (sarcoma), total mastectomy is indicated.

MASTALGIA (“Pain in the Breast”) xx 45% of women report breast pain, 21% severe. xx An entity that is ubiquitous; has an unknown aetiology, and a poorly understood. xx Mastitis, carcinoma presenting with only mastalgia (8%). xx Patients who are on HRT, caffeine, tobacco, large pendulous breasts, etc.

Types xx Cyclical—65%. xx Noncyclical—30%. xx Chest wall pain—5%.

xx xx xx xx

Cause has to be identified. Malignancy has to be ruled out. Avoid coffee and stress. Proper support to breasts.

Tietze’s syndrome:

Costochondritis of second costal car­ti­­lage, commonly seen in females, mimics mastalgia.

TRAUMATIC FAT NECROSIS It may be due to either direct or indirect trauma (trauma may not be noticed many times).

Pathogenesis Capillary ooze causes triglyceride in the fat to dissociate into fatty acids. It combines with calcium from the blood resulting in saponification which causes inflammatory reaction and later presents as a non­progressive swelling in the breast.

Features xx Painless swelling in the breast which is smooth, hard, nontender and adherent to breast tissue. xx It is nonprogressive, nonregressive. xx Investigations:  FNAC shows chalky fluid with fat globules.  Mammography to rule out malignancy. xx Differential diagnosis: Carcinoma breast. xx Treatment: Excision.

Saying ‘no’ to something is actually much more powerful than saying ‘yes’. — Tom Hanks

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Fig. 8.20: Galactocele.

A

Treatment xx Aspiration of the content. xx Excision (submammary incision). xx Abscess when formed should be drained under general

anaesthesia under cover of antibiotics.

MASTITIS Types

1. Subareolar. 2. Intramammary. 3. Retromammary (submammary).

Subareolar Mastitis

B Figs 8.19A and B: Traumatic fat necrosis.

GALACTOCELE xx Seen in lactating women. xx Occurs during cessation of lactation. Often up to 10 months

after lactation.

xx It is due to the blockage of lactiferous duct resulting in

enormous dilatation of lactiferous sinus.

xx It is the infection under the areola due to cracks in the nipple

or areola. It results from an infected gland of Montgomery or a furuncle of the areola. There is blockage of the ducts of these glands. xx Often it is associated with duct ectasia—causing formation of abscess, sinus and fistula. xx It is common in nonlactating women. xx Risk factors are – diabetes, smoking, nipple cracks.

xx It contains milk and epithelial debris within. xx It is a retention cyst in subareolar region attaining large size.

Clinical Features xx Lump in the lower quadrant of the breast which is usually

unilateral, large, soft, fluctuant, with smooth surface.

xx It is usually nontender. xx It may get precipitated, inspissated or get calcified. When

it is calcified it mimics carcinoma breast. If it gets infected it will form an abscess. xx When it is cystic other cystic swelling in the breast should be ruled out.

Investigations xx Ultrasound. xx FNAC. Aspiration shows thick, creamy, greenish/brown

fluid.

Fig. 8.21: Diagram showing subareolar, intramammary and retromammary abscess.

Breast

Fig. 8.23: Typical breast abscess with features of acute inflammation.

Clinical features: Fig. 8.22: Subareolar abscess.

Clinical features xx Red, inflamed, edematous areola with a tender swelling underneath. xx Nipple retraction may develop. Differential diagnosis Paget’s disease of the nipple. Treatment xx Under cover of antibiotics pus is drained by making a subareolar incision.

xx Continuous throbbing pain in the breast and high grade fever. xx Diffuse redness, tenderness, warmness and brawny indura-

tion in the breast.

xx Purulent discharge from the nipple. xx Entire breast may get involved eventually. xx Occasionally tender fluctuant swelling (10%) may be felt;

ulceration and discharge can occur at a later period. Tender axillary lymph nodes may be palpable. xx It is difficult to differentiate initial stage of mastitis (stage of cellulitis) from stage of breast abscess formation. When it is treated with antibiotics without incision and drainage eventually it may get organised to form a nontender, hard breast lump with sterile pus inside—stage of antibioma formation.

Intramammary Mastitis (Breast Abscess)

Differential diagnosis:

a. Lactational abscess of the breast: Commonly seen in lactating women. Usually up to 6 months of lactation period. It occurs in 3% of breastfeeding mothers.

Inflammatory carcinoma of breast.

Precipitating factors

Investigations xx Blood total and differential count.

Cracked nipple Retracted nipple Improper cleaning of the nipple Inadequate milk sucking by baby or milk expression causing stasis ™™ Infection from the mouth of the baby ™™ Haematoma getting infected ™™ ™™ ™™ ™™

Mode of infection: Bacteria (Staph. aureus—most common) enters the breast during sucking through the cracked nipple. Occasionally, it can be from haematogenous spread. Staphylococcus epidermidis, streptococci, anaerobic bacteria also can cause acute mastitis. Gram-negative and other bacterial infections can supervene later. Staphylococcus aureus causes clotting of milk in the blocked duct and multiply. Duct initially gets blocked by epithelial debris or by retracted nipple. Initially it begins in one quadrant but later involves entire breast.

Fig. 8.24: Breast abscess in a male patient. Breast abscess eventhough is uncommon in males, it can occur in puberty and middle age.

When arms are raised fully above the head, visible signs of breast carcinoma frequently becomes more apparent. —Hugh Auchincloss

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SRB's Manual of Surgery xx US breast to identify an abscess, its location, size, loculi.

US guided aspiration can be done; pus should be sent for culture and sensitivity.

Treatment: xx Antibiotics—cephalosporins, flucloxacillin and amoxicillin. xx Repeated US guided aspirations (using 18 gauge needle

with saline lavage) can be tried which avoids surgery and scar—ideal and standard now. xx Drainage under general anaesthesia, a counter incision may be needed. It is not advisable to wait till the formation of abscess. Often takes very long time to heal after surgery causing distress to patient and surgeon as well. Indications for drainage in mastitis/breast abscess Mastitis not resolving with antibiotics in 48 hours Persistent fever and progression of mastitis Brawny induration Do not wait for abscess to form (fluctuation to develop) ™™ ™™ ™™

Complications: xx Antibioma formation. xx Sinus formation, skin necrosis, milk fistula formation. xx Recurrent infection, bacteraemia, septicaemia. Note:

• • • •

Proper antibiotics are needed. Support to breast is done to relieve pain. Milk from affected breast should be removed either manually or using breast pump. Occasionally milk suppression may be needed if milk fistula or recurrent abscess develops. It is achieved by giving bromocriptine (2.5 mg BD for 2 weeks) or stilbestrol.

Treatment: xx Antibiotics. xx Repeated aspirations. xx Drainage and later cone excision of the duct is done.

Retromammary Mastitis xx It is due to tuberculosis of the intercostal lymph nodes or

ribs beneath or suppuration of the intercostal lymph nodes.

xx Breast is normal.

Causes ™™ ™™ ™™ ™™ ™™

Tuberculosis of intercostal lymph nodes Tuberculosis of ribs beneath Suppuration of intercostal lymph nodes Empyema necessitans Infected haematoma

Investigations: xx xx xx xx

Chest X-ray, FNAC, ESR. Peripheral smear. US of breast and chest wall. Often CT scan chest may be needed.

Treatment: xx Cause has to be treated. xx Drainage through submammary/retromammary incision. Note:

• • • • • •

Mastitis of infancy (Witch’s milk) is due to maternal hormone in infant blood. It usually subsides but may cause suppuration. Mastitis of infancy affects both sexes equally. Mastitis of puberty is common in boys, is invariably unilateral with tender, swollen and inflamed breast. Mastitis of mumps is usually unilateral and can occur in both sexes. Bacterial mastitis is seen in adult women, commonly lactating and is due to staphylococci infection. Subareolar mastitis is due to infection of gland of Montgomery or due to areolar furuncle.

ANTIBIOMA If intramammary mastitis is not drained but only treated by antibiotics, pus localises and becomes sterile (flaques) with a thick fibrous tissue cover and it is called as antibioma. A

B

Figs 8.25A and B: (A) Incision and counter-incision for breast abscess; (B) Drain should be placed after incision and drainage in such abscesses. Often gauze drain can be used.

b.  Nonlactational abscess of the breast:  It commonly occurs in duct ectasia and periareolar infections. Common organisms are bacteroides, anaerobic streptococci, enterococci and Gram-negative organisms. It is commonly recurrent with tender swelling under the areola.  It is common in diabetes mellitus and immunosuppression.

Features xx Previous history of mastitis treated with antibiotics. xx Swelling which is painless, smooth, nontender, hard, fixed

to breast tissue without involving the pectorals and chest wall. xx Differential diagnosis: Carcinoma breast (Scirrhous carcinoma breast). xx Investigations: FNAC; mammography; US breast. xx Treatment: Excision (Submammary incision). Later antibiotics are given. It should be sent for histology.

Breast DUCT ECTASIA xx It is dilatation of lactiferous ducts due to muscular relaxa-

tion (myoepithelial relaxation) of duct wall with periductal mastitis. xx It is also called ‘plasma cell mastitis’ as periductal inflammation contains plasma cells. xx Commonly many ducts are involved. xx Hormonally induced myoepithelial relaxation with poor ductal absorption of secretions and desquamated cells causing obstruction are the probable other causes and features.

Features xx Greenish discharge or creamy/paste like from the nipple. xx Indurated mass under the areola which is often tender. xx Retraction of nipple which occurs at later stage of the

disease. Slit like retraction of nipple due to fibrosis occurs. Eventually it forms an abscess and fistula. Often they are bilateral and multifocal. More common in smokers—in relation to arterial path­ology. Common in multiple pregnancies, perimenopausal age, hyperprolactin status. xx May present as mastalgia. xx Axillary nodes may be palpable as nonspecific. xx Secondary bacterial infection (anaerobic) is common. xx Differential diagnosis: Carcinoma breast. xx Investigations:  Discharge study, FNAC.  Mammography. xx xx xx xx

MONDOR’S DISEASE (Henri Mondor— Paris, 1939) xx Mondor’s disease is spontaneous thrombophlebitis of the super­ ficial veins of the breast and anterior chest wall. xx Cause is not known. History suggestive of injury or infection is not observed. xx Presents as a thrombosed subcutaneous cord (2–3 mm sized) which is attached to the skin. xx On raising the arm above, a narrow, shallow subcutaneous groove appears alongside the cord like thrombosed vein. xx The thoracoepigastric vein, the lateral thoracic vein, and the superior epigastric vein—are involved. The upper, inner portions of the breast are never involved. xx Trauma, infection, surgery may be the cause but clearly not proved and so controversial. xx Rarely penile Mondor’s disease and Mondor’s in the arm are observed. xx It is often a self-limiting disease without any recurrence, complication or deformity. xx It often mimics the lymphatic permeation of carcinoma breast. xx Restriction of arm movements, brassiere support and anti-inflammatory drugs may be needed. Occasionally refractory cases need surgical excision of involved segment of vein.

TUBERCULOSIS OF THE BREAST xx It is relatively rare. Even though it is rare, often seen in India (4% of benign breast diseases). It may be due to high resistance offered by mammary gland tissue to the survival and multiplication of the tubercle bacillus, a resistance similar to that offered by spleen and skeletal muscle. xx Usually associated with active pulmonary tuber­culosis. xx Infection reaches through blood or retrograde lymphatic spread from lymph nodes of axilla. xx Common in lactation. xx Nipple and areola are not commonly involved. xx Lump—irregular ill-defined; Peaud’ orange; discharge, sinus, matted axillary nodes often with sinus are the features. xx Presents as a swelling in the breast with cold abscess, sinuses and a typical bluish appearance of surrounding skin with matted lymph nodes in the ipsilateral axilla.

Fig. 8.26: Duct ectasia—ductography.

Treatment xx It is important to stop smoking. xx Cone excision of involved major ducts (Adair-Hadfield

operation).

xx Antibiotics. xx Melhem Novel modified breast ductal system excision.

Fig. 8.27: Tuberculosis of breast showing undermined lesion.

Transillumination in a case of duct papilloma may reveal an opacity in the line of the duct due to pent-up blood. —William J Moore

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SRB's Manual of Surgery xx Differential Diagnosis: Carcinoma breast. xx Investigations:  FNAC.  Frozen section biopsy is useful to differentiate from carcinoma.  Excision biopsy.

Treatment xx Antituberculous drugs—INH, rifampicin, ethambutol,

pyrazinamide.

xx Drainage of cold abscess. Note:

•

Mastectomy is not done.

BREAST CYSTS xx They are cavities lined by epithelium in the breast containing fluid. It arises from destruction and dilatation of breast lobule and terminal ductules. It is due to nonintegrated stromal and epithelial involution. xx Cyst may be microscopic or macroscopic. It contains straw coloured or green or opaque fluid. xx Incidence is very high (1 in 14 females). It is common after the age of 35 years up to menopause. It is uncommon after menopause. Hormone replacement can cause cyst formation in old women. xx Cyst size varies with menstruation due to influence of ovarian hormones. xx Cysts can be multiple (50%). Often bilateral. xx Cysts can be recurrent (50%). xx Risk of breast cancer in breast cyst is very less (0.1%). But incidental associated carcinoma may be present in 3% of breast cysts. xx Clinically—smooth, soft, fluctuant often transilluminating welllocalised swelling may be felt. xx Differential diagnoses are—Bloodgood cyst, haematoma, cystic necrosis in a carcinoma, Brodie’s disease, galactocele, lymph cyst, hydatid cyst. xx Investigations—US of breast; FNAC. Mammography to rule out associated carcinoma.

A

B Figs 8.29A and B: Ultrasound look of breast cysts—simple and complex type. Note:

• • • • • • • •

Fluctuation in the cyst is checked by examiner standing behind the patient. Mammogram should be done if patient is more than 35 years. 21 Gauge needle is used for aspiration. Fluid is sent for analysis (cytology); evidence says that if fluid is clear no need to send for cytology but in practice it is commonly sent and safer to send also. All fluid which is altered should be sent for cytology. After aspiration one should examine for the residual lump. FNAC of this residual lump should be done. Cyst when recurs (30%) reaspiration should be done. Patient should be examined for refilling of the cyst in 6 weeks.

Other cystic swellings of the breast Fig. 8.28: Retention cyst in areola.

Treatment xx Aspiration for two times. xx Surgical excision is done if cyst recurs after two aspirations or if there is bloody discharge or residual mass if felt after aspiration.

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Bloodgood cyst Breast abscess Hydatid cyst Galactocele Serocystic disease of Brodie Cystic necrosis in carcinoma breast Lymph cyst Haematoma in breast

Breast GALACTORRHOEA xx It is secretion of milk not related to pregnancy or lactation. xx It is always bilateral.

xx It can be diffuse—involving all quadrants or small well

localised hard subareolar nodule.

Primary galactorrhoea is due to: xx Stress and other factors. It is physiological in puberty or menopause. Reassurance is the treatment. Secondary galactorrhoea is due to: xx Dopamine receptor blocking agents like haloperidol, methyldopa, chlorpromazine, metoclopramide or by hyperprolactinaemia due to pituitary tumours. It enhances the prolactin activity. xx Hypothyroidism. xx Drugs like oral contraceptives, atenolol, clonidine, ranitidine. xx Ectopic prolactin secreting tumours usually from lungs (bronchogenic carcinoma). xx Chronic renal failure.

Management xx Estimation of serum prolactin, T3, T4, TSH, CT/MRI head. xx Bromocriptine therapy. xx Treatment of cause. Causative drug should be stopped and different drugs should be used for the needed condition. Note: Witch’s milk is secretion of milk in both male and female infants due to maternal hormonal effects in foetus. It lasts up to three weeks after child birth.

GYNAECOMASTIA (Greek—Women Breast) xx It is hypertrophy of male breast more than usual due to

increase in ductal (epithelial) and connective tissue (stromal) elements often attaining features of female breast. xx It can be unilateral or bilateral. Bilateral can be symmetrical or asymmetrical.

Fig. 8.31: Right-sided gynaecomastia (well-localised—puffy nipple).

Aetiology xx Oestrogen excess—increased estradiol secretion due to

testicular tumour (Leydig cell) or nontesticular tumours from adrenal cortex, lung, liver; hyperthyroidism (increases conversion of androgen to estrogen), liver diseases, oestrogen therapy for prostate cancer. xx Androgen deficiency—aging, Klinefelter’s/Kallmann syndromes, eunuch, ACTH deficiency. xx Secondary testicular failure—cryptorchidism, orchitis, trauma, CRF, etc. xx Drugs (25%):  Increases estrogen activity (digitalis, anabolic steroid)/ estrogen synthesis (reserpine, theophylline, frusemide).  Inhibition of testosterone synthesis—cimetidine, phenytoin, spironolactone.

Features Initially there will be florid proliferative stage of ductal epithelium with oedematous stroma without acini (1 year); later there will be quiescent stage with ductal dilatation and stromal fibrosis. xx Always one should examine genitalia and liver. xx It is physically embarrassing; psychologically devastating. Fig. 8.30: Gynaecomastia—right side breast (diffuse type). Compare with opposite side to note the difference in size. xx It is nonphysiological stimulatory oestrogen excess or

inhibitory androgen deficiency. There is nonphysiological hypertrophy of male breast attaining the size of female breast with increase in connective and ductal tissues.

Types Neonatal gynaecomastia is due to action of placental estrogen Pubertal (25%) in young boys is due to excess estrogen level in relation to testosterone. It is usually unilateral. Here breast tissue will be more than 2 cm in diameter in nonobese young male ™™ Senescent in old is due to fall circulating testosterone causing elative hyperestrinism ™™ ™™

In the presence of troubles some people grow wings; others buy crutches.

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SRB's Manual of Surgery Prepubertal—may also be seen in girl child It can be: ™™ Puffy nipples ™™ Pure glandular ™™ Adolescent hereditary ™™ Adult—most common ™™ Androgenic Simon’s classification of gynaecomastia: Group 1—Minor visible type without skin redundancy Group 2 A—Moderate without skin redundancy Group 2 B—Moderate with minor skin redundancy Group 3—Gross pendulous breast ™™

xx Breast irradiation to prevent gynaecomastia in prostatic

cancer patients who are on oestrogen therapy.

xx Causative drugs should be stopped. xx Testicular tumours, hyperthyroidism should be treated if

they are the causes.

xx Testosterone can be given if hypogonadism is the cause. xx Endoscopic assisted subcutaneous mastectomy is done and

under trial mainly for cosmetic purpose.

Note:

• •

Rarely gynaecomastia may turn into malignancy. Gynaecomastia is a differential diagnosis for male breast cancer. 80% of Klinefelter’s syndrome shows gynaecomastia; it has got very high-risk (20 times) of developing carcinoma.

DUCT PAPILLOMA

Differential Diagnosis xx Pseudogynaecomastia—adipose tissue deposition as a part

of obesity; needs liposuction. xx Pectoral muscle hypertrophy. xx Lipoma, dermoid, haematoma.

Presentations xx Diffuse enlargement of breast occupying all quadrants. xx Often well-localised, small, firm or hard nodule under the

areola which is often painful and tender. Causes

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Idiopathic—25% Teratoma testis—3% Ectopic hormonal production in bronchial carci­noma Anorchism, after castration Adrenal and pituitary disease Leprosy, because of bilateral testicular atrophy Drugs (25%): Stilbestrol, digitalis, cimetidine, spiro­nolactone, INH, phenothiazides Liver diseases and liver failure—10% Klinefelter’s syndrome (XXY Trisomy), Kallman syndrome Primary or secondary hypogonadism Hyperthyroidism Renal diseases, dialysis induced (1%)

Investigations Relevant to the cause, e.g. liver function tests, DNA study, hormone assay, FNAC, USG breast.

Treatment xx Well-localised type which is symptomatic or patient is

psychologically worried is treated by surgical excision using circumareolar incision. xx Large diffuse gynaecomastia needs Gaillard Thomas submammary incision for excision. xx Reduction mammoplasty; nipple reduction surgeries. xx Drugs—tamoxifen, clomiphene, androgens (dihydrotestosterone), danazol, testolactone as aromatase inhibitor—but less useful. Drugs are given only for 6 months. Gynaecomastia more than 2 years duration is less likely to show benefit from drugs.

™™ ™™ ™™

It is the most common cause of bloody discharge from nipple It is usually single, from a single lactiferous duct It blocks the duct causing ductal dilatation

xx They are epithelium lined true polyps of breast lactiferous ducts. xx Usually, it is 10 mm

1–10 mm

50% cases (5 fold). xx 5% of male breast cancers are DCIS. xx Minor ductal epithelial proliferation is the typical histology. xx Invasive ductal cancer forms in the same breast and same quadrant of DCIS unlike LCIS. DCIS is an anatomical precursor of invasive DC. xx Presence of > 25% of DCIS component is present in the main invasive tumour or if DCIS is present elsewhere in the surrounding breast tissue, it is called as extensive in situ component. xx Nipple discharge and often small swelling are main presentations. xx US assisted FNAC and mammography are the needed investigations. xx Risk of lymph node spread in DCIS is less than 4%. So axillary dissection is not necessary. xx Sentinel Lymph Node Biopsy and proceed is the preferred method.

Score 5–7 conservative surgery + Radiotherapy Score 8–9 total mastectomy Nottingham Prognostic Index (NPI): ( 0.2 × Tumour size in cm) + Lymph node stage + Tumour grade NPI score—5.4 Poor prognosis with 15% survival

Management of DCIS ™™ ™™ ™™ ™™ ™™ ™™

FNAC confirms the disease but will not differentiate from DCIS and invasive carcinoma Mammography, US breast, MRI breast Routine metastatic work up Breast conservative surgery with RT to breast and axillary dissection after SLNB (if +ve) Hormone therapy (tamoxifen) prevents both local recurrence and development of new primary breast carcinoma Total mastectomy is done in DCIS when—positive margin after wide local excision; two or more primary tumour; when radiation to breast is not possible (collagen diseases); tumour/breast size ratio is not appropriate for conservative surgery and DCIS in pregnancy. Skin sparing mastectomy (SSM) may be ideal in such occasions with immediate TRAM/LD flap.

Types of Carcinoma Breast 1. Scirrhous carcinoma: It is 60% common. It is hard, whitish, or whitish yellow, noncapsulated, irregular, with cartilagi-

Fig. 8.38: Specimen of carcinoma breast. Cut section showing tumour tissue of scirrhous type (most common type).

Breast nous consistency. It contains malignant cells with fibrous stroma. 2. Medullary carcinoma (5%): Also called as ‘encephaloid type’ because of its brain like consistency. It con­tains malignant cells with dispersed lymphocytes.  Medullary variant with some features of pure form shows

uniformly high grade aggressive tumour cells with negative ER, PR, HER2 NEU cell surface receptors (triple negative). They express molecular markers of basal/myoepithelial cells and so now termed as basal-like breast cancers.

3. Inflammatory carcinoma/Lactating carcinoma/Mastitis carcinomatosis:

Most aggressive type of carcinoma breast. It is 2% common. It is common in lactating women or pregnancy. It mimics acute mastitis because of its short duration, pain, warmth and tenderness.  Clinically, it is a rapidly progressive tumour of short duration, diffuse, painful, warm often involving whole of breast tissue with occurrence of peau d’ orange, often extending to the skin of chest wall also.  More than 1/3rd of skin over the breast is involved; diffuse lymphoedema is due to tumour emboli within dermal lymphatics. Underlying localised palpable mass need not be evident clinically. It should be differentiated from other LACB with skin involvement where underlying palpable mass is well evident.  Mammography may not show any finding except skin thickening. Inflammatory carcinoma of breast is a clinical diagnosis.  Ductal or lobular invasive type with cancer cells in dermal lymphatics is the histology.  It rapidly metastasises to chest wall, bone and lungs.  It is always stage IIIB carcinoma (T4d). FNAC confirms the diagnosis—it contains undifferentiated cells. Punch biopsy is ideal and better which shows undifferentiated cells.  Total count is normal. Treatment  External radiotherapy and chemotherapy.  Salvage surgery whenever possible.  It has got worst prognosis. Differential diagnosis  Acute mastitis—total count is increased here.    

4. Colloid carcinoma: It produces abundant mucin, both intraand extracellularly carrying better prognosis. 5. Paget’s disease of the nipple I believe it has not yet been published that certain chronic affections of the skin of the nipple and areola are very often succeeded by the formation of scirrhous cancer in the mammary gland…. In the majority (the affection) had the appearance of a florid, intensely red, raw surface…like the surface of very acute diffuse eczema. —James Paget, 1874  It is superficial manifestation of an intraductal carci­noma. The

malignancy spreads within the duct up to the skin of the nipple and down into the sub­stance of the breast. It mimics eczema of nipple and areola.

 In Paget’s disease, there is a hard nodule just underneath the

areola, which later ulcerates and causes destruction of nipple. Histolo­gically, it contains large, ovoid, clear Paget’s cells with malignant features. Paget’s hyperchromatic cells are located in rete pegs of epidermis containing intracellular mucopolysaccharides as clear halo in cytosol.

Differences between Paget’s disease and eczema of nipple Paget’s disease

Eczema

1. Unilateral

1. Bilateral

2. Edges are distinct

2. Edges are indistinct

3. Itching absent

3. Itching present

4. Seen in menopausal women

4. Occurs during the time of lactation

5. Vesicles absent

5. Vesicles present

6. Nipple is usually destroyed

6. Nipple is usually intact

7. Underlying lump is usually present

7. No underlying lump

Fig. 8.39: Paget’s disease of the breast.  It is 2% common. 90% is invasive ductal carcinoma. 70%

shows mass underneath nipple and areola.

 Breast conservation surgery (BCS) is difficult here; hence,

MRM is needed.

6. Tubular, papillary, cribriform are other types of duct carcinomas. 7. Atrophic scirrhous carcinoma:  Seen in elderly females. It is a slow growing tumour which has

got better prognosis.

 FNAC is diagnostic.  Mastectomy or curative brachytherapy (using breast moulds)

is the treatment of choice.

 It is curable.

8. Lobular carcinoma in situ:

 It originates in terminal duct lobular unit only of female breast

showing its distension and distortion.

 It is 12 times more common in white females. Predominantly

perimenopausal.

 It is 3–5% common. High chance to predispose to invasive

cancer. 35% of LCIS may develop invasive lobular carcinoma either in same or contralateral breast; 65% may develop invasive ductal cancer (same side/opposite side/both sides). LCIS is a marker/predictor of increased risk of invasive breast cancer; not an anatomical precursor unlike DCIS. It is now advocated as a risk factor for developing breast cancer.

Accountable, dependable, reliable are qualities that make a person responsible.

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SRB's Manual of Surgery  It is multifocal, bilateral (50%).  It is an incidental pathological entity. Classical type carries

     

better prognosis; pleomorphic type does not so; occasionally mixed ductal and lobular in situ may be seen. Clinically it does not form a lump. Need not be detected by mammography, as it does not provoke calcification. 50% cancers can develop in the contralateral breast. Immunohistochemistry using e-cadherin antibody shows positive reaction in lobular carcinoma. It has poor prognosis due to bilateral, multifocal nature and difficulty in identifying it. Tamoxifen (risk reduction in premenopausal) or raloxifen (postmenopausal) often with bilateral total mastectomy is the treatment.

Biological Behaviour and Clinical Features of Carcinoma Breast Most common site is upper outer quadrant (60%) because breast tissue is more in this quadrant.

9. Disease of Reclus: It is a rare intracystic papil­liferous carcinoma of breast presenting as a cystic swelling with bloody discharge from the nipple.

Grading of the Tumour xx It is based on nuclear pleomorphism; tubule formation; mitotic rate. xx It can be—well-differentiated (grade 1); moderately differentiated (grade 2) and poorly differentiated (grade 3). Tumour doubling occurs in 6 months with reaching 1 cm in size in 30 doublings. Breast cancer more than 1 cm has its own blood supply and so high chances of systemic spread and so systemic therapy is a must.

Fig. 8.40: Mass in the upper outer quadrant—is the most common site of the carcinoma breast.

Elston-Ellis Modified Bloom-Richardson Grading System Nuclear pleomorphism: Score 1—relatively small uniform nuclei; score 2—intermediate pleomorphic nucleoli; score 3—relatively large prominent nucleoli ™™ Mitotic count: Score 1—< 10% mitoses in 10 HPF; score 2—1020% mitoses; score 3—>20% mitoses ™™ Tubule formation: Score 1—>75% cells in tubule forms; score 2—10-75% cells in tubule forms; score 3—< 10% cells in tubule forms ™™

Grade

Score

Favourable Unfavourable Grade I Grade II Grade III

1 Up to 3 3–5 6–7 8–9

™™ ™™ ™™

Well differentiated low grade—grade 3, 4, 5 Moderately differentiated intermediate grade—grade 6, 7 Poorly differentiated high grade—8, 9

Presentation of carcinoma breast ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Lump in the breast which is hard, painless (most common). At least tumour should become 1 cm to clinically palpable Nipple discharge is the second common presentation Ulceration and fungation Axillary lymph node enlargement; supraclavi­cular lymph node enlargement Chest pain and haemoptysis Bone pain, tenderness, and pathological fracture Pleural effusion, ascites Liver secondaries, secondary ovarian tumour Pain in the lump in 10% cases

Fig. 8.41: Carcinoma breast over the most common site—upper outer quadrant—more visible on raising the arm.

Cutaneous Manifestations of Carcinoma Breast xx Peau d’orange: Due to obstruction of dermal lymphatics,

openings of the sebaceous glands and hair follicles get buried in the oedema giving rise to orange peel appearance. xx Dimpling of skin due to infiltration of ligament of Cooper. xx Retraction of nipple due to infiltration of lactiferous duct. xx Ulceration, discharge from the nipple and areola. xx Skin ulceration and fungation. xx Cancer-en-cuirasse: Skin over the chest wall and breast is studded with cancer nodules appearing like an armour coat. xx Tethering to skin.

Breast

Fig. 8.42: Quadrants of breast. Carcinoma is more common in upper outer quadrant as more breast tissue is located in this quadrant.

Fig. 8.45: Peau d’orange appearance of skin.

Fig. 8.46: Lump (painless) in the breast is the commonest presentation; here lump is in inner quadrant. Fig. 8.43: Carcinoma breast with extensive skin involvement.

Fig. 8.44: Cancer-en-cuirasse with malignant nodules in the chest wall and skin.

Fig. 8.47: Bloody discharge from the nipple in carcinoma of breast.

Have a heart that never hardens and a temper that never tires and a touch that never hurts.

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SRB's Manual of Surgery Axillary group of nodes are: 1. Anterior along lateral thoracic vessels (Pectoral). 2. Central embedded in fat in the centre of the axilla. 3. Posterior along subscapular vessels. 4. Lateral along axillary vein. 5. Apical lies above pectoralis minor tendon in continuity with the lateral nodes and receive efferents from all the groups. Spread to these lymph nodes occur by lymphatic permeation. Groups 1st and 2nd are commonly involved. Groups 3rd and 4th are rarely involved. Finally Group 5th is involved.

Fig. 8.48: Ulcerated carcinoma breast with peau d’orange. Note the lymph node enlargement.

Spread restricted to level I nodes carries better prognosis. Spread to level II has poor prognosis. Spread to level III indicates worst prognosis.

Spread into the Deeper Plane xx Into pectoralis major muscle (is confirmed by observing

the restricted mobility of the swelling while contracting the PM muscle). xx Into latissimus dorsi muscle (extending the shoulder against resistance). xx Into serratus anterior (by pushing the wall with hands without flexing the elbow). xx Into the chest wall (breast will not fall forward when leaning forward, and while raising the arm above the shoulder, breast will not move upwards as it is fixed to the chest wall).

Fig. 8.50: Carcinoma right breast with ulceration in the primary (P) with axillary lymph node secondaries (S). xx Interpectoral, lies between pectoralis major and minor

muscle (Rotter’s nodes). Presently involvement of these lymph nodes are considered due to retrograde spread. These lymph nodes are cleared during Patey’s mastectomy.

xx From axillary lymph nodes spread occurs to supra­clavicular

lymph nodes by lymphatic embolisation.

Fig. 8.49: Advanced carcinoma left breast involving entire breast with nodularity.

Lymphatic Spread xx It occurs through:

 Subareolar Sappey’s lymphatic plexus (presently its

significance is discounted).  Cutaneous lymphatics.  Intramammary lymphatics.

xx Lymphatic drainage of the breast is predominantly through

axillary (75%) and internal mammary lymph nodes.

xx Through dermal lymphatics, it may spread to opposite breast

or to opposite axillary lymph nodes.

xx Spread may occur into internal mammary lymph nodes of

same side and then to mediastinal lymph nodes.

xx Contralateral internal mammary lymph nodes can also get

involved by retrograde spread.

xx Fixed enlarged axillary nodes can cause lymphoedema due

to lymphatic block; venous thrombosis and venous oedema due to venous block; and severe excruciating pain along the distribution of the median and ulnar nerves (rare in radial nerve) with often significant sensory and motor deficits due to tumour infiltration of the cords of brachial plexus (medial cord often lateral cord).

Breast Once axillary lymph nodes get fixed, it can result in lymphoedema of the upper limb. It develops gradually. Compression of nodes on axillary vein can cause sudden onset of venous oedema of upper limb (Venous edema develops faster, and is more proximal with bluish discolouration of the skin of the upper limb. It may lead to venous gangrene and so the compres­sion has to be relieved early by radiotherapy).

Breast is in subcutaneous plane, but its extension, axillary tail of Spence passes through an opening in the deep fascia (foramen of Langer). Often it is difficult to differentiate between lymph node in pectoral region and tumour invasion of axillary tail. Mobility will be indepen­dent if it is a lymph node, but if it is an axillary tail tumour, it is along with the primary tumour in the breast.

Fig. 8.51: Carcinoma breast right sided causing extensive oedema (lymphoedema) in right upper limb.

Fig. 8.52: Carcinoma breast involving axillary tail of Spence.

Haematogenous Spread Causes of lymphatic block in carcinoma breast

Treatment of lymphoedema of arm

• Involvement and fixation of the axillary nodes level I, II and III

• Elevation of limb • Elastic stockings • Pneumatic compression

xx Bone (most common) (70%)

 Lumbar vertebrae, femur, ends of long bones, thoracic

vertebrae, ribs, skull, in order.

 They are osteolytic lesion often with pathological frac-

ture.

• After levels I, II and III dissection • Drugs like diuretics and benzopyrones

 Presents with painful, tender, hard, nonmobile swelling,

• After radiotherapy to axilla

 70% of secondaries in bone in a women is due to carci-

• Inoperable fixed nodes in axilla • Recurrent axillary disease

with disability. noma breast.

 Spine secondaries can cause paraplegia.

• May be associated with canceren-cuirasse • Secondary infection Effects of lymphatic obstruction • Peau d’orange • Brawny oedema of arm—indurated, painful, non-pitting— occurs in fixed nodes in axilla • Elephantiasis chirurgens—after radical mastectomy or radiotherapy to axilla • Cancer-en-cuirasse—seen in locally advanced carcinoma of breast. Skin of chest wall is studded with hard fixed nodules like armour coat (of soldiers) • Lymphangiosarcoma after radical mastectomy or MRM (StewartTreve’s)

Fig. 8.53: Carcinoma breast with rib secondaries.

Mammary fistula presents as a recurrent abscess that points and discharges on to the areola and continues to discharge for weeks at a time.  —Sir Headly Atkins

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SRB's Manual of Surgery Transcoelomic Spread Through mediastinal lymph nodes, it may spread into peri­ toneal cavity causing secondaries in liver, peri­t oneum, ovary (Krukenberg secondaries—occurs in menstruating age groups. During ovulation, cells get attached over the ovarian capsule). Note:

Present concept of Krukenberg tumour is haemato­g enous and lymphatic modes of spread. Older concept of transcoelomic spread is no longer well-accepted.

Recurrent Carcinoma of Breast xx It is recurrence of breast cancer after initial curative therapy;

A

B

Figs 8.54A and B: (A) Pathological fracture of the humerus due to metastatic secondaries from the carcinoma breast. (B) Intramedullary nailing as a treatment for pathological fracture.

Fig. 8.55: Osteolytic secondaries involving ischium and pubic bones.

recurrence can occur in months or years after initial therapy; it may occur in the same original site (local recurrence) or elsewhere in the body at distant site (distant recurrence). xx In local recurrence, lump or ulceration or nodules which are hard and fixed can appear at the local site; if patient has undergone breast conservative surgery then nipple discharge, destruction of nipple areolar complex may develop. xx Recurrence can also occur at axillary or neck (supraclavicular) nodes as palpable, hard often fixed and fungating mass. xx Distant recurrences are of features of metastatic disease in the bone, lungs, liver or brain. xx Factors which are of poor prognostic one are risk factors for recurrence—tumour size/spread/stage, histologic/nuclear grade, receptor status. xx It is evaluated by trucut biopsy from local area, FNAC of the nodes, CT chest, MRI brain, isotope bone scan and PET scan. Treatment differs in individual patients depends on the type and site of recurrence—wide local excision, nodal clearance, RT, chemotherapy, hormone therapy, immunotherapy. Recurrence carcinoma carries poor prognosis.

Features of bone secondaries ™™ ™™ ™™

Pain Swelling Pathological fractures

xx Liver—either through blood, occasionally through transcoe-

lomic spread.

xx Lung—causes malignant pleural effusion and ‘cannon ball’

secondaries. xx Brain—causes increased intracranial pressure, coning. xx Adrenals and ovaries. Common sites of distant spread in carcinoma breast ™™ ™™ ™™ ™™ ™™ ™™

Bones—70% (lumbar vertebrae, pelvic bones, long bones) Lungs and pleura—20–30% Soft tissues—5–15% Liver—10–12% Brain—2–5% Adrenals—2–5%

Fig. 8.56: Recurrent carcinoma breast. Note: Dominant breast mass is three-dimensional, distinct from surrounding tissue of same breast, asymmetric in relation to other breast.

Breast Breast Self-examination (BSE) Breast self-examination plays a major role in early detection and intervention of breast carcinoma. This under­lines the importance of advocating self-examination of the breast. Ideally done once a month just after the menstruation, as during this time breasts are less engorged. In postmenopausal age group it is done at monthly regular intervals. ™™ Examine both breasts ™™ Remind the patient that 90% of breast lumps are not cancer. ™™ Better way is in lying down position with arm raised with a mattress support behind ™™ Palpation should be using the fingers over all quadrants of the breast ™™ If any doubtful swelling is palpable, consult the surgeon ™™ American Cancer Society recommends monthly BSE after 20 years of age ™™ Nursing mother should perform BSE just after feeding the baby

xx There is 5 fold increase in 2nd breast cancer on opposite side in a female, who has had breast cancer on ipsilateral side. xx LCIS, multifocal breast cancer, family history are other risk factors. xx Choudary Millis criteria that help to differentiate primary contralateral breast cancer from metastatic—in situ change, different histological pattern, different differentiation shown in opposite breast, clinically or by evaluation ipsilateral tumour has not shown any features of spread. xx It is investigated like any breast cancer, staged accordingly and treated. xx If tumour on the opposite side is metastatic then it will show separate histology and differentiation with mammography showing less infiltrative, diffuse, without microcalcifications but with oedema. If it is metastatic, it is stage IV disease.

TNM STAGING OF CARCINOMA BREAST (AJCC 7th EDITION, 2010) Primary Tumour (T)

Fig. 8.57: Self-examination of breast is done in lying down position.

Bilateral Breast Cancer xx It is separate primary breast cancer on the opposite side in a patient who is having or treated for ipsilateral breast cancer. xx It can be synchronous or metachronous.

Tx Primary tumour cannot be assessed (already treated elsewhere without documentation). T0 – No evidence of primary. Tis – Carcinoma in situ. Tis (DCIS) Ductal carcinoma in situ. Tis (LSCIS) Lobular carcinoma in situ. Tis (Paget’s) – Paget’s disease of the nipple not associated with invasive carcinoma or with DCIS/LCIS in the parenchyma T1 – Tumour less than 2 cm (20 mm) T1 mi – Microinvasion 1 mm or less in greatest dimension T1a – 1 – 5 mm T1b – 5 – 10 mm T1c – 10 – 20 mm T2 – 20 – 50 mm in greatest dimension T3 – >50 mm in greatest dimension T4 – Any size with direct extension to the chest wall or skin or both. T4a – Tumour of any size extending into the chest wall, not including only pectoralis muscle invasion/adhesion (chest wall means ribs, intercostal muscles and serratus anterior but not pectoral muscles). T4b – Ulceration or ipsilateral satellite nodules and/or oedema including peaud’orange of the skin which do not meet the criteria for inflammatory carcinoma. T4c – T4a and T4b. T4d – Inflammatory carcinoma.

Regional Lymph Nodes (N)

Fig. 8.58: Bilateral breast cancer operated.

Nx – Regional nodes cannot be assessed N0 – No regional nodes involved N1 – Metastases to mobile ipsilateral level 1 and 2 axillary nodes N2 – N2a – Metastases in ipsilateral level 1 and 2 axillary nodes which are fixed to one another (matted) or other structures N2b – Metastases only in clinically detected ipsilateral internal mammary nodes and in the absence of clinically evident level 1 and 2 axillary nodes

Wise man has got the art of knowing what to overlook.

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SRB's Manual of Surgery N3 — N3a – Metastases to ipsilateral infraclavicular lymph nodes (level III axillary) with or without level 1 and 2 axillary lymph node involvement. N3b – Metastases to ipsilateral internal mammary lymph nodes with clinically evident level 1 and 2 axillary lymph nodes involvement. N3c – Metastases to ipsilateral supraclavicular lymph nodes with or without axillary or internal mammary lymph node involvement.

Note:

• • •

T1 includes T1mi T0 and T1 with nodal micrometastases are excluded from stage IIA and is classified as stage IB. If patient presents with M1 prior to neoadjuvant systemic therapy, the stage is considered as stage IV and will remain stage IV regardless of response to neoadjuvant therapy.

Molecular subtypes of carcinoma breast ™™

Note: Clinically detected is defined as detected by imaging studies (excluding lymphoscintigraphy) or by clinical examination and having characteristic highly suspicious for malignancy or a presumed pathologic micrometastases based on the fine needle aspiration biopsy with cytologic examination. Confirmation of clinically detected metastatic disease by fine needle aspiration without excision biopsy is designated with f suffix.

™™

™™ ™™

Distant Metastases (M) M0—No clinical or radiological evidence of distant metastases cM0(i+)–No clinical or radiological evidence of distant spread metastases but deposits of molecularly or microscopically detected tumour cells in circulating blood, bone marrow or other non-regional nodal tissue that are no larger than 0.2 mm in a patient without symptoms or signs of metastases. M1—Distant detectable metastases as determined by classic clinical and radiographic means and/or histologically proven larger than 0.2 mm.

™™ ™™

™™ ™™

Note:

• • • • •

Mx is removed in 7th edition of TNM staging. c: stage given by clinical examination of a patient. p: stage given by pathologic examination of a surgical specimen. y: stage assessed after chemotherapy and/or radiation therapy; in other words, the individual had neoadjuvant therapy. r: stage for a recurrent tumor in an individual that had some period of time free from the disease.

IIA

IIB IIIA

IIIB

IIIC IV

DNA microarrays (gene) analysis Oncotype Dx – 21 gene assay (16 cancer related and 5 normal genes) ™™ Mammaprint – 70 genes are analysed ™™

Note:

Stage Groups Stage 0 IA IB

Basal-like (15–25%): ER–ve, PR–ve and HER2–ve; also called triple negative breast cancer (TNBC). Most BRCA1 breast cancers are basal-like TNBC. They are high grade, aggressive with poor prognosis. Common in black and young individuals; high incidence of lung and brain secondaries. Luminal A (50%): ER+ HER2 –ve and low grade. They are slow growing and occur in postmenopausal women. They respond well hormone therapy. Luminal B (15–20%): ER+ PR+ve Her2 +ve (triple positive) but often high grade. They respond to chemotherapy. Her2 rich (10%): ER –ve. Poorly differentiated, aggressive with higher incidence of brain secondaries. Treated with chemotherapy and trastuzumab. Laptinib is used if brain metastases are present as trastuzumab will not cross the blood-brain barrier. Normal breast like (5%): ER +ve, Her2 –ve. Luminal ER–/AR+: recently identified androgen responsive subtype which may respond to antihormonal treatment with bicalutamide. ERBB2/HER2+: has amplified HER2/neu. Claudin-low: a more recently described class; often triplenegative, but distinct in that there is low expression of cell-cell junction proteins including E-cadherin and frequently there is infiltration with lymphocytes.

TNM status Tis N0 M0 T1/T1 mi N0 M0 T0 N1 mi M0 T1/T1 mi N1mi M0 T0 N1 M0 T1 N1 M0 T2 N0 M0 T2 N1 M0 T3 N0 M0 T0 N2 M0 T1 N2 M0 T2 N2 M0 T3 N1 M0 T3 N2 M0 T4 N0 M0 T4 N1 M0 T4 N2 M0 Any T N3 M0 Any T any N M1

Manchester staging and Columbia classification are obsolete (not used now). Readers can refer 4th edition if needed. Manchester staging is—1. Mobile tumour in the breast; no deeper fixation; skin if involved lesser the size of the tumour; lymph node spread is absent. 2. Same as stage 1 with mobile discrete axillary nodes. 3. Fixed to pectoralis major or skin involvement more the tumour size or fixed/adherent node. 4. Tumour fixed to chest wall/involvement same or opposite supraclavicular nodes, opposite axillary nodes, opposite breast, cancer en cuirasse, distant blood spread.

Differential diagnosis for carcinoma breast ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Fibroadenosis Traumatic fat necrosis Tuberculosis of breast Bloodgood cyst Filariasis breast Mastitis Antibioma Galactocele Mondor’s disease Cystosarcoma phyllodes

Breast Investigations in Carcinoma Breast xx Mammography.

™™

™™ ™™ ™™ ™™ ™™ ™™

Benign lesions are smooth, rounded with well-defined margins with weak internal echoes and compressibility. It can be elliptical, hyperechoic/hypoechoic smooth lesion. Cyst is anechoic, oval/round, well circumscribed lesion. Disadvantage is lesions less than 1 cm may not be identified. FNAC can be done under US guidance. It is cheaper, easily available and there is no risk of radiation. It is preferred method of screening in young females where mammography is not done and in pregnancy and early lactation. US of axilla also can be done to assess axilla and to do guided FNAC of node.

Fig. 8.59: Mammography in carcinoma breast. Findings ™™ ™™ ™™ ™™

Size and location of mass lesion Microcalcifications signify malignancy Soft tissue shadow is irregular Spiculations

xx Bilateral mammography is done to identify multicentricity,

to have guideline for assessing eventual chemotherapy or RT in LABC. xx Stereotactic mammography guided biopsy is very useful. xx LCIS may be missed in mammography. xx Fifty per cent of breast cancers can be seen on mammography before they are palpable. xx It is noninvasive with less radiation exposure. xx Five per cent false-positive rate in mammography; hence, biopsy is a must. xx Mammogram is used during follow-up period after conservative breast surgery and of opposite side. xx Ideally specimen mammography is a must after conservative breast surgery to assess the completion; and after core biopsy to confirm the sample tissue. xx Ultrasound of breast:  To find out whether the lesion is solid or cystic.

Fig. 8.60: Ultrasound picture of right breast showing breast mass.

Ultrasound of breast To look for whether the lesion is solid or cystic, margin of the lesion, internal echoes, retro-tumour acoustic shadowing, compressibility, dimensions. ™™ Irregular margin, irregular internal echoes, irregular posterior shadowing, noncompressibility, ratio between anteroposterior to width (lateral/horizontal) dimensions more than 1 are the features of carcinoma. Doppler will show high frequency signals with continuous flow. It is hypoechoic with more vertical taller growth. ™™

Fig. 8.61: Ultrasound breast is basic noninvasive simple investigation to assess breast lump. xx FNAC (Martin and Ellis 1930): It is very useful in diag-

nosing the carcinoma breast. US guided FNAC is also used. But negative results are difficult to interpret because it may

If you don’t know where you’re going, you may miss it when you get there.

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SRB's Manual of Surgery be due to sampling errors and so requires further diagnostic methods. FNAC of opposite breast, lymph nodes, opposite axillary lymph nodes are also often required. It is done with 23 gauge needle using FNAC aspiration special syringe (aspiration gun). With the lump held firmly, the needle is passed into the lump and with negative pressure continuous aspiration is done until adequate material comes through the needle (suction pressure of 40 cm of H2O is created into the syringe). Needle with syringe is removed without negative pressure. Material is collected on a slide; a smear is made using 100% alcohol. Cytology is studied after staining it under microscopy. xx Minimum six aspirations are done. xx Giemsa, Papanicolaou, hematoxylin and eosin stains are used. xx Repeat FNAC can be done for further 2 times. xx But it gives only cytological diagnosis. Receptor study cannot be done. xx It is difficult to differentiate between in situ and invasive breast cancer by FNAC.

xx Corecut/Trucut biopsy:

 It is done under local anaesthe­sia. It gives clear histo-

 

 

Advantages FNAC is least painful, can be done on OP basis, reliable and cheaper. Malignant deposits will not occur along FNAC track (only contraindication for FNAC is testicular tumour). Note:



logical evidence and also confirms DCIS (FNAC cannot confirm DCIS). This allows proper neoadjuvant/primary chemotherapy, receptor status of the tumour. Wide bore needle biopsy with vacuum is also used. 14–18 gauge spring loaded needle is used. Multiple punctures are needed. US guided biopsy is also done. Large core biopsy is done using 6–14 gauge needle; single puncture is sufficient; large single sample of tissue is obtained. Vacuum-assisted core biopsy is also done. Stereotactic mammographic/MRI/US guided core biopsy are also used in small/impalpable lesions. Stereotactic core biopsy is done in prone position with compressed breast. Under local anaesthesia, 3 mm incision is made and 11 gauge core needle is passed under digital mammographic guidance. Multiple core biopsies are taken using vacuum. A clip may be placed under guidance at the site of the lesion as marker. Mammography of core biopsy specimen is done to confirm the sample tissue. If stereotactic biopsy is inconclusive then a wire localised surgical excision should be done. Core needle biopsy is the method of choice. Image guided biopsies

It is done when lump is not clearly palpable. ™™ US guided core needle biopsy. ™™ Stereotactic mammographic core needle biopsy. ™™ Mammography guided wire localisation using needle sheath over the tumour and through an incision under local anesthesia hook is reached and biopsy is done. It is used if core needle biopsy fails in localising nonpalpable lesion. ™™ MRI guided core needle biopsy.

FNNAC is Fine Needle Non-Aspirating Cytology.

xx Frozen section biopsy: If FNAC fails even after two trials

Fig. 8.62: FNAC of breast lump. Reliability of FNAC and mammography FNAC

Mammography

Sensitivity (true positivity)

90–98%

90%

Specificity (without falsepositive)

98–100%

90%

False-negative

2–10%

10%

False-positive

Near 1–5%

10%

FNAC scoring C0 : No epithelial cells C1 : Scanty epithelial cells, benign C2 : Benign cells C3 : Atypical cells C4 : Suspicious cells C5 : Malignant cells

or in cases of negative FNAC, then on table frozen section biopsy is done for diagnosis. Frozen section biopsy also has got drawbacks. It has got 20% false-negative results. So its use at present is under debate eventhough it is practiced in few oncocenters. It is not ideal method. xx Excision biopsy:  It is done only when FNAC is inconclusive and a facility for frozen section is not available. Incision should be planned in such a way that it will be included in eventual mastectomy. xx Edge biopsy:  Done only when there is ulceration and fungation. Diathermy should be avoided in incision biopsy as it may distort the histology of tumour and study of hormone receptor status may not be possible. xx Oestrogen receptor study:  They are oestrogen sensitive receptors, which are cytosolic, glycoprotein present in the breast and tumour tissue. It is an important indicator of prognosis of carcinoma breast.  Tissue for receptor study is sent at low tempe­rature in

Breast ice flasks. It is assessed by quantitative analysis (Frozen –70°).  If value is more than 10 units (f/mols) per n gram of tissue it is called as ER +ve status. ER positivity is common in postmenopausal women (60%) compared to premenopausal women (30%). If value is less than 10 units per gram of tissue it is called as ER –ve status. In ER +ve status –– Prognosis is good. –– Hormone therapy including tamoxifen is more beneficial. –– Response to treatment is better. In ER –ve status –– Prognosis is poor. –– Hormone therapy is not very beneficial (but used) as compared to ER +ve patients. –– Response to treatment is not good. xx Progesterone receptor (PR status) study or Her 2 Neu receptor status or cErb B2 (growth factor receptor study) are other studies done at present to plan the therapy and assess the prognosis.  Her 2/Neu receptor (Human epidermal growth factor receptor 2 Neu oncogene [Neuropilin 2]) is a tyrosine kinase receptor and is associated with ER negative, high grade, tumours. It carries poor prognosis. Over expression of Her 2/Neu shows good response to adriamycin. xx Study of discharge from the nipple.  Nipple discharge is usually unilateral in carcinoma breast. Ductal lavage may be useful in some patients. Microcatheter of 1 cm length is introduced gently into the ductal opening. 10 ml saline is infused through the catheter. Fluid is withdrawn into the syringe and cytological analysis is done. xx Sentinel lymph node biopsy (SLNB):  The first axillary node draining the breast (by direct drainage) is designated as the sentinel lymph node (SLN). SLN is first node involved by tumour cells and presence or absence of its histological involvement, when assessed will give a predictive idea about the further spread of tumour to other nodes. The incidence of involvement of other nodes without SLN is less than 3% and so if SLNB is negative nodal dissection can be avoided but regular follow-up is needed. SLNB is done in all cases of early breast cancers, T1 and T2 without clinically palpable node.  It is not done in clinically palpable axillary node as there is already distortion of lymphatic flow due to tumour. It is also not done in multifocal and multicentric tumours, as there is involvement of many lymphatic trunks from different places of breast, and chances of false-negative is high.  Sentinel node is localised by preoperative (within 12 hours prior) or perioperative injection of patent blue





 





(Isosulfan vital blue dye 2.5–7.5 ml) or 99m TC radioisotope labelled albumin (one mCi on previous day)/ sulphur colloid (6 hours before) near the tumour (peritumour area) or into subdermal plexus around the nipple. Marker will pass through the sentinel node which can be visually detected as blue staining or with a hand held gamma camera; and is biopsied with a small incision made directly over it. Frozen section biopsy or touch imprint cytology is done for presence of malignant cells. If there is no involvement of sentinel node by tumour then further axillary dissection is not required as skip lesions (skipping sentinel node) occur only in less than 3% cases. Detection rate of sentinel node for blue dye and radioisotope is 90% and 98%, respectively. Subdermal/ subareolar injection of radioisotope has got better sentinel node localisation than peritumour injection. But better imaging is obtained by peritumour injection and so peritumour injection is usually practiced. Radioisotope tracer injection done in the early morning of the day of surgery into peritumour area and perioperative injection of patent blue dye in subareolar region—as a combined method is often used in many centres. After injection of patent blue, breast is massaged continuously to enhance the uptake. Incision is made after 5–7 minutes between pectoralis major and latissimus dorsi to identify blue stained lymphatics which are traced to 2–3 blue lymph nodes. Hand-held radio-probe is used to identify the sentinel node which is later excised. Often 2–3 nodes are removed. Paraffin section histology is better than frozen section to identify positive sentinel lymph node. If report comes negative immunohistochemistry test is done to confirm that lymph node is negative for tumour. Sentinel lymph node biopsy should be done before wide local excision of the primary tumour. Wide local excision of the primary tumour is done after SLNB in the same sitting. SLNB is less invasive than axillary dissection. It is ideal in early invasive carcinoma. Positive SLNB is again classified as macrometastasis (> 2 mm) or micrometastasis (< 2 mm). SLNB is contraindicated in patients who are allergic to vital blue dye or radio-colloid, in pregnancy and in inflammatory carcinoma of breast. Complications of SLNB are rare. They are—blue tattooing of skin which gradually fades; blue—green urine and stool for short period; allergic reactions; anaphylaxis (0.1%); seroma formation. Blue dye binds to oxyhaemoglobin and so artificially registers in oximeter as hypoxaemia.

Note:

Facility for SLNB is not available in many centres.

It is better to light a small candle than to curse the darkness.

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B

Fig. 8.63: Sentinel lymph node biopsy (SLNB) of breast. Note: Spread by skipping the sentinel node is less than 3%. xx Axillary sampling:

 It is often done with an adequate axillary incision. 10–15

nodes are removed for sampling. It is not commonly practiced now (Minimum 10 nodes should be removedlevel I nodes). xx MRI of breast:  To differentiate scar from recurrence.  To image breasts of women with implants.  To evaluate the management of axilla and recurrent disease.  It is useful in screening females with high-risk group and young women and in pregnancy.  T1 and T2 weighed images are taken.  Irregular mass with spiculations, changes in skin and nipple, lymphoedema are the findings in carcinoma breast.  Lesion indeterminate by US/mammography is assessed by MRI.  Ionising radiation is not there with MRI.  It is the method choice of imaging breasts in pregnancy.  It is better in dense breasts.  Patient lies in prone position with breasts placed over breast coils; both precontrast and postcontrast (gadolinium) MRI are taken.

A Fig. 8.64A

C

D Figs 8.64B to D

Figs 8.64A to D: MRI of breast is ideal method to assess or identify recurrence after BCS or after breast implants. (A) T1 weighted with contrast; (B) T1 weighted; (C) T1 weighted with contrast and fat suppressed; (D) MRI perfusion image (Courtesy: Dr Raghavendra Bhat, MD, Radiologist, Balmatta Scan and Research Centre, Mangaluru).  Disadvantages are—it is costly; nonavailability; not

sensitive for premalignant lesions. It cannot be done in patients who are having incompatible metal prosthesis in the body. It is not accurate if done within 9 months of the radiotherapy for carcinoma breast. xx Tumour markers: CA 15/3 (normal value < 40 U/ml of serum) are used mainly during follow-up period. CEA, CA 15-3, CA 27-29 may be useful. xx MRI spine/pelvis show osteolytic secondaries in the bone like vertebra and pelvic bones. xx Radioisotope bone scan to look for secondaries in bone in

Breast visceral metastases in patients with symptoms or signs of metastatic disease. xx CT scan of chest, abdomen and brain whenever needed.  CT is said to be more useful to detect secondaries in these regions. xx Chest X-ray:  To look for pleural effusion, cannon ball secondaries in lungs, mediastinal lymph nodes, secondaries in rib. xx Ultrasound abdomen:  To look for liver secon­daries, ascites, ‘Krukenberg’ tumour. xx X-ray spine shows osteolytic secondaries. xx Ductography:  It is contrast study of ducts of breast in case of unilateral nipple discharge. Fine cannula is passed under vision carefully through the duct opening into the duct and 0.2 ml of dilute water-soluble contrast media is injected into the duct. Craniocaudal and mediolateral X-ray films are taken. Contrast irregular filling defect may be observed. xx Breast ductal endoscopy:  It is useful in direct visualisation of the tumour in DCIS and invasive ductal carcinomas. But it is technically difficult and demanding. xx Thermography:  It is not very sensitive test (50%). Malignant tumours are hypervascular and so transmitted temperature is detected through different thermographic methods. xx Blood count, complete liver function tests are needed.

A

Triple assessment includes: ™™ ™™ ™™

Clinical assessment-history (age) and examination. Radiological imaging US/MRI/ mammography (after 40 years). Cytological or histological analysis FNAC/core biopsy- pathology.

Newer investigation modalities for carcinoma breast Stereotactic core biopsy using computer mam­mography Vacuum-assisted biopsy using 11-guage biopsy probe (becoming popular) ™™ Needle localised biopsy under mammographic guidance ™™ I125 – seed localisation biopsy ™™ ™™

B Figs 8.65A and B: Isotope bone scan is a must in LABC/T3 disease.

advanced cases. It is not done routinely in early carcinoma of breast. Indications for whole body bone scan in carcinoma breast ™™ ™™ ™™ ™™

T3, T4 advanced disease Advanced nodal disease Bone pain, bone swelling, pathological fracture Chest/liver secondaries

xx PET scan:

 It may be an effective single scan for bone, soft tissue or

Treatment Treatment of carcinoma breast It is usually through a combined approach ™™ Surgery ™™ Radiotherapy ™™ Hormone therapy ™™ Chemotherapy

A. Surgeries for Carcinoma Breast xx Total (simple) mastectomy:

 Along with the tumour, entire breast, areola, nipple, skin

over the breast, including axillary tail are removed. There is no axillary dissection. Often the patient is sub­jected to radiotherapy later (External) to axilla. Pectoral fascia

The place to improve this world is first in one’s own heart, head and hands.

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SRB's Manual of Surgery is removed along with breast specimen; breast tissue superficial to axillary fascia is removed. xx Total mastectomy with axillary clearance:  Commonly used procedure. Total mastectomy is done along with removal of axillary fat, fascia and lymph nodes. Level I and II axillary nodes are removed along with total/simple mastectomy.

Fig. 8.69: Gray incision for mastectomy in carcinoma breast which extends to opposite side.

Fig. 8.66: Horizontal incision for total mastectomy. Fig. 8.70: Greenough incision for mastectomy.

Fig. 8.67: Oblique incision extending into the anterior axillary fold for radical mastectomy. Fig. 8.71: Kocher’s incision for mastectomy.

A

B Figs 8.68A and B: Stewart incision for mastectomy.

Fig. 8.72: Orr incision for mastectomy.

Breast coracoid process to clear level II nodes. Medial and lateral pectoral nerves should be preserved (otherwise atrophy of pectoral muscle occurs). Later from the apex of axilla level III nodes are cleared. Nerve to serratus anterior, nerve to latissimus dorsi, intercostobrachial nerve, axillary vein, cephalic vein and pectoralis major muscle are preserved. Wound is closed with a suction drain.  Scanlon’s operation: It is a modified Patey’s operation wherein instead of removing pectoralis minor, it is incised to approach the affected level III lymph nodes.  Auchincloss modified radical mastectomy: Here pectoralis minor muscle is left intact and level III lymph nodes are not removed—commonly done now.

Fig. 8.73: Rodman incision for mastectomy.

Mastectomy specimen should be carefully inspected and sent to pathology department

xx Modified radical mastectomy [MRM]:

 Patey’s operation: It is total mastectomy along with clear-

ance of all levels of axillary nodes and removal of pectoralis minor muscle. It is enblock dissection of breast and axilla. An elliptical incision is made from medial aspect of the second and third intercostal space enclosing the nipple, areola and tumour extending laterally into the axilla along the anterior axillary fold. Upper and lower skin flaps are raised. Breast with tumour is raised from the medial aspect of the pectoralis major muscle. Dissection is proceeded laterally with ligating pectoral vessels. Once dissection reaches axilla, lateral border of pectoralis major muscle is cleared with level I nodes. Pectoralis minor is divided from

A

B

D

xx Specimen is sent in formalin for histology. xx It is sent in saline in low temperature for ER/PR/Her 2 neu status study (histochemistry). xx Specimen mammography is often done. xx Tumour grading, tumour clearance, nodal involvement—its number and capsular breach are assessed histopathologically. xx Halsted Radical Mastectomy* (Complete Halsted) (RM): Structures removed are:  Tumour.  Entire breast, nipple, areola, skin over the tumour with margin.  Pectoralis major and minor muscles.  Fat, fascia, lymph nodes of axilla.  Few digitations of serratus anterior.

C

E

Figs 8.74A to E: Different steps of Patey’s mastectomy with incision, flap raise, dissection in breast and axilla and specimen after surgery.

Failure is the only opportunity to begin again more intelligently.

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SRB's Manual of Surgery Structures retained are (ABC) ™™ ™™ ™™

Axillary vein Bells nerve (nerve to serratus anterior) Cephalic vein

Complications are lymphoedema and eventual lymphangiosarcoma (after 3 to many years later) of the limb. Note:

Hangensen and Stout (1943) criteria were used in identifying the clinically inoperable cases (for Halstead’s RM) in olden days: Extensive oedema of skin over the breast and/or arm; satellite nodules; supraclavicular or internal mammary nodes; inflammatory carcinoma of breast; distant spread.   William Stewart Halsted (1852–1922) pioneered in radical mastectomy, surgeries for inguinal hernia, invented the use of surgical gloves, mosquito haemostat forceps, mattress suture, use of cocaine and anaesthetic agent, developed resident program in surgery. He did cholecystostomy to his mother using kitchen knife as emergency. He gave his own blood to his delivering sister (who became critical) to save her life and it is one of the earliest blood transfusions.

xx Conservative breast surgeries:

a. Wide local excision: It is removal of unicentric tumour with 1 cm clearance margin. Incision is made directly over the tumour. Skin flaps should not be raised. Normal breast tissue of 1 cm clearance with excision of tumour is done. Pectoral fascia is usually not opened in wide local excision unlike in total mastectomy. The specimen is marked after placing in orientation grid and mammography of the specimen is done followed by frozen section biopsy to look for clearance. At least 1 mm clearance is needed for adequacy. Margins where clearance is less than 1 mm need re-excision at that particular margin. If margins show no clearance then patient requires probably total mastectomy. So prior consent for mastectomy should be taken. Drain is not placed; deeper cavity is usually not closed/obliterated as small seroma gets absorbed without any problem. Skin is closed cosmetically. It is often called as lumpectomy or partial mastectomy; but better term is wide local excision. It is ideal

Fig. 8.75: Note the original Halsted and modified Halsted incision.

Fig. 8.76: Complete Halsted operation—radical mastectomy with removal of fat, lymph nodes, pectoralis major, pectoralis minor, entire breast with tumour and skin over the breast, nipple and areola.

Breast breast conservative surgery. Along with this, axillary dissection through separate incision and RT to breast and chest wall area is given.

b. Quadrantectomy: It is removal of entire segment/quadrant with ductal system with 2–3 cm normal breast tissue clearance. It is not advocated now as it is proved that there is no outcome benefit between wide local excision and quadrantectomy. Quadrantectomy is done as a part of QUART therapy (by Umberto Veronesi from Milan, Italy) along with axillary dissection (level I and II) through separate incision and RT to breast area.

xx Toilet mastectomy:  In locally advanced tumour, tumour with breast tissue and whatever possible is removed to prevent further fungation. But its use and significance is under question. It is often done after giving chemotherapy. xx Extended radical mastectomies:  It includes radical mastectomy + removal of internal mammary lymph nodes of same side with or without opposite side. It is not done at present. xx Skin sparing mastectomy (SSM/Key hole mastectomy) is becoming popular with different approaches. xx Lumpectomy/partial mastectomy is better called as wide local excision which includes removal of tumour with gross rim (1 cm) of normal breast tissue.  Small (< 0.5 cm), unicentric, low grade tumour of breast may be treated with lumpectomy with RT. But it is technically difficult to assess such indications. Stereotactic wire localisation, lumpectomy with clearance, specimen mammography and proper follow-up are the needed principles in such situations. One should achieve negative margin of 1 mm on frozen section and with post-excision mammography of retained breast to confirm adequacy of excision. Presently term ‘lumpectomy’ is rarely used to such procedure which basically is wide excision with 1 cm clearance. Patient always needs postoperative adjuvant RT and chemotherapy if poor prognostic factors are present.

A

B

Complications of MRM/mastectomy Injury/thrombosis of axillary vein Seroma—50–70% Shoulder dysfunction 10% Pain (30%) and numbness (70%) Flap necrosis/infection Lymphoedema (15%) and its problems Axillary hyperaesthesia (0.5–1%) Winged scapula Occasionally if on table injury occurs to axillary vein, it should be repaired by vascular suturing using 5 zero polypropylene ™™ Numbness over the medial upper part of the arm can occur due to intercostobrachial nerve injury ™™ Pectoral muscles atrophy if medial and lateral pectoral nerves are injured ™™ Weakening of internal rotation and abduction of shoulder occurs due to injury to thoracodorsal nerve ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Lymphangiosarcoma (Stewart-Treve’s syndrome) of upper limb can deve­lop in patients who have developed lymphoedema after mastectomy with axillary clearance. Usually, it occurs 3–5 years after development of lymphoedema. Such patient may require forequarter amputation. It has got poor prognosis. It presents as multiple subcutaneous nodules.

C

D Figs 8.77A to D: (A to C) Mastectomy specimen with dissected axillary nodes. (D) Organ specimens removed during Patey's operation. Note the pectoralis minor, axillary area and tumour with breast tissue.

He who is afraid of doing too much always does too little.

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Fig. 8.78: Postmastectomy lymphoedema. Note the mastectomy scar.

B. Radiotherapy in Carcinoma Breast Indications: xx Patient who undergo conservative breast surgery, breast is irradiated after surgery. xx After total mastectomy, external irradiation is given to axilla. xx Patients with higher risk of local relapse after surgery: a. Invasive carcinoma. b. Extensive in situ carcinoma. c. Patients under 35 years. d. With multifocal disease. xx In bone secondaries, to palliate pain and swelling. If there is pathological fracture in the bone, internal fixation has to be done along with external irradiation. xx Inflammatory carcinoma of breast. xx In atrophic scirrhous carcinoma of breast, as a curative radiotherapy. xx As preoperative radiotherapy, to reduce the tumour size and downstage the tumour, so that the operability is better. xx More than 4 positive lymph nodes in the axilla, pectoral fascia involvement, positive surgical margins, extranodal spread or in patients with axillary status not known/not assessed. External radiotherapy is given over the breast area, axilla (in selected patients like if axillary dissection is not done or more than 4 positive axillary nodes), internal mammary and supraclavicular area ™™ Total dosage 5000 cGY units ™™ 200-cGY units daily 5 days a week for 6 weeks

Principles: xx It is used in ER/PR positive patients in all age groups (earlier it is used in perimenopausal age groups). xx It is relatively safe, easy to administer. xx It gives prophylaxis against carcinoma of opposite breast. xx It is useful in metastatic breast carcinoma. xx Hormone therapy (tamoxifen) is useful in breast cancer in elderly (positive ER) after wide local excision or occasionally as tamoxifen alone. xx It is now not used in ER negative patients. xx Menopausal status; nodal status; chemotherapy used are not factors to defer the use of hormone therapy. xx Hormone therapy reduces the recurrence rate and so probably improves the life span and quality of life. Includes: xx Oestrogen receptor antagonists—tamoxifen. xx Ovarian ablation by surgery (Bilateral oophorec­tomy) or by radiation. xx LHRH agonists (Medical oophorectomy). xx Oral aromatase inhibitors for postmenopausal women. xx Adrenalectomy or pituitary ablation. xx Progesterone receptor antagonist. xx Androgens—Inj testosterone propionate 100 mg IM three times a week. xx Aminoglutethimide—blocks the synthesis of steroids by inhibiting conversion of cholesterol to preg­ne­nolone— medical adrenalectomy. xx Progestogens, e.g. medroxyprogesterone acetate. Tamoxifen xx It is an antioestrogen. It blocks cytosolic oestrogen receptors. xx Dose is 10 mg BID or 20 mg OD for 5 years. xx Half life of tamoxifen is 7 days; it takes 4 weeks to show its benefits. It reduces the cholesterol and also cardiovascular morbidity. Adverse effects: xx Tamoxifen flare—flushing, tachycardia, sweating, genital itching, vaginal atrophy and dryness (premenopausal), vaginal discharge (postmenopausal), fluid retention, weight gain. xx Occasionally it causes bone pain which should be differentiated from pain due to bone metastasis. It is due to loss of bone density in premenopausal women. xx It increases the incidence of endometrial cancer. xx DVT (3%), pulmonary embolism, CVA, TIA, cataract, fractures.

Radiotherapy in carcinoma breast To chest wall • T3 tumour >5 cm • Residual disease-LABC • Positive margin/close surgical margin of 1 cm, +ve axillary nodes, high nuclear grade, vascular/lymphatic invasion, ER/Pr –ve with over expression HER2 Neu, then adjuvant chemotherapy.

Stage III

Neoadjuvant chemotherapy + MRM + RT + CT + Hormone therapy.

Stage IV

Hormone therapy (Trastuzumab/Lapatinib) with chemotherapy using taxanes or capacetabine + palliative mastectomy (toilet mastectomy if needed when fungation is present)

70%

III

40%

IV

20%

indicator.

xx Age: Younger the age worser the prognosis. xx Sex: Carcinoma male breast has got worser prognosis

compared to female breast. Because of early spread in carcinoma male breast. Lymph node—as a prognostic factor

™™

Causes of death in carcinoma breast

90%

xx Spread to axillary nodes is the most important prognostic

Malignant pleural effusion as secondaries from carcinoma breast ™™

I II

™™ ™™ ™™ ™™ ™™ ™™

Number of nodes: >2 carries poor prognosis Location of nodes Capsular invasion Extranodal status Size of the node: >2.5 cm has poor prognosis More than 4 nodes/level III (apical nodes) involvement has got worst prognosis (5-year survival is 30%) and also decides for radiotherapy to axilla.

xx Stage I and II has got better prognosis. xx Atrophic scirrhous has got best prognosis. xx Medullary carcinoma has got better prognosis than scir-

rhous carcinoma because of lymphocytic infiltration. Invasive carcinoma has got worser prognosis. Inflammatory carcinoma breast has worst prognosis. ER +ve tumours has got better prognosis. Differentiation also decides prognosis. Presence of elastic fibres in histology has got better prognosis. xx Tumour proliferation stages, growth factor and oncogene factors. xx Tubular, colloid, papillary types has got better prognosis. xx Tumour grade, growth factor and oncogene factors. ErbB2—Her-2/Neu positive has got poor prognosis. ErbB1 with overexpression of epidermal growth factor (EGF), TGF alpha and cathepsin D has got poor prognosis. xx DNA flow aneuploid status has got poor prognosis. Low S phase fraction (< 5%) has got good prognosis. xx Size of the tumour—tumour size less than 1 cm has got better prognosis. xx p53 tumour suppressor gene (guardian gene) shows bad prognosis. Prognostic factors are classified as: xx Host factors: Age; sex; menopausal status; family history; previous breast cancer; immunosuppression; nutrition. xx Tumour factors: Tumour size; nuclear grade; staging; receptor status; DNA nature; spread, etc. xx xx xx xx xx

When you get angry, you lose more than your temper.

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Features

Prognosis—5-year survival

Very low-risk primary

DCIS; tubular

>90%

Low-risk primary

Node negative; favourable microscopy

70–90%

High-risk primary

Node positive; unfavourable microscopy

2.5 g/dl Serum-ascitic fluid albumin gradient is 250/cumm AFB in ascitic fluid is seen only 1.016 Glucose 3 cm in depth.

IV – Laceration

Parenchymal disruption 25–75% hepatic lobe; 1–3 Couinaud segments.

V – Laceration – Vascular

Parenchymal disruption more than 75% or more than 3 Couinaud segments. Major hepatic veins or retrohepatic venacaval injuries.

VI – Vascular

Hepatic avulsion.

for trauma) CT scan of chest and abdomen (CT is ideal). xx Diagnostic peritoneal lavage. 10 ml gross blood on initial aspiration, > 1,00,000 cu mm RBCs, > 500 WBCs, and presence of enteric contents suggest positive DPL. Diagnostic peritoneal aspiration only can also be done. xx Hb%, PCV, blood grouping and crossmatching. Adequate amount of blood (5-10-15 bottles of blood) must be kept ready for transfusion, i.e. requires massive transfusion. xx Arterial blood gas analysis. xx Coagulation profile. xx Thromboelastography (TEG) is dynamic form of assessing the coagulation status on table. xx Arteriography to visualise the bleeding branch/vessel in the liver and embolisation can be tried.

Treatment General measures xx IV fluids, blood transfusion (massive), FFP. xx Have both central venous access, and peripheral venous access. xx Bladder catheterisation has to be done to measure the urine output. xx Factor VII—proconvertin (SPCA—0.6 mg/ml up to 4.8 mg); very effective, makes INR normal; but very expensive. Initial conservative nonoperative management xx It is done in—nonprogressive liver injuries in patients who are haemodynamically stable, low grade (I-III) liver injury, need of less than 2 units of transfusion, without peritoneal signs, normal mental status. xx However, CT abdomen (absence of extravasation of contrast during arterial phase can be treated nonoperatively) and repeat CT or regular ultrasound follow-up is a must. xx Replacement of lost blood; prevention of sepsis; regular monitoring by haematocrit, liver function tests, prothrombin time are needed. xx Angiographic embolisation increases the success rate of nonoperative therapy. xx Intensive care unit (ICU) management for 2–5 days; repeat CT scan after 5 days; bedrest to be continued; patient can have normal activity only after 3 months.

xx When at any time patient’s condition worsens, he should be taken up for laparotomy. xx Success rate of nonoperative treatment is 85% in grade I-III injuries; 40% in grade IV–VI injuries. It is the associated injuries which decides the success. xx Intervention radiology methods like angioembolisation through hepatic artery are used especially when there is pseudoaneurysm. But life-threatening hepatic necrosis and gallbladder necrosis can occur. Gallbladder necrosis warrants cholecystectomy.

Specific treatment xx Push (direct compression); plug (plugging the deep track injuries using silicone tube or SB tube); Pringle's manoeuvre; pack (liver wound is directly packed with mop). Damage control surgery initially Phase I – Laparotomy control of bleeding by various methods, closure with pack. Phase II – Resuscitation, managing metabolic insult (hypothermia with temperature 5 cm. Treatment: xx Prior radiotherapy is given to reduce the size and then hemihepatectomy is done. xx Surgery is done when size is large, symptomatic, impending rupture or any other complications. Enucleation or anatomical resection with inflow control is needed. xx xx xx xx xx

Note:

It has got very little or no malignant potential.

2. Hepatic adenomas

Fig. 11.21: Solitary benign cyst of the liver. It is a rare entity. Polycystic liver also can occur. Polycystic liver is associated with polycystic kidney disease. Condition is a rare differential diagnosis for hydatid cyst, hepatoma, and solitary secondary. xx It is congenital in origin and enlarges by ectasia. xx Involution of a large haemangioma can occur forming a

dense fibrosis which mimics metastasis. xx It may compress over gastroduodenum to cause abdominal

pain and vomiting. Acute thrombosis with sudden onset of pain and fever may mimic liver abscess; but symptoms subside gradually in 3–4 weeks. xx Spontaneous rupture is very rare. xx Differential diagnoses – HCC, vascular solitary secondaries, hepatic adenoma, liver abscess. xx In children it is 10–15% of liver tumours. They are multifocal, often involves other organs also. Large one can cause AV shunting leading to CCF. Large childhood hepatic haemangiomas have got 70% mortality due to rupture, DIC, thrombocytopenia. It is confirmed by MRI. It is treated by embolisation, radiotherapy and often resection. xx Cavernous haemangioma, consumption coagulopathy, thrombocytopenia is called as Kasabach-Merritt syndrome.

xx They are common in females (10:1). They present as a solitary nodular lesions in the liver. xx It is said to be due to use of oral contraceptive pills (OCPs). xx It is uncommon in males, but can occur with androgen use. xx It is relatively rare compared to FNH and haemangioma. xx It is commonly solitary; but 20% of cases can be multiple; situation where > 10 adenomas are present is termed as adenomatosis. Multiple adenomas are not related to OCP intake and not more common in females. Multiple type may occur in glycogen storage disease type I. xx Upper abdominal pain (65%) is the commonest presentation. xx AFP is normal but rises if there is malignant transformation. xx They might turn into malignancy, hence resection is advised. xx US, CT scan are diagnostic but angiography is needed prior to resection, as it is vascular. xx MRI is ideal tool. xx Haemorrhage is more common. xx Hepatic adenoma cells are larger, contain glycogen and lipids. They are devoid of bile ducts whereas FNH contains bile duct components. xx Surgical resection is the needed treatment. Limited resection is needed. It is better to do resection prior to pregnancy. In adenomatosis either hemihepatectomy or transplantation may be required. xx OCP should be stopped. Indications for surgical resection ™™ ™™

Rupture of adenomas—50% If there is possibility of turning into malignancy (large adenomas)

Note: Kupffer cells are not present in hepatic adenomas.

3. Focal nodular hyperplasia (FNH) xx It is a benign condition of unknown aetiology, seen in females showing focal overgrowth of func­tioning liver tissue with fibrous stroma support.

Liver xx It is hyperplasia of liver containing all components of liver in disorganized pattern. xx It is 8 times more common in females. xx It contains hepatic cells as well as Kupffer cells which is characteristic. xx It is 2nd most common benign tumour. xx Usually it presents as solitary nodule. xx A sulphur colloid liver scan is diagnostic, shows ‘hot spot’ with a spoke wheel pattern—85%. xx It is a harmless condition. xx CT scan shows central scar with stellate distri­bution of the blood vessels, Kupffer cell activity, without calcifications with homogeneous mass lesion in arterial phase enhancement. xx Telangiectatic FNH and hyperplastic with adenomatous FNH are non-classic forms of FNH, which are 20% common and more common in men. xx It is totally benign tumour; but often difficult to differentiate from fibrolamellar type of HCC. AFP is normal. xx It also should be differentiated from HCC, hepatic adenoma, nodular regenerative hyperplasia of liver (NRH). xx Vague pain abdomen may be the presentation. xx Rupture, bleeding are very rare. xx Histologically it can be typical (with central scar) or atypical (without central scar)—15%. xx Usually it does not require any treatment. OCP should be stopped. Note:

tropical Africa, Taiwan. In Mozambique it is often seen in younger age group—below 30 years. xx Male to female ratio is 4:1. xx It is usually unicentric but occasionally can be multicentric. xx Right lobe is commonly involved.

Fig. 11.22: Hepatocellular carcinoma (HCC/hepatoma) is usually solitary, common in right lobe, attains large size.

Von Meyenburg’s complexes are benign liver malformations that originate from embryonic bile ducts that fail to involute with cystic dilatation. It mimics metastatic liver disease. MRI is essential to diagnose.

Aetiology

PRIMARY MALIGNANT TUMOURS OF THE LIVER

xx Hepatitis B and hepatitis C virus infection. It is more

1. Hepatocellular carcinoma/Hepatoma/HCC (80%). 2. Cholangiocarcinoma (20%). 3. Hepatoblastoma in infants and children. Hepatoblastoma occurs within 2 years of life. It is most common primary malignant tumour of liver in children. It is common in male child. It is derived from fetal or embryonic hepatocytes. Serum AFP is elevated in 90% of cases. CT scan shows vascular mass with speckled calcification. It is highly sensitive to chemotherapy (vincristine, doxorubicin, 5FU). If it is resectable, it is the initial choice of therapy. Liver transplantation is also beneficial.

HEPATOCELLULAR CARCINOMA (HCC/HEPATOMA)

xx HCC is a primary malignant tumour of the liver with hepa-

tocellular differentiation. xx Its incidence is increasing; becoming 4th most common

malignancy worldwide. HCC is the commonest primary liver malignancy (90%). But in the liver, secondaries is the most common malignancy (20 times more common than primary). xx It is common in cirrhotics and hepatitis B and hepatitis C virus infection. xx It is common in Japan, Mozambique, South East Asia,

xx Aflatoxin B1, a product of fungus aspergillus. It is powerful

carcinogen. common in individuals who have chronic positive status for HBs Ag and chronic carriers. Vertical transmission of virus at birth raises HCC rate. In Europe, Japan, USA, HCV infection is more common cause. It is not necessary to develop cirrhosis to cause HCC. It is the infection which is the cause. xx Alcoholic cirrhosis. It is co-carcinogen. xx Clonarchis sinensis infestation. xx Smoking. xx Haemochromatosis, α1 antitrypsin deficiency. xx Hepatic adenoma—potentially malignant. xx Environment related chemicals like DDT, nitrite and nitraterelated food products; trichloroethylene (dry cleaning solvents), biphenyls, carbon tetrachloride, herbicides, solvents like dioxane. xx Tannins, griseofulvin, bush tea (pyrrolizidine), rice toxins. xx Anabolic steroids, polyvinyl chloride.

Pathology Gross It is highly vascular with indistinct margin. Often it is well demarcated by fibrous tissue. Haemorrhage and necrosis are common. xx Hanging type of tumour—tumour attached to normal liver by a small vascular stalk—always very well resectable.

Every job is self portrait of the person who did it.

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SRB's Manual of Surgery xx Pushing type of tumour—large, well demarcated, displaces

normal vasculature—resectable. xx Infiltrative type of tumour—indistinct, infiltrative—often difficult to resect. Other macroscopic classifications of HCC Unifocal –– Expanding with sharp demarcation – portal vein invasion is high –– Pedunculated – type 1 is intrahepatic; type 2 is extra­hepatic –– Spreading type – without a clear demarcation (Engel’s type) ™™ Multifocal – synchronous ™™ Indeterminate – different features in different parts of the liver ™™ Diffuse

Okuda staging system (1984) for HCC Parameter

NCCN classification ™™ ™™ ™™

Nodular Massive Diffuse

Note: • Small HCC nodule is less than 2 cm in size. • PV extension as tumour thrombosis indicates inoperability and cause portal hypertension. • Infiltration into hepatic veins is not common but when it occurs, tumour thrombus extends rapidly into IVC and right atrium. • Invasion into biliary system causes haemobilia and obstructive jaundice. • Lymphatic spread occurs to hilar nodes, celiac nodes, pericardial nodes, paracaval nodes. • Local infiltration into diaphragm and adjacent organs can occur. • Blood spread occurs to lungs, bones, meninges, kidney and adrenals. • Dysplastic nodules and hepatic adenomas are premalignant conditions. • Histologically it can be well/moderate or poorly differentiated tumour. • Variants of HCC are – fibrolamellar (good prognosis); mixed hepatocellular cholangiocellular (poor); clear cell variant (better); giant cell variant; (bad) sarcomatoid variant (carcinosarcoma).

Fibrolamellar Variant of HCC (FL HCC) xx xx xx xx xx xx xx xx xx

xx

FL HCC occurs in younger age group. Incidence is equal in both sexes—5% common. It does not show any elevated levels of serum AFP. Tumour marker for FL HCC type is increase in serum vitamin B12 binding protein and increase in neurotensin levels. It is not related to viral hepatitis or cirrhosis. Left lobe is commonly involved. It involves lymph nodes more commonly than HCC. CT scan shows characteristic central scarring. Fibrous stromas with thin hyaline bands are typical. Sheets of welldifferentiated hepatocytes are seen which are sandwiched between collagen and fibroblasts. It is fairly resectable (50–75%) with better prognosis than HCC.

0

Stage one—0 points

50 %

1

Stage two—1–2 points

Ascites

Absent

0

Stage three—3–4 points

Present

1

Serum

3 mg %

1

Serum

3 mg %

1

Staging of HCC (AJCC)

Okuda classification – (Okuda staging is different) Multifocal Indeterminate Spreading Expanding

Stage

Tumour size

™™

™™ ™™ ™™ ™™

Points

T0 – No tumour T1 – Solitary tumour without vascular invasion T2 – Solitary tumour with vascular invasion/multiple tumours equal or less than 5 cm T3 – Multiple tumours, more than 5 cm (T3a)/tumour invading major branch of portal or hepatic veins (T3b) T4 – Tumour with direct invasion of adjacent organs other than gallbladder or to visceral peritoneum N0 – No regional nodes are involved N1 – Regional nodes are involved M0 – No distant spread M1 – Distant spread is present

Cancer of liver Italian group scoring (CLIP scoring) Parameters Child Pugh’s stage Tumour morphology— Gross

AFP ng/dl

Values A B C Uninodular less than 50% of extension Multinodular less than 50% of extension Massive—extension more than 50% of liver Less than 400 More than 400 No Yes

Portal vein thrombosis Total scores 0–6 Early disease with potential long-term survival 0–3 Advanced stage 4–6

Scores 0 1 2 0 1 2 0 1 0 1

Chinese university prognostic index (CUPI) scoring system uses TNM staging, symptoms, ascites, bilirubin, alkaline phosphatase, AFP. It is used mainly for HBV induced HCC.

Clinical Features xx Painless mass in right hypochondriac region with loss of

appetite and weight. Liver is hard, smooth/irregular and often massively enlarged. Cirrhotic liver may be nodular. xx Acute presentation is not uncommon, when the tumour undergoes necrosis and haemorrhage. Both types of presentations mimic amoebic liver abscess (Haemoperitoneum is also known).

Liver xx Jaundice when present is commonly due to hepatic dysfunc-

tion, but occasionally due to compression of bile ducts. xx Ascites (40%) often it is massive, splenomegaly and features of portal hypertension may be present. xx Hepatic thrill and bruit—25%. xx Fever (10–20%) may be present due to tumour necrosis. xx Dull aching pain in right upper quadrant is common. xx Features of chronic liver disease—jaundice, dilated veins, palmar erythema, gynaecomastia, testicular atrophy, etc. xx Liver failure sets in once tumour replaces the functioning liver parenchyma or portal vein gets occluded by tumour thrombus. xx Gastrointestinal bleeding may be the presentation in 10% of cases due to portal hypertension or portal vein invasion by tumour. xx Occasionally may present with paraneoplastic syndromes. 1%; hypercalcaemia, hypoglycaemia, hyperlipidaemia, hyperthyroidism, erythrocytosis, sexual changes like gynaecomastia, precocious puberty, testicular atrophy and porphyria cutaneous tarda. Presentations Asymptomatic – incidentally identified Symptomatic – abdominal pain (capsule stretching, tumour necrosis), weight and appetite loss, jaundice, mass abdomen Symptoms due to complications – Bleeding HCC can cause life threatening spontaneous haemoperitoneum after an attempt of biopsy; jaundice (in 10% of HCC) due to obstruction by tumour of main intrahepatic ducts or CHD at porta hepatis or by tumour infiltration of biliary system or by haemobilia or due to underlying cirrhosis; oesophageal varices causing haematemesis with portal hypertension Symptomatic due to metastasis – from pulmonary metastases, bone metastases (10%) Paraneoplastic syndrome (1%)

Differential diagnoses for HCC ™™ ™™ ™™ ™™ ™™ ™™

Investigations xx Ultrasound abdomen—very useful method. It shows

hyperechoic mass; mosaic pattern with thin halo and lateral shadows. Extent, tumour thrombi extension can be made out. xx CT scan abdomen (CECT) more reliable and ideal (hypodense, mosaic, vascular lesion with irregular margin).  reveals the size, location and extent, vascularity, portal vein invasion, nodal status, portal vein thrombosis.  helps to assess operability. xx Tumour markers—α fetoprotein (AFP). AFP will be raised more than 100 IU; as high as 1000 IU is possible in HCC. PIVKA II is des γ carboxy prothrombin protein induced by vitamin K abnormality/antagonists 2. It is increased in 80% of HCC patients. AFP is usually more than 400 IU in 70% of HCC patients. AFP –L3 (serum lens culinaris agglutinin reactive fraction of AFP, DCP (des γ carboxy prothrombin) and glypican-3 are other tumour markers used. AFP begins to rise once vascular invasion by the tumour starts, hence it becomes insensitive in detecting early tumour. xx Celiac angiography/CT angiography—it shows the vascularity of the tumour, tumour blush, arterial pattern of the liver and tumour; venous phase can show portal vein invasion or thrombosis and invasion/spread to IVC. Angiogram is essential while planning for hepatic resection. xx Liver function tests like serum bilirubin, albumin, enzymes (alkaline phosphatase, transaminase, 5’ nucleotidase) including prothrombin time. Note:

Spread of Tumour

•

xx Lymphatic spread: It can spread to other part of liver through

lymphatics within the liver, to the lymph nodes in the porta hepatis and other abdominal lymph nodes later. Often spread occurs directly to cisterna chyli. xx Blood spread: To lungs, bones and adrenals often can occur. xx Direct infiltration: To diaphragm and neighbouring structures.

A

Secondaries in liver Liver abscess – amoebic Polycystic liver disease, hydatid cyst Benign tumours of liver Cholangiocarcinoma Hepatosteatoses

B Figs 11.23A and B: CT pictures of hepatoma. In right lobe and left lobe.

•

Preoperative liver biopsy is not recommended now. Biopsy is relatively contraindicated in any candidate for resection, as there is a significant risk of haemorrhage and peritoneal implantation of tumour cells. In case of potentially resectable tumour one should proceed to surgical exploration without tumour biopsy. Biopsy is done only in inoperable advanced cases wherein palliative therapies are undertaken to establish the diagnosis as in a typical images with normal AFP. Liver biopsy is done after controlling prothrombin time if it is elevated (by Inj vitamin K IM or IV 10 mg for 5 days; FFP transfusion). US/CT guided core liver biopsy is useful in non-surgical therapies and mandatory before clinical trials. It is better than FNAC as it reveals tissue architecture. Problems with the core liver biopsy are spillage of tumour and bleeding (due to hypervascularity, associated thrombocytopenia and reduced liver dependent clotting factors like prothrombin). Such problems may be minimal in FNAC. Patients with high suspicious of HCC by clinical and imaging methods and who are appropriate for surgery may be taken up for surgery without a preoperative biopsy. In case of portal vein infiltration by tumour a portal vein biopsy may be done to exclude the patient for surgery or transplantation.

xx Contrast MRI/CT scan 1–2 weeks following intrahepatic infusion of lipiodol (ethiodized oil emulsion 5–15 ml) with contrast agent through hepatic artery is very useful. Such Lipiodol enhanced

Adversity is better teacher than prosperity—James Thurber. If aim is ended most be ended in this life—Rabindranath Tagore

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xx xx xx xx xx xx

CT/MRI even though is ideal and gold standard, but not practiced commonly; during selective angiogram lipiodol is injected into the hepatic artery which is taken up by the tumour, follow-up CT can be done to assess tumour in 2–4 weeks. MRI—T2 weighted studies are useful for small HCC. MR angiography is also done to see tumour thrombus in portal vein, hepatic vein and IVC. Ascitic tap when ascites is present for cytology. Laparoscopic evaluation and laparoscopic US is useful for proper assessment of the tumour. Investigations in relation to hepatitis B and hepatitis C virus infections. Metastatic work up—HRCT of chest is essential. FDG – PET scan and bone scans are useful in detecting the early metastatic diseases. Surveillance screening for high-risk group like cirrhosis is done using USG once in 6 months and AFP.

Treatment Definitive Treatment xx When limited to one lobe, hemihepatectomy is done (Removal of 70% liver is compatible with life). Laparoscopic resection is becoming popular. It is done only to Child’s grade A and favourable Child’s B group patients. It is the treatment of choice for operable HCC in non-cirrhotic patients. There is no regenerative capacity in cirrhotic patients with poor coagulation status, portal hypertension, varices, and ascites. xx In cirrhotic patients with HCC, total hepatectomy with orthotopic liver transplantation is required. Now it is found that even resection candidates will do better by transplantation than resection. But waiting period for transplantation is long. To bridge this waiting period for transplantation radiofrequency ablation, transarterial embolisation, ethanol/acetic acid injections are used. Indications for transplantation in HCC ™™ ™™ ™™ ™™ ™™

Patient who is not a candidate for resection Tumour less or equal to 5 cm Tumour less than 3 in number Tumour without portal/hepatic vein invasion Tumour without extra hepatic spread

Note:

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30% of liver tissue or at least two segments should be retained in liver resection when underlying liver is normal; hepatic reserve is assessed by indocyanine green clearance test and CT or MR volumetry. MELD (Model for End Stage Liver Disease) score is used for resectability using creatinine, bilirubin, PT- INR. Milan’s criteria are tumour less than 5 cm or number less than 3 with each less than 3 cm. University of California Sanfracisco criteria – single tumour < 5cm; < 3 tumours but total diameter less than 8 cm and largest one should be less than 4.5 cm. Involvement of extrahepatic tissues or nodes or portal vein tumour thrombus formation, distant spread are contraindications for liver resection. Liver mass which is confirmed by CT/MRI and serum AFP is >500 ng/dl is almost diagnostic and resection treatment can be started without tissue diagnosis.

Adjuvant Therapy xx Systemic chemotherapy using intravenous adriamycin (doxo-

rubicin), cisplatin, carboplatin, mitomycin C, 5 fluorouracil. xx Octreotide is used along with other chemotherapeutic agents.

It decreases the size of the tumour.

xx Neoadjuvant (preoperative) chemotherapy also practiced to

increase the operability/resectability of the tumour. xx Newer treatments are tried using tamoxifen, interferons,

EGFR antibody, interleukins, I131 lipiodol, Yttrium90 microspheres, etc.

Palliative Treatment xx Radiofrequency ablation (RFA): It is thermal ablation of

the tumour by passing 18G needle into the middle of the tumour and passing electric current of 500 kHz. This creates frictional heat causing sphere of necrosis. Maximum zone of necrosis which can be created is 7 cm for a 5 cm tumour. This causes adequate cyto-destruction of the tumour. Tumour close to vessels and biliary tree, tumour more than 3–5 cm and multicentric tumours are difficult to manage by radiofrequency ablation. One course ablation takes around 20 minutes. It can be done percutaneously under US or CT guidance or through laparoscopy. Percutaneously it can be done on outpatient basis. It can be repeated several times. Tumour less than 3 cm, tumour deep in parenchyma, tumour away from hilum is ideal for radioablation. xx Percutaneous ethanol or acetic acid injection: (Rule of 3 is used here—indicated in HCC not >3 cm and not >3 nodules). Ethanol injection is minimally invasive, can be injected using fine needle, and is cheaper. Local recurrence is lower with acetic acid injection than ethanol. But radiofrequency ablation has got better result than ethanol/acetic acid injection. RFA is costly and not available in many centers. xx Trans-arterial chemotherapy (TAC) using Adriamycin/ cisplatin/mitomycin through gastroduodenal artery. It is often given along with lipiodol to make drugs to stay longer time in the liver tissue so that better results are achieved. This regional chemotherapy is much more successful in HCC. xx Trans-arterial embolisation (TAE) using gelfoam, microspheres, gelatin sponge, or chemoembolisation (TACE). TACE is combined TAE with chemotherapy using lipiodol, doxorubicin, mitomycin and cisplatin. TACE can be conventional or Drug eluted beads (particles) TACE [DEB-TACE]. xx Microwave or cryoablations similar to RFA. xx As it is considered that tumour tissue exclusively gets its blood supply from hepatic artery, ligation of hepatic artery can be a good palliation (to achieve tumour necrosis) for HCC. Normal tissue will still have its blood supply from portal vein. xx Transarterial I131 lipiodol, Yttrium 90 microspheres. xx Targeted Iodine 131 with lipiodol injection into hepatic artery is used as targeted RT as adjuvant therapy after liver resection. It is also makes disappearance of the portal vein thrombosis in HCC and used as neoadjuvant therapy prior to liver resection. Neoadjuvant therapy in HCC Large primary tumour—downstaging/downsizing may make resection possible ™™ Transarterial chemoembolisation (TACE) ™™ Chemotherapy and radiotherapy ™™ Hepatic artery infusion of chemotherapy (HAI) ™™ Radioimmunotherapy ™™ Fractioned radiotherapy ™™ Transarterial 90Y microspheres (TARE- Transarterial radioembolisation)

Liver Treatment strategies for HCC ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Surgical resection, only 20% have resectable liver Liver transplantation Radiofrequency ablation Percutaneous ethanol/acetic acid injection Transarterial embolisation/chemoembolisation Microwave/cryoablation Transarterial radiotherapy Transarterial Yttrium90 microspheres/I131 lipiodol Hepatic artery ligation Adjuvant systemic chemotherapy Immunotherapy/hormone therapy/growth factors

Extra-abdominal: xx Melanoma. xx Carcinoma breast, lung, thoracic oesophagus, bladder,

prostate. xx Testicular and adrenal tumours. xx Follicular carcinoma thyroid (FCT).

Commonly secondaries in liver are multiple, multiple in one lobe or in both lobes. It can be solitary (rare).

Classification Colorectal

Hepatoma/hepatocellular carcinoma/HCC ™™

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Common aetiologies are aflatoxins, hepatitis B and hepatitis C virus infection, alcoholic cirrhosis, haemochromatosis, smoking, hepatic adenoma, clonorchis sinensis, polyvinyl chloride Unicentric and right lobe involvement is more common Fibrolamellar variant is common in left lobe, not related to hepatitis or cirrhosis without AFP level raise. There are increased serum vitamin B12 binding capacity and neurotensin levels Invasion to portal veins is common and it has got negative prognosis with lesser chances of resection or transplantation. It may cause portal vein thrombosis and so splenomegaly It can be multifocal/indeterminate/spreading/expanding— Okuda classification Presents as large, smooth, hard liver mass—later jaundice, fever, pain and tenderness, ascites and bruit over mass Spreads by lymphatics, blood and direct extension Mimics amoebic liver abscess, secondaries, hydatid cyst, polycystic liver disease LFT, CT scan, raised AFP, liver biopsy are the investigations Liver mass, confirmed by CT/MRI and serum AFP > 500 ng/dl is almost diagnostic and treatment can be started without tissue diagnosis Liver biopsy is done (FNAC) only in patients with nondiagnostic level of AFP and not a candidate for curative surgery but only for palliation Hemihepatectomy is the treatment in early operable growth Liver transplantation is the good surgical option Hepatic artery ligation/intra-arterial chemotherapy/chemoembolisation/percutaneous ethanol or acetic acid injection/ radiofrequency ablation/chemotherapy using adriamycin, carboplatin, gemcitabine—are palliative procedures

xx Colorectal carcinoma has got special interest in relation to its secondaries in liver. It carries good prognosis. xx Secondaries can be synchronous or metachronous. xx Resection of secondaries in liver often gives good outcome. xx PET scan is done to identify occult extrahepatic metastases. CEA is reliable indicator of spread or recurrence. xx Resection, chemotherapy, intra-arterial chemotherapy are therapeutic modalities. xx Contraindications for liver resection are—extrahepatic spread, nodal involvement along with primary, short disease free interval less than 1 year, four or more secondary deposits, bilobar spread, CEA more than 200 ng/dl, secondary more than 5 cm in size, involved histologic margin. xx Colorectal liver secondaries show good prognosis when secondary are solitary, and with absence of all poor prognostic indicators. xx 5 FU with irinotecan or oxaliplatin, bevacizumab (anti-vascular endothelial antibodies) are also useful.

SECONDARIES IN THE LIVER It is the commonest malignant tumour in liver. The incidence of primary : secondary : : 1 : 20. Secondaries are common malignant tumours ™™ ™™ ™™

In bone In liver In brain

Fig. 11.24: Secondaries in liver—solitary type from colonic primary.

Neuroendocrine

Causes Abdominal: Carcinoma in stomach, colon, pancreas, small bowel, kidney, abdominal oesophagus, rectum, and carcinoids.

Gastrinoma, glucagonoma, somatostatinoma, nonfunctioning neuroendocrine tumours can cause liver secondaries. xx These tumours are slow growing. xx Main symptoms are often due to secreting peptides causing different clinical syndromes.

The best bridge between despair and hope is a good night’s sleep.—E. Joseph Cossman

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SRB's Manual of Surgery xx Hormonal assay, CT abdomen, CT angiogram are needed. xx Hormone controlling therapies, chemotherapy and cytoreduction using liver resection gives good 5-year survival up to 75% in these patients.

xx Clinical features of primary tumour, e.g. stomach, colon—  Stomach: Vomiting; visible gastric peristalsis; palpable

stomach mass.  Colon: Constipation/diarrhoea; palpable mass; features

of obstruction.

Non-colorectal and Non-neuroendocrine xx These are aggressive primary tumour causing liver secondaries like from stomach, pancreas, small bowel, oesophagus, gallbladder, melanoma, urinary bladder and prostate. xx They carry poor prognosis. xx Treatment is chemotherapy. Early primary like—in stomach with isolated liver secondaries without extrahepatic spread can be benefited with liver resection. xx But overall prognosis is guarded.

Other Classifications xx Precocious: Secondaries are presented/identified before primary is suspected—carcinoid, colorectal cancer. xx Synchronous: Both primary and secondaries are identified at the same time—carcinoma stomach. xx Metachronous: Secondaries develop much later may be long time after the treatment for primary—melanoma, breast carcinoma.

Route of Spread a. Direct spread: Stomach, colon, gallbladder, bile ducts. b. Hepatic artery: Melanoma. c. Portal vein: Carcinoid tumours, other GIT malignan­cies. d. Lymphatic spread: Breast, lung.

 Pancreas: Jaundice; steatorrhoea; itching; palpable

gallbladder.  History of earlier surgery: Like mastectomy/wide exci-

sion of the melanoma.  Testis: Fullness; hard mass; loss of testicular sensation.

Clinical features of secondaries in the liver ™™ ™™ ™™ ™™ ™™

Poor general condition Palpable liver which is hard, multinodular with umbilication Clinical features of primary Ascites ± Jaundice ±

Differential Diagnosis xx Multicentric hepatoma. xx Macronodular cirrhosis. xx Polycystic liver disease, hydatid cyst of liver.

Investigations xx Primary is identified by—gastroscopy, colono­scopy, contrast

X-rays, CT scan.

Clinical Features xx They are multiple, hard, nodular, with nodule showing

umbilication due to central necrosis. xx Patient may have jaundice depending on the extent of liver

involvement. xx Loss of appetite and weight. xx Ascites. xx Pain in liver secondaries is due to stretching of liver capsule/

tumour necrosis. Often pain may be of primary tumour. A

xx Rectovesical secondaries—‘Blumer shelf’. xx Supraclavicular lymph node enlargement–Virchow’s node

(Troisier’s sign).

C

B

Figs 11.26A to C: Secondaries in liver are multiple and often with umbilication. CT picture shows multiple secondaries with ascites. On table photo of multiple liver secondaries with umbilication. xx Liver biopsy is done, only if primary is not identified by

any of these methods. Fig. 11.25: Secondaries in liver. Note the multiple lesions (nodules) in both lobes of the liver.

xx Liver function tests. xx Ultrasound abdomen—multiple hypo- or hyperechoic

lesions; site of possible primary; nodal status; ascites.

Liver xx Tumour marker: CEA. xx MRI/CT scan whenever resection is indicated. xx Laparoscopy often with laparoscopic US is very useful to

detect small secondaries.

Treatment xx Chemotherapy is the treatment of choice. xx Surgery has a definitive role if primary is from the colon,

kidney. xx If the primary growth is in the colon, then a palliative hemi-

LIVER CYSTS

CONGENITAL LIVER CYSTS Simple Liver Cyst xx It is 3% common. It is common in males (2:1). xx Solitary simple cyst is congenital; developing from abnormal intrahepatic bile duct in utero. xx 1/4th of simple cysts are symptomatic only at 4th or 5th decade. xx It is thin bluish walled cyst in one or other lobe containing clear fluid. Simple cyst will never communicate with biliary system. If communication is found, it should be cystadenoma.

colectomy is done. Along with that if a solitary secondary in the liver is present, it can be resected. If secondaries are in single lobe, hemihepatectomy is done. Criteria for selection for liver resection in secondaries in liver, when primary is in colon are: ™™ Stage of the primary ™™ Type of primary resection ™™ Size of the largest liver secondary ™™ Number of secondaries ™™ Segments involved ™™ Associated liver disease like cirrhosis

xx Palliative procedures for other primaries like—for carci-

noma stomach—palliative partial gastrectomy/anterior gastrojejunostomy; for carcinoma pancreas—triple anastomosis/ERCP stenting. xx Depending on the site of primary, drugs vary.  For carcinoma stomach, mitomycin and 5FU are given.  For carcinoma colon, 5-FU, oxaloplatinum/VEGF or EGFR antibodies used with folinic acid. xx Hepatic artery ligation or therapeutic embolization with clot/ gel foam can be tried to relieve pain. xx Intra-arterial chemotherapy is tried with little success. Methods other than resection available to ablate the tumour locally in secondaries in liver ™™ Microwave therapy ™™ Radiofrequency ablation ™™ Laser hyperthermia ™™ Ultrasound or electrolyte therapy

Overall outcome is poor in liver secondaries. They die of malignant cachexia, infection, liver failure. Causes of massive enlargement of liver Hepatoma Secondaries in liver when primary is from melanoma, carcinoid tumour ™™ Syphilitic enlargement of liver (hepar lobatum) ™™ ™™

A

B Figs 11.27A and B: Simple liver cysts—CT pictures in two different patients.

xx 50% present with abdominal pain. Hepatomegaly is common. Jaundice can be present. xx Differential diagnoses are—hydatid cyst, cystic neoplasms and solitary secondary with tumour necrosis. xx US shows anechoic lesion with smooth margin. xx CT scan shows nonenhancing thin lesion. MRI shows hypointense T1 image and hyperintense T2 image. xx Aspiration confirms the diagnosis. Aspiration will not cure the cyst as it recurs 100%. xx Treatment is—aspiration with sclerosant therapy where the recurrence rate is 20%. Deroofing with partial excision of cyst wall, by laparoscopic or open method has recurrence rate of 10%. Complete excision has very less recurrence rate but surgical mortality of 2% is present.

Polycystic Liver Disease xx It is autosomal dominant condition associated with polycystic kidney disease in 40% of cases. xx It arises from biliary epithelium but does not communicate with biliary system. xx Usually they are asymptomatic. xx Hepatomegaly, pain abdomen, jaundice and portal hypertension are the presentations. xx Haemorrhage, biliary obstruction, Budd-Chiari syndrome, rarely malignant transformation—are the complications. xx Liver function is well preserved and so liver failure will not occur. xx US, CT, MRI are investigations done. xx Treatment: Percutaneous aspiration with sclerosant injection, deroofing of all cysts, resection, liver transplantation.

NEOPLASTIC LIVER CYSTS xx They are acquired cysts. xx They are common in females.

A superior man is modest in his speech, but exceeds in his actions.

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They attain large size; multiloculated with papillary projections. 10% of neoplastic cysts are malignant. Cystadenoma is benign containing mucinous or bilious fluid. Cystadenocarcinoma contains haemorrhagic fluid. AFP, CEA are normal; CA 19/9 is elevated.

Hepatobiliary (Hepatic) Cystadenoma xx Incidence is 5% of biliary intrahepatic cysts. xx 50% are in right lobe; 30% are in left lobe; 15% bilateral. xx Cystadenoma without mesenchymal stroma is equal in both sexes and occurs in 5th decade. It is not associated with cystadenocarcinoma. xx Cystadenoma with mesenchymal stroma is common in young females and is often associated with cystadeno­carcinoma. xx It is septated, multiloculated, whereas if cavity contains debris it suggests malignancy. It is surrounded by a smooth and thick fibrous capsule. It contains internal septations and intraluminal papillary projections and lined by cuboidal or columnar biliary epithelium.

existing intrahepatic haematoma causing mixture of bile and blood. Cyst is pseudocyst in liver without an epithelial lining. xx It may resolve spontaneously or may cause abdominal pain, jaundice. It may present months or years later. xx CT scan, old history of liver trauma may be helpful. MRI is diagnostic. xx Treatment is conservative. Often deroofing or cyst excision with ligation of biliary ductule may be needed but technically demanding. Differential diagnosis of space occupying lesions in the liver Hepatoma Amoebic liver abscess ™™ Secondaries in the liver ™™ Cysts of the liver ™™ Haemangioma ™™ ™™

PORTAL HYPERTENSION (Gilbert and Villaret first coined the term portal hypertension in 1906)

Definition

A

B

Figs 11.28A and B: Hepatic cystadenoma of right lobe of liver—CT picture and on table look (Courtesy: Dr Ashfaque Mohammed, DNB, KMC, Mangaluru).

It is sustained elevation of the portal venous pressure more than 10 mm of Hg. Normal portal venous pressure is 5–10 mmHg. It is also defined as elevation of the hepatic venous pressure gradient (HVPG) > 5 mmHg. HVPG is the difference between the wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHPV). When HVPG is more than 10 mmHg, porta systemic shunting develops; when it becomes more than 12 mmHg, risk for variceal bleeding increases; often it will be as high as 20 mmHg in bleeding oesophageal varices.

xx It originates from—congenital aberrant bile duct/embryonic foregut cells/peribiliary endocrine cells. xx MRI is diagnostic. US/CT scan is also useful. xx ERCP is done to identify communication with biliary system; usually to proximal left hepatic duct. xx Treatment—enucleation of entire cyst with surrounding rim of normal liver tissue. Hepatic resection is also an option. xx Note: Aspiration/deroofing, partial excision, sclerotherapy should not be done.

Hepatic Cystadenocarcinoma xx It presents as large palpable smooth liver with abdominal pain. xx It carries better prognosis than HCC or cholangiocarcinoma. It can be:  Cystadenocarcinoma arising from pre-existing cystadenoma with mesenchymal stroma, which occurs only in young females, carries good prognosis.  Cystadenocarcinoma without mesenchymal stroma not associated with cystadenoma, which is common in males and is more malignant.  Cystadenocarcinoma without mesenchymal stroma occurring in women. xx Resection is the treatment. It carries good prognosis.

TRAUMATIC LIVER CYST

xx It is an acquired cyst of liver after liver injury in a blunt abdominal trauma. Biliary duct which is injured will cause bile leak into the

Fig. 11.29: Anatomy of the portal system.

Causes There is increased portal resistance and altered portal blood flow. Increased resistance may be presinusoidal, sinusoidal, postsinusoidal. xx Presinusoidal  Extrahepatic – Portal/splenic vein thrombosis.

Liver  Intrahepatic – Schistosomiasis, sarcoidosis, congenital

hepatic fibrosis, primary biliary cirrhosis. xx Sinusoidal – Cirrhosis, haemochromatosis, Wilson’s disease, non-alcoholic steatohepatitis (NASH). xx Postsinusoidal – Budd-Chiari syndrome, constrictive pericarditis, veno-occlusive disease. Note

• • • • • • • • •

Left sided portal hypertension (sinistral) can be caused by isolated splenic vein thrombosis, which is often caused by adjacent pancreatitis. A rise in portal pressure stimulates portasystemic circulation. Portal vein carries 75% of blood flow to liver with all nutrients to maintain its integrity and gives 50% oxygen supply to liver. 25% hepatic arterial blood flow gives remaining 50% of oxygen supply to liver. Portal hypertension causes compensatory portosystemic venous collateral formation, altered intrahepatic circulation and increased splanchnic blood flow. High pressure portal blood is diverted via coronary (left gastric vein), short gastric and oesophageal veins into azygos venous system. There is dysregulation of compensatory increased hepatic arterial flow response in relation to decreased portal vein flow. 30% of varices patients will bleed; 30% of them will die of bleed; 30% of patients with cirrhosis will develop portal hypertension; 30% of them have variceal bleed in 2 years; 70% of patients who had bleeding once, will rebleed later. Variceal bleed accounts for 7% of upper GI bleed. In western country, more than 90% cases cirrhosis is the cause. In India, extrahepatic portal vein obstruction (33%) and extrahepatic periportal fibrosis (33%) is becoming more common. As liver is normal in these two conditions, patients get better cure rate by shunt surgery. Small varix is 5 mm.

Sites of Portosystemic Collateralisation 1. Lower end of oesophagus, between left gastric and short gastric veins with azygos vein resulting in oesophageal varices— commonest.

2. Umbilicus, between paraumbilical vein and anterior abdominal vein resulting in caput medusae. 3. Lower end of rectum, between superior haemor­rhoidal vein and inferior, middle haemorrhoidal vein resulting in piles. 4. Retroperitoneum (vein of Retzius). 5. Bare area of the liver.

Presentations ™™

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xx General—weakness, tiredness, anorexia, weight loss,

abdominal pain, jaundice, oedema, pruritus, spontaneous bleeding and bruises, impotence, muscle cramps, palor, cyanosis, hypotension. xx Features of variceal bleeding—anaemia, haematemesis, melaena, shock. Bleeding may be from gastric/oesophageal varices or portal gastropathy. xx Features of encephalopathy—memory loss, altered behaviour and mental status, asterixis (flapping tremor/liver flap), unconsciousness, foetor hepaticus. xx Features of liver cell failure—gynaecomastia, palmar erythema, leuconychia, testicular atrophy, spider angioma, parotid enlargement, cyanosis, and tachypnoea. xx Features of porta systemic shunting—see above; venous hum. xx Ascites and generalised anasarca with oedema scrotum and abdominal wall and limbs. Ascites is a sign of hepatic decompensation. xx Decreased urine output features of renal failure—hepatorenal syndrome. xx Splenomegaly causing hypersplenism; hypersplenism occurs in 30% of cases with features of leucopaenia (WBC 2.5 cm) ↓ Cholecystitis ↓ Suppuration and adhesion over the duodenal wall ↓ Communication of gallbladder into the duodenum (Spontaneous bilioenteric fistula) ↓ Gallstones pass into the duodenum forms a bolus (‘Rolling stone gather mass’) ↓ Blocks narrow part in the ileum. ↓ Gallstone ileus

xx A rare entity with cholecystoduodenal fistula causing gallstones from gallbladder to pass into the duodenum leading to duodenal obstruction.

CHOLECYSTOSES xx Cholecystoses are chronic inflammatory conditions of gallbladder with cholesterol deposits. xx It is due to defective transport of the absorbed cholesterol which accumulates in mucosa. There is also increased absorption of cholesterol by gallbladder epithelium. xx Cholecystoses gallbladder is more prone for infection. xx It may precipitate stone formation. xx It is a premalignant condition.

Clinical Features xx Pain abdomen and features of intestinal obs­truction. xx Stones may perforate the ileum to cause peritonitis. xx It is 1% of all intestinal obstruction overall; 25% of obstruction in elderly. xx Recurrent episodic obstruction due to moving stone bolus is typical—tumbling obstruction.

Investigations

A

xx Plain X-ray abdomen in erect posture shows air in the biliary tract (branching gas pattern, pneumobilia) and multiple air fluid levels. xx U/S abdomen. xx CT is diagnostic.

Figs 12.45A and B: (A) Types of cholecystoses. (I) Cholesterosis, (II) Cholesterol polyposis, (III) Cholecystitis glandularis proliferans, (IV) Diverticulosis of gallbladder, (V) Fistula; (B) Cholesterosis of gallbladder. It is a premalignant condition.

Treatment

Types

xx Laparotomy, enterotomy, removal of gallstones and closure of enterotomy is done. Enterotomy is done not at the site of obstruction but more proximal to the site of obstruction and stones are milked towards the enterotomy site. If bowel is found ischaemic at the impacted area, resection and anastomosis is done. xx Laparotomy and crushing of stones with fingers to relieve the obstruction is only occasionally useful. xx Cholecystectomy, correction of fistula with T-tube drainage can be done in same sitting if patient’s general condition is good. Other-

I. Aggregations of cholesterol crystals in the mucosa or submucosa—cholesterosis (Strawberry gallbladder). Lipoid contents are present in large foamy cells which has phagocytosed cholesterol. Here cystic duct is normal. Disease occurs only in gallbladder. It is a premalignant condition. II. Cholesterol laden polypoid projections in the mucosa—cholesterol polyposis (Gallbladder polyp). III. Granulomatous thickening and hyperplasia of the gallbladder— cholecystit is glandularis proliferans.

B

Ability may get you to the top, but it takes character to keep you there.

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SRB's Manual of Surgery IV. Diverticula formation in the wall of the gallbladder— diverticulosis of gallbladder. V. Gallbladder wall fistula.

Clinical Features xx Features of acalculous cholecystitis like dyspepsia, positive Murphy’s sign.

Investigations xx US abdomen. xx OCG. xx Isotope study.

Treatment Cholecystectomy—always should be done whether it is symptomatic or not as it is potentially malignant.

DISSOLUTION THERAPY FOR GALLSTONES Indications xx xx xx xx xx

It is stones in the CBD and biliary tree.

Classification i. Primary—Rare—brown pigment stones. ii. Secondary—Common—black pigment stones/cholesterol stones. It is seen in 15% of gallstone disease; 75% are cholesterol stones, 15% are pigment stones. Primary stones They are formed in CBD and biliary tree itself, and are multiple, often sludge like, commonly pigment or mixed type, extends into hepatic ducts (Brown pigment stones). Causes: xx Defective pathophysiology of biliary tree causing stasis, biliary dyskinesia, benign biliary stricture, sclerosing cholangitis, biliary dilatation, choledochal cyst. xx Congenital conditions like Caroli’s disease, choledo­chal cyst. xx Infections and infestations like clonorchiasis, ascariasis. xx Others: Low-protein diet, malnutrition, obesity, females, old age. Note:

Functioning gallbladder with cholesterol stone. Single stone less than 1.5 cm. Radiolucent stone. Old age. Patients who are not fit for surgery. Contraindications

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CHOLEDOCHOLITHIASIS

Nonfunctioning gallbladder Stone more than 1.5 cm Radio-opaque stone Multiple stones

Stasis and bactibilia are the main causes of primary CBD biliary tree stones.

Secondary biliary stones xx They are from gallbladder (gallstones) pass through cystic duct to CBD. Here CBD and biliary tree are otherwise normal. xx Secondary stones are better and easier to manage than primary stones. xx Commonly gallstones get impacted in supra­duodenal portion of CBD.

Drugs Used xx Chenodeoxycholic acid (for 2 years). xx Ursodeoxycholic acid (15 mg/kg/day). They inhibit absorption of cholesterol from the gut and synthesis of cholesterol in the liver. They inhibit HMG CoA— a rate limiting step in cholesterol synthesis. Ursodeoxycholic acid also inhibits absorption of cholesterol in GIT. Other methods used Citrate Monoterpenes Percutaneous infusion of methyl-tertiary butyl ether (MTBE) into the gallbladder using a catheter ™™ Extracorporeal shock wave lithotripsy (ESWL)—not popular ™™ ™™ ™™

Problems with Dissolution Therapy xx xx xx xx xx

Drugs should be given for a long time. Results are not good. Expensive. Causes side effects like diarrhoea, pruritus. Hepatic dysfunction. Overall results are not good by dissolution therapy.

Fig. 12.46: Multiple stones removed from common bile duct and hepatic ducts. They cause cholangitis. After stone removal, patient needs choledochoduodenostomy/sphincteroplasty/choledochojejunostomy. Note:

• • • • •

Black pigment stones are common in—haemolytic diseases, cirrhosis, ileal resection, fasting for long time, TPN for long time (home TPN). Intrahepatic stones are common—biliary sepsis, biliary stasis, parasitic infection, malnutrition. Retained stones mean—if stones are found in CBD within 2 years of cholecystectomy. Recurrent stones mean—if stones are found in CBD 2 years after cholecystectomy. 5% of CBD stones can be asymptomatic

Gallbladder Clinical Features

Investigations

xx Incidental CBD stones along with jaundice/without jaundice. xx Pain: It may be biliary colic; nonspecific abdominal pain;

xx US abdomen may show gallstones, dilated CBD >8 mm

pain of ascending cholangitis, pain of pancreatitis. xx Jaundice—most common clinical manifestation. xx Fever with chills and rigors. Charcot’s triad of ascending cholangitis ™™ ™™ ™™

Intermittent pain (may be colicky) Intermittent fever Intermittent jaundice

Stone moves proximally and floats, obstruction is relieved and symptoms subside (Intermittent features). Stone in CBD due to impaction Causes obstruction Jaundice

Pain

Stasis

Infection, bacteraemia and fever

xx Reynold’s pentad of acute obstructive cholangitis (suppura-

tive cholangitis—5%).

which suggests biliary obstruction. Sensitivity for CBD stones is only 65%. xx CT scan is the most sensitive investigation for CBD stones; it shows stones, location, ductal stricture or block, ductal dilatation, intrahepatic biliary changes and stones. Helical CT cholangiography is also useful but bilirubin level should be normal which is the limitation. xx MRCP is noninvasive investigation which delineates biliary tree anatomy and pathology clearly; but it is not therapeutic. xx Blood: Total count may be raised; LFT deranged with raised bilirubin (direct) and alkaline phosphatase. PT INR and platelet count should be done. Serum amylase and lipase should be done to rule out associated pancreatitis. xx EUS (endosonography) is useful and accurate but it is invasive. xx ERCP identifies pathology, site of block, stones, etc. (95% sensitivity). It is therapeutic also for extraction of biliary stones and stenting. xx PTC is done only when indicated like in those with previous gastrectomy, failed ERCP. PTC is not routinely needed. PTC can be therapeutic also in extracting the stones and stenting.

Treatment xx Injection Vit. K 10 mg IM once a day for 5 days or FFP

Sometimes obstruction persists causing ™™ ™™ ™™ ™™ ™™

Persistent pain Persistent fever Persistent jaundice Shock (toxicity) and Altered mental status

Here biliary tree contains pus. xx Pain and tenderness in epigastrium and right hypochondrium. xx Steatorrhoea and darkening of urine. xx Pruritus.

infusion to correct the prothrombin time. xx IV antibiotics (cefoperazone, cefotaxime). xx Correction of dehydration. xx IV mannitol daily 200 ml BD to prevent hepatorenal

syndrome. xx ERCP—Therapeutic, i.e. endoscopic papillotomy (sphinc-

terotomy) and stone extraction through Dormia basket or balloon catheter; or fragmenting the stone and extraction; or removal through baby endoscope. CBD stent is placed in situ.

Complications xx xx xx xx xx xx

Liver dysfunction and biliary cirrhosis. White bile formation and liver failure. Suppurative cholangitis. Liver abscess. Septicaemia. Pancreatitis if CBD stone is near sphincter of Oddi blocking drainage of bile and pancreatic duct. Differential diagnosis

Obstructive jaundice due to other causes: ™™ Carcinoma of head of pancreas ™™ Carcinoma of periampullary region ™™ Carcinoma of biliary tree ™™ Biliary stricture ™™ Viral hepatitis

Fig. 12.47: Plain X-ray showing stents in CBD and pancreatic ducts. It was placed in a patient who presented with recurrent pancreatitis with block/stricture in both terminal CBD and pancreatic duct. Later patient underwent choledochojejunostomy and pancreaticojejunostomy.

Typhoid Mary: Salmonella typhi infection with chronic cholecystitis acting as a carrier. Mary was a cook who spread typhoid to many people.

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Fig. 12.48: ERCP showing CBD stones. Endoscopic view of stenting is also seen. Complications of sphincterotomy ™™ ™™ ™™ ™™

Bleeding Sepsis Perforation Pancreatitis

Once CBD stones are extracted through ERCP, laparoscopic cholecystectomy is done. xx In open cholecystectomy  After the removal of gallbladder, on table cholangiogram is done through cystic duct using water-soluble iodine dye to see any stones in CBD. Using stay sutures choledochotomy is done (opened longitudinally) to remove stones in CBD.  False results/failure of intraoperative cholangiogram (IOC) is possible if air is trapped, if there is contrast leakage, if quick flow of contrast into the duodenum, if there is spasm of sphincter of Oddi. Indications for choledochotomy (After open cholecystectomy) ™™ U/S shows stone in CBD ™™ Palpable stone in CBD ™™ CBD diameter >8–10 mm ™™ Recent history of jaundice, and with raised serum alkaline phosphatase level ™™ On table cholangiogram shows stone (done using C-arm image machine) ™™ Failure of stone extraction by ERCP prior to cholecystectomy. ™™ When in doubt

Fig. 12.49: Diagram showing placement of T-tube in CBD after choledocholithotomy. Note the separate drain placed in the cholecystectomy bed to drain fluid, blood, bile.

choledochoscope. Retained stones can also be removed through ERCP. xx After open cholecystectomy, on table ERCP can be tried if there are indications for CBD intervention case of secondary CBD stone/s and if ERCP was not done prior to cholecystectomy. If secondary stone is retrieved by this method, open exploration of CBD can be avoided. xx Intraoperative ultrasound (IOUS) or intraoperative choledochoscope is very useful to confirm that all stones are removed. xx Laparoscopic CBD exploration is becoming popular with availability of expertise and high technology imaging and instruments. Methods to confirm the removal of T-tube Clamp the T-tube, after 10–14 days and observe 48 hours for development of pain, jaundice and fever ™™ Confirm free flow of dye in T-tube cholangiogram ™™

Management of retained CBD stones ™™ ™™ ™™

 After choledochotomy, stones are removed using Des

Jardin’s choledocholithotomy forceps. Bake’s CBD dilator is used to confirm the CBD patency.  T-tube (Kehr’s) is then placed in the CBD and kept for 14 days.  After 14 days a postoperative T-tube cholangiogram is done to see for free flow of dye into the duodenum, so that T-tube can be removed.  If T-tube cholangiogram shows persistent stone, it can be extracted after 6 weeks, through a basket (Dormia) or catheter (Fogarty) through the track or through a

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Small stones may spontaneously pass down. Heparinised saline or bile acid flushing through the T-tube. (Wash 250 ml of normal saline with 25,000 IV heparin for 5 days) Burhenne technique (Canada)—after 6 weeks once T-tube track gets matured, track if needed, is dilated using graduated dilators. Either using Dormia basket or Fogarty catheter or choledochoscope, stone is removed through T-tube track under fluoroscopic guidance (C-arm) ERCP and stone removal in 3 weeks Reoperation if everything fails, either transduodenal sphincteroplasty or choledochojejunostomy ESWL with endoscopic sphincterotomy/extraction/lavage/ stenting Through percutaneous transhepatic route, cholangioscope is passed and CBD is visualised, stone is identified and removed using Dormia basket or Fogarty catheter Laparoscopic choledocholithotomy Open choledocholithotomy often with choledochojejunostomy

Gallbladder Contd... ™™

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Figs 12.50A and B: (A) T-tube cholangiogram showing retained stone in the CBD (Courtesy: Dr Navin Chandra Shetty, HOD, Department of Radiodiagnosis, KMC, Mangaluru); (B) T-tube cholangiogram showing dye in the duodenum and visualisation of normal biliary tree without any obstruction.

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Treatment of Primary CBD Stones xx Difficult and is associated with more complications.

Preferred procedures: xx Transduodenal sphincteroplasty (open method), or xx Open choledochoduodenostomy, side-to-side, or xx Open choledochojejunostomy—Roux-en-Y method.  These procedures attain complete drainage of bile.  Postoperatively they may often require long-term antibiotics.

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Indications for choledochoduodenostomy/choledochojejunostomy: ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Multiple CBD calculi with distal narrowing (Funnel syndrome). Papillary stenosis. Impacted calculi. Biliary sludge—symptomatic. Residual stones. Sphincter of Oddi dysfunction/stenosis. Primary CBD stones. Previous choledochotomy. Marked CBD dilatation.

Prerequisite for choledochoduodenostomy: xx CBD should be more than 1.4 cm and stoma should be 2 cm. Advantages of choledochoduodenostomy are: xx Bile leak is minimal/not there. xx Beneficial as a permanent remedy in multiple stones/sludge/ stenosis/strictures/intrahepatic stones. Problem with choledochoduodenostomy: xx Sump syndrome. Note: Roux-en-Y choledochojejunostomy is equally good as choledochoduodenostomy.

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Silent/asymptomatic gallstone is one which is identified on routine investigation where there are no specific relevant symptoms related to gallstones. Chances of developing symptoms in a silent gallstone is 5% in 5 years and 20% in 15 years. Presently ultrasound is ideal investigation for gallstones. To see gallbladder function or confirm cholecystitis radioisotope HIDA/PIPIDA scan is ideal. Cholecystitis can cause jaundice due to cholangitis. But other causes of jaundice should be ruled out—CBD stones/Mirizzi syndrome. Limey gallbladder is gallbladder filled with toothpaste like mixture of calcium carbonate and calcium phosphate. Plain X-ray shows dense radio-opaque gallbladder shadow (opacified gallbladder). Porcelain gallbladder is one where gallbladder wall is calcified because of chronic cholecystitis. It is potentially malignant. It should be removed either by open or laparoscopic method. Cholesterol stone occurs when there is alteration in levels of cholesterol, lecithin and bile salts. This altered bile has got more cholesterol than adequate micelle and is called as lithogenic bile. Here bile is in supramicellar zone. Cholesterol stone is radiolucent but causes acoustic shadow in U/S Mixed stones are most common—90%. ‘Gallstone is a tomb stone erected to the memory of the organism within it’—Moynihan’s aphorism. Saint’s triad: Gallstones—colonic diverticulosis—hiatus hernia. Complications of gallstones: Acute cholecystitis, chronic cholecystitis, empyema gallbladder, mucocele of gallbladder, perforation and peritonitis, secondary CBD stones, cholangitis, pancreatitis, Mirizzi syndrome, gallstone ileus, pericholecystic abscess and carcinoma of gallbladder. Black pigment stones are more common in gallbladder; brown pigment stones are common in CBD. Cholesterol stones are common in Western countries; pigment/ mixed stones are common in Asian countries. Acute acalculous cholecystitis is 5% common. It occurs after stress, major surgeries or in cholecystoses. Xanthogranulomatous cholecystitis is a rare pathological condition. Gallbladder is thickened with chronic inflammation. It is yellow xathogranulomatous in nature. It often extends to adjacent organs. It is due to reaction to penetrated bile. Residual/retained bile duct stones are one which is present in CBD within 2 years of initial surgery—cholecystectomy. They are usually missed secondary bile duct stones. Recurrent bile duct stones are one which is present 2 years after the initial surgery—cholecystectomy and CBD exploration. They are primary biliary stones. Salmonella cholecystitis (Typhoid Mary—a cook in New York transmitted typhoid through her infected faeces and urine) causes typhoid gallbladder. It can cause acute or chronic cholecystitis. Salmonella itself may predispose stone formation. Patient may be silent typhoid carrier.

Remember Gallstones are commonly radiolucent (90%). Multiple stones are usually faceted because of exertion of equal pressure in a compact gallbladder. ™™ Plain X-ray shows radio-opaque lesion to the right side of the vertebra below rib cage. It should be differentiated from kidney stones. In lateral view X-ray, gallstone will be in front of the vertebra whereas kidney stone overlaps the vertebra. Often gallstone has got central radiolucent area—seagull sign/Mercedes Benz sign. ™™ ™™

Contd...

SUMP SYNDROME It is commonly observed after choledochoduodenostomy rarely after choledochojejunostomy. CBD distal to the choledochoduodenostomy acts as a reservoir with stasis of food particles, bile, stones and sludge. Often it causes cholangitis and narrowing of the stoma of choledochoduodenostomy. Conversion to end-to-end Roux-en-Y choledochojejunostomy is required.

Commitment is what transforms a promise into reality.

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SRB's Manual of Surgery Exceptions to the rule are: xx Double impacted stone—one in CBD and one in cystic duct, with mucocele of gallbladder. xx Large stone in Hartmann’s pouch. xx Empyema gallbladder with CBD stone.

SURGICAL JAUNDICE (Obstructive Jaundice) Definition It is the jaundice that develops due to biliary obstruction, partial or complete or intermittent. It causes conjugated hyperbilirubinaemia. Normal serum bilirubin level is 0.2–0.8 mg%. Scleral icterus is visible when serum bilirubin level exceeds 2.5 mg%.

Pathophysiology in Obstructive Jaundice Fig. 12.51: Technique of choledochoduodenostomy for CBD stones. Note the site of possible occurrence of Sump syndrome.

Bilirubin metabolism and enterohepatic circulation ™™

COURVOISIER’S LAW (SIGN) xx ‘In a patient with jaundice if there is palpable gallbladder, it is not due to stones’.

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Aged red cells get lysed in the reticuloendothelial cells and breakdown into haem and globin. Haem is divided into globin and bilirubin. Bilirubin is combined with albumin and transported to liver. In the liver bilirubin get separated from albumin and conjugated to bilirubin glucuronide by glucuronyl transferase. This conjugated bilirubin glucuronide is water soluble and can be excreted in kidney (So in obstructive and hepatic jaundice bile pigment – bilirubin is seen in the urine). This conjugated bilirubin is excreted through biliary canaliculi reaching intestine. In the intestine, it is converted into stercobilinogen and urobilinogen by intestinal bacteria. 70% of this is absorbed in the colon and brought back to liver as enterohepatic circulation. Unabsorbed stercobilinogen colours faeces brown. Circulating urobilinogen is taken up by kidneys for excretion. If direct bilirubin in the serum is more than 0.4 mg%, then bilirubin is seen in urine. Normal urinary urobilinogen is 100–200 mg/day. It is absent in obstructive jaundice. Normal faecal stercobilinogen is 300 mg/day. It is also absent in obstructive jaundice. In obstructive jaundice urine contains bilirubin and bile salts but urobilinogen is absent; stool is devoid of stercobilinogen.

Fig. 12.52: Courvoisier’s law—“In a patient with jaundice if there is palpable gallbladder it is not due to stones”. In stone disease gallbladder is contracted and fibrotic and so nondistensible. xx In obstruction due to CBD stone, gallbladder does not distend because it is chronically inflamed, thickened, fibrotic, contracted and nondistensible. xx In malignancy, like carcinoma of head of the pancreas or periampullary carcinoma, gallbladder will be distended and palpable to the right of rectus muscle in the right hypochondrium, as non-tender, globular, smooth, soft, dull mass which moves with respiration and with horizontal mobility. Rule may not be useful in ™™ ™™ ™™

Absence of gallbladder Intrahepatic gallbladder Previous cholecystectomy

Fig. 12.53: Sclera of the patient with obstructive jaundice is greenish yellow in colour. xx Obstructive jaundice, often called as surgical jaundice occurs due to intrahepatic or extrahepatic biliary outflow obstruction. It leads into cholestasis which means conjugated hyperbilirubinaemia; probably due to impaired bile flow and impaired bile formation. Bile acid secretion into the gut is impaired causing defective absorption of fat and fat-soluble vitamins like vitamin K; this, in turn causes poor synthesis of prothrombin and conversion of

Gallbladder prothrombin to thrombin causing widened PT and PT INR. Factors II, VII, IX, and X are vitamin K-dependent clotting factors. PT indicates the extrinsic pathway of coagulation; whereas partial thromboplastin time represents the intrinsic pathway. Bile acid stasis causes hepatocytes injury. Fat malabsorption causes steatorrhoea and also deficiencies of vitamins A (visual problem, thick skin), D (osteomalacia), E (peripheral neuropathy, cerebellar ataxia, posterior column dysfunction), K (bleeding tendencies). Cholestyramine and colestipol, used to treat pruritus, bind to bile salts and can exacerbate these vitamin deficiencies. Persistent cholestasis may be associated with deposits of cholesterol in the skin (cutaneous xanthomatosis), occasionally in bones and peripheral nerves. xx Bilirubinostasis (bile plugs) cause hepatocytes degeneration, small duct and ductular obstruction, pericholangitis, oedema, bile leak, liver infarction and biliary cirrhosis. xx Obstruction may be due to benign conditions like biliary tree stones (most common cause) or strictures or sclerosing cholangitis; or due to malignant conditions like carcinoma of pancreas or cholangiocarcinoma. Extrahepatic obstruction may be luminal (stones, infestations [ascariasis, clonorchis sinensis and schistosomiasis]) or mucosal/wall (growth, stricture [post-inflammatory, postsurgical or post-RT], primary sclerosing cholangitis) or external compression (pancreatitis, pancreatic tumour, compression by nodal mass). xx Intrahepatic cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane. Causes include hepatocellular disease (e.g. viral hepatitis, drug-induced hepatitis/cholestasis (thiazides, chlorpromazine), biliary cirrhosis. In hepatocellular disease, interference in the 3 major steps of bilirubin metabolism–uptake, conjugation and excretion usually occur. Excretion is the rate-limiting step and is usually impaired to the greatest extent. As a result, conjugated bilirubin predominates in the serum. xx The lack of bilirubin in the intestinal tract is responsible for the pale stools in biliary obstruction. The cause of itching (pruritus) associated with biliary obstruction is not clear; may be related to the accumulation of bile acids in the skin; or may be related to the release of endogenous opioids. xx Severe biliary obstruction causes cell damage usually in 1 month and, if unrelieved, may lead to secondary biliary cirrhosis. Acute cholangitis is another complication associated with obstruction of the biliary tract and is the most commonly seen in stricture, most often at the level of the CBD. Bile here is usually sterile. Bile flow obstruction → stasis → colonization and multiplication of bacteria → concomitant increased intraductal pressure → reflux of biliary contents → bacteremia, septicaemia → septic shock. If recurrence of biliary colic after cholecystectomy occurs, one should think of possible choledocholithiasis.

Effects of Obstructive Jaundice xx In liver: Enlarged green bile stained liver (hydrohepatosis)

shows dilated intrahepatic biliary radicles. Once intraductal CBD pressure increases bile secretion from liver is reduced causing formation of ‘white bile’ in CBD. Biliary cirrhosis may develop later. xx In the biliary tree: Recurrent inflammation—cholangitis— fibrosis can occur. xx In bowel: Absence of bile from bowel impairs digestion, reduces fat absorption making faeces bulky and fatty.

Vitamin K absorption is reduced causing fall in prothrombin level raising PT-INR. xx Retention of bile salts and bile pigments in blood and body fluids occurs. xx Altered coagulation profile; hepatorenal syndrome and renal failure; sepsis.

Classification of Causes of Obstructive Jaundice 1. Congenital: Biliary atresia, choledochal cyst. 2. Inflammatory: Ascending cholangitis, sclerosing cholangitis. 3. Obstructive: CBD stones, biliary stricture, parasitic infestation. 4. Neoplastic: Carcinoma of head or periampullary region of pancreas, cholangiocarcinomas, Klatskin tumour. 5. Extrinsic compression of CBD by lymph nodes or tumours.

Fig. 12.54: Different causes of obstructive jaundice (surgical jaundice). Benjamin’s (1983) classification of biliary obstruction Type 1: Complete obstruction ™™ Tumours—pancreatic, cholangiocarcinoma ™™ CBD ligation—iatrogenic ™™ Primary/secondary liver tumours Type 2: Intermittent obstruction ™™ Choledocholithiasis ™™ Periampullary tumour ™™ Choledochal cyst ™™ Bile duct papilloma ™™ Hemobilia ™™ Duodenal diverticula Type 3: Chronic complete obstruction ™™ Bile duct stricture ™™ Congenital ™™ Traumatic ™™ Post-radiotherapy ™™ Chronic pancreatitis ™™ Cystic fibrosis Type 4: Segmental obstruction ™™ Traumatic ™™ Sclerosing cholangitis ™™ Cholangiocarcinoma, intrahepatic biliary stones (hepatolithiasis)

You are the sole master of your thought processes.

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SRB's Manual of Surgery Clinical features Severe jaundice. Pruritus, more on the back and forearms. Fever, may or may not be present. Loss of weight. Loss of appetite. Pain in right hypochondrium, palpable gallbladder, hydrohepatotic palpable, smooth, soft, non-tender liver are other features. ™™ Courvoisier’s law may suggest inflammatory/neoplastic cause. ™™ Charcot’s triad/Reynold’s pentad as presentation in cholangitis. ™™ Steatorrhoea (more fatty stool) due to improper absorption of fat soluble vitamins. ™™ ™™ ™™ ™™ ™™ ™™

Investigations for Obstructive Jaundice xx Serum bilirubin. Normal value is less than 1.0 mg%. Both direct and indirect bilirubin are assessed. Direct is increased in obstructive jaundice, i.e. conjugated hyperbilirubinaemia. van den Bergh’s test is done. xx Serum albumin, globulin and A:G ratio. Normal S. albumin is more than 3.5 gm%. xx Prothrombin time. Normal value is 12–16 seconds. It is significant if it is more than 4 from the control or more than one and half times the control. It is corrected by injection vitamin K, 10 mg IM OD for 5 days or by FFP—5–10 units. xx Serum alkaline phosphatase, SGPT, SGOT, 5’ nucleotidase. xx Total count may be raised with neutrophilia in inflammatory conditions. Serum alkaline phosphatase (ALP) and γ glutamyl transpeptidase (GCT) are relevant enzymes in biliary obstruction; especially ALP/GCT ratio is more relevant in differentiating between obstructive jaundice and hepatitis. xx Ultrasound abdomen. xx ERCP to visualise the site of obstruction, brush biopsy, bile sample for analysis. xx PTC to decompress, assess proximal dilated obstructed biliary system if ERCP fails; dine polythene catheter can be kept in situ to have biliary drainage; PTC—stenting across the obstruction can be done under image (C-arm) guidance. xx MRCP—Noninvasive diagnostic tool. It shows 96% sensitivity; 99% specificity. xx CT scan in case of tumours to assess operability.

specificity. But it may also increase in other causes of biliary obstruction and cystadenoma. xx Endoscopic US (EUS): It is done through endoscope. It is more accurate in assessing pancreatic mass, staging of the disease, to identify involvement of portal venous system, CBD stones. It is also useful in EUS-guided FNAC, celiac axis neurolysis, EUS-guided immunotherapy. xx Intraductal US (IDUS): It is very useful in assessing tumour stage, tumour margin in bile duct cancer. It is also used in assessing pancreatic duct to differentiate pancreatic cancer and chronic pancreatitis. xx CT/MR angiogram or venogram to assess vascularity and portal venous system in malignancy. xx Urine tests: Fouchet’s test for bile pigments, Hay’s test for bile salts and test for urobilinogen in urine. Fouchet’s test: 10 ml of urine + 5 ml of BaCl2 + pinch of MgSO4 causes formation of BaSO4 which is filtered over a filter paper and few drops of Fouchet’s reagent is added. Green or blue colour signifies presence of bile pigments in the urine. Hay’s test for bile salt: Sprinkle sulphur to 2 ml of urine. In presence of bile salts sulphur sinks to the bottom. Ehrlich’s test: 5 ml of freshly voided urine + 1 ml of Ehrlich reagent (p-dimethyl amino benzaldehyde) and wait for 5 minutes. Formation of red colour signifies presence of urobilinogen in urine. Normally it is present in traces; in obstructive jaundice, it is absent; and in haemolytic jaundice, it is in excess. Preoperative preparation of patient with obstructive jaundice Proper diagnosis and assessment Injection vitamin K IM 10 mg for 5 days Fresh Frozen plasma—often requires 6 bottles or more Adequate hydration is most important 5/10% dextrose Blood transfusion in case of anaemia Oral neomycin, lactulose Mannitol 100–200 ml BD IV to prevent hepatorenal syndrome Repeated monitoring by doing prothrombin time, electrolytes Antibiotics like third generation cephalosporins. Calcium supplements as calcium chloride IV Preoperative decompression is indicated if bilirubin is > 12 mg%, sepsis, hepatorenal syndrome, severe malnutrition or cardiopulmonary disease. ™™ Correction of coagulopathy, prevention of renal failure, infection, hepatic encephalopathy and electrolyte imbalance (correction of hypoglycaemia and dilutional hyponatraemia due to water retention; avoiding isotonic saline infusion). ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Treatment of Obstructive Jaundice xx CBD stones—ERCP stone removal, choledocholitho­tomy, Fig. 12.55: CT scan showing hydrohepatosis due to obstruction below, in a patient with obstructive jaundice. xx Tumour markers: CA 19/9 is useful for carcinoma pancreas

(more than 70 units/L) with 70% sensitivity and 90%

transduodenal sphincteroplasty, choledochojejunostomy or choledochoduodenostomy. xx Carcinoma periampullary or head of pancreas—Whipple’s operation or triple bypass or ERCP stenting. xx Biliary stricture—Stenting, choledochojejunostomy, Rouxen-Y hepaticojejunostomy.

Gallbladder xx Klatskin tumour—Radical resection or palliative stenting. xx Biliary atresia—Kasai’s operation or liver transplan­tation. xx Choledochal cyst—Excision, hepaticojejunostomy, mucosal

resection. xx Management of pruritus: Pruritus may be due to retention

of bile salts which activates the release of histamine in skin, central mechanism or by release of endogenous opioids. It is often difficult to treat. Once cause is treated and obstruction is relieved, pruritus will regress. Drugs and therapies used are—cholestyramine (ion exchange resin binds bile salts in intestine inhibiting their absorption), rifampin, ondansetron, gabapentin, sertraline, ursodeoxycholic acid, antioxidants, phototherapy, plasmapheresis.

Postoperative Management xx Monitoring with prothrombin time, bilirubin, albumin, creatinine, electrolyte estimation. xx FFP or blood transfusion. xx Antibiotics. xx Observation for septicaemia, haemorrhage, pneu­monia, pleural effusion, bile leak. xx Care of T-tube and drains. xx T-tube cholangiogram in 10–14 days. xx TPN, CVP line, nasogastric tube, urinary catheter.

2. Inflammatory: Stricture following recurrent attacks of cholangitis due to:  CBD stones.  Parasites—Ascaris lumbricoids, Clonorchis sinensis.  Primary sclerosing cholangitis. 3. Malignant: Due to cholangiocarcinoma. 4. Traumatic. Bismuth classification of biliary stricture I. II. III. IV. V.

Low CBD stricture with stump (proximal to stricture) > 2 cm Middle CBD stricture with proximal stump < 2 cm Hilar. Confluence of right and left hepatic ducts is intact Separated right and left hepatic ducts Stricture involving intrahepatic ducts

Clinical Features xx xx xx xx

Obstructive jaundice. Pain abdomen. Features of ascending cholangitis. Profuse persistent bile leak.

CBD STRICTURES (BILIARY STRICTURES) Causes 1. Postoperative (80% common)  After cholecystectomy [open or laparoscopic, more common following laparoscopic (0.8%) than open method (0.35%)].  Biliary surgery.  Gastrectomy.  Liver surgery.  Duodenal and pancreatic surgery.

Fig. 12.56: ERCP picture showing stricture and passing stent into CBD.

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B

C

D

E Figs 12.57A to E: Bismuth classification of stricture CBD.

If there is no struggle, there is no progress—Frederick Douglas. Try and fail, but don’t fail to try—Stephen Kaggwa

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Features

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xx Common in young men (70%). xx Intermittent jaundice. xx Abnormal liver functions. xx Weight loss, pain, fever, pruritus. xx Features of ulcerative colitis in case of PSC (70%). xx PSC may be associated with retroperitoneal fibrosis, mediastinal fibrosis, Riedel’s thyroiditis, orbital pseudo-tumour. xx Hepatic duct confluence is most severely strictured segment in PSC.

Figs 12.58A and B: CBD stent and imaging after placement.

Investigation Causes of postoperative stricture ™™ ™™ ™™ ™™ ™™

Too much traction to the GB during ‘ Fundus first cholecystectomy’ Blind application of artery forceps in Calot’s to control bleeding Anomalies of biliary tree Inflammatory adhesions at Calot’s triangle Injury during other surgery like gastrectomy

Note:

Hogarth Pringle’s manoeuvre is ideal to control bleeding on table by applying pressure using thumb and fingers over the Foramen Winslow.

Investigations xx xx xx xx xx

Ultrasound abdomen. Liver function tests. ERCP. On table cholangiography. MRCP.

Treatment xx ERCP stenting. xx Choledochoduodenostomy or jejunostomy. xx Roux-en-Y hepaticojejunostomy—ideal.

SCLEROSING CHOLANGITIS xx It is fibrous thickening of the CBD and biliary ductular wall, associated with multiple strictures with dilata­tion in between the strictures. Both extra- and intrahepatic ducts are involved. xx They have increased risk of developing cholangio­carcinoma.

Types 1. Primary sclerosing cholangitis is one wherein no cause is found and is associated with ulcerative colitis, Sjögren’s syndrome, Crohn’s disease, Graves disease. It eventually leads to biliary cirrhosis. Primary sclerosing cholangitis (PSC) is an idiopathic, progressive, chronic, cholestatic pathology with diffuse inflammation, sclerosis,

xx ERCP shows beaded appearance of biliary tree. xx LFT is altered. xx Liver biopsy is needed to identify the severity of hepatic fibrosis.

Treatment xx xx xx xx

Stenting. T-tube drainage. Large dose steroids. Immunosuppression therapy—methotrexate, azathioprine, tacrolimus, cyclosporine. xx Ursodeoxycholic acid is beneficial. xx Liver transplantation. xx Median survival in PSC after diagnosis is 10 years.

GALLBLADDER POLYP xx Its incidence is 5% in routine US abdomen; 10% in cholecystectomy tissue specimen. xx It is usually less than 10 mm in size, pedunculated appearance. xx Sessile polyps are often more than 10 mm in size. xx 30% are multiple. xx Gallbladder polyp more than 10 mm in size, associated with gallstones, age above 60 years, symptomatic, sessile polyp and multiple polyps—are indications for surgical intervention. xx CT scan should be done if malignancy is suspected on US. xx It is treated by laparoscopic cholecystectomy. Histology is a must to confirm benign nature and to rule out carcinoma.

BENIGN BILIARY PAPILLOMA xx It is the most common benign biliary tumour. xx 50% occurs close to ampulla presenting as obstructive jaundice. xx Benign adenoma (soft), benign inflammatory pseudotumour and cholangiocarcinoma—are differential diagnosis. xx ERCP, CT scan, EUS, LFT—are the investigations. xx Treatment—papillotomy, wide local excision.

Gallbladder CARCINOMA GALLBLADDER xx It is more common in India (Patna) and Asian countries. It is also common in Chile. xx It is common in females and elderly. Male:Female = 1:3.

Aetiologies for Carcinoma of Gallbladder xx 3% of gallstones with cholecystitis will develop carcinoma

of gallbladder. xx 90% of carcinoma of gallbladder is associated with gall-

stones. Risk of developing carcinoma in gallstone disease is 7–10 times more than general population. Relative risk is less if stone size is less than 2 cm; if stone size is 2–3 cm in size, it is 2.5; it is 10 or more if stone size is more than 3 cm. xx Choledochal cyst, anomalous pancreaticobiliary duct junction (20%), cholesteroses of gallbladder, gallbladder polyp more than 1 cm in size or more than 3 in number or adenomatous polyp, PSC. xx Chronic typhoid carriers, carcinogens, inflammatory bowel disease, hepatitis B and hepatitis C virus infection. xx Porcelain gallbladder is more prone for malignant transformation (25%) and 90% of them are inoperable tumours. xx Nitrosamines. xx Polypoid lesions (GB polyp), xanthogranulomatous cholecystitis.

Gross Types of Carcinoma Gallbladder xx Polypoid/papillary—better prognosis. xx Scirrhous/nodular. xx Proliferative/infiltrative.

Microscopy xx Commonly it is adenocarcinoma (90%); occasionally squa-

mous cell carcinoma, adenosquamous or carcinoid tumour can occur. xx 25% show only localised disease; 35% have lymph node spread; 40% have distant spread at the time of first diagnosis. xx It is very aggressive tumour.

Spread of Carcinoma Gallbladder xx Direct spread to liver (segment IV and V), bile duct,

duodenum, colon and kidney. xx Lymphatic—lymph node of Lund, periportal nodes, peripancreatic and periduodenal nodes. xx Blood spread—to liver, lungs and bones. xx Perineural spread is also known to occur. Staging of carcinoma gallbladder Nevin’s staging: Stage I – Intramural Stage II – Spread to muscularis propria Stage III – Spread to serosa Stage IV – Spread to cystic lymph node of Lund Stage V – Direct spread to adjacent organs/metastases

TNM staging for gallbladder cancer (AJCC) Tumour (T)

Metastases (M)

TX Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1 Tumor invades lamina propria or muscular layer T1a Tumor invades lamina propria T1b Tumor invades muscular layer T2 Tumor invades perimuscular connective tissue; no extension beyond serosa or into liver T3 Tumor perforates the serosa (visceral peritoneum) and/or directly invades the liver and/ or one other adjacent organ or structure, such as the stomach, duodenum, colon, pancreas, omentum, or extrahepatic bile ducts T4 Tumor invades main portal vein or hepatic artery or invades at least two extrahepatic organs or structures

M0 – No distant spread. M1 Distant spread.

Nodes (N) Nx Regional lymph nodes cannot be assessed N0 Regional lymph node metastasis N1 Metastases to nodes along the cystic duct, common bile duct, hepatic artery, and/or portal vein N2 Metastases to periaortic, pericaval, superior mesenteric artery, and/or celiac artery lymph nodes

Staging Stage 0- Tis, N0, M0 Stage I – T1,N0,M0 Stage II – T2, N0, M0 Stage III A – T3, N0, M0 Stage III B – T1 to T3, N1,M0 Stage VI A – T4, N0 or N1, M0 Stage IV B – Any T, N2, M0; Any T, any N, M1 Note: Stage I is Localised; Stages II to IV B are unresectable.

Features of Carcinoma of Gallbladder xx Pain in right hypochondrium, mass in right upper abdomen

which is hard and nontender. Jaundice is common. Significant weight loss in short duration, anorexia Acute presentation of cholecystitis. Palpable nodular liver secondaries, ascites. It is common in places where there is more prevalence of gallstone disease—Patna, Bihar xx It is common in females. xx Incidentally confirmed as carcinoma gallbladder histologically after cholecystectomy for chronic cholecystitis. xx Three clinical presentations – 1. Clinically obvious type with pain, obstructive jaundice, mass. 2. Early GB cancer mimics GB stone disease. 3. Atypical as unusual features. xx xx xx xx xx

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SRB's Manual of Surgery nostomy is done. Open approach rather than laparoscopic is ideal for carcinoma gallbladder. xx Hemihepatectomy with cholecystectomy with nodal clearance. xx During laparoscopic cholecystectomy, any suspicious of GB cancer, procedure should be converted into open cholecystectomy.

B

A

Fig. 12.60: Extended cholecystectomy technique. xx If patient has undergone laparoscopic cholecystectomy and

histology confirmed carcinoma, then staging should be done. All port areas should be re-excised to prevent port site recurrence. Often extended resection of segment IV and lymph nodes may be needed. Spillage of bile during laparoscopic cholecystectomy is common (30% in non-malignant GB, 50% in carcinoma GB). xx Chemotherapy either systemic or intra-arterial, and adjuvant radiotherapy but with poor success rate.

Prognosis xx Overall prognosis for carcinoma gallbladder is poor due to

C Figs 12.59A to C: Specimen of gallbladder after extended cholecystectomy. Note the liver margin cleared of carcinoma, stone in the gallbladder and lymph nodes cleared.

early spread and aggressive nature of the tumour. xx 5-year survival is only 5%. Muscle invasion, nodal and

distant spread carry poor prognosis. In stage T1 simple and extended cholecystectomy will not make difference in prognosis. In T2, stage extended cholecystectomy is very much beneficial which gives 60% 5-year survival rate. T3 and T4 carry poor prognosis.

Investigations xx xx xx xx xx xx xx

Ultrasound abdomen. CT abdomen to see operability. US-guided FNAC. Liver function tests. MRCP. Laparoscopy. CA 19-9 is elevated in 80% of cases.

Treatment xx Cholecystectomy with resection of liver segments IV and

V—extended cholecystectomy with perihepatic nodal clearance. At least 2 cm margin in the liver from the gallbladder bed should be cleared. All pericholedochal lymph nodes should be removed. Frozen section biopsy from cystic duct stump should be done to identify for the existence of microscopic tumour. If present, CBD resection and hepaticojeju-

A

B

Figs 12.61A and B: (A) Gallbladder showing proliferative carcinomatous lesion; (B) Gallbladder showing scirrhous carcinoma with pre-existing gallstones and cholesteroses.

Gallbladder CHOLANGIOCARCINOMA (Bile Duct Carcinoma) xx It is associated with sclerosing cholangitis, clonor­chiasis infestation, Caroli’s disease or choledochal cyst. xx It is an aggressive adenocarcinoma which presents as obstructive jaundice. xx It commonly occurs at the hepatic duct confluence.

Risk Factors for Cholangiocarcinoma xx Primary sclerosing cholangitis (PSC): Here commonly it is extrahepatic, usually at the confluence. xx Choledochal cyst. xx Hepatolithiasis. xx Hepatitis B and C are risk factors for intrahepatic cholangiocarcinoma. xx Lynch syndrome II. xx Multiple biliary papillomatosis. xx Previous biliary enteric anastomosis. xx Clonorchis sinensis infestation. xx Thorotrast, nitrosamines, dioxin.

Classification I xx Intrahepatic—10%. xx Perihilar—65%. xx Distal—25%.

Classification II—Pathological Sclerosing (80%); nodular; papillary.

Classification III xx Upper third—from porta to cystic duct – 50%. xx Middle third—from cystic duct to upper margin of first part of the duodenum—25%. xx Lower third—from upper margin of first part of duodenum to ampulla—20%. xx Diffuse—5%. Classification of perihilar cholangiocarcinoma (Bismuth) ™™ ™™ ™™ ™™

Type I : Below the confluence of RHD and LHD Type II : Reaching the confluence of RHD and LHD Type III : Involving CHD and RHD/LHD Type IV : Involving confluence and both RHD and LHD or multicentric tumour

Features xx Main presentation is painless obstructive jaundice of short duration. xx Palpable liver either smooth and soft (hydrohepatotic) or hard nodular (secondaries). xx Weight loss and anorexia is typical and significant.

Investigations xx ERCP and choledochoscope. xx Liver function tests. xx PTC.

xx Ultrasound abdomen, CT scan. xx MR scan—Best investigation. MRCP to see duct; MRI to see nodes; MR angiogram to see vascularity. Assessment should be done to check the operability of tumour by— assessing the spread in bilateral hepatic duct up to secondary radicles, both hepatic arterial spread, portal vein encasement, hepatic lobe atrophy, distant spread. American Joint Cancer Committee/Union for International Cancer Control 7th edition, TNM staging for perihilar cholangiocarcinoma Primary tumor (T)

Regional lymph nodes (N)

Tx Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1 Tumor confined to the bile duct, with extension up to the muscle layer or fibrous tissue T2A Tumor invades beyond the wall of the bile duct to surrounding adipose tissue T2B Tumor invades adjacent hepatic parenchyma T3 Tumor invades unilateral branches of the portal vein or hepatic artery T4 Tumor invades main portal vein or its branches bilaterally; or the common hepatic artery; or the second-order biliary radical bilaterally; or unilateral second order biliary radicals with contralateral portal vein or hepatic artery involvement

NX Regional lymph nodes cannot be assessed N0 No regional lymph node metastases N1 Regional lymph node metastases present (including nodes along the cystic duct, common bile duct, hepatic artery, and portal vein) N2 Metastases to periaortic, pericaval, superior mesenteric artery, and/or celiac artery lymph nodes

Note: TNM staging defers for intrahepatic, perihilar and distal cholangiocarcinoma.

Distant metastases (M) M0 No distant metastases M1 Distant metastases present Staging Stage 0 Tis N0 M0 Stage I T1 N0 M0 Stage II T2A-B N0 M0 Stage IIIA T3 N0 M0 Stage IIIB T1-3 N1 M0 Stage IVA T4 N0-1 M0 Stage IVB Any T N2 M0 Any T Any N M1

Treatment xx When operable, portal region clearance with hemihepatectomy can be done. Intrahepatic type is treated with hemihepatectomy. Perihilar is treated with hemihepatectomy or extensive bile duct resection, nodal clearance, caudate lobe removal, cholecystectomy. Distal tumour is treated with Whipple’s pancreaticoduodenectomy. xx Most often it is inoperable. Stenting can be done to relieve jaundice, through PTC or ERCP or on table. xx Chemotherapy—5 FU; Gemcitabine, cis platin. xx Chemotherapy, with external beam radiotherapy (ERBT).

KLATSKIN TUMOUR xx It is cholangiocarcinoma at the confluence of the hepatic ducts and common hepatic duct above the level of the cystic duct (20% of cholangiocarcinomas). xx Klatskin tumour is classified as 4 types—I: Just at or below the confluence; II: At the confluence; III: at the confluence extending along the RHD; IV: at the confluence extending along the LHD.

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SRB's Manual of Surgery xx It causes obstructive jaundice with hydrohepatosis without enlargement of gallbladder. xx Management is like cholangiocarcinoma.  Hilar resection with hepaticojejunostomy.  Segment III left hepaticojejunostomy—Blumgart’s.  Longmire’s left hepaticojejunostomy after left liver lobe resection.  Cattell’s hepaticojejunostomy.  Smith’s mucosal graft hepaticojejunostomy.  Palliative PTC with stenting/ERCP stenting, intraoperative stenting. Metal stents show long period of patency (12 months) than polyethylene stents (4 months).

b. Internal:  Cholecystoduodenal fistula causing gallstone ileus.  Cholecystoenteric fistula.  Cholecystocholedochal fistula. External biliary fistulas are difficult to manage, often dangerous, but many a times resolve spontaneously.

Investigations xx xx xx xx

Fistulogram. ERCP. Electrolyte estimation. Liver function tests.

Treatment xx xx xx xx xx

Total parenteral nutrition (TPN). Antibiotics. Blood transfusion. Electrolyte management. Care of the fistula wound with regular dressing, using zinc oxide cream has to be done to protect the skin. xx Later continuity of biliary system has to be restored by open surgery or through ERCP and stenting.

A

B

Figs 12.62A and B: (A) Resected specimen of Klatskin tumour (Courtesy: Dr Arunkumar, MCh); (B) Klatskin tumour. Cholangiocarcinoma ™™ ™™ ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

It is an uncommon tumour of elderly. 1 in 100,000 is the incidence Primary sclerosing cholangitis is the commonest association. 20-fold increased risk Choledochal cyst, Caroli’s disease, pyogenic cholangiohepatitis, Clonorchis sinensis, opisthorchis viverrini infestation, hepatolithiasis, hepatitis C, Lynch syndrome II, bile duct adenoma and papillomatosis are other causes Chemical carcinogens like thorium, nitrosamines, diosmin also can cause Intrahepatic cholangiocarcinoma is 10% 60% cases are proximal to cystic duct CBD junction Features are jaundice, pain, hepatomegaly, cachexia, early satiety and weight loss It is adenocarcinoma type Lymph node spread is common Resection along with liver/resection along with pancreas are surgical options But surgical resection is possible only in 5% of cases Stenting/bypass are palliative options Doxorubicin, cis platin and I131 anti-CEA antibodies are adjuvant therapies Condition has got 90% mortality in one year

BILIARY FISTULAS Types a. External: Usually occurs as a complication of surgery following:  Gastrectomy.  Cholecystectomy open or laparoscopic.  CBD surgery.  Pancreatic surgery.

HEMOBILIA xx It is bleeding commonly from the liver or occasionally from the gallbladder into the biliary tract. xx There is abnormal communication between a blood vessel and a bile duct or any part of the biliary tree.

Causes xx Accidental trauma, iatrogenic trauma (50%). In accidents hemobilia is more commonly caused by blunt trauma than by penetrating one. xx Percutaneous diagnostic and therapeutic proce­dures. xx Vascular diseases of the hepatic artery—10%. xx Malignant liver diseases > common (5%) than benign. xx Portal hypertension. xx Parasitic liver diseases like hydatid disease. xx Gallstones rarely erode into hepatic artery causing life-threatening hemobilia. xx Blood and necrotic material drains into the biliary tree causing gastrointestinal bleeding. As bile inter­feres with coagulation a fatal haemorrhage can occur. xx Arterial hemobilia is more common. Portal venous hemobilia is rare. Hepatic artery aneurysm is common cause. xx Early rapid presentation can occur; but delayed, after weeks/ months/years, presentations are known to occur which is often difficult to suspect and diagnose. xx These recurrent clots can cause pancreatitis, cholangitis, anaemia, cholecystitis.

Clinical Features xx Pain which is colicky in nature. xx Obstructive jaundice. xx Haematemesis and melaena.

Gallbladder CHOLECYSTECTOMY

Triad of Sandblom/Quincke’s in hemobilia ™™ ™™ ™™

Jaundice—60% Pain—70% Upper GI bleed with melaena (90%), haematemesis (60%)

All three features of triad are seen only in 20% of cases.

Investigations xx LFT. xx US abdomen. xx Selective arteriography—test of choice in detecting bleeding site in 90% of cases. CT angiogram is useful. xx Upper GI scopy—useful only in 10% of cases. Note: ERCP is usually not indicated.

Treatment xx xx xx xx

Aim: To stop bleeding and to relieve biliary obstruction. Antibiotics. Blood transfusions. Selective arterial embolisation. Transarterial embolisation (TAE) shows 90% success rate. It is the choice therapy with least morbidity. Coils and glue are used. xx Surgical intervention is only rarely indicated in failed TAE. Laparotomy, ligation of bleeding vessel or hepatic artery, excision of aneurysm, hepatic resection—are the procedures done. Hemobilia is often a fatal condition.

It is the surgical removal of gallbladder. Prophylactic cholecystectomy is done in ™™ ™™ ™™

Diabetic patients Congenital haemolytic anaemia Patients who has underwent bariatric surgery

Indications xx xx xx xx xx

Gallstones—symptomatic. Cholecystitis—acute, chronic. Acalculous cholecystitis. Empyema gallbladder. Mucocele gallbladder.

Approach xx Open  Right subcostal incision (Kocher’s).  Right paramedian.  Horizontal incision.  Mayo-Robson incision.

xx Laparoscopic approach.

Note:

Bilhemia: It is different very rare entity wherein bile flows into the hepatic or portal venous system due to raise in intrabiliary pressure more than that of portal or hepatic venous pressure. It may be due to trauma, iatrogenic or gallstone eroding into the venous system. Large quantity of bile enters the venous system and later to lung becoming fatal. If flow is low which is common, subsides spontaneously. ERCP is diagnostic. Treatment is stenting. Septicaemia and mortality is common.

WHITE BILE xx xx xx xx

It is double misnomer. It is neither white nor bile. It is opalescent. It is mucous secreted by the lining of biliary tree. It signifies severe obstruction due to stone (impacted in the CBD), or carcinoma head of pancreas or periampullary region. xx It is on table finding during surgery. xx It means liver is unable to secrete bile due to raised intraductal pressure, and so can anticipate hepatic failure. xx Indicates a poor prognosis.

A

B

Figs 12.64A and B: (A) Incisions for open cholecystectomy and laparoscopic cholecystectomy; (B) Kocher’s incision used for open cholecystectomy.

OPEN APPROACH CHOLECYSTECTOMY Technique After opening the abdomen, colon is pushed down­wards and stomach medially. Duct—first method: Here Calot’s triangle is dissected. Cystic artery is identified and ligated. Cystic duct is ligated close to the gallbladder. Gallbladder is separated from gall­bladder fossa and removed. Haemostasis is maintained. Fig. 12.63: Demonstration of white bile on table. It is not white but opalescent. It is not bile but it is mucus.

Fundus—first method: It is done in difficult gallbladder due to dense adhesions. Fundus is separated from the liver bed. Dissection is carried

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proximally until cystic duct and cystic artery are identified, which are then ligated. Drain is placed, which is removed after 72 hours. On table cholangiogram is a must after cholecystec­tomy.

Complications of Cholecystectomy xx Complications can occur either in open method or in laparoscopic method. xx Open method is done through either right para­me­dian incision or Kocher’s incision (right subcostal).

It is the most popular method to remove gallbladder. It is the gold standard treatment for gallstone.

Position xx Supine, head end up and right side up.

Anaesthesia—general.

Ports xx 10 mm port in umbilicus to pass 10 mm telescope. xx 10 mm port in midline epigastrium as working channel. xx Two 5 mm ports at midclavicular and anterior axillary line

in subcostal region.

Procedure

Fig. 12.65: Ligation of cystic duct and cystic artery while doing cholecystectomy. Complications which can occur in both: ™™ Infection and subphrenic abscess ™™ Bleeding from cystic artery, and from liver bed ™™ Injury to CBD or hepatic duct ™™ Bile leak and biliary fistula formation ™™ Biliary stricture formation ™™ Injuries to colon, duodenum, mesentery

After creation of pneumoperitoneum with 12–14 mm pressure, 10 mm umbilical port is inserted. Telescope is passed. Under vision remaining ports are passed. With lateral 5 mm port, gallbladder grasper forceps is passed and fundus of gallbladder is held and pushed up towards the diaphragm. With middle 5 mm port grasper is passed to hold Hartmann’s pouch. With 10 mm port dissector is passed using reducer. Calot’s triangle is dissected. Cystic duct is identified. Adhesions are released. First posterior dissection is completed. Cystic artery is above and deep to cystic duct. Cystic duct is clipped or ligated. Cystic artery is also clipped. Gallbladder is dissected off the liver bed using cautery (hook/spatula)/harmonic scalpel. Gallbladder is removed through 10 mm working port with reducer or using a sterile bag. Any bleeding points are coagulated. If needed, saline wash is given to the bed. If infected, if gallbladder is opened, if there are adhesions, if there is oozing from gallbladder bed, a tube drain is placed through lateral 5 mm port. All ports are removed. Umbilical port is sutured in layers. Other ports are sutured. Patient is asked to take oral food in 24 hours and can be discharged in 24–48 hours.

Fig. 12.67: Rouvier sulcus on the undersuface of liver is a guideline during laparoscopic cholecystectomy wherein dissection in Calot’s should be always kept in front of it to avoid CBD/hepatic duct injury.

Problems Fig. 12.66: Diagram showing the partial cholecystectomy wherein GB is removed at Hartmann’s pouch, distal to Calot’s triangle. It is done when there is dense adhesions,with difficult surgical plane.

xx xx xx xx

Difficult Calot’s triangle. Dense adhesions. Bleeding. Anomalies of cystic duct, cystic artery.

Gallbladder

A

surgery (OPUS), and single port incision less conventional equipmentutilising surgery (SPICES), natural orifice transumbilical surgery (NOTUS). It needs general anaesthesia, specialised umbilical large trocars which accommodates working instruments along with flexible laparoscope, rotatable instruments, articulating handles, harmonic scalpel. Here through a large 2.5 cm umbilical vertical incision dissection is done by open method to reach peritoneal cavity. Specialised port in which one can pass 10 mm telescope and two 5 mm instruments for work is used. Instruments are angled and flexible to meet the ergonomic principles to certain extent. Dissection of gallbladder is done in similar fashion like four- port technique. Specimen is easily retrieved through umbilical port as it is wide enough. If difficulty arises any time, one can add additional ports as required.

B

C Figs 12.68A to C: Photos of laparoscopic cholecystectomy showing cystic duct, gallbladder, Calot’s triangle and clipped cystic duct.

A

Complications xx xx xx xx xx xx

Bile duct injury—0.8%. Bleeding. Bile leak. Infection, cholangitis, septicaemia. Subphrenic abscess formation. Injury to colon, duodenum, mesentery.

B Figs 12.70A and B: Single incision laparoscopic surgery (SILS) for cholecystectomy.

Advantages xx There is no visible scar like a traditional multiport. xx Faster recovery time, early return to work. xx Cosmetically better.

Disadvantages Fig. 12.69: Post-cholecystectomy bile leak with fistula. It is common and problematic complication after cholecystectomy.

SINGLE INCISION LAPAROSCOPIC SURGERY (SILS) IN CHOLECYSTECTOMY SILS is an advanced minimally invasive surgical procedure wherein surgeon operates exclusively through a single umbilical entry port. It is also called as single port access surgery (SPA), one port umbilical

xx Expensive trocars and instruments—cost factor. xx Skilled work, learning curve. xx Dissection against normal surgical ergonomics.

Complications xx Umbilical wound pain, infection. xx Umbilical hernia. xx Because of limited visibility time consuming.

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SRB's Manual of Surgery xx During learning curve complications of cholecystectomy and conversion rate may be more. Note:

Waltman-Walter syndrome: It is compression of IVC due to collection of fluid in subphrenic space during post-cholecystectomy period. It mimics coronary thrombosis.

BILE DUCT INJURIES Causes xx xx xx xx xx

Cholecystectomy—open or laparoscopic. Trauma. Instrumentation—ERCP, baby endoscope, chole­do­choscope. Other surgeries—pancreatic, duodenal, gastric. Anomalous biliary system increases the risk of injury.

Strasberg classification

™™

™™ ™™

™™

It classifies injuries in relationship to the confluence and also includes vascular injuries. ™™ Type A: It refers to cystic and/or gallbladder bed leaks ™™ Type B is a complete or incomplete stenosis caused by a surgical staple ™™ Type C represents lateral tangential injuries ™™ Type D refers to complete section of the common bile duct emphasizing their distance to the confluence as well as the concomitant injuries of hepatic artery and portal vein ™™ Type E is late bile duct stenosis at different lengths to the confluence Note: Bismuth classification (for open surgery/pre-laparoscopic era) is discussed under biliary stricture earlier.

Presentations

Classifications

™™

Hannover classification (2007)

Class A: Bile leak from the cystic duct or an accessory duct showing continuity with the common bile duct Class B: Section/injury of an accessory duct/sectorial ducts aberrant right hepatic duct with no continuity with the common bile duct with occlusion Class C: Leak/open drainage from a sectorial duct/aberrant right hepatic duct with no continuity with the common bile duct Class D: Partial section/lateral injury of an extrahepatric duct bile duct with no complete loss of continuity with the rest of the bile duct system Class E: Complete section/circumferential injury of the bile duct with subtypes according to the length of the stump at various levels –– E1- Stricture/injury at more than 2 cm distal to bifurcation. –– E2 – Stricture/injury less than 2 cm distal to bifurcation. –– E3 – Stricture/injury at bifurcation –– E4 – Stricture/injury involving right and left hepatic ducts –– E5 – Complete obstruction of entire bile duct

Note: Only right and left partial injuries are not included in this classification

xx Fever, pain, features of bile stasis like cholangitis, jaundice. xx 10% of laparoscopic bile duct injuries are identified on table; 30% with bile leak; 25% with obstructive jaundice; 30% with cholangitis. Patients with bile leak present early; with formed biliary stricture presents with jaundice and cholangitis months or years later.

Complications xx xx xx xx xx xx

Investigations xx xx xx xx xx

Stewart-Way classification This classification involves four strata based on the mechanism and anatomy of injury. ™™ Class I: It refers to the incomplete section of bile duct with no loss of tissue. It has a prevalence rate of 8% ™™ Class II: It is a lateral injury of the common hepatic duct that leads to stenosis or bile leak. It is the consequence of thermal damage and clamping the duct with surgical staples. It has a prevalence of 2% with a concomitant hepatic artery injury in 20% of cases.T-tube related injuries are included within this class ™™ Class III: It is the most common (60%) represents the complete section of the common hepatic duct. It is subdivided into type IIIa, remnant common hepatic duct; type IIIb, section at the confluence; type IIIc, loss of confluence; and type IIId, injuries higher than confluence with section of secondary bile ducts. Associated injury of right hepatic artery occurs in 25% of cases ™™ Class IV: It is right (65%) and accessory right (25%) hepatic duct injuries with associated injury of the right hepatic artery (60%). Occasionally it includes the common hepatic duct injury at the confluence (5%) besides the accessory right hepatic duct lesion (prevalence of 10%)

Biliary fistula with electrolyte imbalance. Biliary peritonitis, septicaemia. Subphrenic abscess formation. Biloma formation. Severe malnutrition, deficiencies. Late—biliary cirrhosis, portal hypertension.

xx xx xx

LFT, coagulation profile. US abdomen, fistulogram. Dynamic CT scan will delineate the anatomy of injury. ERCP is useful if injury is only partial where stenting can also be done. PTC is the investigation of choice to identify site, nature, extent of stricture. It also facilitates drainage and stenting. Hepatobiliary scintigraphy may be useful. MRCP may be useful to identify ductal anatomy. CT arteriography is useful to identify associated hepatic artery or portal vein injury which is 20% in association with CBD injury.

Management xx General: antibiotics, nutrition, TPN. xx Conservative: Small partial injury to CBD may resolve spontaneously or with the help of ERCP, sphincterotomy and stenting is done. xx Management of biliary duct injury on table (during laparoscopic cholecystectomy/open): Conversion into open surgery with a lengthy subcostal/bucket handle incision. Intraoperative cholangiogram should be done. Partial injury of CBD less than 30% of circumference is treated with primary repair with a T-tube in place. Extensive injury more than 30% of the circumference or cautery injury or complete CBD transection should be treated with Rouxen-Y choledochojejunostomy. Isolated hepatic duct injury less than

Gallbladder 3 mm in size should be ligated. More than 3 mm in size should be reimplanted or Roux-en-Y hepaticojejunostomy should be done. If facility for surgical repair is available, patient should be sent to a higher centre after placing a drain with abdomen closure. xx Management of bile duct injury identified at a later period: In such a situation it is better to wait for 6 weeks for the inflammation to subside which facilitates easier identification of proximal CBD. After proper assessment of injury, Roux-en-Y choledochojejunostomy or Roux-en-Y hepaticojejunostomy is done. xx Hepp-Couinaud approach: Here hilar plate is meticulously dissected; left hepatic duct is anastomosed to Roux jejunal loop to create hepaticojejunostomy often with creation of proximal ‘access loop’ for future endoscopic approach. Complications are—recurrent cholangitis, bile leak from stoma, hemobilia, stenosis of biliary enteric anastomotic site (10%, occurs often after many years).

POST-CHOLECYSTECTOMY SYNDROME (15%) xx Recurrent, new or persistent symptoms after cholecystec­tomy in patients who have no demonstrable abnormality is called as postcholecystectomy syndrome. xx It may be due to loss of reserving function of the gallbladder or continuous bile flow into the duodenum may be causing oesophagitis/gastritis or diarrhoea and colicky pain. 20% causes are other than due to hepatopancreatic biliary problems. xx However importance lies in ruling out the other causes of the symptoms like peptic ulcer, hiatus hernia, pancreatic diseases, residual CBD stone, cystic duct remnant, papillary stenosis. xx True post-cholecystectomy syndrome is treated with proper counseling, psychiatric evaluation and drug therapy. It should be evaluated thoroughly. Causes of post-cholecystectomy syndrome Gallbladder

Residual or reformed gallbladder Stump stones in cystic duct Neuroma in the stump Slipped stones into the peritoneum Clips applied to cystic duct

Biliary tree

Residual stone in CBD Biliary dyskinesia Stricture Dilatation without obstruction Fistula Cholangitis Malignancy

Liver

Fatty liver, hepatitis, cirrhosis Sclerosing cholangitis

Pancreas

Pancreatitis, stones Carcinoma pancreas Sphincter of Oddi dyskinesia

Contd...

Contd... GIT

Oesophagitis / hiatus hernia/ achalasia cardia Duodenal diverticula IBS, constipation, incisional hernia Mesenteric ischaemia

Cardiac

Coronary heart disease

Others

Adrenal tumour Thyrotoxicosis Intercostal neuralgia Arthritis Psychiatric diseases

BILIARY DYSKINESIA Biliary dyskinesia is motility disorder of either gallbladder or sphincter of Oddi. Patient presents with features of biliary colic without any evidence of gallstone disease. It can be: Gallbladder dyskinesia:  Here CT scan, gastroscopy, ERCP are normal. CCK is injected intravenously after filling gallbladder with radionuclide labeled Tc99m, gallbladder ejection fraction is assessed after 20 minutes. If it is less than 35%, then it is called as gallbladder dyskinesia.  It is treated with laparoscopic cholecystectomy. xx Sphincter of Oddi dysfunction:  It is also known as biliary sphincter dyskinesia or pancreatic sphincter dyskinesia. It is benign acalculous obstruction to bile and/or pancreatic flow across sphincter of Oddi causing cholestasis, pancreatitis and pain.  It may be due to trauma, congenital anomalies.  In occurs in 1% of cholecystectomy patients. Condition is common in females.  Normally CCK relaxes sphincter by decreasing its pressure. After IV injection of CCK, if CBD diameter becomes more than 12 mm or if there is increase in CBD diameter in response to CCK on US evaluation it suggests dysfunction of sphincter of Oddi. If basal sphincter pressure, on study, increases more than 40 mmHg it also suggests the same.  Milwaukee’s classification: Type I: Any one of the following features—unexplained biliary pain for more than 6 months after cholecystectomy, ERCP showing CBD >12 mm, delayed bile drainage >45 minutes, altered liver enzymes. Type II: Unexplained biliary pain for more than 6 months after cholecystectomy + with any one of the other criteria. Type III: Only unexplained biliary pain for more than 6 months after cholecystectomy, without any of other criteria.  ERCP/MRCP/sphincter of Oddi manometry, IV cholangiography are the investigations.  Treatment: Endoscopic sphincterotomy, botulinum toxin injection into the sphincter, nifedipine, transcutaneous electric nerve stimulation to raise serum vasoactive intestinal peptide (VIP) level which decreases the sphincter pressure.

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Spleen CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™

Surgical Anatomy Functions of the Spleen Splenunculi Splenic Injury Splenomegaly Hereditary Spherocytosis Immune Haemolytic Anaemia

™™ T halassaemia ™™ Sickle Cell Disease ™™ I diopathic Thrombocytopaenic Purpura ™™ Thrombotic Thrombocytopaenic Purpura ™™ Splenectomy

SURGICAL ANATOMY xx It is a wedge-shaped organ lying mainly in left hypochondrium, along the long axis of 10th rib. xx Hilum of spleen transmits splenic vessels and nerves. The visceral surface is related to stomach, splenic flexure of colon, kidney. xx Spleen in English means “ill temper”. Galen called it as organ of mystery.

Ligaments of Spleen Spleen is suspended by two ligaments (a) lienorenal ligament, (b) gastrosplenic ligament. xx Lienorenal ligament transmits blood vessels to spleen. The tail of pancreas lies in this ligament, which can be damaged during splenectomy. xx The gastrosplenic ligament contains short gastric vessels which supply the left half of greater curvature of stomach. xx Phrenicocolic ligament comes in contact with lower pole of spleen, which may be damaged during mobilization of splenic flexure of colon.

Blood Supply Splenic artery is the branch of coeliac artery but may arise from aorta or superior mesenteric artery, blood flow is 300 ml/mt. Splenic vein joins the superior mesenteric vein at right angle behind the neck of pancreas to form the portal vein. Splenic parenchyma contains white pulp and red pulp. White pulp lies in centre surrounding the central artery, which is a branch of trabecular artery. It is made up of lymphatic nodules with germinal centres and periarterial lymphatic sheaths with a network containing

™™ Overwhelming Postsplenectomy Infection ™™ Splenic Artery Aneurysm ™™ Splenic Abscess ™™ Hypersplenism ™™ Splenic Cyst ™™ Atraumatic rupture of spleen

lymphocytes and macrophages. White pulp is surrounded by marginal zone which contains end arteries from central and peripheral peniciliary arteries. Marginal zone contains marginal sinus which filters the materials from the white pulp. Immunoglobulins secreted by white pulp enter marginal zone and into main bloodstream. Red pulp is located outer to marginal zone. Red pulp contains cords and sinuses. Central artery gives reticular branches which open into these sinuses and cords wherein particles are phagocytosed. Commonly central artery eventually ends in these cords and sinuses. Few end branches of the central artery directly enters the pulp vein. Cords and sinuses eventually drain into pulp vein. Blood circulating through these cords and sinuses are called as ‘open’ circulation (90%). Blood passing through white pulp but not entering these cords and sinuses are called as ‘closed’ circulation (10%). Spleen is palpated under left costal margin during inspiration. It has to enlarge 2–3 times its normal size to become palpable.

FUNCTIONS OF THE SPLEEN Spleen has got two groups of functions: 1.  Cellular function. xx Removal of non-deformable intracellular substances from deformable cells is called as “pitting”. Heinz bodies/Howell-Jolly bodies, Pappenheimer siderotic bodies are removed by this method from RBCs. Post-splenectomy patients will show these bodies in the RBCs in peripheral smear. In splenunculi, these bodies will be absent even after splenectomy. xx Removal of aged/abnormal red cells is done by a process of “culling”. RBCs which loose osmotic balance and membrane integrity is called as non-deformable and they are removed by this method.

Spleen

Fig. 13.1: Architecture of spleen showing red pulp (peripheral); white pulp (central); open and closed circulation; marginal zone and sinuses and trabecular artery and vein.

Fig. 13.2: On table photo of splenunculi with splenomegaly. Splenunculi should be removed otherwise disease will recur.

xx Half-life of platelets is 10 days. In splenomegaly 80% of platelets may be sequestered in spleen causing thrombocytopenia. Normally spleen is reservoir for platelets. 1/3rd of total platelet mass is present in spleen. In pathological status like immune diseases phagocytosis of platelets in spleen is accelerated by many folds. xx Splenomegaly and hypersplenism can cause neutropenia. Neutrophil half-life is 6 hours. xx Bacterial clearance also occurs in spleen by phagocytosis. After splenectomy, patients are more prone for OPSI.

xx After splenectomy, they undergo hyperplasia and lead to

2.  Immunologic functions like synthesis of antibody IgM; formation of lymphocytes; production of tuftsin, opsonins, properdin and interferons. Functions of spleen ™™

™™

™™ ™™ ™™

™™

Response to antigenic challenge—by secreting antibodies like IgM, tuftin, opsonins, properdin, interferons. These agents make bacteria and other organisms more vulnerable to phagocytosis. All bacteria including the capsulated types, virus and fungi are destroyed efficiently. Destruction or correction of abnormal cells like old RBCs, target cells, siderocytes, spherocytes or removal of inclusion bodies or parasites from the RBCs by culling and pitting. Phagocytosis of foreign substances. As platelet reservoir. Erythrocyte production: In fetal life, it is an important site of RBC production till 5th month of gestation. In adults erythropoiesis in spleen occurs only if marrow production is inadequate, e.g. in myelofibrosis. Iron reutilisation.

SPLENUNCULI (30%) xx These are single or multiple accessory spleens. Sites ™™ ™™ ™™ ™™ ™™ ™™

Hilum of spleen (50%) Near splenic vessels Tail of the pancreas (30%) Splenic ligaments—gastrosplenic/splenorenal Mesocolon Greater omentum

recurrence of the disorder for which spleen was removed. xx Blood peripheral smear, in these patients with splenunculi will

not show Howell-Jolly bodies. Pappenheimer siderotic bodies. xx Accessory spleen can also be occasionally present adjacent

to left ovary or adjacent to left testis. xx All accessory spleens should be removed along with sple-

nectomy while doing for ITP or haemolytic disorders.

SPLENIC INJURY (Rupture spleen) The spleen can rupture as—Trauma to a normal spleen OR to a diseased spleen; Atraumatic rupture of a diseased spleen [pathologic (occult) rupture] and Spontaneous rupture of a normal spleen [spontaneous (idiopathic) rupture].

Causes xx Splenic injury occurs commonly following road traffic

accidents, other blunt injury or penetrating/stab injuries.

xx Most often associated with fracture of left lower ribs, haemo-

thorax, injury of liver (left lobe commonly, occasionally both lobes), bowel, tail of pancreas, left kidney. xx Injury is more common and severe in enlarged spleen, i.e. in malaria, tropical splenomegaly, infectious mononucleosis. xx Spontaneous rupture of spleen can occur in malaria and infectious mononucleosis. xx Larang was used to kill by the murderers in far east where malaria was endemic leading to spleno­m egaly, which ruptured more easily. xx Spleen is the most common solid organ injured in blunt abdominal trauma.

Types of Injury 1. Splenic subcapsular haematoma: After initial injury patient remains asymptomatic for a short period. But this haematoma ruptures later, may be after few days causing torrential haemorrhage.

Success isn’t owned, it’s leased and the rent is due every day. Success is not a destination, it’s a journey

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SRB's Manual of Surgery 2. Clean incised wound over the surface: This can be treated by splenorrhaphy. 3. Lacerated wound. 4. Splenic hilar injury causes torrential haemorrhage, may even cause death. So immediate surgical intervention and splenectomy is done. 5. Splenic injury associated with other injuries (left kidney, left colon, small bowel, pancreas, diaphragm, left lung).

A

B

C

D

Associated injuries ™™ ™™ ™™ ™™ ™™ ™™ ™™

Left lobe liver injury Tail of pancreas injury Left kidney, left colonic injury Small bowel injury Diaphragm and left lung injury Fracture lower ribs—left sided (30%) Left sided haemothorax

Presentation Hilar injury presents with rapid development of shock and deteriorates fast. Even death can occur some­times. Here emergency surgery and splenectomy is mandatory. xx In other types, features of shock (pallor, tachy­cardia, restlessness, hypotension), pain, tenderness and abdominal rigidity in left upper quadrant is seen. xx Later there will be abdominal distension due to haemoperitoneum. xx Dullness in the left flank which does not shift, as the collected blood gets clotted. Dullness without shifting— Ballance’s sign.

Figs 13.4A to D: Types of splenic injury. (A) Subcapsular haematoma; (B) Incised wound; (C) Lacerated wound; (D) Hilar injury. xx Pseudoaneurysm and traumatic splenic arteriovenous fistula formation can also occasionally cause delayed life-threatening haemorrhage. xx Features of other abdominal organ injuries may be present. Signs in splenic rupture Kehr’s sign—pain in left shoulder 15 minutes after foot end elevation ™™ Ballance’s sign—left sided abdominal dullness which will not shift ™™ Saegesser’s tender point between left sternomastoid and scalenus medius ™™ Latent period of Bandet—refer above ™™

A

B

Fig. 13.3: Large subcapsular splenic haematoma.

Figs 13.5A and B: Splenic injury with splenic haematoma.

xx Clot collected under the left side of the diaphragm irritates

Splenosis: Autotransplantation of fragments of splenic tissue may occur within the peritoneal cavity following rupture of spleen.

it and the phrenic nerve causing referred pain in the left shoulder—Kehr’s sign. There may be left sided haemothorax with fracture of ribs. Delayed presentation is also possible due to forma­tion of subcapsular haematoma which later gives way. Initially gets temporarily localized by greater omen­tum, later giving way leading to torrential bleeding. Blood clot temporarily seals off the bleeding which later gets dislodged causing severe bleeding. This time period in between is called ‘latent period of Bandet’.

Note:

Investigations xx U/S abdomen is the investigation of choice, as it is quicker,

cheaper and non-invasive. xx Hb%, PCV, blood grouping and cross matching. xx Adequate amount of blood must be kept ready for transfusion. xx CT scan will show type of splenic injury and its class.

Spleen Contd...

Plain X-ray abdomen. Findings are: ™™ ™™ ™™ ™™ ™™ ™™

Grade III

Obliteration of splenic outline Obliteration of psoas shadow (most important feature) Indentation of fundic gas shadow Fracture of lower ribs Elevation of left side of diaphragm Free fluid in the abdomen between coils of intestine

Expanding subcapsular or >50% surface area or ruptured bleeding subcapsular haematoma / intraparenchymal haematoma. Intraparenchymal haematoma >5 cm or parenchymal laceration >3 cm depth involving trabecular vessels

xx Diagnostic peritoneal lavage (DPL): By subumbilical incision the peritoneal lavage catheter is introduced into the peritoneal cavity. One litre of crystalloid (normal saline) is introduced into the cavity. Patient is turned to both left and right side and fluid is collected back. It is sent for cytology, culture, micro­scopy and biochemical analysis. It is significant when the aspirated fluid contains:  Gross blood of 10 ml.  >100000/mm3 of RBC.  >500/mm3 of WBC.  Bile, bacteria or food fibres.  Amylase > 175 units/dl.

Grade IV

Laceration involving segmental or hilar vessels with >25% devascularization

Grade V

Shattered or avulsed spleen; hilar devascularization with entire spleen separation

Treatment Initial Management xx Central venous line for perfusion and monitoring. xx Transfusion of blood as needed, resuscitation using crystalloids like Ringer’s lactate. xx Antibiotics coverage. xx Urinary catheterisation. xx Nasogastric tube aspiration.

Surgical Management

A

Emergency splenectomy xx It is done through midline/left subcostal incision. Thoracoabdominal extension of incision may be needed for rapid control of bleeding for injury to a large tropical spleen with severe bleeding. Other associated injuries should be looked for and dealt with (injury to left lobe liver/pancreas/intestine/colon).

B Figs 13.6A and B: Lacerated injury over the spleen. Patient underwent splenectomy.

xx Angiogram, for diagnosis and often for angiographic embolisation to reduce the bleeding and to manage splenic injury non-operatively is also becoming routine in many centres.

Complications of Splenic Rupture/Trauma xx xx xx xx xx xx

Blood loss. DIC. Sepsis. Splenic artery pseudoaneurysm. Splenic arteriovenous fistula. Problems of associated injuries like of pancreas.

Partial splenectomy (upper/lower) xx It can be done by retaining either of the upper or lower polar branches of the splenic artery. Splenorrhaphy xx In especially clean incised wound, spleen can be salvaged by suturing the wound carefully with placement of gel foam, topical thrombin, absorbable mesh wrap over the wound. Suture repair, oxidised cellulose, debridement of lacerated spleen—are other methods used. Temporary occlusion of splenic artery is often needed during splenorrhaphy. 10% of splenic injuries undergo splenorrhaphy. Its application is getting reduced due to nonoperative approach in such patients xx But in class IV or V injuries splenorrhaphy is not pos­sible.

Splenic organ injury scale (1994) Grade I

Non-expanding subcapsular haematoma 3 times of upper normal limit. 3. Characteristic finding in CECT. Types 1. Acute interstitial oedematous pancreatitis; it is common with mortality only less than 1%

Contd...

2. Acute necrotizing pancreatitis (10%)—it may be sterile necrosis or infected necrosis (occurs after first week). Sterile necrosis has got < 10% mortality whereas infected necrosis has got more than 40% mortality. CT guided aspiration, Gram’s staining and then necrosectomy is the need Organ Failure ™™ Cardiovascular, renal, respiratory (commonest organ failure in severe AP is respiratory) ™™ Modified Marshall scoring system is used. A score of 2 or more suggests. It is based on PaO2/FiO2 (respiratory); serum creatinine (renal); systolic blood pressure and blood pH (cardiovascular). ™™ Transient is 48 hours Systemic Complications ™™ Exacerbations of pre-existing comorbid conditions Local Complications—Based on CECT findings ™™ Acute pancreatic fluid collection (APFC)—Peripancreatic fluid collection with interstitial pancreatitis, no necrosis, no wall forma­ tion, occurs within 4 weeks ™™ Encapsulated fluid collection with a well-defined inflammatory wall with minimal or no necrosis, occurs more than 4 weeks after the onset of interstitial pancreatitis ™™ Acute necrotic collection (ANC)—Collection containing variable amounts of both fluid and necrosis associated with necrotizing pancreatitis ™™ Walled of necrosis (WON)—Mature, encapsulated collection of pancreatic and or peripancreatic necrosis with a well-defined walled of necrosis Severity grading of acute pancreatitis (AP) 1. Mild AP—No organ failure, no local or systemic complications 2. Moderately severe AP—Organ failure that resolves in 48 hours (transient organ failure) and or local/systemic complications without persistent organ failure 3. Severe AP—Persistent organ failure (> 48 hours), can be single or multiple organ failure Phases of acute pancreatitis 1. Early phase usually lasts for first week commonly with initial systemic response to AP 2. Late phase has got a protracted course of many weeks to months with local complications and organ failure Systemic inflammatory response syndrome (SIRS) Core body temperature 38°C; heart rate >90/minute; respira­ tory rate >20/minute or PaCO2 48 hours the patient is likely to have severe pancreatitis

Determinant-based classification Based on: 1. Local determinant is peripancreatic or pancreatic necrosis which is non-viable tissue located in pancreas alone or in peripancreatic tissue alone or both. It can be solid or semisolid and without a radiologically defined wall; should be detected as areas of nonenhancement on CECT. 2. Systemic determinants as organ failure—cardiovascular, respiratory, renal; is assessed based on SOFA scoring as transient or persistent. Type Mild AP Moderate AP Severe AP Critical AP

(Peri) pancre­ atic necrosis Absent And Sterile And/Or

Organ failure

Infected Infected

Persistent (>48 hours) Persistent

Or And

Absent Transient (1000 Somogyi units) or shows rising titre. xx Amylase creatinine clearance ratio is increased. It is urine amylase/ serum amylase X serum creatinine/ urinary creatinine X 100. Normal value is 1–4%. More than 6% signifies acute pancreatitis. xx Serum lipase more specific than amylase. Serum lipase level after rise persists for longer period than amylase. Pancreas is the only source unlike amylase, hence more specific. CTSI Balthazar, 1990 (Emil J CTSI Mortele et al. 2004 Balthazar) Grade and appearance Score

Grade and appearance

CT Grade– A – Normal pancreas B – Oedematous pancreatitis C- B+ mild extrapancreatic changes D- Severe extrapancreatic changes with one fluid collection E – Extensive/multiple extrapancreatic collections or gas bubbles in or adjacent to pancreas

CT Grade— A – Normal pancreas B – Intrinsic pancreatic abnormalities with or without inflammatory changes in peripancreatic fat C – Pancreatic/ peripancreatic fluid collection or peripancreatic fat necrosis

Necrosis score None < 1/3rd More than 1/3rd less than 1/2 More than half

0 1 2 3 4

0 2

Necrosis score None < 30% >30% One or more extrapancreatic complications

Score 0 2 4 0 2 4 2

4 6

CT SI (CT severity index) – CT grade + necrosis score 0–3= mild; 4–6= moderate; 7–10= severe

Working together is essential for success; even freckles would make a nice tan if they would get together.

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SRB's Manual of Surgery xx Serum lactescence (related to triglyceride met­abolism)—Most specific in hereditary hyperlipidaemia or alcohol pancreatitis. xx Serum trypsin is the most accurate indicator but it is not commonly used. xx Trypsinogen activation polypeptide (TAP) assay in serum and urine reveals the severity of the acute pancreatitis. CRP (>150 mg/L) is also useful. Phospholipase A2, LDH levels are also often assessed. xx Liver function tests: Serum bilirubin, albumin, prothrombin time, alkaline phosphatase. xx Blood urea, serum creatinine. xx Blood glucose (hyperglycaemia is seen). xx Serum calcium level (hypocalcaemia occurs). xx Arterial PO2 and PCO2 level to assess pulmonary insufficiency (or ARDS). xx Urinary lipase estimation. xx Total count, haematocrit, platelet count, coagulation profile. xx Peritoneal tap fluid shows high amylase and protein level (very useful method). Lipase level in ascitic fluid is also useful. xx Plain X-ray shows  ‘Sentinel loop’ of dilated proximal small bowel.  Distension of transverse colon with collapse of descending colon (colon cut off sign).  Air-fluid level in the duodenum.  Renal halo sign.  Obliteration of psoas shadow.  Localized ground glass appearance. xx US abdomen. xx Spiral CT (CECT–contrast enhanced CT) is better—gold standard. It is done after 72 hours. To look for oedema, altered fat and fascial planes, fluid collections, necrosis (non-enhancement area > 30% or 3 cm), bowel distension, mesenteric oedema and haemorrhage. CT-guided aspiration (fluid should be sent for Gram’s stain and bacterial culture); pigtail catheter insertion can also be done. If fluid culture shows bacterial growth with CT showing necrosis, it means it is infected necrosis and needs early pancreatic necrosectomy. CT-guided aspiration and Gram’s staining may need to be repeated. CECT gives diagnosis of AP; assesses the severity; detects local complications. But CECT should be done ideally after first week not in initial period unless diagnosis is in doubt or associated pathology is suspected. Non-enhancement finding is typical of pancreatic necrosis (WON). xx MRI, MRCP—should be done at a later date. xx ERCP is usually not done in acute phase. xx Chest X-ray for effusion and ARDS. xx EUS—to see necrosis, calcifications and to assess CBD.

Fig. 14.7: CECT showing pancreatitis with stones in the duct.

Treatment Treatment of acute pancreatitis ™™ ™™ ™™

Conservative, 70–90% Surgical treatment when indicated, 10–30% Management of complications like acute pseudocyst, abscess, fistula, haemorrhage; systemic complications like ARDS, renal failure, MODS

Conservative Treatment AIM Assessment of haemodynamic status and early resuscitation Aggressive early hydration in first 24 hours using 400 ml/hour crystalloids (Ringer lactate, normal saline) to achieve rapid reple­ tion of the severe volume depletion ™™ Risk assessment stratification ™™ Patient with organ failure or SIRS should have ICU care in anticipa­ tion of ventilator and organ support (haemodialysis) ™™ Prevention or treatment of abdominal compartment syndrome (ACS) which carries high mortality; ACS is intra-abdominal pres­ sure (IAP) more than 12 mmHg. It can occur during fluid therapy also; it requires often decompression by percutaneous catheter insertion or laparotomy ™™ Infection control, electrolyte management Risk assessment stratification ™™ Patient features—Age >55 years; obesity (BMI >30); altered mental status; comorbid conditions ™™ SIRS ™™ Laboratory findings—BUN >20 mg/dl with rising BUN; altered haematocrit; elevated creatinine; CRP > 210/L initially ™™ Radiological features (X-ray initially; CECT later)—pleural effusion, ARDS, multiple or extrapancreatic fluid collections ™™ Scoring system—APACHE II, Ranson’s, Glasgow, Modified Marshall, etc. ™™

xx Rehydration is essential (250–400 ml/hour) as there is lot

Fig. 14.6: CT picture showing features of acute pancreatitis.

of fluid sequestration and 3rd space fluid loss. It is done by using ringer lactate, normal saline, dextrose saline, plasma and fresh blood transfusion/packed cells. xx Pain relief by pethidine and other analgesics. Morphine is not used as it causes spasm of sphincter of Oddi. xx In severe haemorrhagic episodes, fresh frozen plasma and platelet concentrate may be required in anticipation of DIC and haemorrhage.

Pancreas xx Nasogastric aspiration, urinary catheterisation to maintain

and monitor urine output 50 ml hourly. Nasojejunal tube placement for feeding is very useful. xx Antibiotics like third generation cephalosporins, imipenem, meropenem, cefuroxime are used even though its role is not clear but it is commonly used to reduce the anticipated sepsis. Indications for antibiotics ™™ In severe infected necrosis with/without proved culture. ™™ Prophylactic antibiotic therapy, in severe pancreatitis. ™™ In biliary pancreatitis with biliary stones and cholangitis. ™™ Clinically disease is rapidly progressing with deterioration. No role of antibiotics in early pancreatitis. Imipenem, cilastatin, cefuroxime are used.

xx Calcium gluconate 10 ml 10% IV 8th hourly is given as

patient will be hypocalcaemic. xx CVP line is essential to monitor, for rapid fluid therapy and for Total Parenteral Nutrition (TPN) using carbohydrate, amino acids, vitamins, essential elements. xx IV ranitidine 50 mg 6th hourly or IV omeprazole 40 mg BD or IV pantoprazole 80 mg BD to prevent stress ulcers and erosive bleeding. xx Proper electrolyte management with monitoring is needed. xx It is always better to manage the patient in an intensive care set up so that when needed endo­tracheal intubation, ventilatory support, tracheostomy can be done as an emergency basis. Mainly conservative treatment 1) (P)   : Pain relief [pethidine, meperidine (no morphine)]  Protease inhibitors (aprotinin, antisnake venom, EACA etc.), Plasma 2) (A) :  A ntibiotics (ceftazidime, cefoperazone, cefotaxime) imipenem Anticholinergics (to reduce sphincter pressure) 3) (N)  : Nasogastric aspiration, Nasal O2 Nutritional support (TPN) 4) (C) : Calcium gluconate 10 ml 10% 8th hourly Calcitonin CVP line 5) (R) : Rehydration by IV fluids, plasma, blood Ranitidine IV 50 mg 8th hourly Respiratory support (ventilator) Resuscitation when required 6) (E) : Endotracheal intubation Electrolyte management 7) (A) : Antacids 8) (S) : Swan-Ganz catheter for CVP and TPN Somatostatin and its analogue (Octreotide)

xx In case of renal failure haemodialysis is required. xx Somatostatin/octreotide is often used to reduce pancreatic

secretion. xx Anticholinergics, protease inhibitors and calcitonin are other agents used. Their efficacy is not sure. xx Steroid injection in initial phase of shock is beneficial. It is also useful in respiratory distress and ARDS.

xx Nebulisation, bronchodilators are also tried. xx Nasojejunal tube placement and feeding should be started

as early as possible once ileus subsides so that it reduces the infection rate by transmucosal migration of bacteria and it also improves nutritional status. During recovery period nasogastric feeding or jejunostomy feeding can be undertaken. xx Repeated calcium estimation, US examination to see the response is useful. xx Dopamine or low molecular weight dextran (to improve renal perfusion), somatostatin/octreotide (to reduce pancreatic secretion) are also often used. xx Management of complications like acute lung injury, atelectasis, renal failure, GI bleeding, metabolic encephalopathy, electrolyte deficiency as and when needed by repeated observation and evaluation. Other measures: Continuous monitoring, observation, maintaining good urine output 30 ml/hr. The required investigations are repeated to find out the response to treatment like serum calcium, total count, blood urea, creatinine, PaO2, haematocrit, ECG. Uses of octreotide Pancreatic surgeries Variceal bleeding Endocrine pancreatic tumours GI fistulas, pancreatic fistulas Dumping syndrome Carcinoid tumour, acromegaly Acute pancreatitis Dose: 50 µg as loading dose IV 50 µg 1 hour in 5% dextrose as maintenance dose. ™™ ™™ ™™ ™™ ™™ ™™ ™™

Surgery Indications for Surgical Intervention (10% cases) 1. If condition of patient deteriorates in spite of good conservative treatment. 2. If there is pancreatic infected necrosis. 3. In severe necrotising pancreatitis as a trial to save the life of the patient which has got very high mor­tality.

Surgical management of acute pancreatitis Surgery removes intra- and extra-pancreatic necrotic materials, pancreatic fluid, and toxins. It permits preservation of viable pancreatic tissue. Open surgery is the gold standard for infected pancreatic necrosis. xx After opening the abdomen, all necrotic tissue, pus, infected fluid and toxins are removed. 10–12 litres of normal saline wash is given. Drainage tubes are placed liberally. Abdomen is closed in layers—Conventional closed method (necrosectomy, wide debridement, adequate drainage, cholecystectomy, closure). Re-laparotomy is done only on demand later.

Each case has its lesson—a lesson that may be, but is not always, learnt for clinical wisdom is not the equivalent of experience.— William Osler

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SRB's Manual of Surgery xx Laparotomy–necrosectomy–wide debridement–wash–wide packing. Wound is left open. Repeated wash and packings are done until healthy granulation develops – open method. xx Laparotomy–necrosectomy and closure with drain and re-laparotomy later—semi-open method. xx Zip technique can be used to give repeated wash to remove toxins and necrotic tissues until healthy granulation tissue develops in the pancreatic bed—Bradley’s repeated laparotomies and wash. xx Continuous closed peritoneal lavage of the pancreatic bed and lesser sac is done with 10–12 litres of normal saline or hyperosmolar, potassium free dialysate fluid 2 litres/hour using multiple tubes to remove toxic material in the peritoneal cavity/retroperitoneal area until return fluid becomes clear—Beger’s lavage. Procedure is done after initial surgical debridement. xx Extra peritoneal lavage through bilateral flank incisions is also used. But being a blind procedure it is technically difficult and one may not be sure about the adequacy of the procedure. xx Under laparoscopic visualisation, necrosectomy, wash and drainage can be done. But often it is difficult to create pneumoperitoneum in acutely ill patient. But it is increasingly becoming popular. xx A jejunostomy is often done along with these procedures to have early enteral nutrition. xx Endoscopic necrosectomy is often done in some centres. Early endoscopic intervention (within 48 hours) with ERCP, biliary stone removal and stenting in biliary pancreatitis is done and favored in many centres. xx Further management is important to prevent recurrence. Gallstones should be dealt by laparoscopic cholecystectomy in 2 weeks after acute attack during same admission period. Endoscopic sphincterotomy (ERCP) and often stenting may be needed if there are CBD stones.

common; after an attack of severe acute pancreatitis or infection in pseudocyst; said to be seen in alcoholics; with a mortality of 25%. CECT confirmation, CT-guided aspiration and culture, CT-guided catheter drainage or open drainage is needed. Septicaemia, bleeding due to erosion and sloughing of vessel wall can occur.

Fig. 14.8: Beger’s lavage to pancreatic bed. Tubes are placed postoperatively. Continuous saline irrigation through the tube is done until irrigation fluid becomes clear.

Note:

• •

GI fistula either enteric or pancreatic and incisional hernia are the late complications of these surgeries. Localized collection of purulent material without significant necrotic material (considered as pancreatic abscess) is an extremely uncommon entity and so term ‘pancreatic abscess’ is not used now as per revised Atlanta classification 2012. Earlier it was thought to be 5%

Ranson’s prognostic criteria in Ranson’s prognostic criteria in Non-gallstone pancreatitis gallstone pancreatitis score >3 suggests severe AP

A

Figs 14.9A and B: On table photos of acute pancreatitis. Note the typical saponification in the omentum and mesentery.

Glasgow–Imrie prognostic criteria

Acute Physiology and Chronic Health Evaluation (APACHE II) score >8 points predicts 11 to 18% mortality • Equation includes the following factors: age, rectal temperature, mean arterial pressure, heart rate, PaO2, arterial pH, serum potassium, serum sodium, serum creatinine, haematocrit, white blood cell count, Glasgow coma scale score.

On admission: • Age >70 years • TC >18,000/cu mm • Blood sugar >220 mg% • LDH >400 IU/L • AST >250 IU/100 ml

On admission: • Age >55 years • TC >16,000/cu mm • Blood sugar >200 mg% • LDH >350 IU/L • AST >250 IU/100 ml

On admission: • Age >55 years • TC >15,000/cu mm • PaO2 16 mmol/L (No response to IV fluids) • Blood sugar >200 mg% (no H/O diabetes)

Within 48 hours:

Within 48 hours:

Within 48 hours:

• • • • •

• • • • • •

• • • •

Haematocrit drop >10% BUN rise >2 mg% Serum calcium 5 mEq/L Fluid sequestration >4 L

Haematocrit drop >10% BUN rise >5 mg% PaO2 < 60 mmHg Serum calcium 4 mEq/L Fluid sequestration >6 L

B

Serum calcium 200 U/L

APACHE II modified (1996) LFT is added in biliary pancreatitis APACHE – O (Toh 1996) Obesity is added

Pancreas Note:

• • •

•

Decrease serum calcium level is worst prognostic indicator of pancreatitis. These scoring systems differ for non-gallstone pancreatitis and gallstone pancreatitis. Other scoring systems which are often used are APACHE II (Acute Physiology And Chronic Health Evaluation II) and SAP (simplified acute physiology) scoring systems. Twelve variables are used to assess in APACHE II scoring. C- Reactive Protein (CRP) > 210 mg/L in first 4 days and >120 mg/L in one week; phospholipase A2 assay; pancreas related protein; interleukin-6; polymorphonuclear elastase > 120 µg/L; serum ribonuclease assay—are other parameters used to assess the severity.

COMPLICATIONS OF ACUTE PANCREATITIS ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Shock—Hypovolemic and septic Respiratory failure and ARDS—Common in 7 days Septicaemia—Common after 7 days Hypocalcaemia Disseminated intravascular coagulation (DIC) Acute renal failure Pancreatic pleural effusion (left sided 20%) Pancreatic pseudoaneurysm Pancreatic ascites Colonic stricture Pseudocyst of pancreas Chronic pancreatitis Splenic vein thrombosis Abdominal compartment syndrome (ACS) Pancreatic endocrine (15%) and exocrine (20%) insufficiency as late sequelae can occur.

xx Acute fluid collection  It is collection of fluid in or near the pancreas during an attack of acute pancreatitis with an ill-defined or lacking fibrin wall or granulation tissue.  It is 40% common; it usually occurs at peripancreatic area, occasionally intrapancreatic.  More than 50% of acute fluid collection regress spontaneously, remaining may form pseudocyst of pancreatic necrosis.  CT-guided aspiration at one puncture site is often necessary to confirm that it has not infected. xx Acute pseudocyst  It is collection of fluid with pancreatic juice in or near the pancreas localised by thin fibrin wall or granulation tissue.  Occurs in 2 weeks, usually resolves spontaneously.  Fluid can be removed percutaneously under guidance or through an endoscope. xx Pancreatic pseudocyst  It is collection of fluid in a false cavity which commonly contains brownish pancreatic enzyme rich fluid, lined by granulation tissue but not true epithelium with an organised thick fibrous covering.  It is commonly located in peripancreatic region, in lesser sac. It can be often intrapancreatic or in other places in the peritoneal cavity. It can be multiple also.

 It usually forms 4 weeks after an attack of pancreatitis—a

chronic entity.

 It is usually sterile but can get infected.  Pseudocyst may rupture to form pancreatic ascites.  It may cause pancreaticopleural fistula when once it erodes

into left side pleural cavity or it may erode into splenic vessels causing life-threatening haemorrhage.

xx Pancreatic necrosis infected. (Walled of necrosis/WON)  It is focal/diffuse area of non-viable pancreatic parenchyma with peripancreatic fat necrosis.  It is initially sterile but eventually gets infected.  It contains paste/putty like material.  It may form pseudocyst, abscess or may be replaced by fibrous tissue during healing.  It can be sterile or infected necrosis.  It is confirmed by CT-scan and CT-guided aspiration usually at one site; collected fluid should be sent for culture.  Infection of necrotic area usually occurs within 4 weeks. It is ideally conventionally treated with laparotomy, debridement is done by removing all necrotic tissue with adequate drainage for remaining viable exocrine function. Often repeat laparotomies are done once in 3 days until all necrotic materials are cleared and jejunostomy is done in final approach.  Laparotomy and debridement done once with continuous lavage; antibiotics with percutaneous drainage/only surgical drainage without debridement/debridement using minimally invasive methods—are unconventional approaches.  It may slough off the pancreatic/splenic vessel wall to cause torrential haemorrhage. Walled of necrosis (WON) may be single or multiple (60%). It is commonly in head/body or tail. But often entire gland may be involved (25%).  Walled of necrosis (WON) may rupture into viscera or extend into other part of the abdomen. Features of sepsis, tender palpable mass in the epigastrium with leukocytosis are observed. xx Respiratory complications  Thay are often severe and life-threatening. It is due to distension of abdomen, diaphragmatic elevation, pleural effusion, reduced surfactant (lecithin) activity in alveoli due to lecithinase, severe pain, pleural effusion (left), intravascular coagulation in lungs and ARDS. Arterial blood gas analysis should be done. Often it needs ventilator support. xx Pancreatic pseudoaneurysm  It is due to enzymatic digestion (elastase) of the wall and weakening and aneurysmal dilatation of the splenic (50%) or gastroduodenal vessels (15%) or inferior and superior pancreaticoduodenal arteries (10%).  It may rupture and cause life-threatening haemorrhage or may rupture into stomach or duodenum to cause massive upper GI bleed or may rupture into pancreatic duct causing haemosuccus pancreatitis.  It is diagnosed by CT angiogram.  It is treated by critical care, blood transfusion, emergency angiographic embolisation or by open surgery and ligation of the involved vessel. It carries high mortality. xx Pancreatic fistula  It can occur due to ductal wall disruption and necrosis or after surgical intervention for acute pancreatitis (necrosectomy).

In case of chronic pancreatitis jaundice supervenes in only fifteen percent of cases, but diabetes is present on thirty percent. — Richard B Cattell

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It may be internal into bowel or external to skin. Fistula may be low (< 200 ml) or high (> 200 ml) out put. It can be straight or curved. It is confirmed by biochemical analysis, ERCP, CT fistulogram. If fistula persists for 6 months then sphincterotomy, resection of fistula with pancreatic resection, pancreaticojejunostomy is done.

xx Emphysematous pancreatitis  It is gas in pancreatic parenchyma, a dangerous type and can be diagnosed by CT scan. Criteria to find out systemic failure in acute pancreatitis ™™ ™™ ™™ ™™ ™™ ™™ ™™

Cardiac: Hypotension; pulse > 130/minute; arrhythmias, ECG changes. Pulmonary: PaO2 > 60 mm Hg; ARDS. Renal: Urine output < 40 ml/hour; increase in blood urea and serum creatinine. Metabolic: Falling serum calcium; magnesium and albumin. Haematologic: Fall in haematocrit; DIC. Gastrointestinal: Severe ileus; sequestration of fluid. Neurologic: Irritability; confusion; localising features.

xx It is lined by fibrin layer but no endothelium, hence called

as pseudocyst.

xx It contains typically brownish fluid with sludge like necrotic

material. It can get infected to form infected pseudocyst or pancreatic abscess. xx Amylase level in the cyst fluid is very high (>5000 units/ml).

Types Depending on whether it communicates with pan­creatic duct or not it is classified as: 1. Communicating pseudocyst. 2. Noncommunicating pseudocyst. It can be xx Acute pseudocyst. xx Chronic pseudocyst. D’Egidio classification of pseudocyst

xx It is localized collection of sequestered pancreatic fluid,

Type I: After an attack of acute pancreatitis. Normal duct anatomy; no fistula/communication. ™™ Type II: After an attack of acute on chronic pancreatitis. Abnormal duct anatomy without stricture; 50% chances of fistula. ™™ Type III: After an attack of chronic pancreatitis, abnormal anatomy with stricture; always communicating. It appears like retention cyst.

xx It can occur after trauma and recurrent chronic pan­creatitis. xx Collection usually occurs in the lesser sac in rela­tion to

Sarle’s classification

PSEUDOCYST OF PANCREAS usually 3 weeks after an attack of acute pancreatitis.

stomach, but can occur in relation with duodenum, jejunum, colon, splenic hilum. xx About 50% of acute pancreatitis leads to pseudo­cyst formation, but among that 20–40% will resolve spontaneously.

™™

™™ ™™ ™™ ™™

Necrotic pseudocyst in acute pancreatitis. Retention cyst in chronic pancreatitis . Intrapancreatic retention due to pancreatic duct dilatation . Extrapancreatic retention cyst due to rupture into peripancreatic tissues.

Sites of pseudocyst L esser sac—commonest, i.e. between colon and stomach In relation to: ™™ Duodenum ™™ Jejunum ™™ Colon ™™

™™

Splenic hilum

Nealon and Walser classification I – Normal duct; no duct communication into pseudocyst. II – Normal duct with communication. III – Normal duct with stricture without communication. IV – Normal duct with stricture with communication. V – Normal duct with abrupt duct termination. VI – Chronic pancreatitis without duct cyst communication. VII – Chronic pancreatitis with duct cyst communication.

Note:

• •

It is not a true cyst as there is no epithelial lining. 75% of cystic lesions of pancreas are pseudocysts; Others are—cystadenomas, IPMNs, cystic necrosis of adenocarcinoma, congenital polycystic disease.

Clinical Features xx A swelling in the epigastric region which is hemi­spherical,

Fig. 14.10: Pseudocyst of pancreas. xx Initially cyst wall is thin (unformed), but later it gets fibrosed

and thickened (formed) (matured).

smooth, soft, not moving with respira­tion, not mobile, upper margin is diffuse but lower margin well defined, resonant or impaired reso­nant on percussion, with transmitted pulsation confirmed by knee-elbow position. xx If it is infected, it will be tender mass and patient will be toxic with fever and chills. xx Because stomach is stretched towards the abdominal wall, Ryle’s tube passed will be felt per abdomi­nally (Baid test).

Pancreas duct; stones if present are removed from the duct; 5 French pancreatic stent is placed which is removed in 6–8 weeks. Confirmation of resolution of pseudocyst is done by follow-up CT. This procedure is suitable only in communicating pseudocyst; it is safer and effective.  Transmural endoscopic or EUS-guided stent placement to the pseudocyst; guided needle aspiration is done initially on the visible bulge; then endoscopic stent is placed to allow internal drainage; stent is removed after 8 weeks endoscopically. Recurrence rate is high; necrosectomy is not possible.  Percutaneous drainage under USG guidance–It is technically easier; catheter drainage is done after placing the catheter under guidance in large pseudocyst; high recurrence, infection, displacement and blockage of catheter are common.  Simple US-guided aspiration has got high recurrence and failure rate; so it is not practiced routinely.

Differential Diagnosis xx xx xx xx xx xx

Aortic aneurysm. Retroperitoneal cyst or tumour. Cystadenocarcinoma of pancreas. Cyst of the liver. Mesenteric cyst. Hydatid cyst.

Investigations xx US abdomen (commonly done procedure), US reveals

the size and thickness of the pseudocyst. Size less than 6 cm indicates that one can wait for spontaneous resolution. Endosonography (EUS) is very useful. xx CT scan is ideal and study of choice. It is two times more sensitive than US. It demonstrates size, shape, number, wall thickness, contents, pancreatic duct size, and extent of necrosis in pancreas, calcification and atrophy in chronic pancreatitis, regional vessels, pseudoaneurysm, splenic/ portal vein thrombosis. xx MRCP delineates the ductal anatomy and its abnormality. xx ERCP is done to find out the communication. xx Barium meal (lateral view) shows widened vertebrogastric angle with displaced stomach (Not usually done now). xx LFT, serum amylase platelete count, PT INR. xx EUS-guided aspiration and analysis of fluid for amylase and CEA. Amylase will be high with normal CEA in pseudocyst; amylase will be normal/low with high CEA >400 ng/ml in mucinous neoplasm.

3. Surgical drainage– It is either open or laparoscopic method. Indications for surgery/intervention ™™ ™™ ™™ ™™ ™™ ™™ ™™

Size more than 6 cm Formed pseudocyst Infected pseudocyst Cyst persisting after 6 weeks/progressive cyst Multiple cysts/cyst due to trauma Communicating cysts/cyst with severe pain Thick-walled pseudocyst

Fig. 14.12: CT scan showing typical pseudocyst of pancreas.

Fig. 14.11: Vertebrogastric angle.

Treatment 1. Conservative—Observation, follow-up using repeat USG at regular intervals. 50% of pseudocysts show spontaneous resolution. 2. Interventional—Needs ERCP to delineate ductal anatomy, pancreatic duct stones, mainly communication into the pseudocyst. It is Guided—Endoscopic/EUS/US-guided drainage  Transpapillary—Through side viewing endoscopy, pancreatic

sphincterotomy is done; guidewire is passed into the pancreatic

A

B

Figs 14.13A and B: CT scan showing pseudocyst of pancreas both single and multiple. Note the cyst cavity and the thick cyst wall. Patient needs drainage procedure either cystogastrostomy or cystojejunostomy.

Doing the surgery may be easier, but it is managing the patient which counts finally.

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SRB's Manual of Surgery Surgery xx Cystogastrostomy: At laparotomy, anterior wall and posterior wall of the stomach is opened. Brownish fluid is aspirated. The thick capsule of pseudocyst is opened. All fluid with necrotic material are sucked. Fluid should be sent for cytology, culture and sensitivity and amylase estimation. Cyst wall always should be biopsied. Cyst cavity should be washed with normal saline after breaking septae. Pseudocapsule is anastomosed to posterior wall of the stomach—Jurasz operation.

Other procedures xx Cystoduodenostomy. xx Cystojejunostomy is done in large cyst, recurrent cyst. xx If infected, cystogastrostomy with external drainage is done using Malecot’s catheter (Smith operation). xx Laparoscopic cystogastrostomy is becoming popular, effective and less invasive. xx Along with cystojejunostomy, pancreaticojejunostomy should be done if there is ductal stricture and dilatation and communication with pseudocyst. xx Distal pancreatectomy with pseudocyst removal if cyst is in distal part. Complications of pseudocyst ™™ ™™ ™™ ™™ ™™ ™™ ™™

A

B Figs 14.14A and B: Pseudocyst of pancreas aspiration of table. Note the brownish-black colour of the fluid aspirated.

Note:

• • • • •

A

Rupture—3%—into bowel or peritoneum Infection, commonest—20%, abscess Bleeding from the splenic vessels—7% Cholangitis Duodenal obstruction Portal/splenic vein thrombosis and segmental portal hypertension Cholestasis due to CBD block

B

Figs 14.15A and B: (A) Cystogastrostomy for pseudocyst of the pancreas; (B) Cystogastrostomy procedure. Anterior layer of the stomach is opened to visualize the bulge in the posterior wall. Aspiration of it shows brownish black coloured fluid, typical of pseudocyst of the pancreas.

• • • • •

Roux-en-Y cystojejunostomy is better with lesser recurrence rate than cystogastrostomy. Pseudopseudopancreatic cyst: It is a mass in epigas­tric region due to pancreatitis formed by bowel, omentum which clinically mimics a pseudocyst of pancreas. But fluid collection is absent. Small cyst can be drained through endoscopy. But debridement is not possible. Bleeding and cyst leakage are other problems. CT-guided percutaneous catheter placement is done in critically ill patients, infected pseudocyst, unfit patients, cyst in pelvis/mediastinum. Improper drainage, recurrence and fistula formation are the problems. External drainage is done when cyst is infected, haemorrhagic or ruptured. Problem with external drainage is formation of fistula (20%). Therapy is decided based on thickness of the wall of pseudocyst; location of pseudocyst; contents of pseudocyst and ductal status. Pseudocysts following trauma and chronic pancreatitis have got lesser chances of spontaneous resolution. Pseudocyst following biliary pancreatitis has got 4 times more mortality than that of alcoholic pancreatitis. Spontaneous resolution rate is 40% for pseudocyst less than 6 weeks; 8% for 6–12 weeks; less than 1% for cyst more than 12 weeks. Presence of significant debris is a contraindication for endoscopic or image-guided drainage.

CHRONIC PANCREATITIS xx It is persistent progressive irreversible damage of the

pancreas due to chronic inflammation. It can be

  Chronic relapsing pancreatitis Chronic pancreatitis

(persistent)   Chronic non-calcifying Calcifying pancreatitis pancreatitis





In the duct In the parenchyma (Stone in the pancreatic duct)

Fig. 14.16: Roux-en-Y cystojejunostomy for pseudocyst of the pancreas.

xx Chronic pancreatitis is more common in males, common in

Kerala (induced by diet, rich in Tapioca).

Pancreas xx Alcohol reduces pancreatic blood flow, alters cell viability,

releases the free radicals, creates pancreatic ischaemia, and activates the pancreatic stellate cells which produce abundant extracellular matrix and collagen. xx Genetic predisposition may be the cause of idiopathic pancreatitis. Mutation in pancreatic secretory trypsin inhibitor causes activation of trypsin causing pancreatitis. xx Hereditary pancreatitis is an autosomal disorder with mutation in trypsinogen gene in chromosome 7. It causes recurrent painful episodes of acute pancreatitis in childhood, leading to chronic pancreatitis and pancreatic cancer in adulthood.

Theories and Concepts in Pathogenesis of Chronic Pancreatitis Fig. 14.17: Calcifications in the parenchyma of the pancreas.

Fig. 14.18: Pancreatic ductal stone removed—specimen. Patient underwent pancreaticojejunostomy. Aetiology ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Alcohol—80% main cause Stones in biliary tree—rare cause Malnutrition, diet Hyperparathyroidism Hereditary (familial hereditary pancreatitis)—Autosomal domi­ nant Idiopathic—20%—as mutation Trauma Congenital anomaly (Pancreatic divisum) Cystic fibrosis Autoimmune pancreatitis Hyperlipidaemia

TIGAR-O Risk Factor Classification 2001 T – Toxic - alcohol/tobacco/dietary/drug. Metabolic-hypercalcaemia/lipidemia/lipoprotein lipase deficiency. I – Idiopathic—early/late onset/tropical –30% G – Genetic mutations—CFTR/SPINK 1. A – Autoimmune primary/with Sjögren/Crohn’s disease. R – Recurrent and severe acute/ischemic. O – Obstructive—pancreas divisum/annular pancreas/stenotic papilla/duodenal obstruction/trauma/pancreatic ductal stones/ choledochocele.

xx Oxidative stress hypothesis—Reactive by-products of hepatic mixed function oxidase activity damage the pancreas through chronic reflux of bile into the pancreatic duct. xx The toxic-metabolic theory—Alcohol is directly toxic to the acinar cell where it brings changes in intracellular metabolism causing pancreatic lipid accumulation, fatty degeneration, cellular necrosis, and eventual widespread fibrosis. xx Stone and duct obstruction theory—Alcohol increases the lithogenicity of pancreatic juice, leading to stone formation. Chronic contact of stones with duct epithelial cells produces ulceration, scarring, atrophy, fibrosis and chronic obstruction of the acini. xx The necrosis-fibrosis theory—Acute and chronic pancreatitis represents a spectrum of disease. Inflammation from acute pancreatitis leads to scarring, extrinsic compression of the pancreatic ductules, obstruction, stasis, atrophy and stone formation. xx The genetic defect of hereditary pancreatitis produces recurrent acute pancreatitis in early childhood, leading to chronic pancreatitis in early adulthood. xx Cellular mechanisms of pancreatic fibrogenesis is due to pancreatic stellate cells which are stimulated and activated by alcohol, oxidative stress, cytokines of acute pancreatitis; activated stellate cells migrate to the periacinar areas to deposit collagen and fibronectin. Transforming growth factor beta 1 is an important mediator of pancreatic fibrosis. xx The sentinel acute pancreatitis event (SAPE) hypothesis—An episode of acute pancreatitis, the sentinel event, sets the stage for the attraction of collagen-secreting stellate cells. xx Heavy, prolonged alcohol use is the most common cause of chronic pancreatitis. Alcohol-related chronic pancreatitis is associated with more severe pain, more extensive calcification and ductal changes, and more rapid progression to endocrine and exocrine insufficiency. Often recurrent episodes of acute pancreatitis for several years are seen in these patients. Some cofactors amplify the effect of alcohol in these patients. Prevalence of some genetic mutations linked with pancreatitis like cystic fibrosis transmembrane regulator (CFTR), serine protease inhibitor Kazal type-1 (SPINK1) has been noted in alcoholic pancreatitis. A high-fat diet and smoking affect pancreatic bicarbonate and water secretion adversely, inducing oxidative stress and increases the rate of pancreatic calcification. xx Tropical pancreatitis is endemic in some regions of India (Kerala), Africa, and South America. Episodic abdominal pain begins in childhood and is followed by rapid progression to endocrine and exocrine insufficiency with pancreatic calculi in non-alcoholic

Carcinoma pancreas should be suspected when an elderly person develops diabetes and in spite of adequate treatment, continues to loose weight. — Robert D Lawrence

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SRB's Manual of Surgery individuals. Dietary toxins (cyanogens in the cassava plant, tapioca) and micronutrients like zinc, copper, and selenium, vitamin A deficiencies, genetic factors, ductal abnormalities are the probable causes of tropical pancreatitis. Linnamarin and its methyl derivative, in acid pH of stomach releases hydrocyanic acid which is cytotoxic in presence of rhodanase releases thiocyanates causing depletion of methionine, damaging pancreas → pancreatitis. Gross look is small, firm fibrotic/adipose type. xx Early-onset idiopathic chronic pancreatitis manifests with severe abdominal pain in childhood, with relatively few structural and functional changes. Late-onset idiopathic chronic pancreatitis manifests in middle and late adulthood, often with minimal pain and pronounced exocrine insufficiency.

Pathology xx It shows atrophy of acini, hyperplasia of duct epithelium, interlobular fibrosis, calcifications, ductal dilatation, with strictures in the duct, focal necrosis. xx There is loss of exocrine function initially and endocrine functions eventually. xx Ductular metaplasia and acinar atrophy along with fibrosis and cyst formation develops. Pathology of chronic pancreatitis ™™ ™™ ™™ ™™

Focal necrosis Segmental or diffuse fibrosis Parenchymal calcification or ductal stones Stricture and/or dilatation of the duct

Spectrum of Chronic Pancreatitis xx Early—pancreatic oedema—chronic inflammation—normal secretory function. xx Moderate—early fibrosis; only few acinar cells—exocrine dysfunction. xx Late—fibrosis—loss of secretory function—diabetes mellitus. xx Complications develop secondary to healing and fibrosis; deposition of inspissated proteinaceous material in the duct; over expression of CTGF and TGF-B1 that stimulate extracellular matrix. Pain hypothesis include: ™™ Acute and chronic inflammation of the pancreas. ™™ Increased pressure within the pancreatic ductal system and parenchyma, ductal dilatation, stasis. ™™ Ischaemia of the parenchyma secondary to increased interstitial pressure. ™™ Over expression of a particular protein in pancreatic nerve fibres. ™™ Pancreatic nerve growth factor released by degenerating acinar cells and its high affinity receptor that promotes nerve growth and repair. ™™ Pain may be due to perineural sheath destruction by toxins, ischaemia and also due to tissue acidosis.

Classification of Chronic Pancreatitis I: Based on main duct dilated or not: xx Large duct disease—main pancreatic duct is dilated. xx Small duct disease—main pancreatic duct, is normal or smaller in size.

II: Staging/classification of chronic pancreatitis (Stages A, B, C) A new classification of chronic pancreatitis, based on combination of clinical signs, morphology and function, is presented (2009 Büchler et al). Specific definition of chronic pancreatitis stage A xx Stage A chronic pancreatitis It is the early stage of chronic pancreatitis where complications have not yet appeared and the clinical exocrine and endocrine function is preserved. Subclinical signs (impaired glucose tolerance, reduced exocrine function but without steatorrhoea) might already be apparent. Stage A is accepted under the following conditions: Pain of any type and degree and/or attacks of acute pancreatitis, no complications, no steatorrhoea, and no insulin-dependant diabetes mellitus. Specific definition of chronic pancreatitis stage B xx Stage B chronic pancreatitis It is the intermediate stage where chronic pancreatitis has led to complications but clinical exocrine and endocrine function is still preserved. The type of complication is specified (e.g. stage B, bile duct). Stage B is accepted under the following conditions: Patients with complications but without steatorrhoea or diabetes mellitus. Specific definition of chronic pancreatitis stage C xx Stage C chronic pancreatitis Stage C is the end stage of chronic pancreatitis, where pancreatic fibrosis has led to loss of clinical exocrine and/or endocrine pancreatic function (steatorrhoea and/or diabetes mellitus). Complications of chronic pancreatitis might or might not be present. The type of exocrine and/or endocrine pancreatic function loss is specified (e.g. stage C, steatorrhoea). Stage C can be sub-classified into three categories: C1: Patients with endocrine function impairment. C2: Patients with exocrine function impairment. C3: Patients with exocrine/endocrine function impairment and/or complications—as they are defined. Stage C is accepted under the following conditions—Patients with clinical manifestation of end-stage functional impairment with or without complications.

Clinical Features xx Pain in epigastric region (80%)

 It is persistent and severe, which radiates to back.

 This pain is due to irritation of retropancreatic nerves,

or due to ductal dila­tation and stasis, or due to chronic inflammation itself.  Two patterns of pain have been described (Ammann and Muellhaupt). Type A pain is short relapsing episodes lasting days to weeks, with pain-free intervals. Type B pain is prolonged, severe, unrelenting pain.  Pain exacerbations need not be always associated with rise in amylase and lipase levels.  There is often a gradual diminish in pain over years due to “pancreatic burnout” by extensive calcifications, exocrine and endocrine insufficiency.

Pancreas Complications of chronic pancreatitis ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Fig. 14.19: Patient will occupy leaning forward position to relieve severe pain of pancreatitis. xx Exocrine dysfunction: Diarrhoea, asthenia, loss of weight

and appetite, steatorrhoea (signifies severe pancreatic insufficiency) (90%), malabsorption. xx Endocrine dysfunction: Diabetes mellitus. Pancreatic diabetes may often be typically brittle because of concomitant glucagon deficiency and requires insulin. xx Mild jaundice is due to narrowing of retropancreatic bile duct and cholangitis. xx Mass per abdomen, just above the umbilicus, tender, nodular, hard, felt on deep palpation, not moving with respiration, not mobile, resonant on percussion.

Investigations ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

™™

Triad of chronic pancreatitis Pancreatic calcification ™™ Steatorrhoea ™™ Diabetes mellitus Triad is found in less than one-third of patients with CP ™™

Mallet-Guys sign: In right knee-chest position, if left hypochondrium is palpated tenderness can be evoked in case of chronic-relapsing pancreatitis. In this position, bowel loops are being shifted to right so as to have a direct palpation of pancreas.

Pseudocyst of pancreas Pancreatic ascites CBD stricture due to oedema or inflammation Duodenal stenosis Portal thrombosis—segmental portal hypertension Peptic ulcer Carcinoma pancreas Pancreatic pleural effusion, pancreatic ascites Pancreatic fistula Splenic vein thrombosis Pancreatics enteric fistula

™™ ™™

Serum amylase—not very useful Blood sugar Liver function tests and prothrombin time US abdomen to see duct dilatation, stones, parenchyma, liver status, CBD (normally, diameter of pancreatic duct is < 3 mm) Endosonography CT scan—CT-guided FNAC ERCP—Chain of lake appearance. Duct is dilated MRCP Plain X-ray shows calcification in 65% of patients Pancreatic secretory juice analysis Pancreolauryl test—pancreatic esterase cleaves fluorescein dilau­ rate after oral intake. Fluore­scein is absorbed and quantified in urine after 2 days. Oral glucose tolerance test Faecal chymotrypsin and elastase analysis Bentiromide test

Investigations presently used are: xx CT scan abdomen: It is 95% reliable; to see pseudocyst,

calcification, ductal stones, duct stricture and dilatation, vasculature, fibrosis, surrounding structures, CBD status. It shows 90% sensitivity; 95% specificity.

Note:

•

Chronic pancreatitis can lead to carcinoma pancreas.

Clinical presentations Stage A: 85%, recurrent/acute episodic pain with weight loss. Stage B: Severe prolonged progressive pain with impaired pancreatic function with cholestasis, pseudocyst, sinistral portal hypertension. ™™ Stage C: Severe exocrine/endocrine deficiency, less severe pain, complications like pseudocyst and obstruction. ™™

™™

Differential Diagnosis xx Carcinoma of head of the pancreas. xx Retroperitoneal tumour.

A Fig. 14.20A

A goal is a dream with a deadline.

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SRB's Manual of Surgery xx MRCP is non-invasive method to see ductal anatomy. xx Endosonography (EUS) to see possible malignant site and to

take FNAC. Site, duct status, stricture, stones, parenchyma, pseudocyst, CBD status, nodes are identified in EUS. Positive five parameters suggest chronic pancreatitis. It also helps in assessing operability.

B Fig. 14.20B Figs 14.20A and B: CT scan abdomen showing features of chronic pancreatitis—calcification, ductal changes, and cyst formation. xx ERCP is useful in chronic pancreatitis to see dilatations,

strictures and altered ductal anatomy. It is mainly to assess structural pathology of the pancreas.

Cambridge grading of CP on ERCP Grade

Main pancreatic duct

Side branches

I: Normal

Normal

Normal

II: Equivocal

Normal

3 Abnormal

IV: Moderate

Abnormal

>3 Abnormal

V: Severe

Abnormal with at least one of the following:

>3 Abnormal

• Large cavity ( >10 mm) • Obstruction • Filling defects • Severe dilatation or irregularity

EUS criteria in chronic pancreatitis—parenchymal

EUS criteria in chronic pancreatitis—ductal

• Gland atrophy

• Narrowing, dilation, irregularity

• Hyperechoic foci

• Calculi

• Hyperechoic stranding

• Side branch dilation

• Cysts, lobularity

• Hyperechoic walls

Rosemont EUS criteria Major: • A—Hyperechoic foci with shadowing and calculi in main pancreatic duct (PD) • B—Lobularity with honeycombing Minor: • Cysts • Dilated ducts ≥3.5 mm • Irregular PD contour • Dilated side branches ≥1 mm • Hyperechoic duct wall, strands • Non-shadowing hyperechoic foci • Lobularity with non-contiguous lobules

xx Secretin cholecystokinin test is the gold standard for assessing pancreatic function. After over night fasting, double lumen tube is placed into the duodenum at the level of ligament of Treitz under C ARM guidance. Gastric and duodenal juices are aspirated. Continuous IV secretin 1 u/kg/hour and CCK are infused in 90 minutes. Sampling of duodenal juice is done in every 10 minutes for one hour for analysis of volume, HCO3, amylase, lipase and proteases. It is to assess functional deficiency. In chronic pancreatitis volume is normal— >2 ml/kg but less bicarbonate content — 80 mEq/L; enzyme levels are normal. xx Pancreolauryl test: After overnight fasting, blood sample is taken. IV secretin is injected 1 u/kg in 3 minutes. Test meal containing bread, butter, tea and fluorescein dilaurate is given to eat. IV metoclopramide 10 mg is injected. Blood samples are taken at 2, 2½, 3 and 4 hours to assess serum fluorescein concentration. It is also quantified in urine after 2 days. xx LFT, prothrombin time is needed to manage the patient. xx Serum trypsinogen 50,000 units). It may be beneficial only in females with idiopathic pancreatitis, small duct disease and pancreas divisum. Other drugs used are—antioxidants, amitriptyline, fluoxitine, octreotide. Novel pain therapies like NGF, antinociceptive agents, mast cell directed therapies are also used. xx Control of diabetes by oral hypoglycaemics or insulin. xx Somatostatin and its analogues. Its role is not clear. xx Repeated ascitic taps for pancreatic ascites. xx Steatorrhoea can be controlled by proton pump inhibitors with 1,50,000 units of oral lipase with low fat diet. PPI inhibits acid in stomach to prevent lipase getting inactivated in stomach.

Persisting pain—main indication Severe malabsorption Suspicion of malignant transformation Multiple relapses Complications like pseudocyst, segmental portal hypertension Biliary obstruction (Wadsworth syndrome) Pseudocyst Pancreatic ductal dilatation > 7 mm Pancreatic ascites/fistula Pancreatic ductal stenosis

Objectives of Surgery xx Pain relief when endotherapy has failed. xx Management of complications. xx Procedure selected is one which shows less morbidity and

mortality.

xx Quality of life (QOL) should be preserved.

Problems and Limitations of Surgery xx Disease is irreversible parenchymal and ductal damage and

so surgery cannot cure or reverse completely.

xx Disease progression cannot be prevented or arrested by

surgery.

xx Risk of development of cancer continues. xx Complications of surgery are a drawback.

Benefits of Surgery in Relation to Pain Relief and Obstruction xx Relieves intraductal, interstitial, intracellular hypertension—

through drainage procedures.

Endoscopic Therapy in Chronic Pancreatitis

xx Entrapped nerves are released and reduction in pancreatic

xx It is used as it has got low morbidity. xx Main indications are—pain relief, ductal stones, main duct stricture, pseudocyst drainage, pancreatic ascites, effusion and fistula. xx It is quite useful for main pancreatic duct obstruction and pseudocyst. It is less useful for biliary stricture. xx Procedures are—pancreatic duct sphincterotomy, main ductal stone extraction using Dormia basket, main ductal stenting in strictures, stricture dilatation, ESWL of main duct stones, minor papillary sphincterotomy. xx Pseudocyst can be treated by transmural stenting across gastric wall if there is visible bulge, distance of cyst wall is less than 1 cm, no major vessel at puncture site. Transpapillary stenting is done if pseudocyst is communicating, if cyst is less than 6 cm, if there is no visible bulge in the stomach. xx Complications are—pancreatitis, stent displacement/occlusion, perforation, bleeding, sepsis, restenosis. xx Advantages of endotherapy are—less invasive, can be repeated, less severe complications, can be used as bridge therapy prior to surgery. xx Disadvantages are—long-term benefits are less (50%). Definitive treatment is delayed. It is not useful in small duct disease; main duct dilatation decides the success rate.

xx Pacemaker—head of pancreas is removed in head coring

enzyme reduces nerve irritation—resectional methods.

procedure (Frey’s) to relieve pain. It is less morbid and acceptable method. xx Resection is better than drainage procedure.

Principles of Surgery xx Pancreatic duct decompression (drainage) reduces the pain and retains the existing exocrine and endocrine functions. But chances of malignant transformation are still high. In significant number of patients recurrence of symptoms (50% recurrence of pain in 5 years) and progression of the disease pathology occurs and it does not give a complete cure. Normal diameter of pancreatic duct 4 mm in head; 3 mm in body; 2 mm in tail of the pancreas. Pancreatic duct diameter more than 7 mm is an indication for surgery (pancreaticojejunostomy). xx Pancreatic resection (total pancreatectomy) is the actually ideal technique which relieves pain, removes entire diseased tissue. But technical difficulty; high surgical mortality (21%); and severe exocrine and endocrine deficiency (brittle diabetes) are the drawbacks. Head

Knowledge is the only treasure that increases on sharing.

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SRB's Manual of Surgery of pancreas is considered as pacemaker of the pancreatitis disease and so pancreaticoduodenectomy (Whipple’s) is the other option to give adequate relief. It is preferred in patients who are having relatively normal body and tail of the pancreas. Occasionally when disease is limited to tail and body then distal pancreatectomy with or without splenectomy often with distal pancreatico-jejunostomy may be done. But it is not beneficial if disease is extensive and diffuse. Resection is the main method of treatment if ductal dilatation is not adequate. xx A combined resection and drainage procedures are also done. Head is decored at various levels and decompressed duct is anastomosed to jejunum.

xx Longitudinal pancreaticojejunostomy after excision of peripancreatic duct tissue—here superficial part of the head of pancreas is removed to achieve improved drainage—Frey procedure. It is done when ductal dilatation is not adequate; head is more than 4 cm thick. Head coring is done with retaining 5 mm thick tissue in front of veins, close to duodenum. It shows 75% pain relief in 3 years.

Surgeries xx Partington-Rochelle operation: Here longitudinal pancreaticojejunostomy is done using almost entire laid open pancreatic duct. Spleen is retained in this procedure. This is now commonly done procedure.

Fig. 14.25: Frey’s procedure. Here head of pancreas is decored and opened duct with decored head is anastomosed to Roux loop of jejunum.

Fig. 14.23: Partington-Rochelle operation. Here spleen is retained and longitudinal pancreaticojejunostomy is done to the opened duct from front. xx Puestow’s operation [Puestow-Gilesby (1958)]—As the duct is dilated more than 8 mm, duct can easily be opened longitu­dinally. After removing all stones from the duct, it is anastomosed to the jejunum as Roux-en-Y anastomosis. In Puestow’s operation spleen is removed.

Fig. 14.26: Decoring of the head with duct part to resect all diseased tissue; it shows good result. But it is technically demanding; bleeds often profusely.

Fig. 14.24: Puestow’s pancreaticojejunostomy. Here spleen is removed. Entire length of dilated duct is opened. Distal pancreas is mobilised up to superior mesenteric vessels. Pancreas with opened duct is telescoped into the Roux loop of jejunum and anastomosed.

xx Duodenal preserving resection of head of pancreas in front of portal vein with jejunal loop anasto­mosis to transected neck of pancreas—Beger procedure. Here extensive resection of head (than Frey’s) is done. xx Total pancreatectomy is indicated when entire gland is diseased. It relieves the pain and also prevents the diseased pancreas from turning into malignancy. Patient has to take insulin and oral pancreatic enzymes permanently (brittle diabetes). xx The cause is treated like cholecystectomy for gallstones. xx Therapeutic ERCP is useful in removal of stones in dilated duct. xx If disease mainly involves head of the pancreas, then pancreaticoduodenectomy can be done—Whipple’s procedure.

Pancreas xx Resection of tail of pancreas with retro­grade pancreatico-jejunostomy—Duval procedure.

Fig. 14.27: Dilated pancreatic duct is laid open; multiple stones are removed and duct is ready for longitudinal pancreaticojejunostomy (LPJ).

A

Fig. 14.28: Pancreatic duct stones—removed during pancreaticojejunostomy.

B

Fig. 14.29: Beger’s procedure. Here head is decored up to the visible portal vein. Neck is transected. Distal end of the pancreas with retained part is anastomosed to Roux loop of jejunum. xx 95% subtotal pancreatectomy. xx Distal pancreatectomy—Spleen, body and tail of the pancreas are removed—Child’s operation.

Figs 14.30A and B: Choledochojejunostomy. It is Roux-en-Y anastomosis. It is done whenever there is complication of biliary stricture after pancreatitis. Often triple anastomosis may be required—pancreaticojejunostomy, choledochojejunostomy and gastrojejunostomy. It is done whenever there is duodenal obstruction, biliary block and pancreatic duct dilatation (drainage procedure). xx When duodenal, biliary and pancreatic obstruction is present— choledochojejunal, pancreaticojejunal and gastrojejunal anastomosis may be needed—triple anastomosis. Only biliary stricture which cannot be managed by ERCP needs choledochojejunostomy.

Listen to the faintest sound; for opportunities knock only once.

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Fig. 14.31: Retrograde pancreaticojejunostomy after resection of the tail of the pancreas (Duval).

Complications of surgery:

xx Pancreatic leak/fistula (10%); infection; bleeding; recurrence; brittle diabetes. xx Pain relief in chronic pancreatitis is achieved by drugs; decompression/drainage surgeries, resection surgeries, epidural analgesia, coeliac ganglion block, operative chemical splanchnicectomy, extra/intra-peritoneal right and left splanchnicectomy, transhiatal bilateral splanchnicectomy, thoracoscopic splanchnicectomy. Post-operative care ™™ ™™ ™™ ™™ ™™

Nutrition—TPN/jejunostomy feed Fluid and electrolyte management Prevention/control of sepsis Proper monitoring Octreotide on table and postoperatively—regular intervals or slow infusion—5 days

Surgery for chronic pancreatitis Drainage • Technically easier • Less mortality 2 cm

III – T4 Any N M0

T3 – E xtension to duodenum or bile duct

IV – Any T Any N M1

T4 – E xtension to portal vein, SMV, SMA, stomach, spleen, colon, celiac axis Nodes—N Nx – R  egional nodes cannot be assessed N1 – No nodal spread N2 – Nodal spread present

Metastases—M Mx – D  istant spread cannot be assessed M0 – No distant spread M1 – Distant spread present

To overcome rigidity of abdomen in refractory cases, with the base of the left hand pressing upon the lower part of the sternum, thoracic respiration is impeded and the abdominal muscles relax. —Neville J Nicholson

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SRB's Manual of Surgery ERCP signs

Important investigations

• • • • •

• Spiral CT/3D CT is ideal—to detect operability, portal vein invasion, size, extent, pancreatic and biliary tree and nodal status • ERCP to take biopsy/brush cytology, stenting, to see the luminal extent of the tumour • MRCP is non-invasive—entire biliary tree is visualised properly • Endosonography (EUS)—to assess size of primary properly; to take endosonographic FNAC • PTC often with PBD if ERCP fails

Abrupt block of pancreatic duct with irregular stricture Pancreatic duct encasement Double duct sign—cut off of both pancreatic and bile duct Parenchymal filling Scrambled egg appearance

Barium meal X-ray

Investigations to stage the disease

• • • •

• • • •

Is rarely done in periampullary carcinoma Rose thorn appearance in hypotonic duodenography Reverse 3 sign in periampullary carcinoma Pad sign—widened C loop of duodenum in carcinoma head of pancreas • Features of Gastric outlet obstruction

3D/spiral CT scan EUS Laparoscopy ERCP

Pre-operative Preparation in Carcinoma Pancreas In operable cases: xx Adequate hydration is important in prevention of dehydration post-operatively. Dehydration is common in obstructive jaundice. xx Glycogen reserve in liver will be inadequate which should be replenished by giving pre-operative glucose orally or intravenously. xx Patient is prone to develop hepatorenal syndrome post- operatively, leading into renal failure due to sludging of the bile salts, due to toxins and sepsis; and so mannitol should be given intravenously for 3 days prior to surgery to flush the kidney (200 ml IV twice a day). xx Injection vitamin K 10 mg IM for 5 days. xx ERCP stenting is done only if serum bilirubin is >30 mg%, severe cholangitis or severe albumin deficit or in inoperable cases to relieve obstruction. Routine ERCP is not advisable as it may contaminate biliary system. Percutaneous transbiliary drainage (PTBD) or cholecystostomy are other options. Whipple’s operation or resections are done 3 weeks later. xx Antibiotics one day prior to surgery—cephalosporins/aminoglycosides. xx Often TPN may be required preoperatively which is also continued postoperatively. xx Pulmonary function study and respiratory physiotherapy to have adequate post-operative pulmonary function. Note:

•

• •

In obstructive jaundice, serum bilirubin level will not go beyond 40 mg%. At this point raised intrabiliary pressure (Normal is 12–22 cm of H2O) to 25 cm of H2O, blocks the formation of bilirubin and secretion of cholesterol and bile acids completely. Maximum production of bilirubin per day possible is 250 mg%. Normal maximum excretion of bilirubin by kidney per day is 210 mg%. So maximum possible raise of serum bilirubin is 40 mg% in obstructive jaundice. Cholangitis in malignant obstruction is rare; but when it occurs it is rather severe form. Pre-operative albumin therapy is usually not done.

xx Whipple’s operation is done by removing tumour with head

and neck of pancreas, C loop of duodenum, 40% distal stomach, 10 cm proximal jejunum, lower end of the common bile duct, gallbladder, peripancreatic, pericholedochal, paraduodenal and perihepatic nodes. Continuity is maintained by choledochojejunostomy, pancreaticojejunostomy and gastrojejunostomy. Few advocate pancreaticogastrostomy into posterior wall of the stomach. Mortality in Whipple’s operation is 2–8%. Original Whipple’s operation (1935) was two staged procedure–initial bypass and a second stage resection with closure of pancreatic stump. In 1941, Trimble performed one stage pancreaticojejunostomy. Complications are delayed gastric emptying (19%); pancreatic fistula (14%); infection (intra-abdominal abscess, wound infection, cholangitis, pancreatitis, pneumonia); bile leak. Mortality is 3%.

xx Traverso-Longmire pylorus preserving pancreatico-duodenectomy (1978): Here duodenum is cut 2 cm distal to the pylorus and continuity is maintained by anastomosing with jejunum. xx Fortner’s regional pancreatectomy (extended Whipple’s) includes resection like Whipple’s along with removal of segment of superior mesenteric vein and clearance of all regional nodes; and portal vein continuity is maintained by a synthetic vascular graft. Even though technically it gives adequate clearance, results are only equivocal.

Treatment Only 10–15% of pancreatic carcinomas (head) are operable. 40–50% are locally advanced. Another 40–50% will have distant spread to liver or lungs. Criteria for resection ™™

Tumour size less than 3 cm

™™

Periampullary tumours

™™

Growth not adherent to portal system

Fig. 14.41: Whipple’s operation.

Pancreas xx Distal pancreatectomy or central pancreatectomy or total pancreatectomy for cystadenocarcinoma of pancreas depending on the extent and size of the tumour.

A

B

Figs 14.42A and B: (A) Specimen of pancreaticoduodenectomy with tumour in the head of pancreas; (B) Resected specimen (after Whipple’s operation) of periampullary carcinoma of pancreas.

Fig. 14.45: Photo showing specimen of distal pancreatectomy.

In inoperable cases: Here mainly to palliate obstructive jaundice, duodenal obstruction and pain.

Fig. 14.43: On table finding in periampullary tumour showing dilated gallbladder and CBD. xx Total pancreatectomy is presently said to be better. It is done along with nodal clearance. Reasons are—possibility of multicentric nature of the disease, higher chance of recurrence after Whipple’s operation, malignant cells may be present in pancreatic duct, morbidity by pancreatic fistula or pancreatitis after Whipple’s operation is not seen here. Mortality in total pancreatectomy is higher 10–20%. Severe, resistant brittle diabetes mellitus may be seen after total pancreatectomy.

Fig. 14.44: Specimen of total pancreatectomy with C loop, head, body and tail of pancreas with spleen. Total pancreatectomy is done in refractory severe chronic pancreatitis and carcinoma pancreas.

xx Roux-en-Y choledochojejunostomy is ideal palliative procedure along with gastrojejunostomy after doing cholecystectomy. Choledochojejunostomy is better than cholecystojejunostomy as CCJ may get blocked either by tumour infiltration or by bile sludge or by inflammation. 30% of periampullary carcinoma/ carcinoma of head of pancreas eventually develop gastric (duodenal) outlet obstruction and so gastrojejunostomy is undertaken. xx ERCP and stenting is done to drain bile. Problems here are recurrent cholangitis, stent blockage and displacement, requirement of repeated stenting procedure. Duodenal stenting for duodenal obstruction is tried. xx Chemotherapy; neoadjuvant chemotherapy. xx Steatorrhoea is treated by enzymes. Control of diabetes is important.

Fig. 14.46: Choledochojejunostomy (CDJ) with gastrojejuno­stomy (GJ) and jejunojejunostomy (JJ). It is a Roux-en-Y anastomosis. CDJ should be 70 cm from the JJ.

Silence is a source of great strength. Silence is the best speech.

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SRB's Manual of Surgery bility and survival. It increases the R0 resection status and reduces the node positive rate. There is less chance of tumour hypoxia (which is more after surgery) by which increases the susceptibility of tumour to chemoradiotherapy; less chance of mucosal anastomotic toxicity. It reduces the tumour burden at surgery; decreases the local or regional recurrence; decreases the chances of pancreatic fistula. But there is no survival benefit.

Post-operative Management in Carcinoma Pancreas

Fig. 14.47: Cholecystojejunostomy—is not a preferred method.

xx Maintenance of proper fluid and electrolyte balance. xx Observation for bleeding and its control by transfusion of blood, fresh frozen plasma (FFP), and prevention of DIC at initial period. xx Injection vitamin K 10 mg IM for 5 days. xx Respiratory care—ideally post-operative ICU care is better. Often ventilator is needed for 24 hours. xx Maintaining adequate urine output—mannitol should be continued. xx Injection octreotide infusion for 5 days to suppress pancreatic secretion so as to prevent leak. xx Antibiotics, nasogastric aspiration. xx Continuous monitoring the patient with pulse/blood pressure/ oxygen saturation/hourly urine output/inspection of drain site/ abdomen distension/by doing HB%, LFT, serum creatinine, bilirubin, arterial blood gas analysis if needed, platelet count, prothrombin time.

Pain Control in Carcinoma Pancreas xx xx xx xx xx

CT-guided 50% of 20 ml ethanol injection into coeliac ganglion. Epidural anaesthesia. Opioids administration. Transthoracic splanchnicectomy—greater splanchnic nerve. Palliative radiotherapy—4000 cGy units.

Prognostic factors in carcinoma pancreas—poor prognosis ™™

Fig. 14.48: White bile. It is neither white nor bile. It is opalescent; and is mucous. It suggests complete obstruction. It is usually observed in carcinoma pancreas. It is peroperative finding.

Adjuvant Therapy xx Adjuvant chemotherapy using gemcitabine—better but

costly; dose is 1000 mg/m2 surface area; 5-fluorouracil; mitomycin; vincristine, cisplatin, docetaxel, oxaliplatin are used along with gemcitabine. xx Radioactive iodine seeds I125 to the field are on trial. External radiotherapy 4000 cGy units to relieve pain and to reduce the tumour size. xx Immunotherapy—specific type to increase the effectiveness of chemotherapy and to improve the cure rate (allogeneic tumour cell vaccine).

Neoadjuvant Chemoradiotherapy Only 20% of pancreatic carcinomas are amenable for surgical resection. Even in these patients in spite of resection, overall outcome is poor. So neoadjuvant chemoradiotherapy is becoming popular [(50 Gy dose of radiotherapy for 5–6 weeks (25–30 fractions) with infusion chemotherapy, then surgical resection)] and under trial to improve the resecta-

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Mean survival rate 6–9 months Growth more than 3 cm Nodal involvement Resection status—R0/R1/R2 Portal vein infiltration Liver/lung secondaries Ascites/Trousseau’s sign/left supraclavicular lymph nodal spread White bile on table carries poor prognosis Associated problems like pancreatitis, diabetes mellitus Liver dysfunction

ENDOCRINE PANCREATIC TUMOURS xx Most common is insulinoma. Others are gastrinoma, glucagonoma, vipoma, pancreatic polypeptidoma. xx They belong to group of tumours called “APUDOMAS”. xx Endocrine tumours are associated with MEN syndrome (Type I Werner’s syndrome). xx They are associated with:  Parathyroid adenoma.  Pituitary adenoma.  Peptic ulcer. xx They are usually multiple, small, 35–50% are malignant and presents with features of endocrine lesion. Commonly occurs in body and tail (except gastrinomas).

Pancreas xx Requires special method to identify. xx MRI, angiogram, hormone assay are the diagnostic methods required. xx Normal islet cells are < 2% of pancreatic mass. They contain α, β, δ, G, D2 and PP cells (pancreatic polypeptide). xx Incidence is 5 per 100000 per year. xx 20% are non-functional. xx Insulinomas are commonly benign; glucagonomas are almost always malignant.

Treatment

INSULINOMAS xx Insulinomas are commonest endocrine pancreatic tumour

(60%) arising from B cells (β cells) of pancreas.

xx They are commonly solitary but 10% can be multicentric and

secrete insulin in excess causing profound hypoglycaemic features. xx Equal in both sexes. xx 90% of insulinomas are 7 µU/ml;

insulin/glucose ratio >0.3 signifies insulinoma. Proinsulin level more than 24% of total insulin signifies insulinoma. Proinsulin level more than 40% of total insulin signifies malignant insulinoma. C peptide level >1.2 µg/ml with glucose level 20% Increased circulating C-peptide Plasma insulin to glucose ratio >0.3 is diagnostic

Differential Diagnosis xx Nesidioblastosis. xx Non-insulinoma pancreatogenous hypoglycaemia.

Fig. 14.50: Passaros triangle.

If you tell the truth you do not have to remember anything—Mark Twain.

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SRB's Manual of Surgery Three points forming Passaros triangle 1. Junction between the head and neck of the pancreas 2. Junction of cystic duct with CBD 3. Junction between the 2nd and 3rd parts of the duodenum

xx Half of them are multiple and malignant (50%). xx It causes severe, multiple peptic ulcers in the stomach,

Remember ™™ ™™ ™™ ™™ ™™

duodenum and jejunum.

xx It is due to hypergastrinaemia causing high levels of acid

Gastrinomas are often associated with MEN syndrome and are multiple Sporadic gastrinomas are often solitary and then are malignant Gastrinoma often secretes ACTH Most common malignant endocrine pancreatic tumour is gastrinoma Gastrinoma causes ulcer of unusual nature (refractory/resistant); unusual recurrence (repeated and multiple); unusual number (multiple); unusual sites (2nd/3rd part duodenum/jejunum); unusual age (young and aged)

secretion. xx Other features are diarrhoea, steatorrhoea, hypo­kalaemia. xx It causes ZES type II. xx When malignant commonly present with secondaries in liver

(80%)/lymph nodes/lungs or bones.

Triad of somatostatinoma ™™ ™™ ™™

GLUCAGONOMAS

Salient features of ulcers in gastrinomas ™™ ™™ ™™ ™™ ™™

Multiple ulcer Resistant ulcer/refractory ulcer Jejunal ulcer Recurrent ulcer Ulcer which is more prone for bleeding and perforation

Investigations Gastrin assay (normal level 15 mEq/hour which is specific of gastrinoma (ZES II). Gastric pH more than 3 rules out gastrinoma. Secretin stimulation test by injecting 2 units/ kg secretin IV and assessing blood samples before and every 5 minutes after injection of secretin for 30 minutes will show rise in gastrin level more than 50% of baseline.

Treatment 60% are curable. xx Enucleation of tumours. xx Distal pancreatectomy. xx Pancreaticoduodenectomy. xx Subtotal pancreatectomy. xx Often total gastrectomy may be required.

Diabetes mellitus Steatorrhoea Cholecystolithiasis

xx xx xx xx xx xx

Arise from α cells of pancreas. Common in body and tail of pancreas. It is common in females. It attains large size of 5–10 cm. It is commonly sporadic. 17% associated with MEN type II syndrome. It is commonly malignant (80%). 80% spreads to liver.

Clinical Features xx xx xx xx xx xx

Necrolytic migratory erythema (65%). Diabetes (90%). Diarrhoea and weight loss. Stomatitis. Anaemia and features of amino acid deficiency. Vulvovaginitis is common. Investigations

™™ ™™ ™™ ™™

MRI, CT scan. Endosonography. Angiogram. Increased serum glucagon level. Fasting glucagon level more than 50 p mol/litre is diagnostic.

Treatment xx Correction of anaemia, protein and amino acid deficiency by enteral/parenteral nutrition. xx Intravenous amino acid infusion to control necrolytic dermatitis. xx Prevention of DVT. xx Distal pancreatectomy. xx Occasionally Whipple’s/total pancreatectomy is needed. xx Enucleation is rarely sufficient for glucagonoma. xx Dacarbazine is specifically effective in glucagonoma. Vipoma ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Arising from D2 cells of pancreas Watery diarrhoea, hypokalaemia, achlorhydria (WDHA syndrome) Also called as pancreatic cholera or Verner- Morrison syndrome, weak—tea syndrome Usually malignant Secretes vasointestinal polypeptide >150 pg/ml Common in body and tail—solitary Distal pancreatectomy is the treatment of choice Prednisolone controls the diarrhoea Octreotide is useful

Pancreas ZOLLINGER-ELLISON SYNDROME Type I: “G” cell hyperplasia with hypergastrinaemia and chronic peptic ulceration. Treatment is partial gastrectomy with removal of “G” cell area. TYPE II: Gastrinomas (see above). Note:

•

• •

Somatostatinoma arises from δ cells of pancreas. It is exceedingly rare. Usually larger than 2 cm and single. It is common in head of pancreas and duodenum. Its association with MEN II syndrome is rare. It is often associated with neurofibromatosis type I and phaeochromocytoma. Presentations are steatorrhoea; diabetes mellitus; gallstones; hypochlorhydria and occasional jaundice. Tumour is commonly malignant and commonly present with nodal and liver spread. Elevated fasting somatostatin level is diagnostic. Treatment is pancreaticoduodenectomy. 20% of pancreatic endocrine tumours are nonfunctional. Nonfunctional means these tumours do not produce hormones or produced hormones will not produce any symptoms. Pancreatic polypeptide tumour (PP tumour) is classified under the non-functioning endocrine tumour as it does not cause any symptoms even though there is high pancreatic polypeptide. It is commonly malignant, often with spread. PPoma occurs predominantly in head of pancreas. Pancreaticoduodenectomy is the treatment.

CYSTIC FIBROSIS It is inherited as an autosomal recessive disease. It causes— 1. Severe exocrine dysfunction—due to blockage of pan­creatic ducts as a result of precipitation of pancreatic enzymes leading to duct ectasia. 2. Chronic pulmonary disease due to blockage of bronchi and bronchioles. 3. Elevated sodium and chloride—in the sweat more than 90 mmol/L. 4. It is common in Caucasians. It is inherited as mutation in cystic fibrosis transmembrane conductance regulator gene in chromosome 7.

Treatment xx xx xx xx xx xx

Low fat and salt rich diet. Correction of malabsorption. Pancreatic enzyme supplements. Antibiotics. Respiratory physiotherapy. If meconium ileus is present, it might require surgery, i.e. BishopKoop operation.

Prognosis is poor. Problems in cystic fibrosis ™™ ™™ ™™ ™™ ™™ ™™ ™™

Meconium ileus Recurrent respiratory infection and complications Sodium deficit Severe malnutrition Sialadenitis, choroiditis Cirrhosis of liver Usually die in childhood or early age group

ANNULAR PANCREAS It is due to failure of complete rotation of ventral bud of pancreas, so that ring of pancreatic tissue encircles the 2nd part of the duodenum causing obstruction. It contains a duct that joins the main pancreatic duct.

Presentations xx xx xx xx xx xx xx xx xx

Chronic pulmonary disease with emphysema, bronchiectasis. Steatorrhoea. Meconium ileus with intestinal obstruction. Salty sweat (while kissing the baby). Poor growth due to malabsorption. Cirrhosis of liver due to bile plugging. Pancreatitis is common. Sialadenitis, choroiditis can occur. Absence of vas deferens in men.

Diagnosis xx DNA study. xx Vomitus when put on an exposed X-ray film will not digest the gelatin in half an hour (wherein in normal individual vomitus contains trypsin which will digest the gelatin of X-ray film and turns white). xx US abdomen. xx Sweat test for sodium and chloride. xx Pulmonary function tests.

Fig. 14.51: Annular pancreas.

Clinical Features xx xx xx xx

Distension of upper abdomen. Bilious vomiting. Visible gastric peristalsis. It is often associated with the Down’s syndrome, and other congenital gut abnormalities.

Types xx Neonatal type—produces symptoms of intestinal obstruction. xx Adult type—presents after the age of 20. Presents with features of duodenal ulcer and bilious vomiting.

Those who wish to sing always finds a song.

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Differential Diagnosis ™™ ™™

Causes

Duodenal atresia. Wilkie's syndrome.

Investigations Plain X-ray abdomen shows double-bubble appearance. ERCP and Radioisotope study. ™™ Barium meal shows obstruction at 2nd part of duo­denum. ™™ ™™

xx Chronic pancreatitis commonly due to dietary factors, familial, hyperparathyroidism. xx Commonly they are multiple and associated with or due to chronic pancreatitis.

Pathogenesis Stricture of pancreatic duct and stasis of pancreatic secretion.

Treatment xx Duodenoduodenostomy—Ideal. xx Duodenojejunostomy. xx Do not resect the ring. Attempt at resection will lead to pancreatic fistula. xx G-J is not done.

ECTOPIC (ACCESSORY) PANCREATIC TISSUE

A

Sites Stomach wall. Small intestine. ™™ Meckel’s diverticulum. ™™ Greater omentum. ™™ Splenic hilum. ™™ ™™

 In the bowel, it may be in the submucous or intra­muscular

plane. It may precipitate intussusception.

 About 30–33% contain islet of Langerhan cells. Often endocrine

pancreatic tumour can arise from ectopic pancreas.

 It may cause upper GI bleed.

B

PANCREATIC DIVISUM xx During development ventral pancreatic bud with distal bile duct is towards right and dorsal pancreatic bud is towards left side. Ventral pancreatic bud forms uncinate process and inferior part of the head of the pancreas. Dorsal bud forms body and tail of the pancreas. Ventral bud rotates clockwise towards left from behind the duodenum to join dorsal bud to form pancreas. Ventral pancreatic bud duct forms main pancreatic duct of Wirsung; dorsal bud duct forms accessory pancreatic duct of Santorini. xx Pancreatic divisum is failure of fusion of ventral and dorsal pancreatic ducts. So that dorsal pancreas drains through duct of Santorini (proximal minor papilla); ventral one drains through duct of Wirsung into major papilla of Vater. xx Its incidence is 10%. xx Here major pancreatic secretion drains through minor papilla causing partial obstruction precipitating pancreatitis.

C Figs 14.52A to C: (A) X-ray showing multiple pancreatic ductal stones; (B and C) CT scan picture showing pancreatic ductal stones. Stones that are removed from the same patient are also shown. Patient underwent longitudinal pancreaticojejunostomy.

Types a. Calculi in the duct:  Here parenchyma is still functioning and less severely affected.  Duct is dilated significantly (more than 3 mm) with multiple large stones in the duct along with multiple strictures.  Duct is having dilatation alternating with strictures—chain of lake appearance.

Pancreas –– Plain X-ray abdomen shows stones placed horizontally at

L1-L2 level. –– US, ERCP, MRCP are other useful investi­gations. –– Blood sugar should be checked. Treatment The duct is opened longi­tudinally and after removing all stones, side-to-side pancreaticojejunostomy is done. b. Calculi in the Parenchyma  Here multiple calcifications occur in the pan­creatic paren­chyma with pre-existing chronic pancreatitis. Gland is fibrosed and severely affected with less functioning capacity.  Plain X-ray, US, ERCP, MRCP are the diagnostic methods. Treatment  Total pancreatectomy.  It is more likely to turn into carcinoma pancreas.

PANCREATIC ASCITES xx It can occur in chronic pancreatitis or as a complication of acute pancreatitis or in ruptured pseudocyst of pancreas or after pancreatic trauma (10%, in children trauma is the cause). xx It may be associated with pleural effusion which can be both sided but commonly on left side. Often pleural effusion and ascites may be massive. It is due to internal pancreatic fistula. xx Incidence is 1%. If not treated mortality is 30%. xx It is due to leakage from disrupted pancreatic duct or ruptured pseudocyst. Anterior disruption causes pancreatic ascites. Posterior disruption causes fluid to travel along oesophageal and aortic hiatus resulting in pleural effusion. xx Pancreatic ascites and fistula are common in pancreatitis due to alcohol intake. It is less common in pancreatitis due to biliary tract disease. xx US, very high amylase and protein levels in ascites fluid, ERCP to identify leak, CT scan are the essential investigations. xx Repeated ascitic tap; pleural tap; TPN; somatostatin or octreotide to reduce pancreatic secretion are tried as conservative therapy for 3 weeks. 50% respond to this therapy. xx If there is no improvement beyond 3 weeks, ERCP stenting of pancreatic duct is done initially. Then resection (better option) or drainage (jejunal loop Roux-en-Y anastomosis directly over disrupted duct) surgery is done. Pancreatic pleural effusion disappears once abdominal cause or ascites is corrected.

PANCREATIC FISTULAE Types

Present ISGPF (International study group of pancreatic fistula) grading system is – Grade 0,A,B,C using various parameters like amylase level of fluid, clinical features, imaging etc.

Causes xx xx xx xx xx xx xx

Whipple’s operation. Pancreaticojejunostomy. Splenectomy. Colonic surgeries. Trauma. After external drainage of the infected pseudocyst of pancreas. After percutaneous drainage of the pseudocyst. Clinical features

Patient is in a catabolic state Skin excoriation ™™ Electrolyte imbalance ™™ Malnutrition ™™ Sepsis. ™™ ™™

Investigations CT scan ERCP ™™ Fistulogram ™™ Amylase estimation of the discharge. ™™ ™™

Treatment Conservative treatment: xx xx xx xx xx

Total parenteral nutrition. Zinc oxide cream for skin excoriation. Correction of electrolyte imbalance. Antibiotics. Octreotide.

Surgery: xx Roux-en-Y anastomosis. xx Resection of fistula with pancreas. xx Endoscopic stenting of the pancreatic duct.

Internal Fistulae xx xx xx xx

Communicating pseudocyst. Pancreatic ascites. Pancreatic pleural effusion. Pancreatic-enteric fistulae.

External and internal fistulae.

External Fistulae

Complications of pancreatic fistulae Septicaemia Malnutrition ™™ Bleeding due to erosion of vessels ™™ Electrolyte imbalance ™™ Severe skin excoriation ™™ ™™

Types a. Low output fistulae 200 ml. (Note: For other GI fistulae it is 500 ml)

It is better to aim at good things and miss it, than to aim at a bad thing and hit it.

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SRB's Manual of Surgery PANCREATIC NECROSIS It is diffuse or focal area of non-viable parenchyma of pancreas, occurs during an attack of severe pancreatitis that is associated with peripancreatic fat necrosis. It occurs in 20% of acute pancreatitis.

Types xx Sterile necrosis is 60% of total pancreatic necrosis. Mortality here is 10%. xx Infected necrosis is 40% of total necrosis. Mortality here is 30–40%, very high. Risk of infection is 25% in one week of acute attack; 35% at the end of 2nd week; and 70% at the end of 3rd week. xx Necrosis extends to retroperitoneal fat, mesentery, retrocolic and perinephric areas.

Pathogenesis xx xx xx xx

Premature activation of proteolytic enzymes. Intrapancreatic vessel thrombosis. Pancreatic microcirculation failure. Release of inflammatory mediators. Mode of infection

™™ ™™ ™™ ™™ ™™ ™™

Haematogenous Reflux through ampulla Mucosal translocation of bacteria From the biliary tree Lymphatic route Transperitoneal spread.

Bacteria 65% are polymicrobial. E. coli is commonest. ™™ Others are—Proteus, Pseudomonas, Klebsiella, staphylococci, Streptococcus faecalis, enterococci, anaerobes, Clostridium welchii. ™™ ™™

xx Intra-abdominal abscess. xx Abdominal dehiscence, incisional hernia after surgery.

PANCREATIC TRAUMA xx It is rare because of its anatomical location—retroperitoneum. xx Its injury is usually associated with injuries to liver/duodenum/ spleen/portal system/biliary system/ kidney. xx Deep force in epigastrium may cause crushing of body of pancreas against vertebra—closed injury. xx Penetrating injury may cause direct sharp injury of pancreas.

Types xx Parenchymal contusion/laceration without duct disruption. xx Parenchymal injury with duct disruption. xx Complete transection of pancreas. xx Massive destruction of pancreatic head. Classification Pancreatic injury Class I Capsular damage; minor parenchymal injury Class II Transection of duct in body or tail—partial or complete Class III Major duct injury in pancreatic head or intrapancreatic CBD injury Duodenal injury Class I Contusion, haematoma, partial thickness injury Class II Full thickness duodenal injury Class III Full thickness duodenal injury with 1. More than 75% circumference injury 2. Extrapancreatic CBD injury Combined pancreatico duodenal injury Type I Class I injury to both organs/class I injury of one organ with class II injury to other Type II Class II injuries of both organs Type III Class III injury to one organ with less severe injury to other Type IV Class III injury to both organs

Grading of pancreatic injury

Diagnosis xx Clinical features. xx CT scan abdomen and CT-guided FNA for Gram’s staining and culture. xx CRP value—> 120 mg/litre; interleukin level; elastase level; urinary TAP assessment.

Treatment xx Antibiotics—imipenem, cefuroxime, ofloxacin, meropenem. xx Percutaneous drainage. xx Laparotomy, necrosectomy, debridement, saline wash, closure with tube irrigations/lavage.

Complications xx Septicaemia, ARDS, renal failure, MODS. xx Pancreatic fistula after surgery.

Grade I – Minor contusion/laceration without duct injury Grade II – Major contusion/laceration without duct injury Grade III – Distal transection or injury with duct involvement Grade IV – Proximal transection or injury with involving ampulla Grade V – Massive disruption of pancreatic head

Features xx xx xx xx

Pain in epigastrium. Features of associated injuries. Features of shock. Rise in serum amylase level is common.

Investigations xx CT scan is diagnostic. xx ERCP to confirm duct disruption. xx Assessment of blood loss and other injuries.

Pancreas Treatment xx Commonly conservative with fluid management; blood transfusions; antibiotics; pain relief. xx Surgery is needed when there is:  Major ductal disruption.  Vascular injury.  Extensive injury to head.  Other organ injury.

Surgeries are

PANCREATIC EXOCRINE INSUFFICIENCY (EXOCRINE PANCREATIC DISEASE) Causes Chronic pancreatitis, cystic fibrosis, pancreatic resections (total or partial), pancreatic duct obstruction by haemochromatosis or α1 antitrypsin deficiency, short gut syndrome, gastric resection, Shwachman Diamond syndrome (congenital entity with pancreatic exocrine insufficiency, cytopenias, skeletal abnormalities).

Proper exploration and haemostasis. In neck transection, distal pancreatectomy with splenectomy. In injury to head, haemostasis and external drainage is done. Pancreaticoduodenectomy is done if there is major injury. Choledochojejunostomy is done if there is CBD injury. Different pancreatic drainage procedures are done to prevent sepsis and fistula. xx Portal system injury carries poor prognosis. It needs repair or intervening graft placement to control and maintain the continuity.

Features

Prognosis

Evaluation

xx Depends on type and class of injury and other associated injuries.

Direct methods:

xx xx xx xx xx xx

Complications ™™ ™™ ™™ ™™ ™™ ™™ ™™

Haemorrhage Septicaemia Pancreatitis—acute/recurrent Pseudocyst formation Pancreatic fistula Pancreatic abscess Pancreatic duct stricture at the site of duct injury as a delayed complication.

CYSTIC LESIONS OF PANCREAS Types 1. True pancreatic cysts:  Congenital.  Not premalignant.  Asymptomatic.  May be associated with cystic diseases of liver, kidney.  Multiple true pancreatic cysts (polycystic disease of pancreas) are common than solitary true cyst. They are lined with cuboidal epithelium and are associated with von Hippel-Lindau disease in 50% of patients. They do not require any treatment. 2. Pseudocyst of pancreas. 3. Cystic tumours of pancreas. a. Serous cystadenoma. b. Mucinous cystadenoma. c. Cystadenocarcinoma. d. Angioma. e. Cystic teratomas. 4. Hydatid cyst of the pancreas.

xx Maldigestion of fat and proteins causing steatorrhoea and weight loss. xx Metabolic bone disease, impaired night vision, fat soluble vitamin deficiencies can occur. xx Vitamin B12 deficiency can occur as decreased intestinal pH prevents transfer of vitamin B12 to intrinsic factor from R factor; it shows positive dual label Schilling test.

It is done by directly collecting the fluid from duodenum using double lumen collecting tubes, one is duodenum to collect pancreatic fluid and other being in stomach to aspirate gastric content so that to avoid it mixing with pancreatic fluid. xx Lundh test (Goran Lundh)—Liquid test meal containing protein, fat and carbohydrate (300 ml) is given orally; duodenal fluid is collected for 2 hours; assessed for enzymes. Normally trypsin level is > 8 mEq/L. It is very low in pancreatic insufficiency. Test is obsolete now. xx Secretin test—Initial test dose of secretin is given 0.2 ug; then full dose of 0.2 ug/kg as a bolus IV dose is given; duodenal fluid is continuously collected with segregations as 15 minutes as 4 groups; in pancreatic insufficiency HCO3 level will be < 80 mEq/L in all four groups; total HCO3 output and volume also analysed. xx Secretin—CCK test is more reliable and accurate than secretin test alone. Both hormones are administered as bolus injection continuously either simultaneously or sequentially; similar assessments are done. Normally duodenal fluid contains more than 80 mEq/L of HCO3 and HCO3 greater than 15 mEq/30 minutes. Indirect methods: These methods are measure of effects of pancreatic insufficiency. xx Serum trypsinogen and trypsin level estimation; trypsinogen level less than 20 ng/ml suggest advanced pancreatic exocrine insufficiency. xx Faecal fat estimation after collecting 72 hours faecal fat and estimation is done for daily fecal fat using Sudan stain. In a person ingesting 100 gm of fat/day, if faecal excretion of fat is more than7 gm/day, it signifies pancreatic insufficiency. It is the most sensitive and specific test. (Presence of neutral fat suggests pancreatic disease whereas split fat suggests small bowel disease).

If you can tell the difference between good advice and bad advice you don’t need to advice—Roger Devlin.

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SRB's Manual of Surgery xx Pancreolauryl test—Fluorescein dilaurate is ingested along with breakfast which is a substrate for pancreatic enzyme cholesterol esterase; depending on the activity of the cholesterol esterase this substrate is cleaved to release proportionate fluorescein; released fluorescein rapidly absorbed from the gut and excreted in the urine. Serum fluorescein and 24-hour urine fluorescein assay gives the quantitative estimation of the pancreatic exocrine function. It is accurate and acceptable test for pancreatic exocrine insufficiency. xx Triolin breath test—Triolin labelled 13C or 14C is administered as test meal; it is hydrolyzed in the gut lumen depending on

the quantity of pancreatic lipase activity; hydrolysed products are absorbed, metabolised and released through pulmonary endothelium as 13CO2/14CO2 which is measured using mass spectrometry or infrared. It is mainly used to quantify steatorrhoea.

Treatment of Pancreatic Exocrine Insufficiency Low fat diet; pancreatic enteric coated tablets during meals, treatment of cause.

Chapter

15

Retroperitoneal Space CHAPTER OUTLINE ™™ Anatomy of Retroperitoneum ™™ Retroperitoneal Fibrosis

™™ Retroperitoneal Swellings ™™ Retroperitoneal Tumours

™™ Psoas Abscess

ANATOMY OF RETROPERITONEUM This is the space between the peritoneal cavity and posterior abdominal wall. It is bounded anteriorly by posterior parietal peritoneum; posteriorly by vertebral column, psoas muscles, quadratus lumborum muscle and tendinous portion of transversus abdominis muscles; superiorly by diaphragm; inferiorly by pelvic levator muscles (by Ackerman). It is real potential space. Diseases of retroperitoneal spaces ™™ ™™ ™™ ™™ ™™ ™™ ™™

Retroperitoneal fibrosis Retroperitoneal cysts Retroperitoneal tumours Retroperitoneal lymphomas Retroperitoneal vascular diseases, e.g. aneurysms Retroperitoneal trauma and haematoma Retroperitoneal infection, e.g. psoas abscess, pyogenic abscess

Diseases of the specific retroperitoneal organs, e.g. adrenals, kidney.

RETROPERITONEAL FIBROSIS xx Idiopathic type (70%) is called as Ormond’s disease

which is associated with mediastinal fibrosis, Dupuytren’s contracture, plantar fasciitis, Peyronie’s disease, Riedel’s thyroiditis, sclerosing cholangitis, mesenteric panniculitis, pseudotumour of the orbit and other fibromatosis. It is nonspecific inflammation of fibrofatty tissue in the retroperitoneum. xx Patient presents with severe and persistent back pain. xx Diffuse fibrosis in retroperitoneum can compress both ureters leading to bilateral hydronephrosis and renal failure. xx Extravasation of urine, ascending lymphangitis, and autoimmune cause are the aetiologies.

Fig. 15.1: Anatomy of retroperitoneal space. xx In 30% cases it is bilateral. Hypertension, lower limb

oedema (lymphatic or venous block), feeble lower limb arterial pulses are common. xx It is like woody fibrous tissue which narrows ureters, vessels and nerves. Ureteric obstruction commonly in lower 1/3rd causing dysuria, frequency, oliguria, renal failure. Venous and lymphatic oedema of limbs can occur. xx It may be localised or generalised. Generalised type (15%) may extend into duodenum, CBD and pancreas. It is not encapsulated but margin is well-demarcated. xx It can also cause vascular compression, both venous and arterial. xx Disease is progressive one.

The lesser the indication, the greater the complication.

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SRB's Manual of Surgery Investigation xx Ultrasound xx IVU—diagnostic: Triad ™™ ™™ ™™

Deviation of middle 1/3rd of ureter medially Hydroureteronephrosis Extrinsic ureteral compression

• •

Only 0.5% of cases present with hypertension. It can be familial, often associated with von Hippel-Lindau disease and RET protooncogene. It may arise from type I cells as chromogranin A positive— NSE positive; or type II cells as S 100 positive with good prognosis. Costello syndrome is mental retardation, benign papilloma; develop embryonal rhabdomyosarcoma. Retroperitoneal cysts are—cysts arising from Wolffian remnants or urogenital tract; RP mesenteric cyst; teratomatous dermoid cysts; RP lymphatic cyst; parasitic cysts.

xx Blood urea and serum creatinine, raised ESR and CRP. xx CT scan.

Treatment xx Drug therapy: Methylprednisolone, azathioprine, penicil-

lamine, tamoxifen. xx Cystoscopic stenting of the ureters to prevent renal failure. xx Symptomatic treatment: If stenting fails, bilateral nephrosxx xx xx xx

tomy is done. Ureterolysis. Lateral repositioning of ureters. Omental wrap after ureterolysis. Vascular bypass graft for vascular encasement. Other causes for retroperitoneal fibrosis (30%)

™™ ™™ ™™ ™™ ™™ ™™ ™™

Methysergide and beta-blocker drugs Urine leak and collection in the space Haematoma, blood collection Advanced malignancy, radiation. Ergot’s alkaloids, dopamine agonists Retroperitoneal surgeries, haemorrhage Trauma, infection

RETROPERITONEAL SWELLINGS Types of retroperitoneal (RP) tumours (0.3–3%) Benign—20% of RP tumours ™™ Retroperitoneal lipoma ™™ Retroperitoneal neurofibroma, neurilemmoma ™™ Retroperitoneal leiomyoma ™™ Extra-adrenal chromaffinomas ™™ Paraganglioma ™™ Mucinous cystadenoma ™™ Haemangiopericytoma Malignant—80% of RP tumours ™™ Retroperitoneal liposarcoma, leiomyosarcoma—50% ™™ Retroperitoneal lymphoma (commonly NHL) ™™ Malignant tumours from specific organs ™™ Germ cell tumours, chordomas ™™ RPLN secondaries with hard nodules

Note:

• •

Tumours of retroperitoneal organs like kidneys, ureters, pancreas, and adrenals are conventionally not included in retroperitoneal tumours. Paragangliomas are of neural crest origin that arises from paraganglionic tissues distributed along the major vasculatures (abdominal aorta in abdomen) or sympathetic chain, may be functioning or nonfunctioning. 20% secrete catecholamines. They may be multiple.

Fig. 15.2: Retroperitoneal tumour can attain very large size often. It causes deviation of ureter laterally often may invade the ureter (In retroperitoneal fibrosis ureter is deviated medially). It may invade or encase the IVC also causing IVC obstruction with features of bilateral oedema feet, dilated lateral abdominal wall vein with upward direction flow of blood.

Features of the Retroperitoneal Mass xx xx xx xx xx xx

It is usually large. Not moving with respiration. Nonmobile. Does not fall forward (confirmed by knee-elbow position). Deeply placed. Resonant on percussion (because of the bowel in front).  In retroperitoneal cyst and sarcoma the swelling is smooth.  In lymphoma it is smooth and firm.  In aneurysm it is pulsatile (expansile pulsation) which will persist even in knee-elbow position.  Confirmation is by U/S, CT scan, MRI.  Most common retroperitoneal benign tumour is lipoma.  Sarcoma (commonest is liposarcoma 40%) which attains a very large size, goes for myxomatous degeneration very early and is aggressive.

RETROPERITONEAL TUMOURS xx Retroperitoneal tumour can be benign or malignant (refer

table above); solid or cystic. Solid tumours are commonly malignant (85%); cystic tumours are usually benign.

Retroperitoneal Space myosarcoma is the most common one. 15% of all sarcomas are of retroperitoneal.

A

Fig. 15.5: Retroperitoneal tumour, on table finding. It was large and inoperable.

Aetiology xx Retroperitoneal tumors may be associated with radiation;

B Figs 15.3A and B: Retroperitoneal tumour—benign lipoma was excised with a loin retroperitoneal approach.

exposures to chemicals like vinyl chloride/thorium dioxide, familial Gardner’s syndrome, familial retinoblastoma or familial neurofibromatosis, Li Fraumeni syndrome, germline mutations of p53 in chromosome 17.

Features xx Tumor arises from fat, areolar tissue, vessels, nerves, skel-

Fig. 15.4: Retroperitoneal leiomyosarcoma, CT picture. xx Malignant retroperitoneal tumour may be mesodermal

(75%), neuroectodermal (24%) or embryonic remnant (1%) in origin. Rarely it can be urologic or metastatic also. Sarcoma is the most common malignancy; in adult—liposarcoma is the most common retroperitoneal sarcoma (50%); leiomyosarcoma is 30%; malignant nerve sheath tumour (5%); fibrosarcoma (5%); malignant fibrous histiocytoma (MFH—10%) can also occur. 20% show neurological deficit; 40% show distant blood spread. In children rhabdo-

etal and smooth muscle, fascia, lymph node and lymphatic systems and tissues of embryologic origin. Sarcomas can be commonly solid, cystic or mixed. Usually tumour develops a pseudocapsule. Liposarcoma often originates from (>30%) perinephric fat. xx Liposarcoma can be well-differentiated (60%) or undiff­ erentiated (dedifferentiated). It spreads along the fascial planes enveloping the organs. Infiltration of organs occurs only at late stage. It shows whorl-like pattern in histology with myofibroblastic or osteoblastic differentiation. Insulin like production by tumour or rapid utilisation of glucose by active tumour causes intermittent hypoglycaemia (paraneoplastic). xx Spread of retroperitoneal sarcoma mainly occurs through blood to lungs and often to liver. Nodal spread occurs rarely (5%). xx Manignant tumours of the retroperitoneum are 4 times common than benign one. xx Retroperitoneum is the 2nd most common site of malignant mesenchymal tumour first site is being lower extremities.

Presentations xx Most patients have initial asymptomatic course with eventual presentation as mass abdomen (90%). Pelvic mass (20%), vague abdominal pain and discomfort (70%), anorexia, fatigue, vomiting,

Time neither subtracts nor divides, but adds to such a pace it seems like multiplication.

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SRB's Manual of Surgery weight loss, fullness in abdomen, back pain due to compression over lumbar and pelvic nerves, leg pain, recurrent episodes of fever—are other features. xx Other presentations are—GI bleeding; intestinal/urinary obstruction (10%); neurological manifestations (20%) by compression or invasion of neurological systems by tumor; iliac vein or IVC compression can cause lower limb varicosities, varicocele, and dilated abdominal veins with venous flow from below upwards, and oedema.

xx MRI is better than CT with near 100% accuracy. It identifies

extent, desmoplastic reaction. Liposarcoma shows decreased signal in T1 and increased signal in T2. MFH shows hetero­ genous signals. xx Retroperitoneoscopy may be ideal to take biopsy. xx IVU shows laterally deviated ureter. Plain X-ray may show soft tissue shadow, obliterated psoas shadow, and often calcification. xx AFP, HCG and other tumour markers are done often. LFT, blood urea and serum creatinine is done. xx Histochemistry is essential in many suspicious types. TNM staging (AJCC 6th edition)

AJCC (6th edition) grading

Tumour (T): Tx: Cannot be assessed T0: No tumour T1: 5 cm or less T2: > 5cm

Low grade High grade

Nodal (N): Nx: Nodes cannot be assessed N0: No nodes N1: Nodes present

A

Metastasis (M): Mx: Distant spread cannot be assessed M0: No metastases M1: Distant spread present

B

C

Figs 15.6A to C: Retroperitoneal tumour presenting as large mass abdomen with all features. CT pictures of the same patient.

Investigations xx CT abdomen—helical contrast CT (commonly used) and

pelvis and CT chest (to see metastases) are essential investigations. xx CT-guided core biopsy; laparoscopic biopsy are needed. FNAC has got limited role.

Fig. 15.7: Retroperitoneal tumour showing encasement of major vessels. It becomes inoperable. Ureter, duodenum, intestines, kidney are other structures which may get infiltrated by tumour.

Staging (AJCC 6th edition): I: T1/T2; N0; M0; low grade II: T1; N0; M0; high grade III: T2; N0; M0; high grade IV: Any T; N1; M1 Note: Nodal spread carries poor prognosis; it is equal to M1 when outcome is considered

Treatment xx Surgery is the main modality of therapy with wide exci-

sion—complete enblock excision (possible only in 30% of cases) is the ideal. Limited resection; debulking (controversial) are other options. Often it needs extensive surgical dissection; resection of adjacent bowel. Wide exposure is the key for successful surgery (lengthy midline/thoracoabdominal). Limiting factors are encasement of major vessels; invasion of ureters; extension into duodenum or pancreas; extensive involvement of mesentery and spread. Proper bowel preparation, colostomy, urinary diversion, adequate blood to replace the lost blood, hypotensive general anaesthesia are the requirements during surgery. Posterior dissection along the IVC, aorta and near spinal canal are the difficult areas of dissection. Complications are—injury to major structures, bleeding, sepsis, and leak. xx Postoperative chemotherapy and radiotherapy is used as adjuvant method. xx Radiotherapy may be external beam RT (5000 cGy); or IORT (intraoperative RT during surgical resection) which reduces local recurrence and radiation enteritis. Problems with RT are radiation injury to kidney, bowel, liver and spinal cord. Preoperative intensity modulated RT (IMRT) is tried. xx Recurrent disease needs re-exploration but often difficult to do complete clearance. xx Mesna, Adriamycin (main drug), ifosfamide and dacarbazine (MAID) are the chemotherapeutic agents used. xx Germ cell tumour, lymphoma (NHL) are treated accordingly.

Retroperitoneal Space Prognosis

Retroperitoneal sarcoma (RPS)

xx Prognosis depends on:  Tumour grade—low or high;  Resectability;  Invasion into organs, veins, nerves;  Size of tumour < 5 cm or > 5 cm or > 10 cm;  Deep location;  Nonliposarcoma in histology—poor prognosis;  Recurrent disease;  Distant spread.  Tumour grade and completeness of resection without distant spread are important prognostic factors.  RP tumours has got overall 40% recurrence rate. Overall survival is 1½ to 2 years.  5-year surrival for well-differentiated tumour is 75%; < 40% for undifferentiated tumours.

™™ Accounts for 15% of all sarcomas ™™ Common presentations are—nontender palpable RP mass (90%);

™™ ™™ ™™ ™™

™™

™™

™™ ™™

™™

™™

™™

A

™™

B Figs 15.8A and B: Retroperitoneal lymph node mass. It could be tuberculosis/lymphoma/secondaries/autoimmune lymph node enlargement. Features of retroperitoneal sarcomas ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Mass per abdomen Pain in the back and compressive features GIT obstruction especially by leiomyosarcoma Compression over the ureter causing hydro­nephrosis Compression over the major veins causing varicose veins Arterial compression features are not common Liver and lung secondaries can occur CT-guided biopsy is ideal method of investigations



™™

™™ ™™

weight loss, pain and discomfort; neurologic (20%); urinary (10%); weight loss (20%); bowel obstruction; paraneoplastic syndrome (hypoglycaemia) 70% present with tumour more than 10 cm; 20% present with metastases Liposarcoma is the most common RP sarcoma; it can be well-differentiated, dedifferentiated, myxoid, round cell, pleomorphic Histological grading is important prognostic factor—high grade carries median survival of 2–3 years; low grade has got survival of 10 years CT scan, CT-guided core biopsy through posterior approach, MRI (extremely accurate)—are the investigations needed. CT chest and abdomen, isotope renal scintigraphy or IVU to check the function of opposite kidney has to be done which may required to be removed A preoperative biopsy is not usually indicated in patients with resectable RPS; but is needed when preoperative therapy alters or lymphoma/germ cell tumours are suspected Open biopsy is also not done in a resectable tumour as it is potentially dangerous, can cause peritoneal contamination. It is done only if CT core biopsy is inconclusive FNAC in RPS is not useful PET scan do not have usual role in screening, diagnosis and staging. It can be used to quantify tumour activity; to assess the response of neoadjuvant chemotherapy and response of newer therapies targeted at specific molecular level to arrest the tumour growth Dutch/memorial Sloan-Kettering cancer centre classification system of RPS (post-surgical) is commonly used: • Stage I – low grade, complete resection, no metastases • Stage II – high grade, complete resection, no metastases • Stage III – any grade, incomplete resection, no metastases • Stage IV – any grade, any resection, distant metastases Surgery is the choice of therapy—monobloc complete surgical resection with dissection outside the pseudocapsule with adequate negative margin is possible only in 50% of cases Often associated visceral organ resection (in 50% cases) is needed— kidney and adrenals (45% cases), colon (25%), small bowel, pancreas (15%), spleen (10%). Need for removal of kidney arises when there is encasement of renal hilar vessels and fascia of Gerota, but not invasion of kidney Adjuvant RT to retroperitoneum is used to prevent local recurrence. It can be—preoperative, intraoperative (IORT), postoperative. It can be external beam (EBRT) or brachytherapy. Advantages of preoperative RT are—well-demarcated gross tumour; radiosensitive viscera is displaced away by tumour itself without adhesions; absence of potential contamination of abdomen cavity; better oxygenated tumour bed. IORT is given as a single large dose (20 Gy) of RT to the retroperitoneum on table after displacing sensitive viscera away. Intensity modulated RT (IMRT) gives 45 Gy RT to planned gross tumour with 1.5 cm margin with intergrated booster doses of 65 Gy at 2.5 Gy per fraction to the margins at high-risk; IMRT has minimal local toxicity like damage to kidney, bowel (stricture), spinal cord. Postoperative RT has more disadvantages and toxicity but allows patient selection in terms of risk of local recurrence Chemotherapy (CT)—no role of neoadjuvant CT. Adjuvant CT may be useful in synovial and myxoid types of liposarcoma. Palliative CT is used in unresectable and metastatic RPS— MAID and AIM regimes are used Specific targeted therapy on tumourogenesis—antiangiogenetic agent, tyrosine kinase inhibitors, and mammalian target of rapamycin inhibitors (MTOR) are used. Trabectedin—synovial sarcoma, myxoid sarcoma, leiomyosarcoma Prognostic factors—tumour grade and completion of surgical resection are the best prognostic factors (not tumour size) Local recurrence is common in 50% of cases. It is usually seen in high-grade liposarcoma. Leiomyosarcoma, malignant peripheral nerve sheath tumours show distant spread commonly along with local recurrence

A man carries success or his failure with him; it does not depend on outside conditions.

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Wide local excision. Often requires removal of adjacent structures like colon, kidney, and spleen Debulking operation as a palliative Enucleation through pseudocapsule. It has got high recurrence rate—not done; may be useful in advanced cases Radiotherapy either brachytherapy or external beam radiotherapy or intraoperative RT Chemotherapy using adriamycin Retroperitoneal NHL is treated by chemotherapy

Fig. 15.10: Psoas abscess.

Differential Diagnosis a. Iliac artery aneurysm. b. Ovarian cyst in females. c. Soft tissue tumours and cysts in the iliac region. d. Hernia.

Fig. 15.9: Large pelvic retroperitoneal tumour.

PSOAS ABSCESS

Investigations xx X-ray spine and chest, CT scan. xx Mantoux test, ESR, peripheral smear. xx Ultrasound abdomen.

xx Abscess in the psoas region in the iliac fossa, is com­monly

due to tuberculosis of spine (T 10) and lymph nodes, retroperitoneal structures, lower intercostal region. xx It can also be a pyogenic abscess.

Clinical Features xx Back pain, fever, spinal tenderness, paraspinal spasm and

restricted spine movement. xx Swelling in iliac fossa which is smooth, nontender, nonmo-

bile, not moving with respiration. xx When it extends across the groin and below the inguinal ligament, it is cross fluctuant across the inguinal ligament. xx Patient has typical psoas muscle spasm in which patient is able to flex his hip but finds it difficult to extend. Swellings which are cross fluctuant ™™ ™™ ™™ ™™

Psoas abscess Ranula Compound palmar ganglion Bilocular hydrocele

A

B Figs 15.11A and B: (A) CT picture of large psoas abscess; (B) On table finding of psoas abscess.

Treatment xx Antituberculous drugs are started—INH, ethambutol, rifam­picin, pyrazinamide. xx Under G/A through lateral loin incision, the psoas region is reached extraperitoneally. The pus is drained and collected for culture and sensitivity, AFB, culture. The wound is closed. All caseating material and diseased parts of vertebra should be removed.

Retroperitoneal Space xx Only lateral approach is advised. In thoracic region—anterolateral decompression with costotransversectomy with bone grafting is the treatment.

C

B

Figs 15.12B and C Figs 15.12A to C: Bilateral large psoas abscess—CT picture. Drainage and placement of Malecot catheters for the same. Note the location of incisions. It is obliquely placed incision above the lateral aspect of groin with extraperitoneal approach.

A

Note: Fig. 15.12A

Posterior approach, i.e. laminectomy—not advised.

It is what a man thinks of himself that really determines his fate.

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Differential Diagnosis of Mass Abdomen CHAPTER OUTLINE

™™ ™™ ™™ ™™

Mass in the Right Hypochondrium Mass in the Epigastrium Mass in the Left Hypochondrium Mass in the Lumbar Region

™™ ™™ ™™ ™™

Mass in the Umbilical Region Mass in the Right Iliac Fossa Mass in the Left Iliac Fossa Mass in the Hypogastrium

In a patient presenting with mass abdomen, generally following clinical features should be assessed care­fully. xx Pain: Site, nature, aggravating or relieving factors, duration of pain, referred pain. xx Vomiting: Type, content, haematemesis, relation to food, frequency. xx Jaundice: It is an important factor in relation to liver, gallbladder or pancreatic masses.

™™ D  istal Rectal Examination for Prostate and Other Conditions

xx Palpation of the mass: Site, extent, surface, tender­ness, consistency, movement with respiration, mobility, borders, plane of the swelling (by leg raising test), presence of other masses.

Fig. 16.2: Abdomen should be inspected by exposing from nipple level to knee level. Inspection is done from foot end and from right side.

Fig. 16.1: Obstructive jaundice in a patient with carcinoma head of pancreas. Note the sclera for discolouration. Severe itching is common in these patients. xx Bowel habits: Constipation, diarrhoea, bloody diarrhoea, furious diarrhoea, tenesmus. xx Decreased appetite and weight. xx Inspection of the mass: Anatomical location, margin, surface, movement with respiration.

xx Often mass needs to be examined for change of position—in sitting, in standing, in side position, after a brisk walk, in knee elbow position for retroperitoneal mass and for puddle sign (but difficult to keep patient in this position). xx Percussion is an important aspect of examination in case of an abdominal mass. Percussion over the mass is important to predict the anatomical location of the mass. If mass is dull, then it is in the anterior abdo­minal wall or in front of the bowel intra-abdominally like liver, spleen, gallbladder. If the mass is with a impaired resonant note, then the mass is arising from the bowel like stomach, colon, small bowel. If the mass is resonant on percussion, then the mass is probably in the retroperitoneal region. Other than this, liver dullness, free fluid in the abdomen should be elicited during percussion.

Differential Diagnosis of Mass Abdomen xx Per rectal examination: It is done to look for any secon­daries in rectovesical pouch, primary tumour or relation of lower abdomen masses (pelvic masses). xx Pervaginal examination is done to assess pelvic masses.

Fig. 16.5: Abdomen mass should be palpated clinically properly.

Fig. 16.3: Superior vena caval obstruction causing dilated veins in the neck, chest wall and shoulder. Note the neck swelling extending into the mediastinum.

Fig. 16.6: Percussion over the mass is absolute need to find out the plane of the mass. Anterior masses are dull on percussion; posterior masses are resonant and mass from bowel has impaired resonance.

A

Fig. 16.7: Digital examination of rectum is a must in patients with mass abdomen to look for secondaries, possible primary and often to assess the mass itself.

B Figs 16.4A and B: Inferior vena caval obstruction causing dilated veins over the lateral aspect of the flank with flow of blood upwards.

Fig. 16.8: Neck should be examined for left supraclavicular lymph node enlargement in all abdominal masses.

Diagnosis of diseases is often easy; often difficult and often impossible—William Harvey

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A

B

Figs 16.9A and B: (A) Different quadrants in the abdomen. They are four in number formed by two lines—one is vertical midline through the umbilicus; another is horizontal line passing through the umbilicus. Quadrants are—right upper, right lower, left upper and left lower, (B) Regions in the abdomen. Regions in the abdomen 1. 2. 3. 4. 5. 6. 7. 8. 9.

Right hypochondrium Epigastric region Left hypochondrium Right lumbar region Umbilical region Left lumbar region Right iliac fossa Hypogastrium Left iliac fossa

Abdomen is divided into nine regions by four lines. 1. Upper horizontal or transpyloric line is mid-way between the umbilicus and xiphisternum. 2. Lower horizontal line is transtubercular line at the level of two tubercles on the iliac crest. 3. Right vertical line is the line through the midpoint of right anterosuperior iliac spine and pubic symphysis. 4. Left vertical line is the line through the midpoint of left anterosuperior iliac spine and pubic symphysis.

MASS IN THE RIGHT HYPOCHONDRIUM

Fig. 16.10: Mass abdomen.

Liver Palpable as Mass in Right Hypochondrium xx xx xx xx

It is horizontally placed. It usually moves with respiration. Upper border is not felt. It is dull on percussion (This dullness continues over liver dullness above). xx Fingers can not be insinuated under right costal margin. Conditions where liver gets enlarged: 1. Soft, smooth, nontender liver:  Hydrohepatosis: It is due to obstruction of CBD causing dilatation of intrahepatic biliary radicles.  Congestive cardiac failure.  Hydatid cyst of the liver: Here mass is well-localised in the liver with typical hydatid thrill. Three finger test: Three fingers are placed over the mass widely. When central finger is tapped fluid movement is elicited in lateral two fingers.

Fig. 16.11: Different causes of mass abdomen.

Differential Diagnosis of Mass Abdomen 2. Soft, smooth, tender liver:  Amoebic liver abscess: Here liver often gets adherent to the anterior abdominal wall and will not move with respiration. Intercostal tenderness, right-sided pleural effusion are common. 3. Hard, smooth liver:  Hepatoma (HCC): Here a large, single, hard nodule is palpable in the liver. But occasionally there can be multiple nodules when it is multicentric. Rapidly growing tumour can be soft also. Hepatoma often can also be tender due to tumour necrosis or stretching of the liver capsule. Vascular bruit may be heard over the liver during auscultation. It mimics amoebic liver abscess in every respect.  Solitary secondary in liver.

xx Kidney mass arising from upper pole of the kidney: It may be due to renal cell carcinoma or hydronephrosis.

A

B

Figs 16.13A and B: Multiple secondaries in liver with umbilication. It is due to central necrosis. Secondaries are the most common malignant tumour of the liver. It could be from GIT or extra-gastrointestinal sites like from breast, lungs, melanoma, thyroid, prostate, kidneys, etc. Patient with liver secondaries has got poor general condition. It should be differentiated from multicentric hepatoma. It is usually treated by palliative chemotherapy. Solitary secondary from carcinoma colon can be removed by segmentectomy.

A

MASS IN THE EPIGASTRIUM

B

Figs 16.12A and B: (A) Hepatocellular carcinoma/hepatoma. It is common in right lobe, unicentric, attains large size; (B) Large upper abdomen mass—could be liver mass, pancreatic mass, retroperitoneal mass. 4. Hard, multinodular liver:  Multiple secondaries in liver: Here hard nodules show umbilication which is due to central necrosis.  Macronodular cirrhotic liver.

Palpable Gallbladder in Right Hypochondrium xx xx xx xx

It is smooth and soft (except in carcinoma gall­bladder). It is mobile horizontally (side-to-side). It moves with respiration. It is located right of the right rectus muscle, below the right costal margin or below the lower margin of the palpable liver. xx It is dull on percussion. Conditions where gallbladder is palpable: 1. Soft, nontender gallbladder:  Mucocele of the gallbladder.  Enlarged gallbladder in obstructive jaundice due to carcinoma head of the pancreas or peri­ampullary carcinoma or growth in the CBD. 2. Hard gallbladder:  Carcinoma gallbladder. 3. Tender gallbladder—empyema GB.

Other Masses in the Right Hypochondrium xx Pericholecystic inflammatory mass: It is tender, smooth, firm or soft, nonmobile, intra-abdominal mass often with guarding.

Palpable Left Lobe of the Liver xx xx xx xx xx

It is in the epigastric region. Its upper border cannot be felt. It moves with respiration. It extends towards left hypochondrium. It is dull on percussion. Conditions where left lobe of the liver is palpable

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Hepatoma Amoebic liver abscess in left lobe Left lobe secondaries Hydatid cyst of the left lobe

Features of Stomach Mass xx xx xx xx xx xx xx xx xx xx xx

It is located in the epigastric region. It moves with respiration. It is intra-abdominal. It is resonant or impaired resonant on percussion. Mass may be better felt on standing or on walking. Mass is often mobile, unless it gets adherent posteriorly. In pylorus mass, all margins are well felt which is mobile with features of gastric outlet obs­truction. Mass from the body of the stomach is horizontally placed without any features of obstruction. Mass from the upper part of the stomach near the OG junction causes dysphagia. Mass from the fundus of the stomach is in the upper part of the epigastric region towards left side. Carcinoma stomach is nodular and hard. It is the most common cause for stomach mass. Leiomyoma of stomach is smooth and firm.

As beds and couches vary in height, the examiner to palpate the abdomen, if need be, must sit on a suitable chair or even kneel upon the floor, no matter how undignified this may appear. — Charles P

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SRB's Manual of Surgery xx Baid test: As the stomach is pushed in front, Ryle’s tube when passed, can be felt per abdomen on palpation.

A

B

C A

B

Figs 16.16A and B: (A) Pseudocyst of pancreas—CT scan picture; (B) Pseudocyst of pancreas presenting as epigastric mass.

Cystadenocarcinoma of the Pancreas Mass is smooth, firm, does not move with respiration, nonmobile, resonant on percussion. Patient com­plaints of back pain.

D

E

Figs 16.14A to E: Carcinoma pylorus causes gastric outlet obstruction with palpable mass above the umbilicus. Carcinoma body of stomach mainly presents as loss of appetite and decreased weight with horizontally placed stomach mass. Carcinoma from fundus of the stomach presents as mass abdomen with loss of appetite and weight. Carcinoma oesophagogastric (OG) junction presents as dysphagia. Carcinoma stomach is one of the common causes of secondaries in liver.

Colonic Mass xx It is due to carcinoma of transverse colon. xx It is mobile, horizontally placed, nodular, hard mass which does not move with respiration. Caecum will be dilated and palpable. xx It is resonant or impaired resonant on percussion. xx Patient will be having bowel symptoms, loss of appetite and decreased weight.

Para-aortic Lymph Node Mass xx Mass in the epigastric region which is deeply placed, nonmobile, not moving with respiration. xx It is vertically placed, above the level of the umbilicus and resonant on percussion. xx Causes for enlargement are: Secondaries, lymphomas or tuberculosis.

Aortic Aneurysm It is smooth, soft, pulsatile (expansile pulsation which is confirmed by placing the patient in knee-elbow position). It is vertically placed above the level of the umbilicus, nonmobile, not moving with respiration and resonant on percussion.

Fig. 16.15: Epigastric mass arising from carcinoma stomach.

Pseudocyst of the Pancreas xx Mass in the epigastric region. It is smooth, soft. It can be tender if it is infected. xx It does not move with respiration. xx It is not mobile. xx It has got transmitted pulsation. It is confirmed by placing the patient in knee-elbow position. xx Lower border is well felt. Upper border is not clear. xx It is resonant on percussion.

MASS IN THE LEFT HYPOCHONDRIUM Enlarged Spleen xx Spleen has to enlarge three times to be palpable clinically. xx It enlarges towards the right iliac fossa from left costal margin. xx It moves with respiration, mobile, obliquely placed, smooth, soft or firm, with a notch on the anterior edge which is directed downwards and inwards. xx Fingers cannot be insinuated over the upper border. xx “Hook sign” is positive, i.e. one cannot insinuate the fingers under the left costal margin. xx It is dull on percussion.

Differential Diagnosis of Mass Abdomen

A

B

Figs 16.17A and B: (A) Hepatosplenomegaly is the common condition (clinical entity). It is due to macronodular cirrhosis with portal hypertension, lymphoma, autoimmune diseases, congestive cardiac failure, hepatoma with portal hypertension, haemolytic diseases, etc. There may be ascites, supraclavicular palpable lymph node and pleural effusion (right-sided); (B) Method of palpating spleen.

A

B

Figs 16.19A and B: Renal (Kidney) punch. Renal angle should be palpated for tenderness. Renal angle is junction of 12th rib and erector spinae. On percussion it is normally resonant as it is occupied by colon. It is replaced by kidney in kidney enlargement. Renal angle should be inspected, palpated and percussed in sitting position from behind.

Palpable Kidney Mass Left-sided Colonic Mass xx It is mobile, nodular, resonant. xx It does not move with respiration. xx It is commonly due to carcinoma colon.

Left Renal Mass from Upper Pole of any Cause It has got features of renal mass.

Left-sided Adrenal Mass xx It does not move with respiration. It is not mobile. xx It is deeply placed mass. Often it crosses the midline. xx It is resonant on percussion. It mimics kidney mass.

Mass Arising from the Tail of the Pancreas Clinical features are same as other pancreatic masses. Causes are pseudocyst in tail of the pancreas and cystadenomas.

MASS IN THE LUMBAR REGION

xx There is fullness in the loin which is better observed in sitting position. xx Mass moves with respiration. It is vertically placed. xx It is bimanually palpable. It is ballotable. xx Renal angle is dull on percussion (normally it is resonant due to colon). xx There is a band of resonance in front due to reflected colon. xx It does not cross the midline.

Conditions Where Kidney Gets Enlarged Hydronephrosis: xx It is smooth, soft, lobulated, nontender mass, nonmobile. Pyonephrosis: xx History of throbbing pain in the loin, pyuria and fever with chills. xx It is smooth, soft and tender kidney mass, nonmobile. Polycystic kidney: xx History of loin pain and haematuria. xx Hypertension, anaemia and features of renal failure. xx Usually bilateral. But one side can present early than on the other side. xx Lobulated smooth surface. Renal cell carcinoma: xx History of mass in the loin, haematuria, fever and dull pain. xx Mass is nodular and hard. xx It does not cross the midline. xx Initially mobile; eventually it infiltrates gets fixed and becomes nonmobile.

Mass from the Ascending Colon on Right Side or Descending Colon on Left Side

Fig. 16.18: Kidney should be palpated bimanually with two hands. Ballotability also should be checked.

xx History of altered bowel habits with decreased appetite and weight. xx Mass is nodular, hard which does not move with respiration and is not ballotable. xx It is resonant or there is impaired resonance on percussion. xx Renal angle is resonant. xx Proximal dilated bowel may be palpable.

After every end is a new beginning and every beginning has an end.

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SRB's Manual of Surgery Adrenal Mass xx xx xx xx xx xx

It is nodular and hard. It does not move with respiration. It is not mobile and often crosses the midline. It is felt on deep palpation. It is resonant in front. It is not ballotable.

Retroperitoneal Tumours xx They are not mobile, resonant and do not fall forward in kneeelbow position. xx They are deeply placed mass which are usually smooth and hard. xx They may be retroperitoneal sarcomas or teratomas or lymph node mass.

Cystic lesions in the abdomen ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Mucocele/empyema of gallbladder Pseudocyst of pancreas Hydatid cyst of liver Congenital nonparasitic cyst of liver Hydronephrosis Mesenteric cyst Ovarian cyst Omental cyst Aneurysm Retroperitoneal cyst Cystadenocarcinoma of ovary Loculated ascites

MASS IN THE UMBILICAL REGION Usual masses are: ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Fig. 16.20: Palpation of mass in knee-elbow position. Mobility and falling forward should be confirmed in knee-elbow position.

Mesenteric cyst Omental cyst Ovarian cyst (pedunculated) Small bowel tumours Extension of masses from other region Transverse colon mass Mass in the body of pancreas Mesentery mass Lymph node mass—secondaries (primary from GIT, testis, ovary, melanoma)/lymphoma/tuberculosis Retroperitoneal tumour

Mesenteric Cyst xx Tillaux triad: 1. Soft intra-abdominal umbilical mass. 2. Mobile in the direction perpendicular to the attachment of the mesentery. 3. Resonant mass. xx May precipitate intestinal obstruction, volvulus.

Omental Cyst xx It is smooth, soft and nontender. xx It moves with respiration. It is mobile in all directions. xx It is dull on percussion.

Small Bowel Swellings xx Small bowel lymphomas. xx Small bowel carcinomas. xx Intussusception.

Intussusception Fig. 16.21: Retroperitoneal tumour.

Retroperitoneal Cysts They are smooth and soft with the same features as retroperitoneal tumours.

xx Mass in umbilical region usually towards left and above the umbilicus. xx Occasionally towards right side. xx Mass is intra-abdominal which is sausage shaped, with concavity towards umbilicus, well-defined, smooth, firm and mobile. xx Mass does not move with respiration. xx Mass contracts under palpating fingers.

Differential Diagnosis of Mass Abdomen xx Often mass disappears and reappears. xx Mass is resonant or there is impaired resonance on per­cussion. xx “Red currant gelly” stool with features of intestinal obstruction may be present.

MASS IN THE RIGHT ILIAC FOSSA

Ileocaecal Tuberculosis xx Mass in the right iliac fossa which is smooth, hard, resonant and nontender. xx It does not move with respiration and has restricted mobility. xx Caecum may be pulled up to lumbar region due to fibrosis.

Amoeboma xx History of dysentery with pain in the right iliac fossa. xx Smooth, hard, well-defined mass in the right iliac fossa which is nonmobile. xx It may or may not be tender.

Psoas Abscess xx It is localised, smooth, soft, nonmobile mass in the right iliac fossa. xx Psoas spasm (flexion of the hip joint) is typical. xx Spine may show gibbus, tenderness, paraspinal spasm. Spinal movements will be restricted. Fig. 16.22: Mass in right iliac fossa. All possible differential diagnosis should be considered and clinically analysed. Common masses are appendicular mass; carcinoma caecum; ileocaecal tuberculosis; lymph node mass; ameboma. ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Appendicular mass or abscess Carcinoma caecum Ileocaecal tuberculosis Amoeboma Psoas abscess Lymph node mass either mesenteric or external Iliac lymph nodes Bony swellings Ectopic kidney Undescended testis (Abdominal) Actinomycosis Crohn’s disease Iliac artery aneurysm Ovarian swelling-ovarian cyst Tubo-ovarian mass Uterine mass like pedunculated fibroid

Appendicular Mass xx It is smooth, firm, tender mass in the right iliac fossa. xx It is not mobile. It does not move with respiration. xx It is resonant on percussion. It is well-localised mass with distinct borders.

Appendicular Abscess It is smooth, soft, tender and dull mass in the right iliac fossa with indistinct borders.

Carcinoma Caecum xx It is nodular, hard, mass in the right iliac fossa. xx It does not move with respiration. xx It is mobile but mobility may be restricted once it gets adherent to psoas muscle. xx Mass is resonant or there is impaired resonance on per­cussion. xx Often features of intestinal obstruction may be present.

MASS IN THE LEFT ILIAC FOSSA ™™ ™™ ™™ ™™ ™™ ™™ ™™

Carcinoma sigmoid or descending colon Bony masses Ovarian/uterine masses Psoas abscess Ectopic kidney Lymph node mass Undescended testis

MASS IN THE HYPOGASTRIUM Bladder Mass xx It is in the midline. It is dull on percussion. Lower border is not felt. xx It can be mobile in horizontal direction. Mass reduces in size after emptying the bladder. It can be felt on per-rectal examination. xx It is either carcinoma bladder (common) or leio­myoma or sarcoma bladder.

Uterine Mass xx It is midline mass which is smooth, hard. xx Lower border is not felt which extends into the pelvis. xx It is felt on pervaginal examination.

Ovarian Mass Pelvic soft tissue mass. In all lower abdomen masses P/R and/or P/V is a must. In all regions parietal masses can occur: xx Benign and malignant soft tissue tumours. xx Common, is lipoma. xx Fatty hernia of linea alba. xx Desmoid tumour. xx Parietal wall abscess. Blaxland ruler test (Athelstan J Blaxland): A flat ruler placed on the lower abdomen just above the anterosuperior iliac spines and pressed firmly backwards. In ovarian cyst, aortic pulsation is transmitted to fingers through ruler; it is not so in ascites.

Smiles are free—don’t save them. The world always looks brighter from behind a smile.

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Carnett’s test The patient, in lying down position, is asked to lift both legs off the bed with knee extended. This puts the abdo­minal muscles into contraction. Intra-abdominal mass becomes less prominent, parietal mass persists as same, but becomes less mobile.



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Fig. 16.23: Looking for minimal ascites in knee-elbow position— Puddle sign.

(para-aortic)/retroperitoneal mass do not show any mobility; cystadenocarcinoma of pancreas may show false mobility (tree top mobility) Percussion is very important method of examination to find out the anatomical plane of the mass. Mass in front of the bowel like liver/spleen/gallbladder/parietal mass are dull on percussion. Mass from the bowel is resonant on percussion like from stomach, small bowel and colon. Retroperitoneal masses like cyst, sarcoma, nodal mass, aneurysm, pancreatic mass are resonant on percussion Succussion splash and auscultopercussion tests are done for gastric outlet obstruction in pyloric stenosis Digital examination of rectum (PR) and left supraclavicular examination for nodes is a must. PR is done to see Blumer shelf secondaries in rectovesical pouch. Pervaginal examination should be done in pelvic mass in females Bladder should be emptied while examining pelvic mass Bimanual examination is done often under general anaesthesia in case of pelvic mass Auscultation for bruit depends on condition and location of mass—over epigastrium, over liver Other relevant systemic examination is a must in examination of mass abdomen—respiratory system, skeletal and neurological systems

Mass that appears and disappears

Investigations for Mass Abdomen xx Haematocrit, liver function tests, renal function tests, stool/ urine examination. xx Ultrasound abdomen. xx Endoscopies-gastroscopy-colonoscopy-ERCP-MRCP. xx Barium studies-Barium meal-Barium enema-Barium meal follow through. xx CT scan-MRI. xx Endosonography. xx Ascitic tap. xx Diagnostic laparoscopy. xx Ultrasound-guided/CT-guided biopsy. xx IVU/RGP/Cystoscopy/Isotope renogram. xx Exploratory laparotomy.

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Pseudocyst of pancreas (communicating) Hydronephrosis (intermittent) Choledochal cyst Intussusception

Srinivasan Costal Sign Srinivasan costal sign is an inspectory finding to assess the acute distended abdomen secondary to surgical or post-operative status or medical causes under treatment. The bilateral costal margin is visualised tangentially on the either side of the abdomen in supine position to appreciate this costal sign.

Note ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Hard mass in the abdomen is commonly malignant Firm mass may be tuberculous, lymphoma or many benign conditions Soft masses are hydronephrosis, pseudocyst, mesenteric cyst, omental cyst, and loculated ascites In tuberculosis abdomen may be doughy due to thickened parietal peritoneum or omentum It is difficult to elicit fluctuation in the mass abdomen as mass cannot be fixed properly Plane of the swelling should be checked by leg raising/head raising test/Valsalva manoeuvre/knee elbow test Bimanual palpation, ballotability, renal angle inspection, palpation and percussion should be done in case of renal mass Intrinsic mobility should be checked. Different mobilities/ movements are—gallbladder shows side to side; stomach lateral; ovarian mass—all over; mesenteric cyst—right angle to line of mesentery; transverse colon mass—vertical; small bowel mass all over; appendicular mass/pancreatic mass/nodal mass

Contd...

B

A

C

Figs 16.24A to C: Srinivasan costal sign: This sign can be appreciated under inspection, the costal margin which is not visible or poorly visible in case of distended abdomen. Once the acute abdomen or distended abdomen secondary to medical cause start settling, the costal margins become visible and prominent, this holds good even in case of fatty protuberant abdomen.

Differential Diagnosis of Mass Abdomen “Prominence of costal margins will be lost in distended abdomen. During therapy, once distension reduces, prominence of costal margins will be visible (during recovery)”.

• •

Acknowledgements With kind permission, from Professor Narayanaswamy Srinivasan, MS, FRCS, who was earlier worked as HOD, General Surgery, Bangalore Medical College; Director of Sanjay Gandhi Accident Hospital and Research Institute, Byrasandra, Bengaluru; Dean and Director of Bangalore Medical College and Research Institute, Bengaluru; Joint Director of Medical Education, Government of Karnataka, India.

DIGITAL RECTAL EXAMINATION FOR PROSTATE AND OTHER CONDITIONS (By kind permission from Professor Laxman Prabhu, MS, MCh, Urologist, Kasturba Medical College, Mangaluru) Rectum is the Dictum

—anonymous

The prostate by virtue of its placement just anterior to the rectum easily tends itself to digital examination. This makes Digital rectal examination (DRE) of the prostate not only easy but an effective method of clinical assessment of prostatic diseases. The prefix ‘digital’ to rectal examination of the prostate became a necessity with the advent of transrectal ultrasound of the prostate (Watanabe et al 1968, 1974) when the two methods of examining the prostate, namely digital (clinician’s forefinger) and sonological per rectum were established as reliable clinical tools. DRE is employed in the following situations specifically with respect to affections of the prostate 1. Grading of benign prostatic enlargements. 2. Local staging of prostatic cancer and in the performance of digitally guided biopsy. 3. In the evaluation of inflammatory disorders of the prostate. 4. To assess the integrity of prostato-membranous urethra in suspected urethral injuries. 5. In the evaluation of ejaculatory dysfunctions.

Note:

•

•

Few generalizations in DRE are essential. The need for a rectal examination is explained to the patient and his consent is taken. The patient is always requested to empty the bladder. During this, urinary samples of initial stream and midstream are collected for culture in sterile wide-mouthed receptacles. Abdominal examination to rule out a distended bladder should always precede examination of the prostate. Findings on DRE of the prostate are unreliable in the presence of a full bladder. Posterior surface of the distended bladder can be erroneously labeled as a large prostate. Uroflowmetry can be performed during voiding to empty the bladder whenever appropriate or if such facility is accessible. It is absolutely essential to ensure privacy. Chaperoning (as insisted while examining a female patient) is not necessary but a caretaker may be allowed to stand next to the patient, especially when the patient is very old and dependent on assistance; presence of a female nurse is better.

•

DRE can be uncomfortable in those patients who are apprehensive and this may persuade the inexperienced clinician to conclude that the patient has a tender prostate. It is recommended that DRE is done only after collecting blood for prostatic specific antigen (PSA) assay as digital manipulation can falsely raise the PSA value ( 150 minutes are other risk factors.

xx Pinkish serosanguineous discharge (salmon-coloured large

quantity of fluid) from the wound. xx Often omentum or coils of intestine are forced out of the wound. xx Clinically burst abdomen can be diagnosed without fail. xx Probing of the wound using gloved finger appreciates dehis-

cence of musculoaponeurotic layer.

B

A

Figs 17.13A and B: Incisional hernia which was repaired earlier has gaped exposing the mesh; (B) Horizontal tension sutures.

Treatment xx Nasogastric aspiration, IV fluids. xx Emergency surgery, i.e. under anaesthesia, wound is opened up properly.  Coils of intestines are replaced into the abdominal cavity. Thorough wash is given. Wound is closed by all layer sutures, passing a nonabsorbable suture material through the red rubber or plastic collar—tension sutures (which is kept for 14 days).  Modified Smead-Jones closure mainly used to prevent burst abdomen—it is interrupted specialised suture used in the closure of abdomen as single layer excluding the skin. Linea alba is held with Allis’ forceps. Number one polyethylene or PDS suture material is used. First bite on one side taken 3 cm away (width) from the margin from outside to inside; it is then passed through the corresponding opposite edge with 3 cm width from inside to outside; later again one small loop of 5 mm width from the edges of each side of the wound from first bite site to second bite site is taken; suture is knotted on the free edge of the first bite side. Full thickness bite holds the suture and maintains the tension in the wound. Smaller loop keeps the linea alba in apposed place. Large curved Ferguson needle

is better to place these sutures. Each suture is placed at 2 cm interval. This is the type of suturing used at present in acute abdominal conditions instead of the retention sutures. Here also it is better to place all sutures under proper vision and knotting is done at the end. At least four knots should be placed. Excessive tension should be avoided. In upper abdomen peritoneum need not be included in the bite; but in lower abdomen as linea alba is indistinct, peritoneum is included in this.  Subcutaneous drain with loose skin sutures are preferred. In severe infection, skin wound is left open and closed as secondary suturing after 14 days.  Problem with immediate closure with forced attempt may cause abdominal compartment syndrome. xx Antibiotics and IV fluids are continued. xx Wound usually heals well without much second dehiscence. Late problem, may be development of incisional hernia. xx Biological dressings, wound vacuum systems are newer modalities used.

Newer present methods of managing the burst abdomen xx If the fascial edges are necrotic, proper debridement of the wound edges is done. One should not attempt forcible wound closure as it will increase intra-abdominal pressure further and re-dehiscence occurs (When fascia is strong and intact primary closure can be done). Wound and contents are covered with absorbable mesh or biological prosthesis like decellularised porcine submucosa and dermis or human cadaveric dermis. They prevent bowel desiccation, bacterial infection. xx Wound vacuum system using—open cell foam, semiocclusive drape over the foam and suction apparatus. It provides immediate coverage, minimises heat loss, by negative pressure it clears interstitial fluid, reduces the bowel oedema and contamination, increases wound blood flow and promotes wound healing. Once wound granulates wound is closed with primary closure or with skin graft or flaps depending on the size of the wound. xx Component separation technique may allow primary fascial closure.

A

B Figs 17.14A and B: Vertical tension sutures.

Truth is what is actually should be. Reality is what is happening. Every reality need not be truthfully right.

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Primary deep fascial closure—deep tension/retention sutures Delayed closure with initial mesh wrap or pack/oppsite or Bogota bag Topical negative (vacuum) pressure closure Delayed skin closure or skin graft over the dehiscence wound once it granulates well. Component separation technique with primary fascial closure Placing drain in subcutaneous plane Suitable antibiotic therapy; fluid management Prevention of abdominal compartment syndrome, haematoma or intra-abdominal abscess formation or sepsis Blood or blood product transfusion; nutrition supplementation

ABDOMINAL WALL TUMOURS B Fig. 17.16B

Figs 17.16A and B: Abdominal wall proliferative ulcer (A) and large tumour, may be fibromatosis of abdominal wall also (B).

A

B

Figs 17.15A and B: (A) Abdominal wall secondaries from carcinoma stomach; (B) Sister Mary Joseph (Nee Julia Dempsey, Mayo clinic USA) metastatic umbilical nodule from carcinoma stomach. xx They are not uncommon but often present late as they are usually asymptomatic. xx Common tumours are lipoma, fibroma, neurofibroma, and fibromatosis. xx Malignant tumours occasionally when occurs, are either from skin or soft tissues. They may be desmoid tumour, soft tissue sarcoma like fibrosarcoma, dermatofibrosarcoma, liposarcoma, umbilical secondaries (Sister Joseph Mary tumour).

A Fig. 17.16A

xx Presents usually as painless progressive swelling. Often ulceration can occur. Attaining large size is also known. It is dull to percuss. On contracting the abdominal wall muscles, swelling becomes prominent and less mobile. xx Differential diagnoses are—abdominal wall abscess, haematoma, intra-abdominal tumours (adherent to abdominal wall). xx US abdomen, CT abdomen is diagnostic. Biopsy is essential. xx Treatment is wide excision with adequate clearance with removal of adjacent skin and musculoaponeurotic layer. Defect is covered with a large mesh.

DESMOID TUMOUR (‘Desmo’ Means Band/Tendon in Greek) xx It is a tumour arising from the musculoaponeurotic layer of

abdomen, below the level of the umbilicus.

xx It is unencapsulated, hard, fibroma, presently classified

under aggressive fibromatosis.

xx 80% of cases occur in women, commonly after deliveries.

It is common over old abdominal operation scars (lower abdomen), may be due to old haema­tomas. Oral contraceptive (OCP) use is more commonly associated with desmoid. xx It is often associated with the familial polyposis colon (FAP), osteomas, odontomes epidermal cysts—Gardner’s syndrome. Desmoid tumour is 1000 times more common in FAP. xx It is a slow growing tumour involving muscle and soft tissue of the abdominal wall, locally spreading, often undergoes myxomatous changes. xx Unlike fibromas, it never turns into sarcoma. xx It is often classified as superficial and deep. It is also classified as abdominal (common in females); extra-abdominal (common in males, common in back, head, scars, chest wall, neck); and peripheral. Histologically it contains multinucleated plasmo­dial giant cells.

Abdominal Wall and Umbilicus Gardner’s syndrome Familial polyposis colon Osteomas ™™ Odontomes ™™ Epidermal cyst—20% ™™ ™™

Management xx The possible association of Gardner’s syndrome is looked for and Barium enema, X-ray, U/S abdomen are done. MRI is useful. Biopsy is done to confirm the diagnosis. xx Wide excision of the tumour with a margin of 2.5 cm is done along with placement of a mesh to the abdominal defect. xx It is moderately radiosensitive. xx Drugs like sulindac and tamoxifen are also used. xx Chemotherapeutic agents like doxorubicin, actinomycin D, dacarbazine, carboplatin are used but with significant toxicity. xx Recurrence rate is high—20–40%.

Fig. 17.17: Recurrent abdominal wall tumour. It may be fibromatosis or recurrent dermatofibroma.

EXOMPHALOS (Omphalocele) xx It is the failure of all or a part of the gut to return to the coelomic cavity during early foetal life, as coelomic cavity has not developed properly.

Fig. 17.18: Exomphalos.

Fig. 17.19: Exomphalos major. Note the liver, small and large bowel. xx Sac covering the content is very thin, consists of three layers—outer amniotic membrane, middle Wharton’s jelly and inner peritoneal layer. Sac may get ruptured during birth. xx Omphalocele is often associated with congenital anomalies of cardiac and genitourinary system—70%. xx Vitellointestinal anomaly, diaphragmatic hernia, malrotation can co-exist, exomphalos, macroglossia, gigantism (EMG) can co-exist in 2/3 of such babies—is called as Beckwith-Weidemann syndrome. xx Chromosomal trisomies—13, 15, 18 and 21, bladder extrophy, imperforate anus, sacral vertebral anomaly, meningomyelocele. xx Abdominal wall defect can be confirmed in utero by US. Amniocentesis and chromosomal analysis can be done. This will allow deciding the possible need for termination of pregnancy, or management plan immediately after delivery. xx Abdominal wall muscle is normally developed but peritoneal layer is hypoplastic.

Types Two types: Differences between exomphalos minor and exomphalos major Exomphalos minor

Exomphalos major

Small sac

Large sac

Defect < 5 cm

Defect > 5 cm

Content is small bowel only

Liver, small and large bowel

Primary closure is possible

Primary closure is not possible

Good prognosis

Poor prognosis

Exomphalos minor: xx Here the sac is small and umbilical cord is attached to the summit, with small bowel as the content. Treatment for E. minor is relatively easier. The sac has to be twisted so as to reduce the content to the peritoneal cavity through the umbilical defect and the abdomen is strapped. Later the defect is closed (Defect is < 5 cm).

Difficulties come not to obstruct, but to instruct.

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aspirin, ibuprofen, pseudoephedrine during 1st trimester and who regularly smoke and take alcohol. xx Umbilicus is normal. The defect is almost always to the right of an intact umbilical cord. Evisceration of the bowel occurs through the defect during intra­uterine life. There is no peritoneal sac and the irritating effect of amniotic fluid causes chemical peritonitis with formation of a thick, oedematous membrane. xx Nonrotation and intestinal atresia are common associations (15%). Cardiac anomaly is not common as in omphalocele. xx After delivery, these infants are more prone for fluid loss, hypothermia, hypovolaemia, sepsis, metabolic acidosis. xx Necrotising enterocolitis is also common in such infants (20%). They are also more prone for paralytic ileus.

Fig. 17.20: Diagram showing differences between exomphalos minor and exomphalos major. xx As there is hardly any properly developed abdomi­nal cavity, it is not possible to reduce the contents to the peritoneal cavity. So initially, relaxing incisions are placed over the lateral abdominal wall and also the subcutaneous layer has to be undermined so as to accommodate, whatever possible contents in the cavity. The contents are not to be forced into the cavity, which in turn may cause intestinal obstruction, respiratory distress, venous engorgement. xx Often a sterile polythene bag (Silastic silo) can be wrapped over the content carefully. Gradual twisting of the bag over the summit at regular intervals over two to three weeks will stimulate the peritoneal cavity to increase in capacity and eventually the contents get reduced. Later the defect is closed properly. xx Antibiotics, IV fluids, nutritional support are required during this period. xx Mortality is higher in spite of all these—due to sepsis, dehydration, hypothermia and respiratory failure. xx Late ventral hernia should be corrected at later period. Management of exomphalos ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Vitamin K injection, TPN Sepsis control with antibiotics Evaluation for other anomalies In E. major when sac is intact application of 0.5% mercurochrome with 65% alcohol to promote granulation tissue formation Prevention of aspiration Prevention of hypothermia Wrapping the content with sterile bag/wrapper Correction of dehydration Definitive surgical procedures like release incisions and closure

GASTROSCHISIS (Belly Cleft) xx It is a defect of the anterior abdominal wall just lateral to the umbilicus. It is common in premature babies. xx It is associated with defect in the involution of 2nd umbilical vein. It is common in mothers younger than 20 years, those who take,

B

A

Figs 17.21A and B: Gastroschisis.

Treatment General: ™™ Fluid management ™™ TPN ™™ Antibiotics ™™ R-T aspiration ™™ Calorie supplement.

Specific: xx Later under GA, intestines are pushed into the abdomen through the defect and defect is closed with interrupted nonabsorbable sutures. Often when bowel is not accommodating in the abdominal cavity, bowel is initially placed in sterile silastic silo bag. In later period, it is pushed into the abdomen gradually. Often a part of the bowel may not be viable, then resection and anastomosis has to be done. xx With proper surgery, nutrition, resuscitation, survival rate is 90% which is better than omphalocele. xx Prolonged postoperative ileus is the common problem in these patients. Exomphalos

Gastroschisis

1. Defect through umbilicus 2. Covered by sac which has three layers 3. Associated with anomalies

1. Defect lateral to umbilicus 2. No peritoneal sac 3. Not associated (except malrotation)

RECTUS SHEATH HAEMATOMA xx Rectus abdominis muscle is supplied by superior and inferior epigastric arteries. Injury to one of these vessels will cause bleeding and haematoma in rectus sheath.

Abdominal Wall and Umbilicus xx Commonly it is due to bleeding from inferior epigastric artery in the lower abdomen. Causes ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Trauma Surgery Spontaneous haematoma, typhoid fever Blood dyscrasias, haemophila, anticoagulant therapy Severe straining and exercises Tetanus and other convulsions Patients on anticoagulants Puerperium.

xx Aspiration will show pus. xx Should be ruled out from intra-abdominal mass, cold abscess, parietal hernia. xx Ultrasound and needle aspiration is confirmative.

Treatment It is antibiotics and drainage under general anaesthesia.

Features xx Common in females. xx Sudden onset of swelling in lower abdomen, which is tender, warm, firm on one side of the abdomen. Swelling does not cross the midline. xx Bluish discoloration over the swelling. xx US and aspiration confirms the diagnosis. xx Should be differentiated from other masses and parietal hernias. xx Coagulation profile is a must. xx CT scan abdomen is often needed.

Treatment xx Usually conservative with analgesics and antibiotics. xx Angiographic embolisation of inferior epigastric artery. xx Occasionally requires drainage of haematoma and ligation of inferior epigastric artery.

ABDOMINAL WALL ABSCESS Causes Infected haematoma Umbilical sepsis spreading into the abdominal layers causing the abscess ™™ Blood spread from distant focus. ™™ ™™

B

A

Figs 17.23A and B: (A) Abdominal wall abscess; (B) Postoperative abdominal wall abscess.

MELENEY’S PROGRESSIVE SYNERGISTIC BACTERIAL GANGRENE OF ABDOMINAL WALL xx It is due to infection by microaerophilic streptococci, staphylococci and other anaerobes of the postoperative abdominal or thoracic wounds. xx It is common in HIV, diabetic and immunosuppressed people. xx Sudden pain, redness, blackening and gangrene of the skin of the abdomen with abdominal wall necrosis. xx Toxicity, septicaemia, renal failure can occur.

Treatment xx Antibiotics like penicillins and metronidazole. xx Excision of necrotic and gangrenous tissue until it bleeds.

B

A

Figs 17.22A and B: (A) Abdominal wall abscess in a child; (B) Abdominal wall infection with a wound.

Features xx Tender, soft/firm swelling which is well-localised, adherent to skin and abdominal muscles underneath and not mobile.

Fig. 17.24: Severe abdominal wall sepsis in a postoperative patient.

A deaf husband and a blind wife are always a happy couple.

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Blood transfusion, nutrition supplement. Maintaining adequate urine output. Management of toxaemia, hyperbaric oxygen and critical care. Skin grafting and coverage, when it granulates well.

DIVaRICATION OF RECTI (DIASTASIS RECTI) xx It is thinning of linea alba in midline in epigastrium. xx Abdominal wall protrudes in midline with prominent divaricated edges of both recti. xx Transversalis fascia remains intact and hence hernia will not be present; so impulse on coughing will be absent. xx Diastasis will become prominent on lifting the head from the bed. xx It does not require any treatment.

Fig. 17.25: Divarication of the recti with visible mass in epigastrium.

Chapter

18

Hernia CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™

Introduction Aetiology Parts of Hernia Classification of Hernia Inguinal Hernia –– Surgical Anatomy of Inguinal Canal –– Classification of Inguinal Hernia –– Indirect (Oblique) Inguinal Hernia –– Direct Inguinal Hernia

–– Recurrent Hernia –– Hernioplasty –– Malgaigne Bulging –– Incarcerated Hernia ™™ Strangulated Hernia ™™ Sliding Hernia ™™ Pantaloon Hernia ™™ Femoral Hernia ™™ Ventral Hernia ™™ Incisional Hernia ™™ Umbilical Hernia

INTRODUCTION Hernia means—’To bud’ or ‘to protrude’, ‘off shoot’ (Greek) ‘rupture’ (Latin). xx A hernia is defined as an area of weakness or disruption of the fibromuscular tissues of the body wall. Often hernia is also defined as an actual anatomical weakness or defect. 75–85% of abdominal wall hernias are groin hernias. 15% of males and 5% of females will develop groin hernia. Presently all hernias in groin are grouped as groin hernias. But in this chapter discussion of the indirect/ direct/femoral hernias are given, in detail as it is still practiced and followed in most of the centres and still it is important when surgical technical aspects are considered. xx Hernia is defined as an abnormal protrusion of a viscous or a part of a viscous through an opening, artificial or natural with a sac, covering it. xx Inguinal hernia is the most common hernia (73%) because the muscular anatomy in the inguinal region is weak and also due to the presence of natural weakness like deep ring and cord structures. Indirect is more common than direct. xx Femoral is 7%; umbilical is 8.5%; others are 1.5% (Excluding incisional hernia). xx In general, incisional hernia is next to inguinal hernia in occurrence–15%.

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Paraumbilical Hernia Epigastric Hernia Spigelian Hernia Obturator Hernia Richter’s Hernia Lumbar Hernia Phantom Hernia Sciatic Hernia Complications of Hernia Surgery Parastomal Hernia

xx Groin hernia is 25 times more common in men than women. Indirect inguinal hernia is commonest hernia in men and women. Femoral hernia s more common in females (10:1); umbilical and incisional hernias are also common in females (2:1).

Fig. 18.1: Common and rare sites of hernias.

In order to achieve a radical cure of inguinal hernia it is absolutely essential to restore those conditions in the area of hernial orifice which exist under normal circumstances. —Edoardo Bassini

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A

B

C

Figs 18.2A to C: Note the clinical look of indirect inguinal (commonest), direct inguinal and femoral hernias.

Fig. 18.3: Large ventral hernia in the lower abdomen.

Fig. 18.5: Epigastric hernia.

AETIOLOGY xx Straining. xx Lifting of heavy weight. xx Chronic cough (tuberculosis, chronic bronchitis, bronchial

asthma, emphysema).

xx Chronic constipation (habitual, rectal stricture). xx Urinary causes

Fig. 18.4: Incisional hernia; common in lower abdomen.

 Old age—BPH, carcinoma prostate.  Young age—stricture urethra.  Very young age—phimosis, meatal stenosis.

xx Obesity.

Hernia xx Pregnancy and pelvic anatomy (especially in femoral hernia

Sac is a diverticulum of peritoneum with mouth, neck, body and fundus. Neck is narrow in indirect sac but wide in direct sac. Body of the sac is thin in infants, children and in indirect sac, but is thick in direct and long-standing hernia.

 

in females). xx Smoking. xx Ascites. xx Appendicectomy through McBurney’s incision may injure the ilioinguinal nerve causing right sided direct inguinal hernia.

Fig. 18.8: Diagram showing the differences between indirect and direct sacs.  Hernia without neck: Those hernias with larger mouth

lack neck, e.g. direct hernia, incisional hernia.

 Hernia without sac: Epigastric hernia—it is protrusion

of extraperitoneal pad of fat.  overings of the sac are the layers of the abdominal wall C through which the sac passes. Contents of Sac  Omentum—Omentocele (Epiplocele). Difficult to reduce the sac later, initially it can be reduced easily.  Intestine—Enterocele—commonly small bowel, but sometimes even large bowel.  Difficult to reduce the sac initially.  Richter’s hernia: A portion of circumference of bowel is the content.  Urinary bladder may be the content or part of the posterior wall of the sac—cystocele.  Ovary, often with fallopian tube.  Meckel’s diverticulum—Littre’s hernia.  Appendix in inguinal hernial sac which is often incarcerated—Amyand’s hernia.  Fluid: Fluid is secreted from congested bowel or omentum. It may be an infected fluid or ascitic fluid or blood from the strangulated sac.

Fig. 18.6: Old appendicectomy scar with direct inguinal hernia. It is due to injury to ilioinguinal nerve during appendicectomy. xx An indirect inguinal hernia occurs in a congenital, preformed

sac, i.e. the remains of processus vagi­nalis. Chances of presence of bilateral preformed sac is 60%. xx Familial collagen disorder—Prune Belly syndrome. xx Acquired herniation is also probably due to collagen deficiency called as metastatic emphysema of Read.

PARTS OF HERNIA Hernia comprises of: xx Covering. xx Sac. xx Content.

Note:

•

Fig. 18.7: Parts of hernia. Note the fundus, body and neck of the hernia.

The Groin even though anatomically not a well-defined area, it includes inguinal and femoral regions; both are separated by medial part of the inguinal ligament. Clinically when hip is completely flexed inguinal and femoral regions touch each other and that area is recognised as groin. Sebaceous cyst, lipoma, neurofibroma are swellings arising from integuments; inguinal and femoral hernias; lymphadenopathy; saphena varix and aneurysms are vascular swellings; ectopic testis, lipoma or hydrocele of the cord, hydrocele of the canal of Nuck (in females) are swellings related to inguinal canal; psoas abscess which is deeper—are groin swellings. Common groin swellings are inguinal and femoral hernias, inguinal lymphadenopathy and saphena varix. Groin pain may be due to hernia, funiculitis, varicocele, lymph node diseases or post surgery pain.

Anything the mind of man can conceive and believe, it can achieve.

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SRB's Manual of Surgery which radiates to the adductor region and even the testicles. Symptoms can often be reproduced by performing sit-ups or crunches or with the patient in “frog position”, in which the patient is supine with knees bent and heels together. It is probably due to torn external oblique aponeurosis or conjoint tendon or transversalis fascia or internal oblique muscle or entrapment of ilioinguinal nerve. MRI may be useful. Sleeping in a prone position with the hip on the affected side flexed and externally rotated can be a cure in some individuals. Many eventually require a definitive treatment consisting of surgical repair followed by a structured rehabilitation.

CLASSIFICATION OF HERNIA A

B

Figs 18.9A and B: Hernial sac containing small bowel (enterocele) and omentum (omentocele) in two different patients.

Classification I (Clinical) 1. Reducible Hernia Hernia gets reduced on its own or by the patient or by the surgeon. Intestine reduces with gurgling and it is difficult to reduce the first portion. Omentum is doughy, and it is difficult to reduce the last portion. Expansile impulse on coughing present.

2. Irreducible Hernia Here contents cannot be returned to the abdomen due to narrow neck, adhesions, overcrowding. Irreducibility predisposes to strangulation.

3. Obstructed Hernia It is an irreducible hernia with obstruction, but blood supply to the bowel is not interfered. It eventually leads to strangulation.

Fig. 18.10: Amyand hernia—is appendix in inguinal hernial sac.

Fig. 18.12: Inguinal hernia presenting with features of intestinal obstruction. Note:

Fig. 18.11: Littre’s hernia with Meckel’s diverticulum as content.

• •

Herniography (by Gullmo): Injection of contrast into the peritoneal cavity and taking films in supine and prone positions to diagnose small protrusions of peritoneal sac is called as herniography. It was earlier also used for diagnosing undescended testis. Gilmore’s groin or hockey groin or Athletic pubalgia or hockey/sports hernia, or groin disruption is a condition of the pubic joint in athletes; presents with chronic groin pain and a dilated superficial inguinal ring. Football and ice hockey players are most frequently affected. Present with pain during movements of sports, particularly hip extension, twisting and turning

•

Garrey’s stricture: Constriction that occurs due to ischaemic narrowing of small bowel which has reduced from an obstructed hernia.

4.  Inflamed Hernia It is due to inflammation of the contents of the sac, e.g. appendicitis, salpingitis. Here hernia is tender but not tense; overlying skin is red and oedematous.

5.  Strangulated Hernia xx It is an irreducible hernia with obstruction to blood flow.

The swelling is tense, tender, with no impulse on coughing and with features of intestinal obstruction.

Hernia Classification III: According to the Contents ™™ ™™ ™™ ™™ ™™ ™™ ™™

Omentocele—omentum. Enterocele—intestine. Cystocele—urinary bladder. Littre’s hernia—Meckel’s diverticulum. Note: Littre described Meckel’s diverticulum in a hernial sac 81 years before Meckel was born. Maydl’s hernia. Sliding hernia. Richter’s hernia—part of the bowel wall.

Classification IV: Based on Sites ™™ ™™ ™™ ™™ ™™

Fig. 18.13: Garrey’s stricture on table. Due to ischaemia, a stricture is formed in the bowel at the constriction ring after reduction. xx Features of intestinal obstruction may be absent in case of

™™ ™™ ™™

omentocele, Richter’s hernia, Littre’s hernia.

INGUINAL HERNIA

xx Strangulation is the most serious complication of hernia;

most common strangulated hernia is indirect inguinal hernia. Highest rate of strangulation is seen in femoral hernia (ratio of strangulated femoral hernia to total number of femoral hernia).

Classification II Congenital—Common It occurs in a preformed sac/defect. Clinically may present at a later period due to any of the precipitating causes like in indirect inguinal hernia. Acquired It is secondary to any causes which raise the intra-abdominal pressure leading into weakening of the area like in direct inguinal hernia.

Inguinal hernia—occurring in inguinal canal. Femoral hernia—occurring in femoral canal. Obturator hernia. Diaphragmatic hernia. Lumbar hernia. Spigelian hernia. Umbilical hernia. Epigastric hernia.

SURGICAL ANATOMY OF INGUINAL CANAL Superficial inguinal ring is a triangular opening in the external oblique aponeurosis and is 1.25 cm above the pubic tubercle. The ring is bounded by a superomedial and inferolateral crus. Normally, the ring does not or just admit the tip of little finger. Deep inguinal ring is a U-shaped condensation of the transversalis fascia, lies 1.25 cm above the inguinal ligament midway between the symphysis pubis and the anterosuperior iliac spine. Inguinal (Poupart’s) ligament: It is formed by the lower border of the external oblique aponeurosis which is thickened and folded backwards on itself, extending from anterosuperior iliac spine to pubic tubercle. Inguinal canal: It is an oblique passage in lower part of abdominal wall, 4 cm long, situated above the medial ½ of inguinal ligament, extending from deep inguinal ring to superficial inguinal ring. In infants both superficial and deep rings are superimposed without any obliquity of the inguinal canal. Inguinal canal in female is called as ‘canal of Nuck’. Contents of inguinal canal ™™ ™™ ™™

Spermatic cord in males Round ligament in females Ilioinguinal nerve

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Vas deferens Artery to vas Testicular and cremasteric artery Genital branch of genitofemoral nerve Pampiniform plexus of veins Remains of processus vaginalis Sympathetic plexus around the artery to vas

Contents of spermatic cord

Fig. 18.14: Inguinal hernia on right side in a child. It needs only herniotomy.

When spermatic cord is rolled transversely beneath the gentle pressure of index finger. Thickening of the cord denotes presence of a hernia. — William E Ladd

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SRB's Manual of Surgery Coverings of Spermatic Cord xx Internal spermatic fascia from fascia transversalis. xx Cremasteric fascia. xx External spermatic fascia from external oblique aponeurosis is seen below the external ring in the scrotum.

A

Fig. 18.15: Structures related to cord in the inguinal canal.

B

Fig. 18.16: Surgical anatomy of inguinal canal.

Boundaries In front: External oblique aponeurosis and conjoined muscle laterally. Behind: Inferior epigastric artery, fascia transversalis and conjoined tendon medially. Above: Conjoined muscle (Arched fibres of internal oblique). Below: Inguinal ligament. Defence mechanism of inguinal canal Obliquity of inguinal canal Arching of conjoint tendon ‘Shutter mechanism’ of internal oblique ‘Ball valve mechanism’ due to contraction of cremaster muscle which plugs to superficial ring ™™ When external oblique muscle contracts, intercrural fibres of superficial ring appose causing ‘slit valve mechanism’ ™™ Hormones ™™ ™™ ™™ ™™

C Figs 18.17A to C: Nerves in inguinal canal: Iliohypogastric nerve (T12, L1) runs between transversus abdominis and internal oblique divides into lateral and anterior branches; anterior branch pierces internal oblique 2 cm medial to anterosuperior iliac spine and later pierces the external oblique 3 cm above the superficial inguinal ring to supply abdominal skin above the pubis. Ilioinguinal nerve (L1) pierces the transversus abdominis near anterosuperior iliac spine, pierces the internal oblique just above the internal ring, and enters the inguinal canal within cremasteric fascia outside the cord supplies medial thigh, base of penis and proximal scrotum. Genital branch of genitofemoral nerve (L1, L2) enters the cord through internal ring supplying the cremaster and scrotum.

Fruchaud’s myopectineal orifice It is an osseo-myo-aponeurotic tunnel. It is through this tunnel all groin hernias occur.

Hernia It is bounded: ™™ Medially by lateral border of rectus sheath. ™™ Above by the arched fibres of internal oblique and transversus abdominis muscle. ™™ Laterally by the iliopsoas muscle. ™™ Below by the pectin pubis and fascia covering it.

Fig. 18.19: Location of direct and indirect inguinal hernia and femoral hernia.

Classification II According to the Extent Fig. 18.18: Fruchaud’s myopectineal orifice is bound—by lateral border of rectus, iliopsoas, conjoint tendon, pectin pubis.

CLASSIFICATION OF INGUINAL HERNIA (EARLIER) Classification I Anatomical Classification (in Inguinal Hernia) Indirect hernia It comes out through internal ring along with the cord. It is lateral to the inferior epigastric artery. Direct hernia It occurs through the posterior wall of the inguinal canal through ‘Hesselbach’s triangle’ (bounded medially by lateral border of rectus muscle, laterally by inferior epigastric artery, below by inguinal ligament). Sac is medial to the inferior epigastric artery.

A

B

xx Incomplete:

 Bubonocele: Here sac is confined to the inguinal canal.  Funicular: Here sac crosses the superficial inguinal ring,

but does not reach the bottom of the scrotum.

xx Complete: Here sac descends to the bottom of the scrotum.

Saddle-bag or pantaloon hernial sac has got both medial and lateral component. Note:

Inguinal hernia is above and medial to the pubic tubercle. Femoral hernia is below and lateral to pubic tubercle.

Newer classification of hernia I. Gilbert Classification Type I: Hernia has got snug internal ring through which a peritoneal sac passes out as indirect sac. Type II: Hernia has a moderately enlarged internal ring which admits one finger but lesser than two finger breadth. Once reduced it protrude during coughing or straining.

C

Figs 18.20A to C: (A) Bubonocele; (B) Irreducible left side inguinal hernia. It is above the upper part of the testis (funicular). Taxis is the method used to reduce it; (C) Bilateral complete inguinal hernia. Here hernia descends up to the bottom of the scrotum.

Great minds have purposes, others have wishes.

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SRB's Manual of Surgery Type III: Hernia has got large internal ring with defect more than two finger breadth. Hernia descends into the scrotum or with sliding hernia. Once reduced it immediately protrudes out without any straining. Type IV: It is direct hernia with large full blow out of the posterior wall of the inguinal canal. The internal ring is intact. Type V: It is a direct hernia protruding out through punched out hole/ defect in the transversalis fascia. The internal ring is intact. Type VI: Pantaloon/double hernia. Type VII: Femoral hernia. Type VI and VII are Robbin’s modifications. II. NYHUS Classification Type I: Indirect hernia with normal deep ring. Type II: Indirect hernia with dilated deep ring. Type III: Posterior wall defect. a. Direct. b. Pantaloon hernia. c. Femoral hernia. Type IV: Recurrent hernia.

A

B

Figs 18.21A and B: (A) Indirect inguinal hernia. Right sided bubonocele and left sided funicular; (B) Complete indirect hernia. Coverings of indirect hernia (from inside out) ™™ ™™ ™™ ™™ ™™

Extraperitoneal tissue Internal spermatic fascia Cremasteric fascia External spermatic fascia Skin

Type I: Anterolateral defect (indirect). Type II: Anteromedial (direct). Type III: Posteromedial (femoral). Type IV: Posterior prevascular hernia. Type V: Anteroposterior defect: Inguino-femoral hernia.

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IV. Classification—Casten’s Staging

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Smoking Obesity Respiratory causes like bronchial asthma, tuberculosis, bronchitis Ascites Previous surgery like appendicectomy which can cause direct inguinal hernia Chronic constipation due to anorectal strictures. Rectal stricture may be due to chronic proctitis (amoebic), tuberculosis of anorectum, previous anorectal surgery, rectal carcinoma or stricture due to lymphogranuloma venereum Urinary problems like benign prostatic hyperplasia (BPH), urethral stricture Straining Multiple pregnancies

III. BENDAVID Classification [Type, Staging, Diameter (TSD) Classification]

Stage 1: An indirect hernia with a normal internal ring. Stage 2: An indirect hernia with enlarged internal ring. Stage 3: All direct or femoral hernias. V. Halverson and McVay Classification Class 1: Small indirect hernia. Class 2: Medium indirect sac. Class 3: Large indirect hernia or direct hernia. Class 4: Femoral hernia. VI. Ponka’s Classification 1. Indirect inguinal hernia: –– Uncomplicated indirect hernia. –– Sliding indirect hernia. 2. Direct hernia: –– Small defect on the medial aspect of the Hesselbach’s triangle. –– Diverticular hernia in the posterior wall with an otherwise intact inguinal floor. –– A large diffuse direct inguinal hernia of the entire floor of Hesselbach’s triangle.

Precipitating causes for inguinal hernia

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Types Three types 1. Bubonocele: Where the hernia is limited to inguinal canal. 2. Funicular: Processus vaginalis is closed just above the epididymis. Contents of the sac can be felt separately from testis, which lies below the hernia.

INDIRECT (OBLIQUE) INGUINAL HERNIA xx This is the most common type of hernia (65%). xx It is more common in younger age group as compared to

direct inguinal hernia which is more common in elderly.

xx It is more common on right side in 1st decade but in 2nd

decade, the incidence is equal on both sides.

xx Hernia is bilateral in 30% of cases. xx Sac is thin in indirect type. Neck is narrow and lies lateral

to inferior epigastric vessels.

Fig. 18.22: Surgical anatomy of indirect hernia.

Hernia

Fig. 18.23: Inferior epigastric artery (IEA) on table look during open inguinal hernia repair. 3. Complete (Scrotal): Testis appears to lie within the lower part of hernia. It can occur in any age group. It occurs in a congenital preformed sac (processus vaginalis). More commonly contents descend into the pre-existing sac, only when there are precipi­tating causes which force the content down. Expansile impulse on coughing ™™ ™™ ™™ ™™ ™™

Hernia Laryngocele Meningocele Empyema necessitans Swellings with intracavitary communications like thorax, cranium, and abdomen like dermoid

Clinical Features xx Prevalence of inguinal hernia is 25% in males; 2% in females. xx It is more common in males (20 : 1 :: Male : Female). xx Patient presents with dragging pain and swelling in the groin which is better seen while coughing and stan­ding; and felt together with an expansile impulse (momentary increase or occurrence of the swelling during the act of coughing). xx In complete type, the content descends down to the scrotum completely. On palpation, one cannot get above the swelling.

Fig. 18.24: Types of indirect inguinal hernia.

A

B

Figs 18.25A and B: Left side indirect inguinal hernia (inguinoscrotal swelling); one cannot get above the swelling on palpation. xx Contents are either small bowel, large bowel, omentum or combination of all these. In females, sometimes ovary and tubes may be the content. In infants, swelling appears when the child cries and is often translucent. xx It is usually reducible, but can go for irreducibility, inflammation, obstruction, strangulation. xx Internal ring occlusion test: Internal ring is located half inch above the mid-inguinal point (center point between anterosuperior iliac spine and pubic symphysis). After reducing the contents, in lying down position, internal ring is occluded using the thumb. Patient is asked to cough. If a swelling appears medial to the thumb, then it is a direct hernia. If swelling does not appear and on releasing the thumb swelling appears during coughing, then it is an indirect hernia confirmed in standing position. xx Ring invagination test: After reduction of hernia, the little finger/ index finger of the examiner is invaginated from the bottom of the scrotum, gradually pushed up and rotated to enter the superficial inguinal ring. The impulse on coughing is felt at the tip of the invaginated finger. This test is done only in males. xx Zieman’s test: The examiner places his index finger on the deep inguinal ring and middle finger on the superficial inguinal ring, ring finger over saphenous opening. The patient is asked to cough or to hold the nose and blow. If the impulse is felt on the index finger, it is indirect hernia. xx Head or leg rising test is done to look for abdominal wall muscle tone and Malgaigne bulgings. Valsalva manoeuvre is also used to check the tone of abdominal wall muscles. xx Abdominal, respiratory, urological examination is done to look for any precipitating factors like chronic bronchitis, ascites, stricture urethra, BPH. xx Per rectal examination is a must. xx Inguinal hernia in females: Increased thickness of labium majus on palpation, when compared to contralateral side. xx Silk glove sign: Index finger is invaginated across scrotum towards the external ring. When patient coughs, inguinal hernia is felt as a slit like sensation.

Hydrocele of canal of Nuck is the most common differential diagnosis for inguinal hernia in females.

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SRB's Manual of Surgery Use five fingers of the hand to complete all tests for hernia ™™ ™™ ™™

Thumb—for deep ring occlusion test Index, middle and ring fingers for Zieman’s test Little finger for superficial ring invagination test

™™ ™™ ™™ ™™

Never forget to examine opposite side Never forget to do per rectal examination Never forget to examine urethra Never forget to check abdominal muscle tone

Rules of hernia examination

Differential diagnosis

Fig. 18.26: Zieman’s test. Index finger on deep ring; middle finger on superficial ring and ring finger over saphenous opening—are placed after reducing the content. Patient is asked to cough and impulse is felt in finger corresponding to the existing hernia.

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Hydrocele—infantile/encysted/large vaginal/bilocular Undescended testis Femoral hernia Lipoma of the cord Hydrocele of the canal of nuck (in females) Inguinal lymph node enlargement Groin abscess

Fig. 18.27: Head or leg rising or Valsalva manoeuvre is important to elicit abdominal muscle tone. Note the bilateral inguinal (direct) and right sided femoral hernias; femoral hernia is rare in males. xx Palpation of bulbar urethra for stricture (thickening/crescent like feel/button like depression).

Fig. 18.28: Left side inguinal hernia in a female. In female, commonest hernia is inguinal hernia; but also femoral hernia is common in females.

Fig. 18.29: Differential diagnosis for groin swellings. Indirect inguinal hernia

Direct inguinal hernia

Can occur in any age from childhood to adult

Common in elderly

Occurs in a pre-existing sac

Always acquired

Protrusion through the deep ring; herniation occurs later

Herniation through posterior wall of the inguinal canal

Pyriform/oval in shape; descends obliquely and downwards

Globular/round in shape; descends directly forward bulge

Can become complete by descending down into the scrotum

Descent down into the scrotum is rare

Contd...

Hernia Contd... Sac is anterolateral to the cord

Sac is posterior to the cord

Ring occlusion test does not show any impulse after occluding the deep ring Invagination test shows impulse on the tip of the little finger

Test shows impulse even after occluding the deep ring

Zieman’s test shows impulse on the index finger Commonly unilateral but can be bilateral Obstruction/strangulation are common Sac should be opened during surgery

Test shows impulse on the middle finger Commonly bilateral

Impulse is felt over the pulp of the little finger

A

B

Rare but can occur Sac is not necessarily opened unless obstruction is present

Figs 18.32A and B: Typical enterocele and omentocele.

Investigations xx Chest X-ray to rule out chronic bronchitis. xx Ultrasound abdomen to find out BPH, ascites. xx Tests relevant to other precipitating causes.

Treatment This method reconstructs the inguinal canal as it is physiologically, with two rings, one abdominal, the other subcutaneous; and with two walls, one posterior and the other anterior, between which the spermatic cord passes obliquely. —Edoardo Bassini, 1887

xx Treatment for inguinal hernia is always surgery. However,

A

B Figs 18.30A and B: Indirect and direct inguinal hernias.

asymptomatic direct hernia patients can wait without opting for any surgical intervention. Precipitating causes should be treated or controlled first like treating asthma, tuberculosis, bronchitis, chronic cough, stopping smoking, treating enlarged prostate by TURP (transurethral resection of prostate), etc. TURP and hernioplasty can be combined together.

Note:

Wearing truss should be discouraged. Usually, elective surgery is done; but if it is irreducible or obstructed/or strangulated immediate surgery is the need; especially strangulated hernia which should be operated as an emergency at the earliest.

A

B Figs 18.31A and B: Indirect and direct sacs of inguinal hernia.

In enterocele

In omentocele (epiploecele)

First part is difficult to reduce but last part is easier. There will be gurgling sound on reduction

First part is easier to reduce but last part is difficult. Has a doughy feeling

Resonant on percussion

Dull on percussion

Peristalsis is seen

No peristalsis seen

Bowel sounds may be heard

Bowel sounds not heard

Fig. 18.33: Large hernia with BPH (benign prostatic hyperplasia) with Foley’s catheter in place as patient presented with retention of urine. He underwent transurethral resection of prostate (TURP) first and later hernioplasty was done.

Usually saphena varix feels softer than a femoral hernia.— Robert Milnes Walker

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SRB's Manual of Surgery xx Lichtenstein open tension free onlay hernia mesh (Prolene

mesh) repair (hernioplasty) is the standard treatment (most commonly done) through inguinal (anterior) approach. Hernial sac should be ligated and excised in indirect sac (herniotomy) prior to mesh placement (hernioplasty). Strengthening of the posterior wall is important in all inguinal hernia repairs whether direct or indirect (Either tissue repair or prosthetic repair is used). xx Bassini’s tissue repair (even though lasted for a century; Bassini is father of hernia surgery) is not commonly used now except in strangulated hernia where mesh is contraindicated. Shouldice tissue repair shows less recurrence, but it is technically demanding. New no mesh tension free tissue repair invented by Professor Mohan Desarda from Pune, India as “Desarda no mesh tissue repair” is becoming popular with less recurrence and least postoperative chronic pain. xx In Western countries, most of the open inguinal hernia surgeries are done under local anaesthesia as day care procedure. In developing countries spinal anaesthesia is commonly used. In infants and children and in adult for TEP (Totally Extraperitoneal Preperitoneal mesh repair) and TAPP (Trans Abdominal Pre Peritoneal mesh repair) general anaesthesia is preferred and ideal. xx In infants and children whether inguinal hernia or hydrocele, herniotomy is done through inguinal approach (Michaelis Plank operation); neither tissue repair nor mesh repair is needed (only herniotomy ideally open; can be through laparoscopy).

Procedure: After cleaning and draping, skin is incised 1.25 cm above and parallel to the medial two-thirds of inguinal ligament. Two layers of superficial fascia (outer Camper`s fascia and inner Scarpa’s fascia) are incised. Superficial pudendal and superficial epigastric vessels are ligated with catgut or cauterised. Self-retaining mastoid or similar retractor is placed to retract the skin edges. External oblique aponeurosis is incised along its long axis parallel to the line of skin incision. Incision is extended on either ends of the incision; medially it is extended to cut the margins of the superficial ring. Upper leaf is reflected above and held with haemostat; using peanut dissection upper leaf is raised adequately to visualise conjoined tendon and lateral rectus sheath. Iliohypogastric nerve is identified above and medially which after piercing the internal oblique enters the external oblique. Lower leaf is reflected downwards to visualise and expose the inguinal ligament. Entire inguinal ligament is dissected medially and exposed with its shelving edge and iliopubic tract. Ilioinguinal nerve is safeguarded which is located in the inguinal canal outside the cord. Cremasteric muscle (box) with its fascia is opened longitudinally as medial and lateral flaps. Genital branch of genitofemoral nerve passes through the cord structures. Care should be taken not to injure it. Cremasterectomy is not done, even though it clearly exposes cord and posterior inguinal wall, it causes hanging testis without support (clapper in bell). If there is a lipoma of the cord it should be excised. Cord structures are dissected. Sac lying anterior and lateral to cord is identified and is pearly white in color. Dissection is usually started from the fundus and extended towards the neck which is identified by the extra-peritoneal fat. The neck is narrow and is lateral to inferior epigastric artery. High dissection beyond the deep ring is done. Sac is opened at the fundus. Finger is passed to release any adhesions. Sac is twisted so has to prevent the content from coming back. It is transfixed using absorbable suture material (chromic catgut 2-0 or vicryl) and is excised (redundant sac) distally. In complete hernia, distal scrotal part of the hernial sac can be left in situ as left open/ lay open) without suture ligating the distal end (Wantz procedure). Direct sac is usually not opened unless it shows adhesions or obstruction. Direct sac should be inverted using vicryl or PDS by taking purse string suture around.

Fig. 18.34: Inguinal hernia in a child; here just herniotomy is required. Repair is not done.

Herniotomy Anaesthesia: Spinal or general anaesthesia or local anaesthesia. Urinary catheterisation is better done in large hernia, direct hernia, sliding hernia and old people.

Fig. 18.35: Incision for inguinal hernia surgery (open surgery through anterior approach).

Hernia

A

B

Figs 18.36A and B: Herniotomy—is usually done in indirect sac of inguinal hernia. After twisting to prevent contents getting in, transfixation is done using vicryl; redundant sac is excised.

prosthetic repair. Strengthening by tissue repair has got various approaches where transversalis fascia or tendinous fascio-aponeurotic upper part is approximated to iliopubic tract or Cooper’s ligament or shelved edge of the inguinal ligament. Upper leaf taken for repair should be tendinous fascio-aponeurotic layer not fleshy red muscle. Non-absorbable monofilament sutures like polypropylene should be used ideally. Prosthetic repair is done by placing mesh or prosthesis by onlay/inlay/sublay/sublay intraperitoneal method. Polypropylene mesh is commonly used with different modifications. Tissue prosthesis like tensor fascia lata or temporal fascia is not used now. But an innovative technique as advocated by Mohan Desarda, live aponeurotic tissue is used as prosthesis in his “Desarda no mesh tissue repair” is said to very effective tissue prosthesis repair. Lichtenstein hernioplasty After herniotomy 15 × 8 cm or suitable sized mesh is selected. Mesh is placed deep to the cord structures; below it is sutured to the inguinal ligament using continuous non-absorbable polypropylene sutures; medially it should overlap 2–2.5 cm over the pubic tubercle. Suture should be ended laterally at the level of internal ring. Mesh on its lateral part is slit onto two tails; 2/3rd upper leaf and 1/3rd lower leaf; slit is done up to the internal ring and cord with ilioinguinal nerve is passed in between the tails; upper leaf is overlapped onto

A Fig. 18.37: Lipoma of the cord should be excised during herniotomy.

Hernia Repair Repair may be Pure tissue repair: Desarda, Shouldice, MacVay (Still very useful repairs) and modified Bassini (not used now) ™™ Prosthetic repair: Lichtenstein, Rives, Gilbert, Stoppa, TEP, TAPP ™™

B

C

Approach for repair may be Anterior (inguinal) approach repair: Bassini’s, Desarda, Shouldice, MacVay, darning, Andrew’s, Wilkinson’s, Cooper’s, Lichtenstein mesh repair, PHS repair, Rives preperitoneal mesh repair Posterior approach repair: Through suprainguinal preperitoneal approach—Nyhus repair (tissue or mesh), Kugel’s, Stoppas, TEP, TAPP

It means repair or strengthening of the posterior wall of the inguinal canal. Strengthening can be done by tissue or

D Figs 18.38A to D: Lichtenstein mesh repair—polypropylene is used; often mesh is trimmed.

In exomphalos, the protruding abdominal contents being covered only by a diphanous membrane, through which viscera are exposed to view, as if exhibited in a show case. — William E Ladd

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SRB's Manual of Surgery the lower leaf in front below and is sutured to inguinal ligament at the level of internal ring. Laterally both leaflets are spread up to anterior superior iliac spine for 6 cm. Above and medially mesh is fixed to conjoint tendon using interrupted non-absorbable sutures. Care should be taken to avoid taking bites from the iliohypogastric nerve. Cord is placed on the mesh and external oblique is sutured using same suture material or delayed absorbable suture. Subcutaneous and skin is closed. Recurrence rate has reduced significantly by prosthetic mesh repair. But incidence of mesh inguinodynia has increased due to entrapment of ilioinguinal or iliohypogastric nerves in the mesh.

•

Even though it is a commonly done procedure at present for inguinal hernia, in adolescents whether it should be used or not is a debate. In children, it is not used. It is not done in strangulated hernia or in presence of sepsis where only tissue repair is done. (Different mesh procedures are discussed at a later part of this chapter).

Note:

Other methods of mesh repair are:

• Nyhus pre-peritoneal mesh repair (sublay). • Gilbert mesh repair (patch and plug). Gilbert’s PHS (Prolene Hernia System) repair (onlay and sublay). • Stoppa’s (Rene S Stoppa) giant prosthesis reinforcement of visceral sac (GPRVS- sublay). • Kugel (Rober D Kugel) groin hernia mesh repair (sublay). Tissue repairs are: • Modified Bassini`s Herniorrhaphy: Conjoined tendon and inguinal

ligament are approximated using interrupted non- absorbable monofilament sutures (polypropylene); medial most stitch is taken from the periosteum of pubic tubercle (called as key or Bassini`s stitch); external oblique is closed and other layers are closed. Bassini originally used silk suture for the repair (1887). He also used triple layer of upper leaf which contains transversalis fascia, transversus abdominis and internal oblique muscles in his repair. Care should be taken not to injure iliac vessels (mainly vein) while taking bite from inguinal ligament. It is often practiced to take bites in inguinal ligament at different levels to prevent tearing of the fibres of inguinal ligament. Laterally repair is done beyond the line of internal ring. Few advocate horizontal mattress sutures starting from conjoined tendon to inguinal ligament and from inguinal ligament to conjoined tendon.

Fig. 18.39: Modified Bassini’s repair: It is approximation of inguinal ligament to conjoined tendon using interrupted non-absorbable sutures.

•

Desarda no mesh tension free tissue repair (Professor Mohan Desarda, Pune, India): It is live external oblique tissue flap reconstruction of the posterior wall of the inguinal canal. He proposed that strength

•

of the inguinal canal depends on the aponeurotic extensions from the transverse abdominis aponeurotic arch normally which is physiologically dynamic and strong and his repair supports this effectively with least complications and recurrence. Shouldice repair: Even though transversalis fascia is thin, it is a tough layer and so double breasting of this fascia using continuous sutures (with non-absorbable material) strengthens the posterior wall of the inguinal wall. It is a multilayered repair. Continuous sutures provide even distribution of tension throughout the repair. It was originated at Shouldice hernia clinic in Toronto by Shouldice (EE Shouldice 1930) where it was usually done under local anaesthesia. Often cremasteric resection is done in Shouldice in order to have proper revelation of the posterior inguinal wall. Cremasteric vessels (located at lateral part of the cord along with genital branch of genitofemoral nerve) need ligation during cremasterectomy (it causes hanging testis/clapper in bell). After doing herniotomy as in any other inguinal hernia, transversalis fascia is incised along the line of the wound from deep ring to pubic tubercle. Upper medial flap is elevated without elevating lower lateral flap. First suture line—Lower lateral flap of fascia is sutured to posterior deep part of the elevated upper flap using continuous sutures from pubic tubercle to internal ring which is tied at deep ring without cutting/ ending. Second suture line—Using same suture which is not cut, free margin of upper flap is sutured to the shelving edge of the inguinal ligament from deep ring towards pubic tubercle. It causes double-breasting of the transversalis fascia. Knot is placed at the end over the pubic tubercle. Fist and second line sutures are done using a single suture material. Third suture line—The conjoined tendon and anterior to the shelving part of the inguinal ligament is sutured from internal ring to pubic tubercle continuously and tied without cutting. Fourth suture line—Same uncut suture is again sutured back continuously between conjoined tendon and anterior fibres of the inguinal ligament to reach internal ring. External oblique aponeurosis is sutured in two layers (5th and 6th suture lines; double-breasting) in front of the cord in original Shouldice repair. Hence, this original Shouldice repair is 6-layered procedure. Suture material used here is 34 gauge fine steel wire (in original Shouldice repair) or polypropylene or polyethylene. Recurrence rate in Shouldice repair is 1%. Berliner modified Shouldice repair—It involves double-breasting of the transversalis fascia like in Shouldice repair and single layer closure of the external oblique aponeurosis without any additional two-layered repair of conjoined tendon to inguinal ligament. Lytle`s repair (William James Lytle): Often internal ring is narrowed by placing interrupted sutures over the medial side of the ring to the transversalis fascia using either silk or polypropylene (to narrow the ring and push the cord laterally).

Fig. 18.40: Lytle’s repair is narrowing of the widened internal ring.

•

Halsted (USA)—Tanner (London) slide operation: To reduce the tension in the repair area, relaxing incision is placed over the lower rectus sheath so that conjoined tendon is allowed to slide downward.

Hernia • •

Abrahamson nylon darning: Continuous intervening network of non-absorbable sutures are placed between conjoined tendon and inguinal ligament to give good support to posterior wall inguinal wall. Koontz`operation (Koontz AR, New York, 1963): In old people after taking consent, orchidectomy is done along with removal of full cord, testis and total closure of posterior inguinal wall by repair so as to reduce the recurrence.

• • •

Fig. 18.41: Tanner slide operation.

sion. Transversalis fascia is cut to reach the preperitoneal space. If it is direct sac, it is dissected without opening and isolated. Sac is inverted using absorbable purse string suture. If it is indirect sac, it is dissected proximally high up, opened and ligated. Transaponeurotic arch (transverse abdominis muscle and transversalis fascia) is sutured below to Cooper’s ligament and iliopubic tract. Nyhus mesh repair is done similarly through this approach by placing mesh and suturing to Cooper’s ligament. Andrew’s operation: It is overlapping of the external oblique aponeurosis. Condon procedure: It is anterior iliopubic tract repair by suturing the transversus abdominis to iliopubic tract from pubic tubercle to deep ring; then extending lateral to the cord. In direct sac relaxing incision is made on the lower rectus before tying all placed sutures. Wilkinson method: Transversus abdominis and internal oblique are sutured to inguinal ligament with continuous monofilament sutures—1st layer; lower free edge of the external oblique is passed above, behind the cord and is sutured to internal oblique surface— 2nd layer; upper free edge of the external oblique is brought down in front of the cord and is sutured to lower visible surface of the external o0blique—3rd layer. It has less recurrence rate.

Complications of tissue repair are: xx Haemorrhage, haematoma, seroma, haematocele. xx Infection, osteitis pubis. xx Post-herniorrhaphy hydrocele, lymhocele. xx Hyperaesthesia over the medial side of inguinal canal due to injury to iliohypogastric nerve—neuralgia (15%). xx Recurrence—10–15% in modified Bassini; 1–5% only in other types. xx Injury to urinary bladder, bowel, ileus. xx Testicular atrophy due to thrombosis of pampiniform plexus of veins, penile oedema—rare.

Fig. 18.42: Darning in inguinal hernia—Abrahamson’s nylon darning.

• •

•

Removal of cord at inguinal region (Hamilton Bailey): Cord is removed from the inguinal canal by ligating both at external and internal ring. But testis is retained [for psychological reason] and closure of inguinal canal by repair is done. McVay operation, 1940 (Cooper’s ligament repair): It is repair by placing interrupted sutures between edge of the transversus abdominis to Copper’s ligament starting from pubic tubercle medially towards femoral sheath and later continued as suture repair between transversus abdominis and iliopubic tract laterally up to the entrance of cord. It is a pure tissue repair. It requires relaxing vertical / curvilinear oblique incision at the lateral border of the anterior rectus sheath from pubic tubercle to a point superiorly for 4 cm. It covers all three groin defects (Myopectineal orifice)—indirect, direct and femoral. Nyhus (original) iliopubic repair: Through suprainguinal approach, a transverse incision is made two fingerbreadths above the pubic symphysis to expose the rectus sheath. Left index finger is passed into the external ring; level of internal ring is confirmed. Anterior rectus sheath is incised horizontally above the level of the deep ring; lateral part of lower end of the rectus is retracted. Posterior rectus sheath is opened. External oblique, internal oblique and transversus abdominis muscles are cut along the length of the inci-

Fig. 18.43: Left sided inguinal hernia repair wound is infected; right side is clean. Technique of local anaesthesia Around 50 ml of xylocaine 0.5% is used. Plain xylocaine 0.5% or xylocaine 0.5% with adrenaline can be used. Plain xylocaine— dose is 2 mg/kg body weight. Xylocaine with adrenaline—is 7 mg/kg body weight. Two methods are used: 1. Nerve block method (Point block): 10 ml of xylocaine is infiltrated 2 cm above and medial to anterior superior iliac spine to block

Language is the dress of thought.

Contd...

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SRB's Manual of Surgery DIRECT INGUINAL HERNIA

Contd... the iliohypogastric nerve. Midinguinal point is infiltrated with 10 ml xylocaine. Pubic tubercle place is infiltrated with 10 ml xylocaine. 10 ml of xylocaine is infiltrated just below the inguinal ligament lateral to femoral artery to block the genital branch of genitofemoral artery. Line of skin incision is infiltrated with 10 ml of xylocaine. Later neck of the hernial sac is infiltrated with 10 ml of xylocaine. 2. Field block method (Shouldice method): Skin of around 4 cm wide area is infiltrated including the subcutaneous plane as first layer from anterior superior iliac spine to pubic symphysis. Skin, subcutaneous and two layers of superficial fascia (Camper and Scarpa’s) are incised. Area deep to external oblique aponeurosis is infiltrated with 10 ml of xylocaine. External oblique aponeurosis is incised. Exposed inguinal canal and hernial sac is infiltrated with 10 ml of xylocaine to continue with the dissection.

Conservative treatment Taxis: Patient is placed in supine position with hip and knee flexed and hip internally rotated. Contents are pushed with one hand directing with other hand ™™ Use of Truss: Rat-tailed sprung truss is used. Measurement is taken from the tip of greater trochanter to third piece of sacrum circumferen­tially –– Complications are discomfort, ulceration, strangulation, inflammation, testicular atrophy, ilioinguinal neuritis, femoral neuritis –– It may be used in elderly people, who are not fit for anaesthesia and surgery –– Conservative treatment should be avoided in hernia as much as possible –– Truss is absolutely contraindicated in femoral and sliding hernia –– Truss increases the surgical bleeding, postoperative oedema, testicular pain ™™

10–15% of the hernias are direct. 50% of direct hernias occur bilateral. 35% of inguinal hernias are direct. It is uncommon in females and children. It is always acquired, due to weakening of posterior wall of inguinal canal. xx Hernia is medial to the inferior epigastric artery with wide neck. Sac is thick and often the medial wall or content may be bladder. xx Direct hernia occurs through Hesselbach’s triangle which is bounded by inferior epigastric artery laterally, lateral border of rectus medially, inguinal ligament below. It is divided into medial and lateral halves by obliterated umbilical artery (medial umbilical ligament). So, direct hernia is classified as medial or lateral depending on which part of the Hesselbach’s triangle, it is arising from. xx xx xx xx xx

Fig. 18.45: Surgical anatomy of direct inguinal hernia.

A

Fig. 18.46: Surgical anatomy of Hesselbach’s triangle. Coverings of direct herniafactors (from inside out) Predisposing

B Figs 18.44A and B: Hernia truss. It is used only when patient is not fit for surgery. It may precipitate strangulation. Before placing truss, contents of the hernia should be reduced completely.

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Extraperitoneal tissue Chronic cough, smoking Fascia transversalis Straining Conjoined tendon Constipation External spermatic fascia Heavy work Skin Previous appendicectomy

Hernia xx Ideally hernioplasty (mesh repair) is done. In case of bilat-

eral hernia, mesh repair can be done on both sides together. Laparoscopic approach (TEP) or suprapubic approach may be better in bilateral cases. Funicular direct hernia (prevesical hernia)

It is also called as Ogilvie’s hernia. It is a type of direct hernia which is prone for strangu­lation. It is a narrow necked hernia with prevesical fat and a portion of bladder, and or intestine that herniates through a small defect in the medial part of the conjoined tendon just above the pubic tubercle. ™™ It occurs in elderly males. ™™ ™™ ™™

Fig. 18.47: Bilateral direct hernia. Note the medial location of the direct hernias. xx Malgaigne bulgings are often seen in these patients on

Giant inguinal hernia Hernia reaches below the mid-level of thigh when patient stands.

examination, more often than in indirect hernia. They are protrusion of abdominal wall muscle during leg raising test as weak, soft, supple, swellings which signifies poor abdominal muscle tone. It is common in old age, obesity; it indicates that hernia requires mesh repair. xx Direct hernia rarely descends into the scrotum and strangu­ lation is not as common as in indirect hernia. But in longstanding cases, it can descend down to the scrotum and strangulation can occur. B

A

Figs 18.49A and B: Giant indirect and direct inguinal hernias. (Courtesy: Prof Ramlingam, KIMS, Narkatpally, Telangana, India).

RECURRENT HERNIA (Inguinal) xx Incidence is 10%. xx If recurrence is within 3 years it is called as early; if after

3 years it is late.

Fig. 18.48: Large bilateral direct hernia. Occasionally direct hernia descends down and becomes complete and then may cause obstruction. Descent is not as common as indirect hernia.

Treatment Surgery: xx Usually direct sac is not opened. xx Care should be taken at the medial aspect due to the

presence of bladder (bladder should be emptied before surgery).

Fig. 18.50: Recurrent inguinal hernia—left sided. Note the scar earlier surgery.

Femoral hernia is never congenital.

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SRB's Manual of Surgery Treatment xx After thorough investigations, the cause of recurrence has

to be treated and later hernioplasty is done.

xx Laparoscopic (TEP/TAPP) approach is better for recurrent

hernia. In open repair, preperitoneal mesh repair is ideal. In elderly people, Koontz orchidectomy or cord excision at inguinal canal may be added after proper prior consent.

Rerecurrent Hernia Fig. 18.51: Recurrent inguinal hernia is 10% common. It is commonly medial recurrence. It is treated by mesh repair. Predisposing factors Preoperative ™™ Smoking ™™ Chronic cough ™™ Constipation ™™ Old age ™™ Anaemia ™™ Hypoproteinaemia ™™ Straining ™™ Increased intra-abdominal pressure of any cause (BPH, carcinoma prostate, stricture urethra) ™™ Ascites Operative ™™ ™™

Tension in the sutures Weak anterior abdominal wall

Postoperative ™™ ™™ ™™ ™™

Infection (50%) Haematoma formation during earlier surgery Retained sac in pantaloon hernia Straining

Recurrence Rate Bassini’s repair—10%. Shouldice repair—1%. Hernioplasty—1 to 3%. Other methods—1 to 5%. True or false recurrences are the types of recurrence. If hernia occurs in inguinal region after inguinal hernia repair it is called as true recurrence. If other groin hernia occurs after inguinal hernia repair like femoral hernia or obturator or other rare types, it is called as false recurrence. But presently hernia is classified grossly as groin hernias and so all recurrences are true recurrences. xx xx xx xx

Clinical Features xx Same as for inguinal hernia. Defect is usually narrow and

so more likely to go in for strangulation. xx It can be medial recurrence or lateral recurrence depending on the location of the sac. Medial recurrence is common as tension in suture line is greatest near the pubic tubercle.

1% common.

Causes Infection, earlier mesh extrusion, failure of treating the precipitating causes.

Treatment xx The cause is treated and mesh repair is done. xx GPRVS (Giant prosthesis reinforcement of the visceral sac)

or TEP through laparoscopy is ideal.

HERNIOPLASTY It is strengthening of posterior inguinal wall in case of indirect hernia or in any large hernia with weak abdominal wall using a supportive material. This allows and supports good fibroblast proliferation which in turn strengthens the weak posterior wall of inguinal canal or abdominal wall. Material used Synthetic: Prolene mesh (white in colour) Dacron mesh, Morlex mesh, Mersilene sheath. ™™ Biological: Tensor fascia lata, temporal fascia and skin. (presently biological materials are not well-accepted as infection is common and its efficacy is not proved).   Prolene mesh is commonly used at present. Non-absorbable interspersed absorbed mesh (Vipro/Ultrapro) are also used nowadays. ™™

Indications xx xx xx xx xx xx xx

Direct hernia. Recurrent hernia. Re-recurrent hernia. Incisional hernia. Old age. Hernia with weak abdominal muscle tone. Sliding hernia.

Complications xx xx xx xx

Infection. Mesh extrusion. Foreign body reaction. Mesh inguinodynia causing hyperaesthesia and pain along the distribution of ilioinguinal or iliohypogastric nerves.

Hernia xx Mesh erosion into bladder, bowel or vessels can occur occasionally (rare).

•

•

Fig. 18.52: Infected mesh after open hernioplasty; it needs removal of the mesh.

Principle

•

xx Size of the mesh should be bigger than the size of the defect. xx Mesh should be fixed above and below to the conjoint tendon and inguinal ligament or abdo­minal wall using interrupted, nonabsorbable sutures. xx Absolute haemostasis and control (prevention) of infection is important.

•

Types of mesh repair ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Onlay repair Lichtenstein mesh repair—a type of onlay Inlay repair—mesh placed at myopectineal level—bridging repair Underlay repair—mesh placed at deeper plane usually in preperitoneal space Gilbert patch and plug repair/Gilbert’s PHS repair (onlay + sublay) Nyhus preperitoneal mesh repair Kugel groin hernia mesh repair Modified Rives preperitoneal mesh repair through inguinal approach Stoppa GPRVS repair TEP mesh repair TAPP mesh repair

Hernioplasty is becoming the prime treatment for inguinal hernia. Note:

• • •

Onlay mesh repair by placing mesh in front. It is sutured above to conjoint tendon and below to inguinal ligament using monofilament non absorbable suture material. Lichtenstein tension free onlay mesh repair (1993) where the cord is encircled with mesh which is often done under local anaesthesia. Suturing of mesh is done similar to onlay mesh repair. It has got less recurrence rate. Nyhus preperitoneal mesh repair: It is done through suprainguinalhorizontal incision above the pubic symphysis and internal ring. Preperitoneum is approached through lateral border of the lower part of rectus muscle by making an opening in the posterior rectus sheath. Mesh is placed in the preperitoneal space deep to the cord, conjoint tendon, and transversalis fascia. Below, it is folded deep to

•

the iliopectineal ligament of Cooper and sutured to it using two or three interrupted non-absorbable sutures. It is sutured to transverse abdominis above and transversalis fascia from deep. Modified Rives preperitoneal mesh repair (Read-Rives) is preperitoneal mesh repair through transinguinal approach. Direct sac, is inverted with sutures. For indirect sac, a high ligation is done. Here mesh is placed in preperitoneal space, folded and sutured below to iliopectineal ligament, above to the transverse abdominis in deeper plane. Often transversalis fascia opened earlier is sutured back using nonabsorbable suture material in front of the placed mesh. Stoppa’s giant prosthesis reinforcement of visceral sac (GPRVS): It is done in large hernias, hernias in elderly, bilateral hernias, recurrent and re-recurrent hernias, hernia with very lax abdomen, and hernia with collagen diseases like Marfan’s syndrome. Horizontal length (size) of the mesh is 2 cm less than distance between two anterosuperior iliac spines and vertical length (size) is distance between the umbilicus and pubic symphysis. Large mesh is placed between peritoneum and lateral, inferior, anterior abdominal wall which stretches in the lower abdomen and pelvis. It is done through lower midline or Pfannenstiel incision. Usually, such large mesh is placed without any anchorage. Gilbert mesh repair (patch and plug): After herniotomy, internal ring is plugged by cone-shaped (umbrella plug) piece of prolene mesh. Later onlay/inlay mesh repair of posterior wall of the inguinal canal is done. Gilbert’s PHS (Prolene Hernia System) repair (onlay and sublay— sandwich technique): It is an open transinguinal approach to place a specially devised mesh in both preperitoneal as inlay and in front as onlay mesh repair. This mesh has got a rounded deeper part which is placed in preperitoneal space and a modified quadrangular part which is placed as onlay. Both parts are connected through a connecting stiff rounded part in between which steadies the mesh in place preventing its displacement. Kugel (Rober D Kugel) groin hernia mesh repair (sublay): It is done through posterior preperitoneal approach with tension free less invasive sutureless repair. Kugel patch contains two overlapping layers of knitted polypropylene mesh which are attached to each other ultrasonically. Near the outer edge of the mesh it has got a polyester spring which stiffens the mesh to unfold. 1 cm of mesh extends outer to the spring which also has radial slits to have easy maneuverability. Anterior layer of the mesh has got single transverse slit to facilitate the insertion. Multiple 3 mm holes through both layers of the mesh are present that allow tissue contact in better way to prevent mesh displacement. Small V shaped triangular cuts on the anterior layer adjacent to these multiple holes act as sutureless anchors. Incision is above the deep ring and lateral to inferior epigastric vessels. Skin, subcutaneous tissue, external oblique aponeurosis is cut; internal oblique and transversus abdominis muscles are split to reach deeper space. Transversalis fascia split vertically to avoid injury to inferior epigastric vessels which are retracted medially. Preperitoneal space is created; indirect sac is dissected off the deep ring from above; proximal part being ligated using absorbable 3 zero vicryl. Direct sac is dissected off the defect without opening; its pseudosac which is modified transversalis fascia is dissected off entirely from the peritoneum behind. Kugel’s mesh patch is placed properly without allowing any tissue bands folding it. Transversalis fascia is sutured with one absorbable suture. Transversus abdominis and internal oblique muscles are not sutured. External oblique aponeurosis is sutured.

xx Transabdominal preperitoneal laparoscopic mesh repair

(TAPP repair): It is mainly used in irreducible and large hernias.

Spigelian line: Runs along the lateral border of rectus sheath and extends from the pubic tubercle to the tip of the 9th costal cartilage. Spigelian fascia: Is the fascia between the aponeurosis of external and internal oblique, transversus abdominis and recuts sheath.

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SRB's Manual of Surgery xx Totally extraperitoneal laparoscopic mesh repair (TEP)—

becoming popular.

Transabdominal Preperitoneal Mesh Repair (TAPP) Using Laparoscope This is used in large indirect hernia or irreducible inguinal hernia. 10 mm umbilical port is used for laparoscope. 5 mm ports are placed one on each side on pararectal point at the or above the level of umbilicus so as to achieve adequate triangulation. Contents of the hernia are reduced. Hernial sac is dissected in preperitoneal plane after making horizontal incision at the upper part of the sac opening. Vas, gonadal vessels, pubic bone, inferior epigastric vessels are identified. Once sac is dissected and excised, a prolene/vipro/ultrapro mesh of 15 × 10 cm sized or smaller is placed in preperitoneal space. It is fixed to pubic bone using tacks. Peritoneum is closed with continuous prolene sutures. Fig. 18.55: Mesh placement in TAPP procedure.

Totally Extraperitoneal Repair (TEP Repair) Using Laparoscope xx This technique is gaining more popularity than TAPP. Through subumbilical incision (10 mm) extraperitoneal space is reached. After CO 2 insufflation, another 5 mm port is inserted 4 cm below the first port in the midline. Third 5 mm port is inserted in the same line 4 cm below or in the right iliac fossa. Dissection is carried out downwards carefully, then medially up to the pubic tubercle, iliopectineal ligament, laterally to iliac vessels, and inferior epigastric vessels. Once adequate space is dissected, 15 × 15 cm mesh is placed and spread. Care should be taken not to have any folding in the mesh. Mesh may be sutured to iliopectineal ligament. Displacement of mesh is not common. Other side also can be done together. Anatomical considerations Preperitoneal space is a potential space in front of the peritoneum, behind the transversalis fascia and anterior rectus muscle. Below in front of the urinary bladder, it is called as space of Retzius (medially), laterally it is called as space of Bogros. Median umbilical fold is formed by urachus in the midline. Medial umbilical ligament is formed by obliterated umbilical arteries, lateral umbilical fold by inferior epigastric vessels. Three fossae are lying in relation to these folds—supravesical and medial fossae are medial to lateral umbilical fold which are sites of direct hernia whereas lateral fossa is lateral to lateral umbilical fold and is site of indirect hernia. ™™ In 1956 Fruchaud described his myopectineal orifice bounded medially by the lateral border of rectus abdominis, laterally by iliopsoas, superiorly by conjoint tendon and inferiorly by pectin pubis. This area is the site of groin hernia which should be covered by mesh of adequate size to strengthen the defect and to prevent the recurrence. Iliopubic tract is analogue of the inguinal ligament, extends from Cooper’s ligament to anterosuperior iliac spine which divides endoscopic view of preperitoneal space into superior compartment (contains inferior epigastric artery, Hesselbach’s triangle, cord structures and is site of inguinal hernia) and inferior compartment (contains femoral canal, iliac vessels, iliopsoas muscle, genitofemoral nerve, lateral femoral cutaneous nerve). External iliac vessels lie in a triangle formed by gonadal vessels laterally, vas deferens medially and peritoneal reflection inferiorly (triangle of doom). ™™

Fig. 18.53: Gibert‘s PHS mesh.

Fig. 18.54: View of indirect hernia laparoscopically during TAPP.

Hernia

Fig. 18.59: TEP after dissection prior to placement of mesh. Direct defect, inferior epigastric artery, pubic symphysis and Cooper’s ligament are clearly seen. Fig. 18.56: Ports used for TEP and TAPP.

Fig. 18.60: TEP after dissection showing indirect sac, inferior epigastric vessels, Cooper’s ligament.

Fig. 18.57: Diagrammatic representations of TEP and TAPP.

Fig. 18.61: TEP mesh placement in preperitoneal space.

Fig. 18.58: Port incisions in TEP.

xx Aberrant obturator artery is an occasional branch of inferior epigastric artery replacing its pubic branch travels across Cooper’s ligament, which during fixation of mesh can cause torrential haemorrhage—circle of death. Triangle of pain is formed by gonadal vessels medially, iliopubic tract laterally and peritoneal reflection below. Genitofemoral nerve and lateral cutaneous nerve of thigh traverse this triangle. Injury to these nerves either by dissection or by tacks cause postoperative pain. Tacks/staplers should not be placed in this triangle.

Smile is the curve which puts everything straight.

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SRB's Manual of Surgery Indications for TEP

Contraindications for TEP

• Recurrent hernia • Bilateral hernia • Indirect/direct/femoral hernia

• Obstructed/strangulated inguinal hernias • Ascites • Bleeding disorders

Landmarks to be identified in TEP

Principles in TEP

• • • • • •

• Head-down supine position • Surgeon standing on opposite side of hernia • Camera person placed on opposite side of hernia • Monitor at foot end • Catheterise/empty the bladder properly prior to TEP • Adequate wide space creation • Careful dissection of cord and sac • Ligate indirect sac • Mesh should not be fixed laterally • Size of mesh is 15 × 15 cm • Two point fixation—one at pubic bone other at Cooper’s ligament by tacks/staplers

Pubic bone midline Inferior epigastric artery Cooper’s ligament Iliopubic tract Cord and vas deferens Psoas muscle and nerves in relation

Difficulties and complications in TEP repair ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Difficulty in dissecting indirect sac. Cord/vas injury Inadvertent opening of the sac/peritoneum and creation of pneumoperitoneum. Injuries to major structures like iliac vessels—0.5–1.0% Displacement of mesh or erosion into structures like urinary bladder—rarely may occur Nerve injury Formation of seroma/haematoma Infection Recurrence

Advantages of TEP repair Approach is totally extraperitoneal Small incision Proper placement of mesh in right space that is preperitoneal space ™™ Peritoneal cavity is intact and not opened ™™ ™™ ™™

Common bacteria in strangulated hernia ™™

E. coli

™™

Anaerobic streptococci

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Anaerobic bacteria

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Klebsiella

Obstruction ↓ Initially venous return is impaired ↓ Congestion of the bowel ↓ Further dilatation of the bowel which becomes purple coloured ↓ Fluid collects in the sac ↓ Eventually arterial blood supply is impaired ↓ Bowel becomes dark, brownish black coloured with flabby and friable wall ↓ Bacteria migrate transerosally and multiply in fluid of the sac ↓ Perforation occurs at the site of constriction ring ↓ Peritonitis occurs. xx Strangulation commonly occurs in the small bowel and also

in large bowel. Occasionally strangulated omentocele also can occur without any intestinal obstruction. xx Strangulation can occur in inguinal, femoral, obturator, umbilical or any hernias. xx Indirect inguinal hernia is more prone for stran­gulation than direct inguinal hernia. It is due to narrow neck, adhesions, narrow external ring in children. xx Part of circumference of the bowel when strangu­lated, is called as Richter’s hernia wherein the patient presents with diarrhoea, toxicity mimicking gastroenteritis. Richter’s hernia is more common with femoral, obturator hernias.

INCARCERATED HERNIA xx Here the lumen of the portion of colon occupying a hernial sac is blocked with faeces. Here scybalous content of the bowel should be capable of being indented with the finger, like putty. xx In incarcerated hernia, sac and contents are densely adherent to each other (contents are fixed to sac). It is always irreducible; often obstructed but may not be strangulated.

STRANGULATED HERNIA Pathology It occurs when blood supply of the contents of hernia is seriously impaired leading to formation of gangrene.

Fig. 18.62: Picture showing strangulated hernia with toxic fluid and site of constriction.

Hernia xx 3% in incidence. Features of strangulated hernia

A

B

Figs 18.63A and B: (A) Strangulated inguinal hernia will be tender and irreducible without impulse on coughing; (B) Hernia with gangrenous omentum. Note the colour of the gangrenous omentum.

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Strangulation during infancy ™™ ™™

Causes of strangulation ™™ ™™ ™™ ™™

Narrow neck Adhesions Irreducibility Long-time, large hernia with adhesions

Maydl’s hernia (Hernia-in-W): Here a loop of bowel in the form of ‘W’ lies in the hernial sac and the centre portion of the ‘W’ loop is strangulated and lies within the abdominal cavity. Thus local tenderness over the hernia is not marked and hernia gets reduced with the strangulated loop in the centre of the “W”. Strangulation in this case is often missed during surgery and may lead to peritonitis due to retained gangrenous loop.

Tense, tender, irreducible No impulse on coughing Shock, toxicity Features of obstruction when there is enterocele Abdominal distension, vomiting Rebound tenderness

Incidence is 4%. Female to male ratio is 5:1 In female infants, the content may be ovary with or without fallopian tube

Taxis xx Often in irreducible hernia, reduction of hernia is tried by elevation, sedation and taxis (i.e. with flexion and medial rotation of the hip, reduction of hernia is tried). xx In obstructed hernia, taxis may be dangerous as during taxis, contusion and rupture of the intestinal wall can occur. Reductionen-masse may mask the gangrenous bowel existing in the sac. Inner gangrenous loop of Maydl’s hernia may be missed. Rupture of the sac extraperitoneally is also a possibility. xx Taxis has no role in femoral hernia and strangu­lated hernia. If tried, contusion, reduction-en-masse and rupture of the sac can occur. Taxis Used in irreducible or partially reducible hernia Trial reduction by flexing and medially rotating the hip It is dangerous in: –– Obstructed hernia –– Maydl’s hernia    (As rupture can occur leading to peritonitis) ™™ No role in femoral and strangulated hernia

™™ ™™ ™™

Fig. 18.64: Maydl’s hernia (Hernia-in-W).

Clinical Features of Strangulated Hernia xx Sudden severe pain, initially over a pre-existing hernia

which later becomes generalised over the abdomen.

xx Persistent vomiting, constipation and distension of the

abdomen.

xx Hernia is tense, severely tender, irreducible and without

any expansile impulse on coughing. Rebound tenderness is diagnostic. xx Features of toxicity and dehydration. xx Electrolyte imbalance. xx Abdominal distension with guarding and rigidity. xx Oliguria.

Fig. 18.65: In an obstructed hernia, if reduction is forced it may get reduced with the sac and ring with the obstructed/strangulated bowel—Reduction-en-masse. xx In strangulated omentum features of obstruction are not present (i.e. vomiting, constipation). Omentum becomes congested, oedematous and black in colour which secretes toxic fluid with secondary bacterial infection. But here, initially the sepsis is slower than that of strangulated intestinal obstruction.

The most important thing that you wear is the expression on your face.

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SRB's Manual of Surgery xx Eventually the infection spreads causing diffuse peritonitis. Downward spread of infection can cause scrotal abscess.

Investigations xx xx xx xx xx

Plain X-ray abdomen in erect posture shows multiple air-fluid levels. Serum electrolytes. Blood urea and serum creatinine. Total count is increased. U/S abdomen.

The viability of the bowel is checked by colour, peristalsis, pulsation, bleeding. ↓ When gangrenous, resection and anastomosis is done and drain is placed.

Strangulation without obstruction ™™ ™™

Richter’s hernia Omentocele

A

B

C

D

Treatment of Strangulated Hernia xx The patient is admitted. xx Ryle’s tube aspiration. xx Intravenous fluids to correct dehydration and electrolyte

imbalance.

xx Antibiotics. xx Catheterisation to maintain adequate urine output. xx Emergency surgery:

E Figs 18.67A to E: Strangulated hernia—left side. It is tense, tender, without any impulse on coughing. Note the incision, discoloured sac, content (gangrenous bowel) and proximal viable bowel. Bassini’s repair is done by placing interrupted non-absorbable sutures. Antibiotics, IV fluids are continued. Drain is removed in 4–5 days. Once the bowel movement begins, oral diet is started (in 5 days). Note: Fig. 18.66: Incision for strangulated hernia is obliquely placed extending to the scrotum. Groin incision is made with incision extending into the most prominent area of the swelling. ↓ Sac is exposed. ↓ Constriction ring and superficial ring is released (cut). ↓ Sac is opened carefully without allowing the spillage of fluid (Usually spillage occurs extraperitoneally) ↓ Fluid is sucked with a suction apparatus. ↓ The bowel is held with fingers so as to prevent it from getting reduced. ↓

During surgery for strangulated hernia mesh is usually not used, only repair is done. Biological mesh can be used.

Postoperative Problems Infection, leak with fistula, septicaemia.

SLIDING HERNIA (HERNIA-EN-GLISSADE) xx Here posterior wall of the sac is not only formed by the parietal peritoneum, but also by sigmoid colon with its mesentery on left side; caecum on right side and often with portion of the bladder (Both sides) (1:2000). xx Rarely small bowel sliding hernia or sacless sliding hernia can occur (1:8000). xx Content of the sac is usually small bowel or omen­tum. xx Sliding hernia occurs exclusively in males. Mainly on the left side (85%). xx It commonly occurs in indirect sac even though femoral and direct sliding hernias are known to occur. xx Bilaterality is extremely rare.

Hernia xx It is seen commonly in adults and elderly. xx Huge hernia can occur which extends into the scrotum and do not get reduced totally.

Fig. 18.68: Sliding hernia with urinary bladder as posterior wall of the sac.

Clinical Features (2%) Large globular swelling in the inguinal region descen­ding into the scrotum, often irreducible.

the peritoneal cavity. Posterior wall of the sac should not be separated from large bowel or bladder. If tried it may lead into faecal or urinary fistulas. Often sac can be excised partially; this partially excised sac can be pushed into peritoneal cavity. Right sided sliding hernia will have caecum and appendix in its posterior wall; caecum should not be separated from posterior wall of the sac which may otherwise create faecal fistula. Appendix should not be removed as it may precipitate sepsis. Appendices epiploicae from sigmoid colon should not be removed as there are chances that they may contain small colonic diverticula which may get opened to contaminate the field. Bladder will be present on medial side of the sac and sac should not be separated; if bladder injury occurs it should be sutured in two layers with vicryl. Inside out purse string suture on the opened sac is applied and the sac with its posterior wall is pushed into the abdominal cavity. Urinary catheterisation is a must. xx Truss should not be used in sliding hernia.

PANTALOON HERNIA (DOUBLE HERNIA, SADDLE HERNIA, ROMBERG HERNIA) xx Here both direct and indirect inguinal sacs are present and clinically present as direct hernia. xx During surgery, indirect sac may be missed and so leads to recurrent hernia through retained (or unidentified) indirect sac. xx Here both medial and lateral sacs straddle the inferior epigastric artery. xx It is one of the causes for recurrent hernia.

Fig. 18.69: Sliding hernia (Hernia-en-Glissade).

Small bowel as the content of sliding hernia can lead to strangulation.

Fig. 18.70: Saddle/Pantaloon hernia. It is on either side of the inferior epigastric artery having both direct and indirect sacs. Infantile hernia

Treatment

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Always Surgery xx Posterior wall of the sac should not be separated from large bowel or bladder. If tried, injury may result to these organs leading to faecal or urinary fistulas. xx Partially excised sac is pushed into the peritoneal cavity with posterior wall and repair is done usually using prolene mesh (Hernioplasty). xx In LaRoque repair deep ring is incised above and below; reefing of the sigmoid colon mesentery is done which forms the posterior wall of the inguinal canal so that entire sigmoid is replaced into

Clinically difficult to diagnose. Often it is diagnosed on table. Processus vaginalis is closed at internal ring and hernial sac either invaginates processus vaginalis as “inverted umbrella" or comes behind processus vaginalis.

FEMORAL HERNIA Surgical Anatomy of Femoral Canal It is the medial, most compartment of the femoral sheath, which extends from femoral ring above to saphe­nous opening below. It contains fat,

It takes 26 muscles to smile, and 62 muscles to frown.

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SRB's Manual of Surgery lymphatics, lymph node of Cloquet. It is 1.25 cm long and 1.25 cm wide at the base. Below it is closed by cribriform fascia. Femoral ring is bounded anteriorly by inguinal ligament; posteriorly by iliopectineal ligament of Cooper, pubic bone and fascia covering the pectineus muscle; medially by concave, sharp lacunar (Gimbernat’s) ligament; laterally by a thin septum separating from femoral vein.

A

Fig. 18.71: Surgical anatomy of femoral hernia.

B Figs 18.73A and B: Hernia; inguinal hernia is above and medial to tubercle, and femoral hernia is below and lateral.

Clinical Features

Fig. 18.72: Femoral triangle.

Aetiology xx Wide femoral canal. xx Multiple pregnancies.

Pathology in Femoral Hernia Through femoral canal, hernial sac descends down vertically up to saphenous opening and then escapes out into the loose areolar tissue to expand out like a retort. Because of its irregular pathway and narrow neck, it is more prone for obstruction and strangu­lation. During surgery, precaution should be taken about the femoral vein and pubic branch of obturator artery (or accessory obturator artery) which often may get injured leading to torrential haemorrhage.

xx Common in females (2:1 ratio), common in multi­para. xx Rare before puberty. 20% occurs bilateral, however, more common on right side. xx Presents as a swelling in the groin below and lateral to the pubic tubercle (Inguinal hernia is above and medial to the pubic tubercle). xx Swelling, impulse on coughing, reducibility, gurgling sound during reduction, dragging pain, are the usual features. xx When obstruction and strangulation occurs which is more common, presents with features of intestinal obstruc­tion—painful, tender, inflamed, irreducible swelling without any impulse. They also present with abdominal distension, vomiting and features of toxicity. xx Often femoral hernia can be associated with inguinal hernia also. xx 40% of femoral hernias present as emergency hernia with obstruction/strangulation. Note:

•

Gaur’s sign: In femoral hernia, distension of super­ficial epigastric and/or circumflex iliac veins occurs due to the pressure by the hernial sac.

Differential diagnosis ™™ ™™ ™™

Inguinal hernia An enlarged Cloquet lymph node of any cause Psoas abscess—psoas spasm with flexed hip but difficulty in extension

Hernia Lipoma Femoral aneurysm Distended psoas bursa (Disappears on hip flexion) Saphena varix—it is enlarged terminal portion of long saphenous vein. It is soft, disappears on lying down, fluid thrill, impulse on coughing and venous hum on auscul­tation are present. There is associated varicose veins on leg ™™ Haematoma in the region ™™ ™™ ™™ ™™

• • • • • •

Hydrocele of femoral hernia occurs when adherent omentum which is the content secretes fluid into the sac. Herniation through a gap in the lacunar ligament (medial) is always strangulated and is called as Laugier’s femoral hernia (L for L). In congenital dislocation of hip, femoral hernia occurs behind the femoral vessels—Narath’s femoral hernia. If sac lies under the pectineal fascia, is called as Cloquet’s hernia. Strangulation and Richter’s hernia are common in femoral hernia. Often on medial side, a portion of bladder forms the wall of the femoral hernial sac—sliding—femoral hernia.

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

2. Mc’Evedy-high operation: A incision is made over the femoral canal extending vertically above the inguinal ligament. Sac is dissected from below, neck from above and repair is done from above. It gives a very good exposure of both neck, fundus of sac and repair is also easier. It is done in strangulated femoral hernia. 3. Lotheissen’s operation: It is through inguinal canal approach (like for inguinal hernia). Transversalis fascia is opened and neck of the sac is identified in the femoral ring. Sac is dissected from above, neck is ligated and repair is done.

Femoral hernia—occurs medial to femoral vein Narath’s hernia—occurs behind femoral artery, in congenital dislocation of hip Hesselbach’s hernia—occurs lateral to femoral artery Serofini’s hernia—occurs behind femoral vessels Laugier’s hernia—through lacunar ligament Teale’s hernia—in front femoral vessels Callison-Cloquet hernia—through pectineal fascia Cooper’s hernia—femoral hernia with two sacs The de Garengeot’s hernia—incarcerated (acute appendicitis) appendix in femoral hernial sac

Fig. 18.75: Different surgical approaches for femoral hernia.

Fig. 18.74: Femoral hernia on right side. Note the location below the inguinal ligament. Femoral hernia is common on right side. It is common in females.

Treatment Approaches 1. Lockwood-low operation: Here sac is approached below the inguinal ligament through groin crease incision (or over the swelling) so that fundus of sac is dissected by direct vision and repair is done from below. Here inguinal ligament is sutured to Cooper’s ligament. standard and ideal (Cooper’s ligament repair).

Fig. 18.76: Femoral hernia repair. Inguinal ligament is approximated to Cooper’s (Iliopectineal line) ligament. In Lotheissen’s repair conjoined tendon is sutured to iliopectineal line.

Love means sharing the same road, wherever it leads.

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A

B

C

D

E

F

Figs 18.77A to F: Strangulated femoral hernia. Note: clinical look, Richter’s gangrenous bowel, resection and Lotheissen’s repair.

Lotheissen’s repair: After herniotomy, conjoined tendon is sutured to iliopectineal line (ligament) by interrupted sutures (2 or 3), using nonabsorbable monofilament sutures. Care should be taken to avoid injury to femoral vein, pubic branch of obturator artery, bladder. It is not as strong as Cooper’s ligament repair. Complications: Bleeding haematoma, abscess formation. 4. AK Henry’s approach: Repair of bilateral femoral hernia through lower abdominal incision. 5. Polypropylene mesh can be buttressed over the femoral canal to close the defect. 6. Laparoscopic mesh repair—TEP/TAPP.

VENTRAL HERNIA

Causes xx Congenital defect. xx Obesity. xx Smoking. xx Chronic cough.

A

Any protrusion through abdominal wall with the exception of hernia through the inguinofemoral region is defined as ventral hernia. Incisional hernia (80%) and primary defects in abdominal fascia which can cause umbilical hernia, epigastric hernia, paraumbilical hernia or Spigelian hernia are grouped under ventral hernia.

B Figs 18.78A and B: Large ventral hernias. It needs proper mesh repair.

Ventral hernia can be: ™™ ™™ ™™ ™™ ™™ ™™

Reducible. Irreducible. Obstructed. Strangulated. Single. Multiple small defects (Swiss cheese hernia).

A

B

Figs 18.79A and B: (A) CT scan showing ventral hernia which is irreducible; (B) Ventral hernias with Swiss cheese multiple defects.

Hernia Additional History to be Collected in Incisional Hernia

A

B

Figs 18.80A and B: (A) Port placement for laparoscopic ventral hernia repair. Left subcostal point is Palmar point; (B) Laparoscopic view of ventral hernia with omentum as irreducible content. Content is released and duval or four-layered mesh is fixed with tackers or sutures. Preoperative preparation xx Proper skin hygiene. xx Respiratory care. xx Control of obesity. xx Antibiotics. Management xx Relevant investigations xx Open mesh repair—inlay; onlay; sublay—retrorectus; underlay. xx Laparoscopic mesh placement—underlay (directly in front of the contents) using dual mesh or four layered mesh.

INCISIONAL HERNIA

xx Details of surgery that patient has undergone earlier. Duration after how long incisional hernia has occurred is important. xx History of wound infection, wound dehiscence, whether surgery done was an emergency or elective, and tension sutures placed or not. xx History of pain, irreducibility and details of precipitating factors to be asked. xx Other precipitating factors are similar to inguinal hernia like smoking, urinary/respiratory/abdominal symptoms.

Predisposing Factors xx Vertical scar, midline scar, lower abdominal scar—may injure the nerves of the abdominal muscles. xx Scar of major surgeries (biliary, pancreatic). xx Scar of emergency surgeries (peritonitis, acute abdomen). xx Faulty technique of closure. xx Poor nutritional status of the patient. xx Presence of cough, tuberculosis, jaundice, anaemia, hypoproteinaemia. xx Malignancy, immunosuppression. xx Smoking in postoperative period. xx Causes which increases the intra-abdominal pressure (BPH, straining, stricture urethra or rectum, ascites). Factors responsible for development of incisional hernia ™™ ™™

xx It is herniation through a weak abdominal scar (scar of

™™ ™™

xx It is common in old age and obese individuals. xx It occurs in 10% of abdominal surgeries; 70% occurs in first

™™

previous surgery).

5 years; 30% occurs in 5–10 years.

™™ ™™ ™™ ™™

Vertical incision has got higher chances of incisional hernia than horizontal incision Layered closure of the abdomen has got higher chance than single layer Continuous closure has got higher chances than interrupted closure Using absorbable suture material has got higher chances of hernia than nonabsorbable sutures Emergency surgical wound has higher chances than elective surgical wound Laparotomy for peritonitis, acute abdomen, and trauma can commonly cause incisional hernia Drainage through the main laparotomy wound may precipitate formation of incisional hernia Chronic cough, smoking, obstructive uropathy, constipation can precipitate incisional hernia Diabetes, old age, malnutrition, malignancy, anaemia, hypoproteinaemia, jaundice, ascites, liver disease, uraemia, steroid therapy, immunosuppressive diseases are other precipitating factors

Features

Fig. 18.81: Incisional hernia adherent to skin. Note the ulceration over the summit. Patient underwent resection and anastomosis with removal of the ulcerated skin with mesh placement.

xx xx xx xx xx xx

Swelling in the scar region. Pain. Impulse on coughing. Gurgling sound. Often bowel peristalsis may be visible under the skin. Eventually features of irreducibility, obstruction, strangulation is seen.

So many languages in the world and a smile speak them all. A warm smile is the universal language of kindness.

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SRB's Manual of Surgery xx Hernia is common in lower abdomen. xx It may be small or large; huge or massive (diffuse). xx Scar, its extent and location, whether healed primarily or

secondarily, skin over the scar and swelling is noted. Details of the swelling with expansile impulse on coughing and examination both in lying down and standing are done. xx Gap cannot be assessed in an irreducible hernia. Type of defects in incisional hernia ™™ ™™ ™™ ™™ ™™

A

Small defect 2 cm Very large defect Massive/diffuse Multiple defects—Swiss cheese pattern

Note:

• •

Size of the defect is important to decide the type of surgical closure in incisional hernia. Midline hernia expels the content more outwards due to contraction of rectus muscles on both sides.

xx Investigations: Always the precipitating factors must be

looked for:

 Chest X-ray.  US abdomen.

 Tests relevant for causes. Complications of incisional hernia: Irreducibility, obstruction, strangulation, incarceration

Preoperative Preparations for Incisional Hernia Surgery B Figs 18.82A and B: Incisional hernia in a patient during straining and during relaxing.

xx Reduction in weight and control of obesity. xx Nutrition, control of anaemia. xx Treatment for diabetes, hypertension, cardiac diseases, respiratory problems. xx Treating the precipitating causes. xx Chest X-ray, U/ S abdomen to be done.

Fig. 18.83: Incisional hernia which is irreducible with visible bowel beneath. Defect is felt and assessed during head rising, by placing fingers over the scar horizontally Size of the defect is very important

Fig. 18.84: CT scan abdomen showing incisional hernia.

Hernia placement is chances of adhesion and GI fistula formation, but still it is found to be safer. Laparoscopic preperitoneal mesh placement is also done for smaller defects. Now dual mesh (PTFE) or four layered mesh are available. Here mesh is placed under the peritoneum deep to the defect after reducing the contents. Mesh is fixed with sutures and tacks. In four-layered mesh, deepest 1st layer is absorbable cellulose which allows new peritoneum to creep underneath. 2nd layer is PDS/PTFE mesh 3rd layer is polypropylene mesh and the last 4th layer is again PDS/PTFE mesh. It is ideal but costly.

xx Massive incisional hernia after reduction might cause IVC compression, paralytic ileus and diaphragmatic elevation with respiratory embarrassment (abdominal compartment syndrome). It is prevented by prior increasing the capacity of peritoneal cavity by creating pneumoperitoneum using CO2 so as to increase the peritoneal pressure by 12–15 cm of H2O, daily for 3–6 weeks. Later definitive surgery is done.

Treatment Strategy for Incisional Hernia xx Mesh repair of the incisional hernia defect is always better

and ideal with less chances of recurrence—retrorectus or sublay is ideal (mesh onlay is not accepted).  Adequate sized mesh is placed either outer to peritoneum (sublay), or occasionally combined sublay and onlay mesh placement, both deep and outer to musculoaponeurotic layer. Onlay/overlay mesh is placement of mesh outer to the abdominal musculoaponeurotic layer which is not advisable in ventral / incisional hernias.  Rive’s Stoppa’s mesh placement for incisional hernia is placing mesh between posterior rectus sheath and rectus muscle—retrorectus mesh placement is easier for dissection and mesh placement.  Commonly polypropylene mesh is used. Other materials used are Dacron, polytetrafluoroethylene (PTFE) mesh, polyglycolic mesh (vicryl mesh) or combined polypropylene and polyglycolic acid mesh (vipro mesh). Drain (suction drain) must be placed after surgery.  Mesh repair is ideal approach for incisional hernia. Prevention of infection/haemostasis and drainage are important.

Note:

•

• •

•

Cattell’s operation: When the defect is less than 3 cm, and if the patient is having adequate abdominal muscle tone, layer by layer anatomical repair is done using monofilament nonabsorbable suture material like polypropylene/polyethylene, ideally with interrupted sutures. Sac should be dissected, ligated and excised prior to repair. Peritoneum and posterior rectus sheath is apposed as first layer and anterior rectus sheath as second layer. Double breasting of the rectus sheath using interrupted nonabsorbable sutures using monofilament suture material. It is overlapping the rectus sheath in two layers with two rows of sutures. Keel operation is done in large defect. Scar is excised and is dissected beyond the margin of the defect. Sac is never opened unless there is obstruction of the content. Sac in inverted using continuous/inter­rupted inverting non-absorbable sutures, layer by layer until the defect margins are apposed together which is then again sutured with interrupted sutures. Keel is inverted beam of the ship. Nuttall’s operation is done for lower midline incisional hernia. Recti attachments are detached from the pubic bones and are crossed over to fix to opposite pubic bones so as to create a firm abdominal wall support by crossed recti muscles.

xx Laparoscopic mesh repair is done for incisional hernia

by placing a mesh under the defect laparoscopically in intraperitoneal plane. The only problem of this underlay

A

B

A

B

Figs 18.86A and B: (A) Keel operation, and (B) Nuttall’s operation.

Different Types of Mesh Repair for Incisional Hernia C Figs 18.85A to C: On table incisional hernia defect also showing mesh placement in retrorectus plane.

xx Outer to peritoneum is ideal method (sublay): Large sized mesh is placed in preperitoneum. It need not be fixed as abdominal pressure keeps it in position (according to Pascal’s law).

Luck is when opportunity knocks and you answer.

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SRB's Manual of Surgery xx Under the peritoneum, directly over the content (underlay): Now it is accepted but there are chances of ad­hesions/fistula formation. It is used in laparoscopic repair. Dual mesh/four-layered mesh is used. xx Overlay mesh placed outer to musculoaponeurotic layer. Here mesh is placed under subcutaneous tissue; it carries high recurrence rate (30%). So it is not recommended. xx Combined inlay and overlay with two layers of mesh. xx Rive’s Stoppa’s method of placing mesh between posterior rectus sheath and rectus muscle widely. Dissection is done at least 10 cm beyond the defect under rectus muscle in front of the posterior rectus sheath; mesh should cover 5 cm beyond the defect all around. Recurrence rate with this is less than 10%. xx Components separation technique is better method in large defects. Here skin and subcutaneous fat are dissected of the anterior rectus sheath → external oblique is incised 2 cm lateral to rectus abdominis → external oblique is separated from internal oblique until posterior axillary line → additional relaxing incisions are made over rectus sheath, internal oblique, transverse abdominis → it is repeated on opposite side → 20 cm mobilisation is achieved → also reinforced with a large mesh. Component separation technique causes often lateral bulges on both sides. If it is done without mesh support recurrence rate is high. Advantage is defect up to 20 cm can be easily brought together. Technique is also called as Autologenous repair by vascularised innervated muscle flaps) (Ramirez, 1990). xx Bridging at myoaponeurotic level outer to peritoneum (inlay): Adequate sized mesh is placed in the defect level bridging the gap to cover preperitoneum. It is better by principle but still shows high recurrence. Surgeries for incisional hernia ™™ ™™ ™™ ™™ ™™ ™™

Mesh repair—commonly done and ideal Component separation technique Layer by layer closure—Cattell’s operation Double breasting of the rectus sheath Keel operation—not commonly used now Nuttall’s operation—not commonly used now

Postoperative Care xx xx xx xx xx xx xx xx xx xx xx

Antibiotics. Analgesics. Nasogastric aspiration. Abdominal binder for support. Prevention of paralytic ileus. Control of obesity and other precipitating factors. Stop smoking and treat other associated causes. Early ambulation. Fluid management, catheterisation. Drain should be kept until drainage becomes minimal. Abdominal binder is used to support abdominal wall during recovery period. Complications of incisional hernia surgery are:

Wound infection, seroma formation Paralytic ileus, abdominal compartment syndrome in large hernias ™™ Wound sinus, enterocutaneous fistula ™™ Infection of the mesh, recurrence ™™ ™™

Additional Problems in Large Incisional Hernia xx While reducing the bulky contents like bowel and omentum, inadequate intra-abdominal capacity leads to increased intraabdominal pressure causing IVC compression, mesenteric oedema followed by stasis of splanchnic bed, paralytic ileus, diaphragmatic elevation and respiratory distress (abdominal compartment syndrome), urinary and bowel disturbances. Abdominal capacity can be raised by creating regular pneumoperitoneum over the period of 3–6 weeks. xx Lordosis and back pain may be presenting feature. xx Sac and contents may get adherent to the thin skin over the summit of the hernia leading to skin ulceration and occasionally fistula formation. xx Often might need resection of the adherent bowel segment. xx Large mesh placement is required. Note:

• •

It is now universally accepted that prosthetic repair is gold standard for all incisional hernia. Prostheses used are polypropylene mesh, e PTFE, Dacron, dual intraperitoneal mesh, biologic grafts. Nonprosthetic repair has got only historical value as recurrence rate is very high (as high as 55%).

UMBILICAL HERNIA Anatomy of Umbilical Region Umbilical ring is a complex structure which is related to linea alba, falciform ligament, obliterated urachus (median umbilical ligament) and umbilical fascia (Richet’s fascia). It is located at the level of L4 and L5 vertebral disc. It is at lower position in infants. It is water shed area for venous and lymphatic drainage—above umbilicus it drains to axillary vein or lymphatics; below to inguinal area. Umbilical skin is supplied by T10 spinal cord. It is the meeting point of four folds of embryonic plate and three systems—GI (vitellointestinal), urinary (urachus), and vascular (umbilical vessels). Umbilical hernia develops due to either absence of umbilical fascia or incomplete closure of umbilical defect. Weakest part in the umbilical cicatrix is upper part where hernia begins.

Features xx Umbilical hernia can be congenital in newborn and infants

(common in males) or acquired in adults (common in females). Congenital umbilical hernia is common in Africa or in African origin people (8 times). Acquired is like any ventral hernia. xx It is herniation through a weak umbilical scar (cicatrix). xx It is common in infants and children, occurs com­monly due to neonatal sepsis. xx Male : female :: 2:1. xx It is seen in 20% of newborn infants. xx Umbilical hernia is common in Down’s syndrome, Beckwith-Weidman syndrome, ascites. xx Presents with a swelling in the umbilical region within first few months after birth, the size increases during crying. It is hemispherical in shape. xx Defect can be felt with finger during crying. xx Occasionally it can go for irreducibility and obstruc­tion which presents with pain, distension, vomiting.

Hernia

B

A

Figs 18.87A and B: Umbilical hernia in a male child and adult. Often it can attain a large size.

Treatment Initially conservative. In 93 to 95% of cases, it disappear spontaneously in few months after birth (masterly inactivity). It can be hastened by adhesive strapping across the abdomen.

Mayo’s operation: Here horizontally opened rectus sheath is approximated as double breasting with upper flap overlapping lower flap in front. It is rarely done today. Sublay mesh repair: In a large umbilical hernia (>3 cm size defect) with a degenerated skin on its surface it is often difficult to retain the umbilicus. When umbilicus is tried to be saved, infraumbilical incision should extend laterally about 2 cm on each side at 3 and 9 o’clock positions. Sac is dissected similarly. Sac is excised after excision of redundant sac. Presently it is standard to use polypropylene mesh as sublay or in retrorectus position and then rectus sheath is closed. Umbilectomy: Unhealthy thin skin over the large umbilical hernia is a real problem. It is better to do umbilectomy in these patients (excision of umbilical cicatrix). It is done only in adult with large umbilical hernia with thinning of umbilical skin. Prior consent and eventual creation of umbilicus is needed. Open dual PTFE and polypropylene mesh placement: Umbilical hernia is dissected similarly through subumbilical incision. Redundant sac is excised. Peritoneum is not closed. A special composite mesh containing wider PTFE on the inner side with little smaller polypropylene mesh on the outer aspect is used. It has also got two additional straps of the mesh attached to the outer part of the main composite mesh which are used to hold and later to fix into the defect anteriorly. This has got excellent results with low recurrence rate. Laparoscopic umbilical hernia repair: It is similar like any ventral hernia repair through laparoscopy which is done under general anaesthesia. It is useful only in large umbilical hernia.

Fig. 18.88: Incision for umbilical hernia repair (infraumbilical)— inferior crease incision. Fig. 18.89: Umbilical hernia dual mesh to place both intraperitoneally and retrorectus plane with straps to fix.

Surgery Indications for surgery ™™ ™™ ™™

If persists even after the age of two years. If the defect is more than 2 cm in size. Acquired/adult umbilical hernia.

Different surgeries are: Primary closure of the defect: An infraumbilical incision is made encircling its lower half. Sac is dissected circumferentially and is released off from the umbilicus and subcutaneous tissue. Sac is opened; contents are reduced; excess part is excised up to the umbilical ring. Defect is closed with interrupted nonabsorbable polypropylene sutures.

PARAUMBILICAL HERNIA (Supra- and Infraumbilical Hernia) xx It occurs commonly in adults. It is a protrusion or hernia-

tion through linea alba, just above or below the umbilicus.

xx It enlarges ovally, often attains a large size and sags downwards. xx Neck of the sac is relatively narrow. Contents are usually

omentum, small bowel, some­times large bowel.

xx It has got tendency to go for adhesion, irreducibility and

obstruction.

Those who can’t hear the music think the dancer’s mad.

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SRB's Manual of Surgery xx Postoperative weight reduction, use of abdominal binder is

required for these patients.

EPIGASTRIC HERNIA (Fatty Hernia of Linea Alba) xx It is 10% common; common in males. xx 20% of epigastric hernias are multiple—Swiss cheese like. xx It occurs usually through a defect in the decus­sation of the

B

A

Figs 18.90A and B: Large ventral hernia front and side views. It needs preperitoneal mesh repair. Predisposing factors ™™ ™™ ™™

Obesity Multiple pregnancies Flabby abdominal wall

Clinical Features xx Common in females (5:1 ratio). xx It presents as a swelling which has smooth surface, distinct

fibres of linea alba, any where between xiphoid process and umbilicus. xx Extraperitoneal fat protrudes through the defect as fatty hernia of the linea alba presenting like a swelling in the upper midline with an impulse on coughing. xx It is sacless hernia. Later protrusion enlarges and drags a pouch of peritoneum, presenting as a true epigastric hernia. xx If the defect is less than 1.5 cm, lateral margin of the defect is formed by only anterior and posterior lamina of the rectus sheath; if the defect is > 1.5 cm, then lateral margin is also formed by rectus muscle. xx Content of true epigastric hernia is usually omen­tum, sometimes it may be small bowel. xx Common in muscular men; manual labourers.

edges, soft, resonant with dragging pain and impulse on coughing. Large hernias can present with intestinal colic due to subacute intestinal obstruction. Eventually strangulation can occur.

Treatment Is always surgery xx Dissection of hernial sac and placement of mesh in retrorectus plane and under the umbilicus is the ideal treatment. xx Often umbilectomy is required and also mesh placement is beneficial (when defect is > 4 cm in size). xx If there is strangulation, resection of bowel segment and anastomosis is done followed by repair of the hernia. xx Mayo’s operation: Through a transverse elliptical incision, sac is identified and dissected. Hernio­tomy is done. Double breasting of the defect in the rectus is done by interrupted nonabsorbable sutures. xx Additional lipectomy (panniculectomy) may be done in case of pendulous abdomen.

Fig. 18.91: Epigastric hernia. Often multiple Swiss cheese defects are seen.

Mayo’s operation ™™ ™™ ™™ ™™

™™ ™™

It is done for umbilical and paraumbilical hernia Once lower flap or umbilicus is raised above, sac is identified, dissected and opened After reducing the contents sac is transfixed using vicryl Rectus sheath is repaired with double breasting using nonabsorbable sutures between superior and inferior fascial margins as ‘vest on pant’ imbrications Skin flap is closed with a drain. Infection, recurrences (30%) are known complications It is not commonly used now

Fig. 18.92: Epigastric hernia showing features of strangulation.

Hernia Clinical features Often asymptomatic. Swelling in the epigastric region which is tender. Pain in epigastric region. It is often associated with peptic ulcer and so pain may be due to peptic ulcer. So gastroscopy is done to rule out acid peptic disease. ™™ Impulse on coughing; defect in the epigastric region are also found. ™™ Irreducibility, obstruction, strangulation as seen in any other hernia can also occur in epigastric hernia. ™™ ™™ ™™

xx Large defect is supported with preperitoneal mesh. xx Complete reconstruction of linea alba is needed from xiphi-

sternum to umbilicus especially in Swiss cheese type using different methods like—interrupted primary closure using polypropylene sutures; modified shoelace technique is used after removing strip of medial margins of the linea alba; double breasting of the linea alba. Interparietal hernias/interstitial hernias

Treatment

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xx Through a vertical incision, sac is dealt with. Defect is closed

with nonabsorbable interrupted sutures.

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Herniation through parietal peritoneum into various layers of the abdominal wall Common in Down’s syndrome, Prune Belly syndrome Often it can attain large size May mimic abdominal wall lipoma; haematoma As neck of the sac is often narrow, can present with irreducibility or obstruction Commonly it is deep to external oblique aponeurosis Types: –– Preperitoneal—between peritoneum and transversus abdominis muscle—20% –– Interparietal/intermuscular—between external oblique and internal oblique; most common—60%. It is commonly associated with inguinal hernia –– Extraparietal (inguinosuperficial)—herniates through external oblique aponeurosis into subcutaneous plane—20% U/S; X-ray abdomen; often CT confirms the diagnosis Through a transverse incision, surgical ligation of sac, repair or mesh placement is the treatment

SPIGELIAN HERNIA xx It is a type of interparietal hernia occurring at the level of arcuate line through spigelian point. Hernial sac lies either deep to the internal oblique or between external and internal oblique muscles. xx It is lateral ventral hernia through Spigelian fascia at any point along its line. Semilunar line of Spigel is a line from pubic tubercle to tip of 9th costal cartilage. It marks the lateral margin of the rectus sheath. Semicircular arcuate line (fold) of Douglas is lower end of posterior lamina of rectus sheath below the umbilicus and above the pubis. Spigelian fascia is area between lateral border of the rectus muscle and external and internal oblique and transversus abdominis muscle. xx Spigelian hernia can occur above (10%) or below (90%) the umbilicus. Below the umbilicus it occurs at the junction of linea semilunaris and linea semicircularis (wider and weaker point). In Spigelian hernia, defect is formed by internal oblique and transversus abdominis muscle. External oblique is outer to the hernial sac.

B

Features

C

D Figs 18.93A to D: Epigastric hernia—incision, sac and defect.

xx Presents as a soft, reducible mass lateral to the rectus muscle and below the umbilicus, with impulse on coughing. Strangulation is common in spigelian hernia. xx Presence of precipitating factors like obesity, chronic cough, old age, multiple pregnancies. xx Common in females after 50 years of age. xx Investigation: Ultrasound abdomen.

We do not remember days, we remember moments.

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SRB's Manual of Surgery Differential diagnosis ™™ ™™ ™™

Abdominal wall lipoma. Soft tissue sarcoma. Abdominal wall haematoma.

Fig. 18.96: Obturator hernia through obturator canal in obturator foramen. Note also the locations of inguinal and femoral hernias.

Fig. 18.94: Spigelian hernia.

xx Referred pain in knee joint through geniculate branch of obturator nerve signifies not only obturator hernia but also strangulation— Howship-Romberg sign (50%). xx On per vaginal examination, tender swelling is felt over the obturator foramen. xx Here strangulation is usually of Richter’s type.

Treatment

Treatment

xx Through a lengthy transverse incision herniotomy and later closure of the defect layer by layer using nonabsorbable interrupted sutures. xx But ideally mesh is required to cover the defect properly. xx Laparoscopic dual mesh placement is also useful.

xx Laparotomy is done and the sac is identified. It is dis­sected and ligated. If strangulation is present (common), resection and anastomosis is done. Broad ligament is stitched over the opening to prevent recurrence. xx Mesh placement is the ideal way of repairing the obturator defect. xx In nonobstructive type, if diagnosed clinically and by CT scan imaging, either TEP (laparoscopic) or lower abdominal midline extraperitoneal approach may be the method to manage the obturator hernia. xx In strangulated hernia, rarely additional exposure in thigh often may be required to reduce the content through a vertical medial pectineus muscle split incision.

A

RICHTER’S HERNIA

B Figs 18.95A and B: Spigelian hernia. On table finding and placement of mesh in same patient.

OBTURATOR HERNIA xx It is hernia occurring through obturator canal between superior ramus of pubis and obturator membrane. It is a rare entity, seen in elderly females (6::1 ratio female to male).

Clinical Features xx Usually presents with features of intestinal obstruction (85%) and more often confirmed only on laparo­tomy. xx Rarely seen as a swelling in Scarpa’s triangle (20%) deep to the pectineus muscle, with limb in flexed and abducted position. Movement of limb is painful.

A

B

Figs 18.97A and B: (A) Strangulated femoral hernia, Richter’s type with perforation. Patient underwent resection and anastomosis; (B) Richter’s hernia.

Hernia It is a hernia in which the sac contains only a portion of the circumference of the intestine (small bowel). It is usually seen in femoral and obturator hernia.

Treatment Repair using fascial flaps or mesh.

PHANTOM HERNIA

Clinical Features xx It mimics gastroenteritis with pain abdomen, diarrhoea, toxicity, vomiting. xx There are no features of intestinal obstruction. xx Constipation does not occur in Richter’s hernia. xx Gangrene (strangulation) of a part of bowel occurs, eventually leading to peritonitis.

Treatment xx Resection and anastomosis is done. xx The type of hernia is treated. xx Mortality increases with delay in surgical intervention.

LUMBAR HERNIA xx It is herniation either through superior or inferior lumbar triangle. xx Superior lumbar triangle (Grynfelt’s/Lesgaft’s triangle) is bounded by sacrospinalis, 12th rib and posterior border of internal oblique. xx Inferior lumbar triangle is bounded by latissimus dorsi, external oblique and iliac crest (triangle of Petit). xx Lumbar hernia is more common through superior lumbar triangle. xx It can be:  Primary.  Secondary, which is due to previous renal surgery, more common.

xx It is a muscular bulge as a result of local muscular paralysis due to interference with nerve supply of the affected muscles, like poliomyelitis. It is common in lumbar region. It is often seen in lower abdomen. Phantom hernia is muscular bulge due muscle paralysis in lumbar region Phantom limb is feeling of pain in amputated toe or limb Phantom tumour is tumour like lesion in lung like interlobar pleural effusion

SCIATIC HERNIA xx It is a rare hernia. xx It is the protrusion of the peritoneal sac through the greater or lesser sciatic foramen. Types Classified based on their relationship to the pyriformis muscle and ischial spine. 1. Suprapyriformis. 2. Infrapyriformis. 3. Subpyriformis.   Sac lies deep to gluteus maximus. Large hernias protrude below the buttock crease.

Diagnosis: Usually on laparotomy for intestinal obstruction. Treatment: Defect is covered by fascia mobilised from pyriformis muscle after reducing the sac contents.

COMPLICATIONS OF HERNIA SURGERY

B

A

Figs 18.98A and B: (A) Lumbar triangles; (B) Lumbar incisional hernia—large. Previous lumbar incision scar is visible. Differential diagnosis Lipoma. Cold abscess. ™™ Lumbar phantom hernia. ™™ ™™

Proper idea of complications of hernia surgery are important as often complications may become more problematic than hernia itself. 20 years back where tissue repair was popular recurrence was the most worried complication. Now since recurrence rates have come down due to standard usage of mesh, mesh related complications have become more common than recurrence. Inguinodynia, mesh extrusion, mesh infection, mesh erosion are the worried problems.

• Complications of open hernia surgery

• Early

• Complications of TEP/TAPP

• Delayed

• Complications of other hernia surgery— ventral/femoral

• Late • Life-threatening

The wind of anger blows out the lamp of intelligence.

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SRB's Manual of Surgery Inguinodynia xx It is chronic inguinal pain seen in post-hernia surgery patients (30%)—whether tissue or mesh repair. xx Causes are—traction, cautery, transection, entrapment. Even though it can occur in both tissue and mesh repair, it is more observed in mesh repair especially in onlay mesh repair. It is due to entrapment of nerve in the suture or in the mesh itself or nerve gets adherent to the mesh during fibrosis (perineural fibrosis) (Mesh inguinodynia). Complications of open hernia surgery

Complications of TEP/TAPP

• Infection • Groin pain; ostetitis pubis • Ischaemic orchitis—due thrombosis of pampiniform venous plexus (0.5%) • Injury to vas • Injury to viscera • Recurrence • Hydrocele formation • Seroma, haematoma • Inguinodynia—neural • Dysejaculation—painful, burning sensation just before/during/after ejaculation due to cremaster dysfunction or vas stricture (0.25%)

• SC emphysema • Pneumothorax, hypercarbia • Vascular • Neural • Visceral • Infection, ileus • Conversion • Recurrence

Immediate

Late/delayed

• Vascular—injury to iliac vessels/ IE vessels • Visceral injury—bowel/bladder • Vas injury • Anaesthetic complications

• • • • • •

Seroma/haematoma Neural complications Intestinal obstruction Bowel adhesion/fistula Testicular atrophy Mesh related complications • Recurrence

xx It may be transient or persistent. xx Nerves involved are—iliohypogastric, ilioinguinal, genital branch of genitofemoral nerve, paravasal nerves. xx Features are—distressing pain in the groin which often radiates to thigh, scrotum and loin. Arch and twist mobility of pelvis reproduce the pain. Bupivacaine injection relieves the pain. Imaging/ nerve conduction studies are of no use. xx Open method has higher (32–38%) incidence of inguinodynia than TAPP/TEP. In open hernia surgery inguinodynia has replaced recurrence as a primary complication. It is distressing discomfort to both patient and surgeon. Incidence is less in posterior or laparoscopic approach.

xx It is treated with analgesics/nerve block (Injection of steroid, local anaesthetic agents, phenol, and alcohol)/transcutaneous stimulation/ cryotherapy/radiofrequency therapy/neurectomy. xx Neurectomy is done via groin or suprainguinal or laparoscopic or laparotomy approach. Commonly groin approach is used. Ilioinguinal, iliohypogastric and genitofemoral nerves are carefully dissected. Nerve which is causing the problem is transected at a point where it comes out of the internal oblique muscle and proximal end should be ligated, otherwise end neuroma may form to cause recurrence of the pain. This ligated stump is buried in the internal oblique muscle. Just neurolysis may be sufficient but chances of re-adhesion are higher with recurrence of symptoms. In difficult cases nerve may be transected through laparotomy/ laparoscopy approach.

PARASTOMAL HERNIA xx It is herniation of intestine on the side of bowel stoma—ileostomy/ colostomy/other stomas. xx Incidence is 8%. xx Classification (Devlin’s): (1) Subcutaneous—intestine herniates along the side of stoma to reach subcutaneous plane—most common. (2) Interstitial—along the side of stoma intestine herniates into intermuscular plane. (3) Intrastomal—bowel herniates between emerging and everted parts of the stoma. (4) Perstomal— herniation occurs between the layers of the prolapsed stoma. xx Features: Pain, features of obstruction, stomal malfunction, swelling which is tender, toxicity. xx Diagnosis: X-ray; CT abdomen. xx Treatment: Surgery is indicated in recurrent obstruction, narrow neck, strangulation, interference with stoma.  Stoma is dissected, hernia content is reduced and defect is repaired. But it shows high recurrence.  Subcutaneous mesh repair as onlay placement after reduction of hernia.  Extraperitoneal mesh repair around the stoma.  Intraperitoneal mesh repair deep to peritoneum surrounding the stoma and defect.

Different types of hernia

1. Gibbon’s hernia—It is hernia with hydrocoele 2. Berger’s hernia—Hernia in pouch of Douglas 3. Romberg hernia—Saddle hernia 4. Obturator hernia—Hernia through obturator foramen (canal) 5. Grynfelt’s hernia—Upper lumbar triangle hernia 6. Petit’s hernia—Lower lumbar triangle hernia 7. Femoral hernia—Hernia medial to femoral vein 8. Cloquet’s hernia—Hernia through pectineal fascia 9. Narath’s hernia—Behind femoral artery, in congenital dislocation of hip 10. Hesselbach’s hernia—Lateral to femoral artery 11. Serofini’s hernia—Behind femoral vessels 12. Laugier’s hernia—Through lacunar ligament

Contd...

Hernia Contd...

Contd...

13. Teale’s hernia—In front of femoral vessels 14. Richter’s hernia—Part of circumference of bowel wall is gangrenous 15. Littre’s hernia—Hernia with Meckel’s diver­ticulum as the content 16. Sliding hernia—Posterior wall of the sac is formed by colon or bladder 17. Maydl’s hernia—‘W’ hernia 18. Phantom hernia—Localised muscle bulge following muscular paralysis 19. Spigelian hernia—Hernia through spigelian fascia

Contd...

20. Mery’s hernia—Perineal hernia 21. Sciatic hernia—Hernia through greater or lesser sciatic foramen 22. Amyand hernia—Appendix in inguinal hernial sac 22. Amyand hernia—Appendix in inguinal hernial sac 23. Beclard’s hernia—Femoral hernia through the saphenous opening 24. Barth’s hernia—Hernia between abdominal wall and persistent vitellointestinal duct 25. Holthouse’s hernia—Inguinal hernia that has turned outwards into the groin 26. De Garengeot’s hernia is incarcerated appendix in femoral hernia

Our greatest glory is not in never falling, but is rising every time we fall.

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Chapter

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Oesophagus CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Anatomy Lower Oesophageal Sphincter Dysphagia Contrast Study of Oesophagus Oesophagoscopy Oesophageal Endosonography Third Space Endoscopy Gastro-oesophageal Reflux Disease ™™ Hiatus Hernia

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Rolling Hernia Reflux Oesophagitis Barrett’s Oesophagus Barrett’s Ulcer Oesophageal Motility Disorders Achalasia Cardia Plummer-Vinson Syndrome Corrosive Stricture of Oesophagus ™™ Schatzki’s Rings

ANATOMY

Anatomical specialities

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Boerhaave’s Syndrome Mallory-Weiss Syndrome Tracheo-oesophageal Fistula Oesophageal Diverticulum Carcinoma Oesophagus Benign Tumours of the Oesophagus ™™ Oesophageal Perforation

Parts

Oesophagus is a hollow muscular tube which begins at the lower edge of the cricoid cartilage (C6 vertebra) and ends at oesophagogastric junction (T12 vertebra). It is 25 cm in length. Upper end is closed by crico­pharyn­geus muscle which is 18 cm from upper incisors. Lower end is 40 cm from the upper incisors (upper jaw is fixed and so is used as the landmark to measure, but not the lower jaw which is mobile). It lies anterior to vertebral column and posterior to the trachea. It lacks serosal layer but is surrounded by a layer of loose fibroareolar adventitia.

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Lacks serosa (other structure without serosa is rectum). Contains 2 different types of muscles (striated and smooth at proximal 1/3 and distal 2/3 respectively) Contains 2 different types of epithelium. Segmental blood supply. Only part of GIT which shows very thinly scattered Meissner’s plexus. Longitudinal arrangement of veins and lymphatics.

It is lined by squamous epithelium throughout the length except the last 3 cm (OG junction) which is lined by columnar epithelium. Submucosa of the oeso­phagus is thick and strongest part.

1. Cervical oesophagus: It extends from cricopharyn­geus which is the horizontal part of inferior constrictor muscle. Upper oblique part is called as thyro­pharyngeus. Gap between the two is called as Killian’s dehiscence which is a site of occurrence of pharyngeal pouch. Cervical oeso­phagus is related to trachea and recurrent laryngeal nerve. 2. Thoracic oesophagus: Lies initially towards the right side. In lower third, it deviates towards the left and continues as abdominal oesophagus. It is related to azygos vein, thoracic duct (which crosses the oesophagus posteriorly from right to left), aorta, pleura and pericardium. 3. Abdominal oesophagus is 2.5 cm long and grooves behind the left lobe of the liver. Three areas of anatomic narrowing Cervical constriction—occurs at the level of crico­pharyngeal sphincter—narrowest point of GIT—15 cm from upper incisor— site of F/B impaction ™™ Bronchoaortic constriction—located at the level of T 4 – 25 cm from upper incisor—site of endoscopic perforation ™™ Diaphragmatic constriction—occurs where oeso­phagus traverses the diaphragm (Level of T10)—40 cm from upper incisor ™™

Oesophagus Arterial supply of oesophagus By inferior thyroid artery, oesophageal branches of the aorta, gastric arteries and inferior phrenic arteries. Venous drainage of oesophagus By inferior thyroid vein, brachiocephalic vein, hemiazygos vein, azygos vein, coronary vein, splenic vein and inferior phrenic vein. Veins are longitudinal and they lie in submucosal plane in lower third and in muscular plane above.

A

B Figs 19.2A and B: (A) Arterial supply and (B) Venous drainage of oesophagus.

xx However, due to longitudinal arrangement of lymphatic plexus in the wall of oesophagus, any group of (neck/thorax/coeliac) lymph nodes can get involved in diseases at any level.

Fig. 19.1: Anatomical relations of the oesophagus. Lymphatic drainage Lymphatic arrangement in oesophagus is longitudinal and so spread of carci­noma to distant lymph nodes occurs early. Longitudinal lymphatics are 6 times more than transverse one There are more lymph vessels in submucosa than blood vessels. Lymph nodes are: xx Paraoesophageal groups located in the wall of the oeso­phagus and are cervical, thoracic, paraoesophageal and paracardial nodes. xx Perioesophageal groups located immediately adjacent to oesophageal wall. They are deep cervical, scalene, paratracheal, mediastinal, diaphragmatic, gastric and coeliac lymph nodes. xx Lateral oesophageal groups receive lymph from para and perioesophageal lymph nodes. xx Upper oesophagus drains into supraclavicular nodes. xx Thoracic oesophagus drains into paraoesophageal and tracheobronchial nodes in thorax. xx Abdominal oesophagus drains into coeliac nodes.

Fig. 19.3: Lymphatic drainage of the oesophagus.

Nerve Supply xx Oesophagus is innervated by vagus. xx It has got both sympathetic and parasympathetic innervation. xx It has got mainly Auerbach’s plexus between longitudinal and circular muscle layers.

Don’t go through life, but grow through life.

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SRB's Manual of Surgery Leugart’s pouch is prolapse of the wall of the oesopha­gus like a diverticulum over a band (Leugart’s band) between the left bronchus and adjacent vertebra.

xx Dysphagia can be oropharyngeal or oesophageal depending

Physiology

geal phase of the swallowing wherein patient also develops cough while swallowing. Dysphagia due to problem in oesophageal involuntary phase of swallowing is specified by food getting stuck in the pathway. But site of “food getting stuck” feeling is not relevant. xx Dysphagia can be progressive or intermittent.

Three types of contractions in the oesophagus: 1. Primary: Progressive, triggered by swallowing. 2. Secondary: Progressive, generated by distension or irritation. 3. Tertiary: Nonprogressive. Presbyoesophagus is less efficient oesophageal peristalsis. Note:

• •

Laimer’s triangle is formed with base above formed by cricopharyngeus and on either side divergent longitudinal oesophageal muscles. Laimer’s triangle is in the posterior part of the oesophagus midline. Collar of Helvetius is the site where oesophageal circular muscle fiber becomes oblique muscle of the stomach.

LOWER OESOPHAGEAL SPHINCTER (LOS) xx It is a high physiological pressure zone located in the lower end of the oesophagus in terminal 4 cm, with a resting pressure of 10–25 mmHg. xx LOS prevents reflux of gastric and duodenal contents. xx It is influenced by food, gastric distension, gastric pathology, smoking, GI hormones, alcohol. xx Normally there is a transient relaxation period where­in reflux (physiological) occurs but then immediately gets cleared by oesophageal clearance mechanism. xx So pathological reflux or GORD can occur due to decreased LOS tone, altered relaxation time, reduced oesophageal clearance mechanism, or other altered mechanical factors. xx Oesophageal clearance mechanism is due to primary oesophageal peristalsis which carries saliva with high bicarbonate content which neutralizes and clears the transient physiological reflux. Manometry with special microtransducers are used to measure the LOS pressure.

on the cause. xx Dysphagia may be due to pathology in voluntary/pharyn-

Causes of Dysphagia Common causes: xx Gastro-oesophageal reflux diseases (GORD/GERD/Hiatus hernia). xx Carcinoma oesophagus: Here dysphagia is of short duration and progressive. 2/3 of the lumen should be blocked by tumour to develop dysphagia. xx Foreign body in oesophagus: It may be coin/bone piece/ denture. It is common in children. It causes acute dysphagia. It may be often life-threatening. xx Carcinoma of pharynx or posterior 1/3rd of the tongue. xx Corrosive strictures: It is usually alkali stricture. Squamous mucosa is resistant to acid effect to certain extent. xx Oesophageal candidial infection: It is becoming common due to immunosuppression in association with HIV infection; steroid therapy; cancer chemotherapy; post-transplant period, etc. Presentation is dysphagia and odynophagia. Oral candidiasis (thrush) is obvious. Endoscopy shows whitish curd-like plaques in the oesophageal mucosa which cannot be moved (whereas food particles can be moved). Barium swallow shows mucosal ulceration and irregular areas. Biopsy confirms the diagnosis. Treatment is oral antifungal as well as topical antifungal therapy.

DYSPHAGIA xx Dysphagia is difficulty in swallowing. Painful swallowing

is odynophagia. xx It can be acute—due to foreign body impaction or acute

infection or chronic due to causes like stricture or carcinoma, etc. xx Associated hoarseness of voice may be present in advanced pharyngeal or post-cricoid carcinomas. At late stage laryngeal carcinoma also can cause dysphagia along with hoarseness of voice.

A

B Figs 19.4A and B: Endoscopic view of oesophageal candidiasis infection. Note the whitish curd-like plaques.

Causes of dysphagia Extraluminal causes

Causes in the wall of oesophagus or other area

Causes in the lumen

• Mediastinal nodes— secondaries/lymphoma/ tuberculosis • Aortic aneurysm • Rolling hiatus hernia • Thyroid enlargement— malignant • Dysphagia lusoria • Congenital anomalies • Mediastinitis/mass

• Carcinoma oesophagus • Corrosive/tuberculous/inflammatory/congenital stricture oesophagus • GERD • Achalasia cardia • Plummer-Vinson syndrome • Oesophageal diverticulum • Carcinoma posterior 1/3rd of tongue/pharynx • Diffuse oesophageal spasm • Congenital anomalies • Retropharyngeal abscess/peritonsillar abscess (Quinsy)/acute tonsillitis/pharyngitis

• Foreign body in the oesophagus—coin/ dentures/fish or meat bone Other causes Cranial causes (neurological): • Bulbar palsy/infarction/hemiplegia • Vertebrobasilar insufficiency

Oesophagus xx Plummer-Vinson syndrome. xx Mediastinal swellings—primary tumours/nodal mass either lymphoma or secondaries or tuberculosis. Rare causes: xx Diffuse oesophageal spasm: They are incoordinated contractions of oesophagus causing chest pain or dysphagia. It is common in distal 2/3rd of the oesophagus. Hypertrophy of circular muscle fibres with very high persistent pressure of 400–500 mmHg is specific. Treatment is calcium channel blockers, vasodilators, endoscopic dilatation and extended oesophageal surgical myotomy up to the aortic arch (very useful especially for dysphagia; not much for chest pain). xx Oesophageal diverticula, Chaga’s disease. xx Dysphagia lusoria (Lusoria means in Latin “sport of nature”): It is a congenital vascular anomaly of aortic root. Aortic arch anomalies are—double arch (40%), right arch and left ligamentum arteriosum (25%), anomalous innominate or common carotid artery or aberrant right subclavian artery (10%). It is due to disappearance of proximal right 4th aortic arch instead of distal portion. All patients having this anomaly (dysphagia lusoria) have got an aberrant right subclavian artery in a transposed position arising from descending aorta that courses posterior to oesophagus. Often there will be a complete vascular ring around trachea and oesophagus. It is categorised based on their specific subclavian anomaly—depends on presence of aneurysm, occlusive disease and compression. Commonly they are asymptomatic. Presentations may be dysphagia, chest pain, stridor, wheeze, recurrent respiratory infection (usually presents after the age of 40). Investigations: CT chest, MRI, chest X-ray, barium swallow (T4 level diagonal impression) and endoscopy (shows pulsating extraluminal compressive mass). Treatment is reconstruction or ligation of aberrant right subclavian artery by sternotomy/by neck approach. xx Thyroid swelling: It is uncommon to develop dysphagia in a thyroid swelling. There will be always dyspnoea when dysphagia develops. Large malignant thyroid or anaplastic thyroid can cause dysphagia with dyspnoea or stridor. xx Boerhaave’s syndrome: It is vertical full thickness tear of lower oesophagus due to vomiting with closed glottis. It is often lifethreatening and emergency. xx Neurological causes like stroke, bulbar palsy, motor neuron disease, Parkinson’s disease, etc. xx Congenital anomalies of oesophagus. xx Drug-induced dysphagia: Drugs like KCl, quinine, NSAID can cause dysphagia. xx Mediastinal fibrosis.

Evaluation of a Patient with Dysphagia xx xx xx xx

Proper history. Haematocrit. Chest X-ray often shows mediastinal mass lesion/foreign body. Oesophagoscopy: Once lesion is detected, it is treated accordingly. Biopsy from lesions, endotherapy if needed should be carried out (like F/B removal; stricture dilatation; sclerotherapy). xx Barium swallow may show irregular filling defect or extrinsic compression. xx CT scan chest is very useful method to identify the anatomical location of the cause (nodes/tumour/aorta/cardiac cause/congenital).

xx xx

xx

xx xx

Extent, spread, nodal status, size and operability of tumour also well-assessed. Oesophageal manometry in achalasia cardia/GERD. 24 hours pH monitoring is ideal and most accurate for GERD. Small pH probe (transnasal catheter) is passed into the distal oesophagus 5 cm proximal to upper margin of LOS under manometry guidance. Probe is connected to a digital recorder worn by the patient for 24 hours. Record is analysed using a computer. A pH less than 4 for more than 4% of total 24 hours period (more than near to one hour in toto in 24 hours) is pathological reflux. It is often assessed by scoring system. Radio-telemetry pH probes are used now without any nasal tube. It is passed and placed on the oesophageal wall using endoscope. Endosonography is very useful in many conditions causing dysphagia. It can assess site, layers of the oesophagus, nodes, spread, etc. properly. Different layers are seen as alternating hyperechoic and hypoechoic bands. Ultrasound abdomen to see abdominal nodes/liver/ascites. MRI study.

Treatment for Dysphagia Depends on cause—modified Heller’s myotomy; oesophageal resection; dilatation; F/B removal, etc.

CONTRAST STUDY OF OESOPHAGUS Types 1. Barium swallow using barium sulphate (thick paste). 2. Using water-soluble contrast like ‘Gastrografin’.

A

B

Figs 19.5A and B: Barium swallow X-rays showing narrowing and irregularity in carcinoma oesophagus.

Indications 1. Barium swallow  Dysphagia due to motility disorder like acha­lasia cardia, diffuse oesophageal spasm.  Dysphagia due to mechanical causes like carcinoma, benign strictures and neoplasms, external compression.  Pharyngeal pouch and other diverticula.  GORD.

Instrumentation is the most common cause of oesophageal rupture.

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SRB's Manual of Surgery 2. Water-soluble contrast radiograph  In suspected oesophageal perforation.  Leaking oesophageal anastomosis.

Important Findings in Barium Swallow xx Achalasia cardia—‘Bird beak’ appearance, as the oesophagus is grossly dilated above an apparent narrowing at the cardia. In longstanding cases—‘sigmoid oesophagus’. xx Diffuse oesophageal spasm—Corkscrew appearance. xx GORD—shows reflux when done in Trendelen­burg’s position. xx Oesophageal carcinoma—irregular stenosing lesion with shouldering (‘Rat tail’ is a fluoroscopic finding). xx Pharyngeal pouch—demonstration of the pouch. xx External compression—indentation of barium column by superior or posterior mediastinal mass, enlarged left atria as in mitral stenosis.

OESOPHAGOSCOPY Indications Diagnostic To identify the lesion and to take biopsy in carci­noma oesophagus. ™™ For diagnosing other oesophageal conditions. ™™

Therapeutic ™™ To remove foreign body ™™ To dilate stricture ™™ To place endostents for inoperable carcinoma oeso­phagus ™™ To inject sclerosants for varices

 Complications are perforation (most common site of perfora-

tion is at the level of cricopharyn­geus), bleeding. 2. Fibreoptic flexible oesophagoscope  It can be done under local anaesthesia. Reflux and hiatus are well identified. Stomach also can be visualised. Easy to pass and perforation is unlikely.  But tissue taken for biopsy is smaller and removal of foreign body is also difficult.

Oesophageal Endosonography xx It is useful method of finding and assessing invol­vement or pathology of diffe­rent layers of oesophagus especially in carcinoma oesophagus. It shows all layers clearly and distinctly and so invasion can be better made out and operability can be decided. xx Endoscopic oesophageal staining using labelled iodine is used to identify early carcinoma in oeso­phagus. Normal mucosal cells contain glycogen which takes up iodine and so stains brown, whereas carcinoma cells will not take up iodine and so mucosa appears pale (not stained).

THIRD SPACE ENDOSCOPY xx It is newer method wherein submucosal or intramural space which is called as 3rd space (first being luminal space and 2nd peritoneal space) is approached for various therapeutic and diagnostic purposes. It is also designated as SuMO (SubMucosal Operation). xx Currently, it is used in upper gastrointestinal area like oesophagus and stomach. Procedures done are – POEM (Per oral endoscopic myotomy) for achalasia cardia, submucosal tunneling tumour biopsy, submucosal tunneling pyloromyotomy for gastroparesis after vagotomy (G-POEM), submucosal tunneling tumour excision (STER). It is said to be safer, effective and less invasive; procedure is fast developing.

GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD/GERD) xx It is a pathological reflux from the stomach into the lower

oesophagus. xx It accounts for 75% of oesophageal pathology (most

common). xx Symptoms may be due to peptic oesophagitis, LOS dysfunc-

tion, aspiration due to reflux, due to late effects like stricture and obstruction. xx It is due to varied anatomical and physiological factors.

Anatomical Factors Fig. 19.6: Oesophageal candidiasis—note the multiple curd-like lesions.

Types 1. Rigid oesophagoscope (Negus type)  It is done under general anaesthesia. Head is extended and head end of the table is tilted upwards, scope is passed behind the epiglottis and cricoid through the crico­pharyngeal opening. This is the most diffi­cult part in oeso­phagoscopy. After that, negotiating through the oesophagus is easier. The lesion is identi­fied and biopsy is taken if required.

xx Obesity. xx Altered length of intra-abdominal oesophagus. Level of

acid exposure is inversely related to length of the intra­ abdominal oesophagus. More the length more the need of intra-abdominal pressure to cause the reflux and so less the reflux with more length. xx Alteration of phreno-oesophageal ligament. xx Altered obliquity of O-G junction (alteration in angle of ‘His’). xx Reduced pinching action (Pinch-Cock effect) of right crus of diaphragm. xx Alteration in normal mucosal rosette at O-G junction. xx Alteration in sling mechanism of gastric musculature.

Oesophagus Physiological Factors

Clinical Features

xx Reduced LOS pressure. Normal resting LOS pressure

xx Fatty dyspepsia. xx Chest pain and heart-burn (pyrosis)—80%—main

is 10–25 mmHg. During swallowing, pressure drops to 1–3 mmHg for few seconds (10 seconds). Resting pressure is increased by gastrin, cholinergic, adrenergic, prokinetic drugs; decreased by secretin, cholecystokinin, glucagon, calcium channel blockers, deriphylline, coffee, fatty meal. xx Altered transient relaxation period in LOS. xx Reduced oesophageal clearance mechanism. Change in oesophageal clearance is due to altered oesophageal body pump (primary peristalsis with 30–80 mmHg amplitude propagative downwards waves; secondary by food bolus), altered salivary bicarbonate neutralizing mechanism of reflux acid, altered mucosal defense mechanism (mucous and surface active phospholipid). xx Delayed gastric emptying due to diabetes, neuromus­cular block, gastroparesis, medications. xx Increased gastric distension and gastric acid hyper­ secretion.

symptom. Pain is more in lying down position and at night. It may mimic cardiac pain/angina. It often begins in the epigastrium and becomes substernal. xx Odynophagia (painful swallowing). xx Appearance of symptoms within seconds of ingestion of food is typical. xx Regurgitation—50%. It is return of oesophageal content. xx Laryngeal symptoms—hoarseness of voice. xx Dysphagia will occur once complications begin. xx Symptoms are more with change of position. xx Chronic cough, shortness of breath and hoarse­n ess— Nocturnal reflux—reflux is return of gastric content. xx Haematemesis. xx Post-prandial fullness, choking, wheezing, recurrent pneumonia are other features. Triad

Note: GERD is not associated with H. pylori infection.

Other Factors xx Alcohol, smoking, stress, lifestyle. xx It is seen in infants and children and also in pregnant women.

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Heart burn Epigastric pain with dysphagia Regurgitation

Typical Symptoms Heart burn, regurgitation, dysphagia mainly; odynophagia, haematemesis often.

Pathogenesis GERD begins from distended fundus due to variety of causes and other anatomical and physiological factors, repetitively unfolding the sphincter to the gastric juice leading to all problems. There is reduced and low LES resistance causing loss of barrier to reflux. It is probably due to gastric distension, delayed gastric emptying, and raised intragastric or intra-abdominal pressure. Gastric distension may be due to overeating or aerophagia. Fundic distension → stretching of fundus → LOS squamous epithelium exposed to acid gastric juice → oesophagitis → increased stimulus to swallow saliva to neutralise oesophagitis → further fundal distension → cycle repeats → sphincter is taken into stretched fundus → effects like erosion, ulceration, fibrosis, mucosal metaplasia. Types Classification I ™™ Symptomatic uncomplicated GORD (NERD—Nonerosive Reflux Disease) ™™ Symptomatic, complicated GORD Classification II ™™ Primary: Incompetent LOS ™™ Secondary: Due to surgery/disease Classification III ™™ GORD with sliding hernia ™™ GORD without sliding hernia Classification IV ™™ Acute – After alcohol intake, stress, burns. ™™ Chronic – Hiatus hernia, postoesophageal surgery.

Atypical Symptoms Cough, hoarseness, wheezing, sore throat, noncardiac chest pain and palatal/dental erosions. It will eventually lead into recurrent pneumonia and pulmonary fibrosis. If pH of the cervical oesophagus is below 4, for less than 1% of time, then respiratory symptoms are due to GERD. De Meester’s scoring system Grade 0 1 2 3 0 1 2 3 0 1 2 3

Features Heart burn None Minimal—occasional episodes Moderate—medical therapy visits Severe—interferes daily activities Regurgitation None Minimal—occasional episodes Moderate—on position and straining Severe—features of aspiration Dysphagia None Minimal—occasional episodes Needs fluid to clear Causes food impaction

Reflux is precipitated by flexion of the trunk—Boot lacing sign.

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SRB's Manual of Surgery Complications xx xx xx xx xx xx

Reflux oesophagitis. Sliding hiatus hernia. Stricture lower-end oesophagus. Oesophageal shortening. Barrett’s oesophagus. Carcinoma (adeno) oesophagus (10% of GERD).

Oesophageal

Extraoesophageal

• • • • •

• Laryngitis • Recurrent pneumonia • Progressive pulmonary fibrosis

Oesophagitis Stricture Barrett’s oesophagus Oesophageal shortening Carcinoma (adeno)

xx Barium study in head down position. xx Endoscopy to exclude other disease and to assess any

mucosal injury—red inflamed mucosa often with ulceration. Sliding hernia can be identified through endoscopy. When patient retches, gastric mucosa will enter the OG junction and ascends upwards to variable distance. xx Mucosal biopsy to confirm metaplastic trans­formation. xx Oesophageal manometry to assess the function of LES. Length and pressure of LOS is important. Transient relaxation period which is increased is most important. xx 24 hours oesophageal pH monitoring—gold standard. PPI should be stopped for 3 weeks prior to pH monitoring.

C

Differential diagnosis ™™ ™™ ™™ ™™ ™™ ™™ ™™

Achalasia cardia Carcinoma oesophagus Peptic ulcer Gallstones Pancreatic diseases Gastritis Cardiac angina

Treatment of Uncomplicated GORD

Investigations

A

xx DeMeester scoring system is used to assess the severity of the GORD. xx 99Tc sulphur colloid mixed with saline scan to study OG reflux and 99Tc HIDA scan to study and detect duodeno-gastric reflux are used.

B

D

Figs 19.7A to D: Gastro-oesophageal reflux disease (GORD) endoscopic views. xx Bernstein test: Instillation of 1:10 HCl into stomach of patient with reflux will reproduce the symptoms; and pH in the lower end of the oesophagus decreases. Later pain disappears with saline infusion. xx Dual probe pH monitoring (one in distal oesophagus and one in proximal oesophagus/trachea) is used to confirm the respiratory complications of GORD.

A. General measure—Lifestyle changes  Control of obesity.  Stop smoking and alcohol.  Avoid tea, coffee and chocolate.  Propped up position.  Small frequent meals. B. Drugs  H2 antagonists; antacids.  Proton pump inhibitors (PPIs)—very effective –– Omeprazole 20 mg—BD for 3–6 months. –– Lansoprazole 30 mg. –– Pantoprazole 40 mg. –– Esomeprazole 20 mg. –– Rabeprazole 20 mg, Ilaprazole 10 mg.  Prokinetic drugs –– Metoclopramide, Domperidone 30 mg. –– Cisapride, Mosapride. –– Itopride 50 mg—does not cause cardiac arrhythmias. –– Defoaming semethicone, alginic acid along with antacids. –– Anticholinergic drugs—pirenzipine. –– Mucosal protector drugs—sucralfate, colloid bismuth. C. Endoluminal therapies for GORD  Endoluminal suturing (Wilson-Cook)  Plexiglass microspheres (PMMA). Microsphere suspended in gelatin is injected through endo­scopic needle. Gelatin gets absorbed and spheres cause a tissue bulking.  Gatekeeper reflux repair system. Endoscopic delivery of preformed radiopaque hydrogel into submucosa.  Stretta catheter. Flexible, soft, 6 mm sized, 65 cm length tube with balloon/basket and 5.5 mm NITI electrode, irrigation and suction  Enteryx injection technique (estrinyl vinyl alcohol)  Endocinch technique  Endoscopic full thickness plication.

Oesophagus D. Surgery  Indications for surgical treatment –– Failure of drug treatment –– Sliding hernia –– Barrett’s ulcer –– Severe pain –– Presence of complications like bleeding/stricture/ shortening, respiratory problems

Surgeries

Antireflux surgery is the only effective long-term beneficial therapy ideally available and considered now. Laparoscopic fundoplication (most popular), Collis-Nissen vertical gastroplasty and fundoplication, resection of OG junction when metaplasia is present, Belsey Mark 4 operation (technically difficult) are the procedures used now. Principles of antireflux surgeries ™™ ™™ ™™ ™™ ™™

Operation should restore the LES pressure twice the resting gastric pressure The adequate length of the intra-abdominal oesophagus should be maintained Apposition of diaphragmatic crurae, reduction of hiatus hernia when present Repaired OG junction should relax during swallowing adequately Tension free fundoplication should be done

Fundoplication xx Nissen’s posterior total fundoplication: Here after narrowing the crus of diaphragm, mobilised posterior part of the fundus of the stomach is wrapped totally 360° around the area of OG junction.

A

after crural repair (otherwise fundoplication may displace into thorax causing paraoesophageal hernia); intra-abdominal length of 2 cm oesophagus is created (not more); fundus of the stomach is known to relax in concert with oesophageal sphincter so only fundus should be used to buttress the sphincter; wrapping should be done only around sphincter oesophagus not around body of stomach; fundoplication should be kept in abdomen without under tension and without displacing into thorax. Nonabsorbable polypropylene sutures are used.  Crural repair is done using interrupted polypropylene sutures.  Fundoplication should prevent sphincter shortening/ unfolding during gastric distension, should preserve normal swallowing ability, allow proper belching and allow vomiting whenever needed.  Bougie; on table and postoperative manometry to assess the pressure of new LOS; on table and postoperative gastroscopy— are commonly used in fundoplication.  Mortality of procedure is very less; other parts of the abdomen can be assessed and addressed like gallstones.  Complications are—gas bloat syndrome (inability to belch); dysphagia; inability to vomit; slippage, proximal migration; paraoesophageal hernia, splenic injury. Floppy Nissen’s fundoplication reduces the incidence of gas bloat syndrome.  Laparoscopic Nissen’s fundoplication is ideal and equally successful.  Transthoracic approach is used for Nissen’s fundoplication in patients who had hiatus hernia repair earlier; who has short oesophagus; in patients who is having sliding hiatal hernia that does not reduce below the diaphragm, associated pulmonary disease, in obese, in patients who are having narrow subcostal angle or barrel-shaped chest. xx Toupet’s partial 180° posterior fundoplication: It is similar to Nissen’s posterior fundoplication; it controls reflux alike Nissen’s but gas bloat is very less. It is commonly done procedure now. Short gastric vessels are divided completely or partially. xx Rosetti Hell anterior fundoplication: Here anterior part of fundus of stomach is used. Superomedial part of the fundus is brought around oesophagus to suture into anterior part of fundus. Here short gastric vessels are not ligated and much less fundus need to be mobilised. xx Dor anterior fundoplication: Here right margin of the fundus is sutured to left margin of the oesophagus; front part of fundus is sutured to right margin of the oesophagus; 2nd row is also sutured to right crus.

B

Figs 19.8A and B: (A) Nissen’s fundoplication; (B) Toupet’s partial fundoplication.  Rudolph Nissen (1959) first did total fundoplication.  Opening the peritoneum over the oesophagus to mobilise the    

lower end of oesophagus. Dissection of the diaphragmatic crura of the oesophagus. Mobilisation of entire fundus by ligating short gastric vessels. Vagi are preserved. In Nissen’s, 60 French bougie wrap is ideal; after complete mobilisation, only posterior part of the fundus is wrapped around

Fig. 19.9: Dor anterior fundoplication. Right margin of the fundus is sutured to left margin of the oesophagus. Front aspect of the fundus is sutured to right margin of the oesophagus. Second row is also sutured to right crus.

Attitude determines altitude.

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SRB's Manual of Surgery xx Watson’s anterolateral fundoplication: 5 cm intraabdominal oesophagus is created with blunt transhiatal dissection. 120° anterolateral fundoplication augments the LOS function during stomach distension. Bougie insertion, division of short gastric vessels are not needed here. xx Lind both anterior and posterior fundoplication of 300° with 60° anteriorly uncovered area is not routinely practiced now. xx Partial fundoplication with mesh wrap around is also used. But complications of mesh like erosion, stricture and adhesions are problems. Fundoplications ™™ ™™ ™™ ™™ ™™ ™™

Nissen’s—total 360° posterior fundoplication Toupet’s—partial 180° posterior fundal/posterolateral Rosetti Hell—total anterior fundal Dor—anterior partial Watson’s—anterolateral 120° partial Lind—posterior and anterior

Note: Other procedures

•

Belsey Mark IV operation (1967): It is plication of oesophagus to the diaphragm through many interrupted mattress sutures so as to push the oesophagus downwards to make it intra-abdominal with adequate length. It is done through left transthoracic approach. 240° fundoplication, creation of intra-abdominal oesophagus, crural sling repair are the techniques. It corrects GERD and also maintains normal eructation and physiological reflux. But long hospital stay and respiratory complications are distressing problems.

Fig. 19.11: Vertical gastroplasty is done to lengthen the intraabdominal oesophagus.

•

Thal’s patch procedure: It is done for localised nondilatable stricture oesophagus. Stricture is incised full thickness longitudinally. Mobilised fundus of stomach is placed and sutured as a serosal patch technique over the defect.

Fig. 19.12: Thal’s patch done for oesophageal stricture due to reflux oesophagitis.

• Fig. 19.10: Belsey mark 4 operation for sliding hiatus hernia. It is done through thoracic approach. Here angle of oesophagus is restored with sutures and partial anterior fundal wrap is done. Then oesophagus is pushed down by oesophago-diaphragmatic plication sutures.

• • •

Hill’s operation: Intra-abdominal fixation of OG junction (cardia) into median arcuate ligament to augment the effect of LOS, to enable the effective oesophageal peristalsis. Procedure is done by transabdominal approach which is assessed by intraoperative manometry. But it is technically difficult, may damage celiac plexus. Placement of Angelchik prosthesis: Annular silicone gel filled angelchik prosthesis with a tape on either end. After insertion around OG junction ends are tied around. Collis’ vertical gastroplasty is done using fundus of stomach. A vertical cut along the line of oesophagus is made on the fundus which is sutured to create extra length of oesophagus and new lesser curvature. It is done whenever oesophagus cannot be mobilised due to oesophageal shortening by a stricture developed as a complication of GORD. Partial fundoplication is added to this usually.

• • • • •

Narbona’s ligamentum teres cardiopexy (commonly done in Spain): Ligamentum teres is mobilised from falciform ligament with its blood supply from left lobe of liver; it is detached from umbilicus and brought around the mobilised lower oesophagus with traction until LOS pressure becomes 15–20 mmHg with manometry; flap end is sutured left of OG junction and anterior wall of stomach. It is more physiological and division of short gastric vessels is not required. Boerema operation: It is fixing OG junction in front into anterior abdominal wall. It is not practiced now. Oesophagogastrectomy is required whenever there is failure of antireflux procedure/metaplasia is present / nondilatable stricture is present. Lower end of oesophagus and proximal stomach is resected with oesophagogastric anastomosis is done through thoracoabdominal approach. Transhiatal oesophagectomy with anastomosis between cervical oesophagus and stomach in the neck is an alternate procedure which can be used in severe extensive disease and stricture. Allison’s procedure: It is transthoracic repair of GE junction to replace the GE junction in its normal intra-abdominal location is one of the earliest procedures done with symptomatic relief but 80% recurrence rate; hence it is not done. Stricture oesophagus due to GERD which is dilatable can be treated by regular oesophageal dilatation and long-term PPI therapy.

Oesophagus Complications of Surgery xx xx xx xx xx xx xx xx

Oesophageal/gastric perforation. Haemorrhage. Pneumothorax/pyothorax. Vagus nerve injury. Cardiac arrhythmias. Sepsis – mediastinitis or septicaemia. Disruption/failure of fundoplication. Gas bloat syndrome.

HIATUS HERNIA

Sliding hernia is commonly associated with GORD (should be discussed like GORD). Here the cardia migrates back and forth between the posterior mediastinum and peritoneal cavity. Saint’s triad ™™ ™™ ™™

Hiatus hernia Diverticulosis Gallstones

Grading of hiatus hernia Grade I-H0 II-H1 III-H2 IV-H3 V-H4

It is the most common type of diaphragmatic hernia. Types of hiatus hernia—classification TypeIhiatus hernia: It is the cephalad displacement of the gastrooesophageal junction through the hiatus into the mediastinum. It is usually small, asymptomatic and reducible. It is commonest type ™™ Type II hiatus hernia: It is superior migration of the fundus of the stomach along side the GE junction and oesophagus into the mediastinum with GE junction in normal intra-abdominal location. It is rolling hernia ™™ Type III hiatus hernia: It is combination of type I and type II ™™ Type IV hiatus hernia: It is the hernia containing other abdominal viscera as content like transverse colon and omentum ™™

Type Normal Sliding Rolling Mixed Massive herniation

Types xx Sliding hernia (85%). xx Rolling hernia (10–12%). xx Combined.

Fig. 19.15: Types of hiatus hernia.

ROLLING HERNIA (PARAOESOPHAGEAL HERNIA) It is herniation of stomach fundus or rarely other abdominal contents colon/spleen through a hiatus, usually towards left side.

Clinical Features Fig. 19.13: Different types of hiatus hernia.

xx xx xx xx xx xx xx

Common in elderly. Abdominal pain and chest pain. Hiccough, early satiety. Regurgitation, postprandial bloating. Cardiac abnormality (arrhythmia). Dysphagia dyspnoea. 40% presents as acute features with perforation/gangrene/bleeding. Complications

A

B

Figs 19.14A and B: Endoscopic view of oesophageal hiatus hernia.

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Gangrene of stomach. Perforation into the mediastinum. Perforation into the peritoneum. Gastric volvulus. Ischaemic longitudinal ulcer in the herniated stomach in rolling hernia is called as Cameron ulcer.

Kindness is a language which the dumb can speak, the deaf can understand.

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Clinical Features

xx Plain X-ray—lateral and PA erect view showing retrocardiac airfluid level. xx Barium meal study very useful. xx ECG. xx 3D CT scan is useful.

xx It is a part of GORD. xx Pain and burning sensation in retrosternal area often referred

Treatment xx Treatment is always surgical.  Excision of sac and repair of the defect.  If it is gangrenous, gastrectomy is required.  Either abdominal or thoracic or laparoscopic approach can be used in treating rolling hernia surgically.  Mesh reinforcement to hiatus to close the defect may be needed.

REFLUX OESOPHAGITIS Types 1. Acute: Following burns, trauma, infection, peptic ulcer. 2. Chronic: Reflux of acid in sliding hernia, after gastric surgery. Reflux is quite common in pregnancy. Site is always in lower oesophagus.

Pathology There is bleeding granulation tissue in lower oeso­phageal mucosa with spasm of longitudinal muscle which pulls the adjacent gastric area upwards into the oesophagus causing sliding hernia. Grading 1. 2. 3. 4.

Mucosal erythema Mucosal erythema + superficial ulceration Mucosal erythema + superficial ulceration + submucosal fibrosis Mucosal erythema + extensive ulceration + para­mural fibrosis

Savary-Miller classification of reflux oesophagitis— grading 1. Single or isolated erosive lesion(s), oval or linear but affecting only one longitudinal folds 2. Multiple erosive lesions, noncircumferential affecting more than one longitudinal fold with or without confluence 3. Circumferential erosive lesions 4. Chronic lesion: Ulcers, strictures and or short oesophagus alone or in association with grade 1–3 lesions 5. Columnar epithelium in continuity with the Z-line, non-circular, star shaped or circumferential, alone or in association with grade 1–4 lesions

Los Angeles classification of reflux oesophagitis—grading A. One or more mucosal break no longer than 5 mm that does not extend between the tops of two mucosal folds B. One or more mucosal break more than 5 mm long that does not extend between the tops of two mucosal folds C. One or more mucosal break that continues between the tops of two or more mucosal folds but which involves less than 75% of the circumference D. One or more mucosal break, which involves at least 75% of the oesophageal circumference

to shoulder, neck, arm. xx Heart burn is common. xx Dysphagia. xx Anaemia.

Diagnosis xx Barium meal X-ray. xx Gastroscopy and biopsy.

Barrett’s ulcer is an ulcer with gastric (columnar) metaplasia in lower oesophagus.

Treatment xx Antacids xx H2 blockers: Ranitidine, famotidine. xx Proton pump inhibitors—Main method and more effective.  Omeprazole 20 mg BD one hour before food (Morning) for 6 months  Lansoprazole 30 mg  Pantoprazole 40 mg  Esomeprazole 20 mg  Rabeprazole 20 mg (can be given with food). xx Prokinetic drugs like metochlopramide, domperi­done, cisapride, mosapride. xx Treating GORD and associated causes. By fundopli­cation and other surgeries. xx Resection in severe cases. Note: Erythromycin is a prokinetic drug (motilin agonist), which acts by binding with motilin receptor on GI smooth muscle cells.

BARRETT’S OESOPHAGUS (Norman Barrett, British, 1950) xx It is the metaplastic changes in the mucosa of the oesophagus as the result of GORD. xx Squamous epithelium of lower end of the oeso­pha­gus is replaced by diseased columnar epithelium (columnar metaplasia). xx There is macroscopic visible length of columnar mucosa with microscopic features of intestinal metaplasia. xx It affects lower oesophagus commonly often middle oesophagus also. xx There is proximally displaced squamocolumnar junction on endoscopy with acid—mucin containing goblet cells that is specialized intestinal metaplasia. There is presence of columnar epithelium lined oesophagus (CELO) with intestinal metaplasia on histology.

Types (Based on Length) a. If the length of metaplasia is more than 3 cm, it is called as long segment Barrett’s oesophagus—classic Barrett type. b. If the length is less than 3 cm, it is called as short segment Barrett’s oesophagus.

Oesophagus Histological Types a. Gastric type: Contains chief and parietal cells. b. Intestinal type: Contains goblet cells. c. Junctional type: Contains mucous glands alike of gastric cardia. Cardia metaplasia is metaplasia at OG junction without any macroscopic change in gastroscopy. This diseased columnar epithelium is more prone for malignant transformation, i.e. when there is intestinal metaplasia, risk of malignant transformation increases (40 times more than general population). More the amount of dysplasia, more is the risk of malignant transformation. Dysplasia may be indefinite; low grade or high grade.

xx

Clinical Features xx Features of GORD. xx Haematemesis. xx Common in men; common in whites. Complications of Barrett’s oesophagus ™™ ™™ ™™ ™™ ™™

Ulcerations and stricture Dysphagia Bleeding Perforation Adenocarcinoma of O-G junction (25 times more common)

Management xx Regular endoscopic biopsy and surveillance for low-grade

dysplasia. Ablation of Barrett’s oesophagus by laser. Photodynamic therapy—through endoscopy. Argon beam coagulation. Proton pump inhibitors—high dose for 3–6 months. Antireflux treatment by surgery. Resection—Always better choice—for high-grade dysplasia. Transhiatal oesophagectomy is preferred. xx Endoscopic mucosal resection. xx xx xx xx xx xx

BARRETT’S ULCER It is an ulcer in columnar epithelium lined Barrett’s oeso­phagus at or just above the squamocolumnar junction. It is more prone for: xx Bleeding. xx Perforation. xx Adenocarcinoma of oesophagus—very high > 40 times. Treatment for Barrett’s ulcer is endoscopic biopsy and resection.

OESOPHAGEAL MOTILITY DISORDERS Primary xx Achalasia, vigorous achalasia. xx Diffuse and segmental oesophageal spasm: It is 5 times less common than achalasia, mainly primary spasm of the oesophageal body, predominantly presenting only as chest pain and less severe

xx

xx

xx

dysphagia. There is hypertrophy of oesophageal wall muscle with degeneration of vagal fibers; Simultaneous multipeak waveforms of high amplitude and long duration with 20 or more simultaneous waveforms out of 10 wet swallows is diagnostic. Often it can be segmental or involve distal 2/3rd of oesophagus. LES resting pressure is normal with normal deglutition relaxation time. Barium swallow shows corkscrew pattern. Treated with nitrates, calcium channel blockers, bougie dilatation, long oesophageal myotomy either video assisted or thoracotomy approach. Nutcracker oesophagus (supersqueeze oesophagus): Common hypermotility disorder with high amplitude peristalsis, equal in both sexes. Severe chest pain (noncardiac), dysphagia without regurgitation, odynophagia are the features. Waves of hypertensive amplitude pressure >180 mmHg often can become very high >400 mmHg; long duration contraction waves >6 seconds with normal LES pressure and LES relaxation. It is treated with nifedipine, nitrates, antispasmodics, occasionally long myotomy. Hypertensive LES: LES pressure is above normal (>26 mm Hg). LES relaxation, amplitude pressure, contraction waves, oesophageal body peristalsis are normal. Botulinum, balloon dilatation, modified Heller’s myotomy are the treatment. Ineffective oesophageal motility disorders: It is irreversible contraction abnormality of distal oesophagus in association with GORD. It is often due to secondary inflammation of oesophageal body following more exposure to gastric contents and poor oesophageal acid clearance. Reflux, dysphagia, heartburn, chest pain, are the features. Manometry shows—sum of total number of low amplitude contractions of less than 30 mmHg and nontransmitted contractions exceeds 30% of wet swallows. Nonspecific oesophageal motility disorders: It shows slow transit incomplete emptying, with normal or hypertensive LES pressure, LES shows incomplete relaxation, decreased amplitude pressure 20% nontransmitted, prolonged waves of >6 secs with abnormal peristalsis. Dysphagia, chest pain reflux and regurgitations are the features.

Secondary xx Neurological—stroke, bulbar palsy, motor neuron disease, multiple sclerosis, Parkinson’s disease, poliomyelitis. xx Muscular—myasthenia gravis, muscular dystrophy, dermatomyositis. xx Autoimmune disorders—systemic sclerosis, polymyositis, SLE, CREST syndrome, scleroderma. xx Eosinophilic allergic oesophagitis, alcoholic neuropathy. xx Endocrine and metastatic diseases.

ACHALASIA CARDIA (Cardiospasm) The symptom—complex in cardiospasm (the term by which oesophageal achalasia was formerly known) is as a rule almost pathognomonic. It may be divided into the three stages—first, cardiospasm without food regurgitation; second, cardiospasm with immediate food regurgitation; third, cardiospasm with dilated oesophagus, the retention of food in the dilated portion and its regurgitation at irregular intervals after taking. — Henry Stanley Plummer, 1908

It is failure of relaxation of cardia (oesophagogastric junction) due to disorganised oesophageal peristalsis, as a result of failure

Never forget that only dead fish swims with the stream.

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xx Achalasia with diffuse oesophageal spasm is called as

‘vigorous achalasia’. xx Presents with progressive dysphagia, which is more for

liquid than to solid food. xx Regurgitation and recurrent pneumonia are common

(60%). xx Walking while eating, chin thrusting, neck and shoulder

extension, Valsalva manoeuvre facilitates emptying of food from the oesophagus. xx Heartburn (50%) is common. Chest pain during meal is common. xx Malnutrition and general ill health. xx Lung abscess formation. xx Odynophagia and weight loss.

Triad

Fig. 19.16: Diagrammatic representation of achalasia cardia.

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Dysphagia Regurgitation Weight loss

Aetiology xx There is absence or less numbered ganglions in myenteric

plexus.  Stress.  Vit B1 deficiency.  Chaga’s disease. It is caused by Trypanosoma cruzi, which is common in South America called as sleeping sickness.  Diffuse oesophageal spasm (Corkscrew oeso­phagus).  Most commonly it is idiopathic. There is degeneration of Auerbach’s myenteric plexus along the entire length of oesophagus more so in LOS. xx There is pencil-shaped narrowing of cardia (O-G junction) with enormous dilatation of proximal oeso­pha­gus, which contains foul smelling fluid and is more prone for aspiration pneumonia. xx Achalasia cardia is a precancerous condition—seven times chances of getting squamous cell carcinoma (8%, after 15 years).

Staging/Grading I: Proximal dilatation 6 cm IV: Sigmoid dilatation

Note: Clinical scoring of achalasia cardia are: 0 No weight loss or dysphagia or retrosternal pain or regurgitation. 1. Weight loss < 5 kg; occasional dysphagia, retrosternal pain, regurgitation. 2 Weight loss 5 –10 kg; daily dysphagia, retrosternal pain, regurgitation. 3 Weight loss >10 kg; dysphagia and regurgitation during each meal; retrosternal pain several times a day.

Investigations xx Barium swallow is diagnostic—shows.

Pathology xx Thickening of circular muscle fibres in distal oesophagus. xx Myenteric inflammation; depletion of ganglion cells; neural fibrosis, reduced nitric oxide and VIP (mediators of LES relaxation). xx Absence of peristalsis; raised LES pressure; failure of relaxation with functional obstruction of OG junction. xx Dilatation of proximal oesophagus with atony.

Clinical Features xx Common in females between 20 and 40 years age group. xx Incidence is 6 per 1, 00,000 population. xx Chest pain occurs in early stage.

A

B

Figs 19.17A and B: (A) Barium swallow X-ray showing features of achalasia cardia; (B) Endoscopic view of achalasia.

Oesophagus Pencil-like smooth narrowing of lower oeso­phagus—Bird beak appearance ™™ Dilatation of proximal oesophagus—cucumber oesophagus ™™ Absence of fundic gas bubble ™™ Sigmoid oesophagus or megaoesophagus ™™

Contd...

Resection of OG junction/transhiatal total oesophagectomy in severe cases—megaoesophagus/metaplasia POEM (Per Oral Endoscopic Myotomy) Forcible dilatation: ™™ Plummer’s pneumotic dilatation ™™ Negus hydrostatic balloon dilatation Drugs: ™™

™™ Botulinum toxin ™™ Nitroglycerin, nifedipine

Surgery xx Modified Heller’s operation (Heller—German, 1913):

Oesophagocardiomyotomy. Success rate is 85%.

Fig. 19.18: Sigmoid oesophagus in achalasia cardia—Barium X-ray and endoscopic view. xx Chest X-ray shows patches of pneumonia. Double medi-

astinal strip of dilated oesophagus is typical with air fluid level in posterior mediastinum on lateral view. xx Oesophageal manometry shows unrelaxed lower oesophageal sphincter with high resting pressure—very useful and gold standard. It shows failure of LES to relax completely during swallowing and complete absence of peristalsis. LES pressure is >35 mmHg. Baseline oesophageal pressure will be high without progressive oesophageal peristalsis with low amplitude muscular tone. Intraoesophageal pressure in relation to intragastric pressure is elevated. xx Oesophagoscopy is done to confirm the diagnosis and to rule out carcinoma oesophagus. It shows totally closed LES (rosette like) with atonic, dilated proximal oesophagus. Biopsy of mucosa at LES should be done.

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B

Figs 19.19A and B: (A) Heller’s cardiomyotomy for achalasia cardia. Only circular muscle layer is cut longitudinally in OG junction until mucosa protrudes out without perforating the mucosa; (B) Heller’s cardiomyotomy—on table look with partial fundoplication (Courtesy: Dr Yogishkumar, Professor of Surgery, KMC, Mangaluru).  Either through thoracic or through abdominal approach, thick-

ened circular muscle fibres are cut longitudinally for about 8–10 cm, 2 cm proximal to the thickened muscle to 1 cm distal to OG junction. Care should be taken not to open the mucosa (anterior myotomy is done now. Original Heller’s is both anterior and posterior myotomies).  Nissen’s or Toupet’s fundoplication is done along with the above procedure to prevent reflux.  Resection is done when failure of myotomy occurs or when megaoesophagus or metaplasia is present. Transhiatal total oesophagectomy with gastric pull up and oesophagogastric anastomosis in the neck is a good option in such patients.

Differential Diagnosis xx Carcinoma oesophagus. xx Stricture oesophagus. xx Scleroderma.

Treatment Treatment for achalasia cardia Surgery: ™™ Modified Heller’s cardiomyotomy with Toupet’s / Dor’s fundoplication –– Open abdominal/thoracic (rare) approach –– Laparoscopic approach—ideal –– Robotic-assisted laparoscopic approach Contd...

A

B

Figs 19.20A and B: Laparoscopic port positions and view of Helller’s cardiomyotomy for achalasia cardia (Courtesy: Dr Roshan, MS DNB, Laparoscopic Surgeon, City Hospital, Mangaluru).

Self-respect — that a cornerstone of all virtue.

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dexterity and three-dimensional vision.

POEM (Per Oral Endoscopic Myotomy) Here using endoscope, methylene blue diluted saline is injected into the submucosa of the oesophagus 15 cm proximal to OG junction; mucosal incision of 2 cm is made proximally to enter submucosal space; adequate tunnel in the space is created; small bleeders are controlled by specialized cautery device; LES myotomy is done using special electric endoknife. Mucosa is closed using clips. It is a novel seemingly effective technique.

•

Botulinum toxin is neurotoxic protein derived from Clostridium botulinum is highly toxic poisonous substance. Very small dose is used for therapeutic purpose. Seven types of toxins are found. A (A1 /A2 /A3) type is used for therapy. It blocks the cholinergic nerve ends reducing the cholinergic acetylcholine release causing flaccid paralysis of muscles. It is used in cosmetic facial line, strabismus, focal dystonia, tremor, tics, muscle spasms, achalasia, smooth muscle hyperactivity, Frey syndrome, and hyperhidrosis.

PLUMMER-VINSON SYNDROME (Paterson-Kelly Syndrome)

Forcible dilatation xx It stretches spasmodic segment. Gradual repeated dilata-

tions are required. Dilatation up to 54 French bougie can be done. Two types of dilatations are used—pneumatic and hydrostatic.  Plummer’s pneumatic dilatation is done using balloons of 30–40 mm diameters. It is inserted over a guidewire. Risk of perforation (5%), need for repeated dilatations are the problems.  Negus hydrostatic dilatation is done to dilate O-G junction. It is not very well-accepted method as chances of perforation is high. Success rate is 65%. 30 mm diameter balloon is inflated for 3 minutes.

Drugs a. Endoscopic injection of botulinum toxin to sphincter—high recurrence rate. b. Calcium channel blocker, nitroglycerin sublingually.

Fig. 19.22: Oesophageal web, endoscopic view. xx Here oesophageal webs are seen in uppermost portion of the oesophagus with spasm of circular muscle fibres. xx Common in patients with long-standing iron deficiency anaemia. xx Common in females. xx Superficial glossitis, cheilitis, koilonychia commonly seen. xx Splenomegaly may be present. xx In oesophageal webs, mucosa is hyperkeratotic, friable, desquamated. xx It is a premalignant condition and presents with severe dysphagia. xx Oesophagoscopy and biopsy is required to rule out malignancy.

Treatment xx Oral iron—ferrous sulphate 300 mg TDS with vitamins. xx Blood transfusion is given when there is severe anaemia (Transfusion of packed cells). xx IV or IM iron therapy. xx Once anaemia comes under control, webs will clear and patient can swallow. Follow-up endoscopy is a must. xx Dilatation of web may be required.

CORROSIVE STRICTURE OF OESOPHAGUS Fig. 19.21: Negus hydrostatic dilator used for achalasia cardia. It has got only 65% success rate. Note:

•

Pseudoachalasia shows features like of achalasia cardia with dysphagia and weight loss, seen in an elderly due to carcinoma. Amylnitrate inhalation causes sphincter relaxation in Achalasia cardia but not in pseudoachalasia.

Features of oesophageal corrosive lesion Acute/immediate –– Severe pain, shock, laryngeal oedema –– Mediastinitis, septicaemia, haemorrhage, perforation ™™ Late/chronic –– Dysphagia –– Stricture—50% ™™

Contd...

Oesophagus Treatment

Contd...

Severe malnutrition Recurrent respiratory infection Oesophageal shortening Malignant changes Tracheo-oesophageal fistula formation Corrosive strictures can be multiple. Damage is more in lower 1/3rd of oesophagus –– –– –– –– ––

xx Corrosives are commonest cause of oesophageal stricture. xx Mainly due to ingestion of alkali (Lye stricture—Lye is strong alkali sodium hydroxide) sodium hydroxide, occasionally due to acid (sulphuric acid, nitric acid). Acid commonly damages the stomach. xx It causes extensive inflammation of the mucosa with perioesophagitis which, if not treated, leads to multiple strictures in oesophagus. xx Sometimes it causes severe life-threatening necro­tising lesion which requires immediate surgical intervention. xx Acute phase lasts for 3 weeks. xx Damage is more in lower 1/3rd of oesophagus. xx Alkali is odourless and tasteless and so large volume is ingested. Alkali causes liquefaction, saponification and thrombosis of vessels and later leading to fibrosis and stricture. Acid causes intense pylorospasm, antral pooling of acid, coagulation necrosis and eschar formation. xx Severity depends on type of agent, its concentration and volume. Phases of tissue injury in corrosive ingestion

Degrees of burns after corrosive oesophageal and gastric burns

Phase 1: Acute necrosis—1–4 days

1st degree: Mucosal hyperaemia and oedema

Phase 2: Ulceration— granulation—4–12 days

2nd degree: Small bleeding, exudates, ulcers, pseudomembrane

Phase 3: Cicatrisation and scarring—3 weeks to 6 months

3rd degree: Mucosal slough, deep ulcers, massive bleed, complete obstruction, charring, perforation

xx Acute phase management:  Neutralisation with vinegar or citrus food if it is alkali ingestion (If pH of the solution is less than 11.5, then damage is less); it is with antacids, milk, egg whites if it is acid ingestion. Early endoscopy is needed to assess the severity and extent.  Emetics and NaHCO3 are avoided as they may precipitate perforation.  In 1st degree burns: 48 hours observation; oral feeds are started once patient swallows saliva painlessly. Regular follow-up endoscopy at 1st, 2nd and 8th months. Stricture, if formed, can be identified by this time.  2nd and 3rd degree burns: They are treated with fluid therapy, antibiotics, nutrition, resuscitation, PPIs, aerosolised steroids, fiberoptic-guided airway intubation if needed/tracheostomy; endoscopic oesophageal stenting, feeding jejunostomy, laparoscopy for evaluation. Unstable patients have high mortality. Laparotomy is done in such patients. If oesophagus and stomach shows full thickness necrosis, resection of these parts is done and end cervical oesophagostomy with jejunostomy is done. When in doubt, re-exploration for second look is done after 36–48 hours to assess the stomach. xx Careful early gentle repeated endoscopy is mandatory. xx Though advocated often for 2–3 weeks, use of steroids is controversial and under debate. xx Antibiotics if there are chances of aspiration or perforation. xx Regular oesophageal dilatation is done for stricture. Stricture is dilated endoscopically using guidewire. Dilators are solid type with gradual increase in diameters. Often radiologic C-arm guidance is needed to pass the guidewire into the stomach. Dilatation should be done up to minimum 16 mm diameter. Pneumatic or balloon dilatation is also practiced. Gum elastic dilators, mercury weighted dilators, Eder-Puestow dilators, Savary-Gilliard dilators, balloon dilators are other dilators used. Earlier, blind dilatation using oesophageal bougies of increased diameters was the practice, which is followed even now in many places, but chances of perforation is more. xx Oesophageal resection in corrosive strictures is technically difficult and may be hazardous. Oesophageal bypass is better and easier, and following later by regular endoscopic surveillance for malignant transformation (5%). Colon is used as replacing conduit as stomach itself may be diseased in corrosive pathology. xx In multiple strictures oesophageal resection and colonic transposition may be advocated if risk of malignancy is considered. Note: Malignancy can develop in corrosive strictures—5%. It is 1000- fold greater than general population.

Causes of stricture oesophagus

A

B

Figs 19.23A and B: Endoscopic view of corrosive injury. Endoscopy should be done very gently in corrosive injury.

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Peptic stricture (oesophagitis induced) Corrosives—most common cause Foreign body Postsurgical, radiotherapy Congenital Infection like tuberculosis Drugs like tetracycline, vitamin C

Happiness comes more from loving than being loved. Happiness is not a destination; it is a method of life and is a way of travel.

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Figs 19.24A and B: (A) Endoscopic view of oesophageal stricture; (B) Oesophageal dilatation is being done endoscopically.

A

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Figs 19.26A and B: (A) Barium swallow X-ray showing Schatzki ring, also shows features of hiatus hernia; (B) Schatzki’s ring—endoscopic view.

Treatment xx Intermittent oesophageal bougienage. xx Antireflux drugs. Note: Ring should not be excised.

BOERHAAVE’S SYNDROME A

B

Figs 19.25A and B: (A) Barium swallow showing stricture at lower oesophagus. It may be due to oesophagitis, congenital, tuberculosis, malignancy, drug induced, etc; (B) Patient underwent total oesophagectomy with colonic transposition. Colon placed in subcutaneous plane.

It is a tear in the lower third of the oesophagus which occurs when a person vomits against a closed glottis, causing leak into the mediastinum, pleural cavity and peritoneum (Refer Table).

Site 2–10 cm of posterolateral part of lower oesophagus.

Investigations

SCHATZKI’S RINGS They are semicircular protrusion of lower oesophageal mucosa located at or just above the oesophagogastric junction (squamo-columnar junction). Its undersurface is lined by columnar gastric epithelium. xx They involve only the mucosa and submucosa of the oesophagus, not the muscle. xx They present with dysphagia and reflux. xx Episodic aphagia can occur causing food bolus or meat bone to get impacted which requires emergency rigid oesophagoscopy to remove the food. 5 ml of 2.5% oral papain every 30 minutes to digest food protein along with 50 mg meperidine iv to dislodge the impacted food bolus can be tried initially.

xx Chest X-ray—shows pneumomediastinum (‘V’ sign of Naclerio). xx MRI/CT chest. xx Total count.

Treatment xx xx xx xx

Nil by mouth. Antibiotics, IV fluids, TPN. Feeding by jejunostomy. Most often surgery with resection may be required (thoracotomy and repair)—left thoracotomy is better. xx When severe mediastinitis occurs, condition has high mortality.

Features of Boerhaave’s syndrome Presentations Sudden onset of symptoms Severe chest pain Pain abdomen Subcutaneous emphysema Shock

Differential diagnosis Myocardial infarction Pancreatitis

‘Crunching effect in the chest’ is called as Hamman’s sign. Mackler’s triad: (1) vomiting, (2) chest pain, (3) subcutaneous emphysema.

Complications Mediastinitis Septicaemia Peritonitis Emphysema

Oesophagus Treatment xx xx xx xx xx xx xx

Conservative, as it is only a mucosal tear. Blood transfusion. IV fluids. Sedation. Haemostatic agents like vasopressin. Endoscopic injection therapy is used if required. Surgery is rarely required.

TRACHEO-OESOPHAGEAL FISTULA (OESOPHAGEAL ATRESIA) Fig. 19.27: Diagrams showing Mallory-Weiss syndrome and Boerhaave’s syndrome.

xx In 85% cases, it is a blind upper end with lower end commu-

nicating with trachea.

MALLORY-WEISS SYNDROME xx It is seen in adults with severe prolonged vomiting, causing

longitudinal tear in the mucosa of stomach at and just below the cardia, leading to severe haemate­mesis. xx Violent vomiting often may be due to migraine or vertigo or following a bout of alcohol. xx Presents with severe vomiting and later haemate­mesis, with features of shock. xx It is common in 1 o’clock position. xx Only 10% of cases involve lower oesophageal mucosa.

xx It may be associated with VACTER anomalies. xx It is a spectrum of anomalies which shares a defect of the

oesophageal continuity with or without a fistula to the trachea or bronchi. V A C TE R

— — — — —

Vertebral defects Anal atresia Cardiac defect (PDA/VSD) Tracheo-oesophageal fistula Radial hypoplasia and renal agenesis

Clinical Features

Investigations xx Gastroscopy, Hb%, PCV, blood grouping. xx During gastroscopy, if stomach is not inflated properly, 50%

cases may be missed. Differential diagnosis ™™ ™™ ™™ ™™

Types (Refer Figure 19.28)

Bleeding peptic ulcer Oesophageal varices Erosive gastritis Carcinoma stomach

xx Incidence is 1 in 4,500 births; common in males (3:1). xx TOF should be recognised within 24 hours of birth. xx Newborn baby regurgitates all feeds and there is continuous

pouring of saliva from the mouth which is a diagnostic feature. xx Cough and cyanosis. xx It is commonly associated with maternal hydramnios (50%).

Investigations xx Obstruction is revealed while passing nasogastric tube. xx Contrast study will reveal fistula and obstruction (Dionosil 1 ml).

Fig. 19.28: Gross classification of TOF – Type A: Atresia without fistula – 8.5%. Type B: Atresia with proximal TOF – 15. Type C: Atresia with distal TOF – 85% (commonest). Type D: Atresia with both proximal and distal TOF – 1.5%. Type E: No atresia but ‘H’ type TOF – 4%.

All are equal in their ignorance.

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SRB's Manual of Surgery –– Treatment: Diverticulopexy/diverticulectomy (excision)

xx Other anomalies are looked for. xx Chest X-ray. xx Echocardiography.

Treatment Surgery xx Child requires feeding gastrostomy commonly. xx Often the procedure is staged one. xx Through right-sided thoracotomy (opposite to the side of

aortic arch), fistula is identified and resected. Lower segment is anastomosed to the blind upper segment. Occasionally if the length is inadequate or the atretic segment is long one, then colonic or gastric transposition is required. Complications of surgery

™™ ™™ ™™ ™™

Pneumonia Leak from the anastomotic site Reflux Dysphagia

+ oesophageal myotomy (Heller’s) + repair of associated hiatus hernia/antireflux procedure. 2. Traction diverticulum: Occurs in mid-oesophagus or in parabronchial region, is due to mediastinal granulomatous disease like tuberculosis.  Traction diverticulum is a true type containing all layers in its wall and is due to traction by the healing fibrosing mediastinal lymph nodes.  It is seen commonly towards right side. It has got wide mouth and it rests on the spine.  Presentation is dysphagia, chest pain and regurgitation.  CT scan (chest), barium study, manometry, endoscopy to assess mucosa with EUS, blood test for tuberculosis (ESR, peripheral smear) are the investigations.  Treatment: Treating the cause like tuberculosis, histoplasmosis. Diverticulum less than 2 cm is observed; progressive symptoms, size >2 cm needs surgery. Surgeries are—diverticulopexy, long oesophageal myotomy.

OESOPHAGEAL DIVERTICULUM

CARCINOMA OESOPHAGUS xx Carcinoma oesophagus is common in China, South Africa and Asian countries. xx It is 6th most common cancer in the world. xx It is less than 1% of all cancers. It is 7% of all GI malignancies. xx It is less common in America and European countries. xx In India, it is common in Karnataka and Orissa. xx When patient presents with dysphagia, often it is fairly advanced and inoperable and only palliation is the possibility. But then surgery is the treatment of choice in early growths.

Aetiology Fig. 19.29: Endoscopic view of oesophageal diverticulum

Types 1. Pulsion diverticulum: Pulsion diverticula are false type containing mucosa and submucosa only; is due to high abnormal intraluminal oesophageal pressure developed due to various motility disorders. a. Pharyngeal pouch through Zenker’s or Killian’s dehiscence (Refer chapter Neck). b. Epiphrenic pulsion diverticulum occurs in lower oesophagus, usually towards right side, due to obstruction in the distal oesophagus or due to incoordinated LOS relaxation. –– Site is within 10 cm of OG junction. It is false type. –– It is associated with nonspecific oesophageal motility disorders and often with achalasia and diffuse oesophageal spasm. Ehler Danlos syndrome and trauma are the other causes. –– It is common on right side with wide mouth. –– Features are of motility disorders like dysphagia, regurgitation, cough, weight loss, chest pain. –– Barium study, CT chest are diagnostic; endoscopic evaluation with EUS, manometry is a must.

Diet, deficiencies (vit. A, C, riboflavin) 5% common Common after 45 years Mycotoxin Alcohol and tobacco Common in men Fungal contamination of food Common in China – Henan province Human papilloma virus (HPV 16,18) In India, common in Geotrichum candidum fungi in China Orissa and Karnataka Achalasia cardia 30% Oesophageal webs 25% Barrett’s oesophagus Plummer-Vinson’s syndrome 15% Corrosive strictures 30% Tylosis* (Hovels-Evans syndrome) Nitrosamines * Tylosis is an inherited disease with thickening of skin of palm and sole

Tylosis Autosomal dominant condition seen from childhood Soles and palms are involved called as palmoplantar keratoderma Waxy, yellow lesions, which do not itch 60% of members of families develop carcinoma oesophagus after the age of 60 ™™ Systemic retinoids are the drugs used for tylosis ™™ ™™ ™™ ™™

Oesophagus Pathology xx Common in:

 Middle third—50%.  Lower third—33%.  Upper third—17%.

xx Lower 3 cm of oesophagus is lined by columnar epithelium,

and so adenocarcinoma is common here. Barrett’s columnar metaplasia which occurs in lower third of oesophagus is also more prone for adeno­carcinoma. xx Squamous cell carcinoma is commonest type in India and Asian countries.

A

B

• •

C

D

•

Figs 19.31A to D: Gross outer look and cut-section of proliferative and indurated lesions of carcinoma oesophagus.

A

B Figs 19.30A and B: Carcinoma oesophagus middle third— pathology specimen, gross and cut section. Note:

In India 90% are squamous cell carcinomas. In western countries, adenocarcinoma is becoming more common. Adenocarcinoma arises from submucosal oesophageal glands/heterotrophic columnar epithelium/Barrett’s oesophagus. H. pylori infection is associated with reduced risk of oesophageal adenocarcinoma (inversely related).

Gross types ™™ ™™ ™™ ™™ ™™

Annular (15%) Ulcerative (20%) Fungating—cauliflower like (60%) Polypoid Varicoid—diffuse submucosal type

xx Lymphatic spread  It spreads both by lymphatic permeation and lymphatic

embolisation.  It can cause satellite nodules elsewhere in the oeso­

phagus, away from the main tumour.  Above in the neck, it spreads to supraclavicular lymph nodes.  In thorax, it spreads to paraoesophageal, tracheobron-

chial lymph nodes to sub­diaphrag­matic lymph nodes.

Spread

 In abdomen, it spreads to coeliac lymph nodes.

xx Direct

xx Blood spread occurs to liver, lungs, brain and bones.

 Lack of serosal layer in oesophagus favours local exten-

sion. In upper third it spreads through muscular layer and gets adherent to left main bronchus, trachea, and left recurrent laryngeal nerve (causes hoarseness), aorta or its branches (causes fatal haemorrhage, but rare).  It may perforate and cause mediastinitis.  It may get adherent to pleura also.  Broncho-oesophageal, tracheo-oesophageal, oesophagoaortic fistulas can occur in advanced cases; it may cause torrential haemorrhage, pulmonary infection. Barium study, contrast dynamic CT, bronchoscopy will help in identifying fistulas. Surgery and radiotherapy are not possible in such situation. It is the terminal stage of the disease. Endoscopic stenting is the better palliation method.

Clinical Features xx Recent onset of dysphagia is the commonest feature. For

the dysphagia to develop, two-third of the lumen should be occluded. xx Regurgitation. xx Anorexia and loss of weight (severe), cachexia. xx Pain-substernal or in the abdomen. xx Liver secondaries, ascites. xx Bronchopneumonia, melaena. xx Features of broncho-oesophageal fistula in carci­noma of upper third oesophagus (30%). xx Left supraclavicular lymph nodes may be palpable.

All things must change to something new and strange.

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SRB's Manual of Surgery xx Hoarseness of voice due to involvement of recurrent laryn-

geal nerve. xx Hiccough, due to phrenic nerve involvement. xx Back pain—due to nodal spread (paraoesophageal/coeliac

nodes).

xx Male to female ratio is 3:1. In adenocarcinoma, it is 15:1. TNM staging and histologic grading for carcinoma oesophagus and esophagogastric junction (AJCC 7th edition) T status – Tumour T0 No primary tumour Tis High-grade dysplasia T1 Invasion into the lamina propria, muscularis mucosae (T1a) or submucosa (T1b) T2 Invasion into muscularis propria T3 Invasion paraoesophageal (adventitia) tissues without adjacent structure spread T4a Invades resectable adjacent structures (pleura, pericardium, diaphragm) T4b Invades unresectable adjacent structures (aorta, vertebral body, trachea)

A

B

Figs 19.32A and B: Barium swallow showing irregular filling defect and shouldering sign in middle third oesophagus.

N status – Nodes N0 No regional lymph node metastases N1 1 to 2 positive regional lymph nodes N2 3 to 6 positive regional lymph nodes N3 7 or more positive regional lymph nodes M status – Metastasis M0 No distant metastases M1 Distant metastases Histologic grade G1 Well differentiated G2 Moderately differentiated G3 Poorly differentiated G4 Undifferentiated

A

B

C

D

Stage groups Stage

Adenocarcinoma

SCC

Location

0

TisN0M0G1

TisN0M0G1

Any

IA

T1N0M0G1-2

T1N0M0G1

Any

IB

T1N0M0G3 T2N0M0G1-2

T1N0M0G2-3 T2-3N0M0G1

Any Lower

IIA

T2N0M0G3

T2-3N0M0G1 T2-3N0M0G2-3

Upper, middle Lower

IIB

T3N0M0Gany T1-2N1M0Gany

T2-3N0M0G2-3 T1-2N1M0Gany

Upper, middle Any

IIIA

T1-2N2M0Gany T3N1M0Gany T4aN0M0gany

T1-2N2M0any T3N1M0Gany T4aN0M0gany

Any Any Any

IIIB

T3N2M0Gany

T3N2M0Gany

Any

IIIC

T4aN1-2M0Gany T4bNanyM0Gany TanyN3M0Gany

T4aN1-2M0Gany T4bNanyM0Gany TanyN3M0Gany

Any Any Any

IV

TanyNanyM1Gany

TanyNanyM1Gany

Any

Investigations xx Barium swallow: Shouldering sign and irregular filling

defect. Rat tail lesion on fluoroscopy is typical.

xx Oesophagoscopy—to see the lesion, extent and type.

Figs 19.33A to D: Barium swallow X-rays showing irregular filling defect at different levels—feature of carcinoma of oesophagus. xx Biopsy—for histological type and confirmation. xx Chest X-ray—to look for aspiration pneumonia. xx CT scan (95% accuracy)—to look for local extension,

nodal status, perioesophageal/diaphragmatic/pericardial (1%)/vascular infiltration, obliteration of mediastinal fat and status of tracheobronchial tree in case of upper third growth. xx Bronchoscopy to see invasion in the upper 1/3rd carcinoma of oesophagus; laryngoscopy to identify vocal cord palsy.

Oesophagus

Fig. 19.34: Endoscopic views of oesophageal carcinomas—at different levels and different gross types. xx Chromoendoscopy, magnification endoscopies are newer

methods. Local topical application of different stains will improve the tissue (tumour) localization, features and diagnoses. Different stains that are used like absorptive (Lugol’s, methylene blue – get absorbed by specific cell membranes), contrast (indigocarmine – permeate into the mucosal crevices showing irregularity and topography) or reactive (Congo red, phenol red – shows colour change due to reaction with cell chemicals). Biopsy is done in these selected areas. xx Oesophageal endosonography—to look for the involvement of layers of oesophagus, nodes, cardia and left lobe of the liver. Nodes smaller than 5 mm can be very well visualised by EUS which may be missed in CT scan. EUS guided transmucosal nodal needle aspiration cytology can also be done.

Fig. 19.35: CT scan chest and abdomen is essential investigation in carcinoma oesophagus to identify operability, nodal status.

xx Ultrasound abdomen—to look for liver and lymph nodes

status in abdomen. xx Endoscopic oesophageal staining with labelled iodine results

in normal mucosa being stained brown, but remains pale in carcinoma (as mucosa in carcinoma will not take up iodine). xx Blood tests: Haematocrit; ESR; Liver function tests. xx Laparoscopy: It is useful to see peritoneal spread, liver spread and nodal spread. It is the only reliable method to detect peritoneal seedlings. Biopsy from different places can also be taken. It will prevent unnecessary laparotomy for anticipated surgical resection. xx PET scan using 18 F-fluorodeoxyglucose (FDG): 18 FDG is given to the patient. FDG enters highly active cells and gets phosphorylated to FDG 6 phosphate. It stays in the cell as end product and gets polarised there. PET with CT scan is used to see response for therapy. xx Video-assisted thoracoscopic approach—to stage oesophageal carcinoma and to identify the operability, nodal status. xx Endoscopic mucosal resection (EMR) is done using double channeled endoscope with tip having a soft plastic cap. Cap is firmly placed over the lesion and suction is created; a snare is brought over the lesion; biopsy specimen is snared off 1.5 cm in size containing mucosa and submucosa. It is basically a diagnostic biopsy tool; but can be therapeutic in early and premalignant lesion. Endoscopic submucosal dissection (ESD, Japan) is now devised using hook cautery and scissors to remove the lesion up to muscularis propria.

Tolerance is another word for indifference.

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SRB's Manual of Surgery xx Newer modalities of evaluation – Flow cytometry, p53

immunohistochemistry, optical coherence tomography, spectroscopy, etc.

Treatment Gastrostomy should not be done as a palliative procedure.

Principles Indications for curative treatment 1. Early growth when patient is fit. 2. When there is no involvement of adjacent perioesophageal structures, bronchus, liver or distant organs.

xx Only 20% of oesophageal cancers present early and becomes curable. In such early growths confirmed with absence of nodal spread, curative surgery is the main approach—radical oesophagectomy. Proximal extent of resection should be 10 cm above the macroscopic tumour and distal extent of resection is 5 cm from macroscopic distal end of tumour. Proximal stomach has to be removed commonly especially in lower 1/3rd of tumour. Sufficient removal of contiguous structures may be needed in curative resection. xx If nodes are present, then multimodal approach should be used like—curative resection; radiotherapy and chemotherapy. Outcome of surgery depends on location of tumour; number, location and size of nodes; tumour grading. xx Lymph node involvement more than 5 carries poor prognosis. If 5 or less nodes are involved then, it is called as curative resection. xx Neoadjuvant therapy by chemotherapy and/or radiotherapy prior to surgery may improve the survival. xx Aggressive chemoradiation also may be used as curative therapy in some patients especially upper 1/3rd growths and in patients who are unfit for surgery. xx In remaining patients (80%) palliation is the main modality of treatment. Palliation therapy is done if patient is not fit for major surgery; if there is blood spread; if there is spread to adjacent organ; if there is peritoneal/liver spread. It is to relieve pain and dysphagia and also to prevent aspiration and bleeding. Palliative therapy (80% cases) Indications where probably curative To palliate therapy is not possible Nodes >5 involvement Invasive, poorly differentiated grade Length of involvement >8 cm Abnormal oesophageal axis in barium study Horner’s syndrome Loss of weight >20% Metastatic disease

Pain Dysphagia Prevent bleeding Prevent aspiration

Fig. 19.36: Carcinoma oesophagus (Endoscopic view).

Approaches for Different Level Tumours Post-cricoid tumour (Squamous cell carcinoma): xx Treated mainly by radiotherapy. Radical radiotherapy— 5000– 6000 rads. xx Often pharyngolaryngectomy is done along with gastric or colonic transposition. But complications are more in this procedure. Free jejunal transfer is the other option. Upper third growth (Squamous cell carcinoma): xx Treated mainly by radiotherapy. xx Commonly it is advanced with left recurrent laryngeal nerve palsy and bronchial invasion. xx If it is early and operable, McKeown three phased oesophagectomy and anastomosis is done in the neck. Initially laparotomy is done to mobilise the stomach. Then thoracotomy through right 5th space is done and oesophagus is mobilised. Through right side neck approach, oesophagus with growth is removed. Anastomosis between pharynx and stomach is done in the neck. xx Split sternum approach oesophagectomy is also practiced. Middle third growth (Squamous cell carcinoma): Ivor Lewis operation (Lewis-Tanner two-phased oesopha-gectomy): After laparotomy stomach is mobilised. Pyloroplasty is done. Through right 5th space thoracotomy is done and growth with tumour is mobilised. Partial oesophagectomy and oesophagogastric anastomosis is done in the thorax. Intercostal tube drainage is placed during closure. Right gastroepiploic vessels should be retained safely (essential). Azygos vein should be ligated securely. Mediastinal nodes should be dissected. Thoracic duct should be ligated if needed. Feeding jejunostomy is better to maintain nutrition. Complications of Ivor Lewis operation–Pulmonary (bronchopneumonia, empyema), anastomotic leak, mediastinitis, oesophagitis and sepsis. If the growth is inoperable, palliative radiotherapy is given.

Oesophagus Complications are leak, fistula formation, delayed emptying, redundancy, peptic ulceration, stricture formation. Colonic polyp and diverticulosis are contraindications for colonic conduit.  Jejunum: Isolated required length of pedicled jejunum is transposed. Jejunal free transfer is also tried; vessels are sutured to internal mammary vessels or to the vessels available the neck. Pedicled jejunum is also supercharged with microvascular anastomoses with internal mammary vessels. It is used as a last option only.

Lower third growth (Squamous cell carcinoma + adenocarcinoma): xx Here through left thoracoabdominal approach, partial oesophagogastrectomy is done with oesophagogastric anastomosis. Often jejunal Roux-en-Y loop anastomosis is done. xx Orringer approach, i.e. transhiatal blind total oesophagectomy with anastomosis in the left side of the neck. Through laparotomy, stomach and lower part of the oesophagus are mobilised. Through left sided neck approach, upper part of the oesophagus is mobilised using finger. Blind dissection is completed by meeting both fingers above and below in the thorax. Later oesophagus is pulled up out above through the neck wound and removed. Continuity is maintained in the neck. It is a palliative surgery.

Fig. 19.37: Transhiatal blind oesophagectomy— on table surgical specimen.

Other Approaches xx Thoracoscopic-laparoscopic oesophagectomy and lymphadenectomy is becoming popular, safer and effective. xx Radical oesophagectomy with 3-field clearance of abdominal/ thoracic and cervical nodes is also practiced in many centres. 3-Field clearance (coeliac, thoracic and neck) is done for mainly squamous cell carcinoma as spread in SCC is upwards. In adenocarcinoma 2-field clearance is sufficient (abdominal—coeliac and thoracic) as spread is downwards. Note:

When oesophagus is removed totally or subtotally an interposition is required between cervical oesophagus/pharynx and distal stomach. Different parts of GI is used for the same.

Oesophageal substitutes:  Stomach: It is preferred one and is based on right gastric and right gastroepiploic arteries. It needs only one anastomosis and take up is well due to good vascularity. But it can cause postprandial fullness with bile or acid regurgitation (>50%). It also needs a pyloroplasty for gastric drainage as vagotomy is done. Entire stomach or tubed part or reverse tubed part can be transposed.  Colon: It is better as there are less postprandial problems. But it needs 3 anastomoses. Left colon is used with ascending branch of left colic artery as isoperistaltic loop. Right colon is used with middle colic artery as base as antiperistaltic loop.

Transposition is done through posterior mediastinum (shortest route), right pleural space (transpleural), retrosternal or subcutaneous route. xx Skinner en bloc resection used to be of practice in olden days in which tumour with oesophagus is resected along with thoracic duct, azygos vein, intercostal vessels crossing the vertebral bodies, pericardium and mediastinal pleura. There is no survival benefit with this procedure. xx Vagal sparing oesophagectomy with HSV is tried to preserve pylorus functioning with avoiding pyloroplasty to reduce the chances of postprandial fullness. But it is technically tedious. xx Lymphadenectomy in carcinoma oesophagus:  Standard: Nodes removed are—paratracheal, parabronchial, carinal, paraoesophageal, posterior mediastinal, paracardial, left gastric, along lesser curve of stomach.  Extended/three field/ultraradical: As like standard above, with bilateral cervical lymphadenectomy, removal of upper mediastinal, coeliac, retroperitoneal, subhepatic nodes. Surgical approaches Ivor-Lewis 2-phase oesophagectomy McKeown 3-phase oesophagectomy Left abdominothoracic approach for lower oesophagus—Sweet approach ™™ Thoracoscopic—laparoscopic ™™ Transhiatal blind approach—Orringer’s ™™ ™™ ™™

Postoperative Management xx xx xx xx xx xx

Fluid and electrolyte management. Antibiotics and proper analgesia. Respiratory care; ICT care; physiotherapy. Prevention of DVT—elevation, exercises, heparin. Monitoring for bleeding, sepsis, leak, oxygen saturation. TPN only during initial postoperative period and early jejunostomy feeding for nutrition.

Palliative Treatment 80% of patients with carcinoma oesophagus, when present first, have fairly advanced tumour and so they are amenable for only palliative treatment. It is to relieve pain, dysphagia and to prevent aspiration and bleeding. Palliation therapy is done – xx If patient is not fit for major surgery. xx If there is blood spread. xx If there is adjacent organ spread. xx If there is peritoneal/liver spread.

Life is half spent before we know what it is. Life is like a beautiful melody; only its lyrics are messed up.

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SRB's Manual of Surgery Different methods are: xx Palliative external radiotherapy  3000 Rads. Severe mucositis, stricture and fistula formation are the complications. xx Intraluminal RT  Brachytherapy (radiation intraluminally). Loading catheter is placed using endoscope and applicator is fixed to mouth to give 1500 cGy radiation with least systemic effects.

A

B

Figs 19.38A and B: (A) Stricture oesophagus after radiotherapy given for carcinoma oesophagus; (B) Oesophageal stent in situ—a look endoscopically. xx Chemotherapy  Cisplatin; methotrexate; 5 FU; palcitaxel, etoposide, bleomycin. Platinum based chemotherapy is beneficial especially in advanced adenocarcinoma of oesophagus. xx Intubation Intubation was described by Symmonds in 1887. It is commonly used method. Guidewire is passed across the growth under X-ray screening or C-arm guidance; flexible introducer and prosthetic tube is pushed across the tumour along the guidewire. It carries 90% success rate. Problems are—tube intolerance, poor drainage, airway compression, reflux, aspiration, displacement, food blockage, tumour overgrowth beyond the prosthesis causing its failure.   Intubation is used for tracheo-oesophageal fistula or external compression. Prosthesis with a sponge-filled balloon is used for fistula closure. Standard tube wrapped with multilayered polyvinyl sponge is other option. It is less expensive, single time, rapid acting.   They can be traction or pulsion tubes. Perforation chance is 10%.

Different tubes used are:  Atkinson tube.  Celestin tube (armoured rubber tube with a long tail)— ideal,

commonly used tube. It is wider proximally. It can be passed through endoscopy or laparotomy.  Souttar tube (coiled German silver wire)—block is first dilated with bougies; tube is passed over small sized bougie and pushed across the block. It is mainly useful for lower oesophagus.  Mousseau-Barbin tube—cheaper but needs laparotomy. After laparotomy, anterior wall of the stomach is opened. MB tube is passed from mouth with the help of anesthetist by stitching its tip to nasogastric tube and pulled down into the stomach. Tip is cut near the cone part. It is sutured to anterior wall of the stomach. Gastrotomy is closed. xx Endoscopic therapy:  Self-expanding metal stents (sems) are passed through endoscope under C-arm guidance. It is the ideal method of palliation. Stent is collapsed during insertion and released once it is placed in proper position. There is no need to dilate

oesophagus more than 8 mm to pass this expanding stent and so chances of perforation is minimal. Uncovered SEMS—here tissues project through the mesh to have a better grip with less chances of migration. But stent occlusion is more. Plastic covered SEMS—it shows less stent occlusion and less friction. Stent migration is more. SEMS may be—stainless wall stent; knitted nitinol Strecker stent; stainless steel covered Gianturco-Rosch stent. Problems of stents are—aspiration, displacement, erosion, bleeding, tumour growth across or beyond mesh, food bolus obstruction, retrosternal pain, need for reinsertion (40%). Mortality is 1–2%.  Endoscopic laser is used to core a channel through the tumour to improve dysphagia (Nd YAG laser; Diode laser). It causes thermal destruction of tumour. It improves dysphagia but needs repeated laser ablation. It may be used more effectively to remove tumour block in previously placed stents. Exophytic tumour less than 6 cm is suitable for laser. Noncontact high power Nd:YAG 50-100 W laser from distal to proximal end facilitates visualisation of lumen and also reduces the chances of perforation. Contact low power Nd:YAG 10-20 W laser is used for fully occluded tumour with less smoke formation and less perforation chance. Success rate of palliation is 85%. Problems are—fever, chest pain, 3% mortality, perforation (2%) and fistula formation—5%, costly, takes one week to relieve dysphagia  Endoscopic bipolar diathermy using a olive tip; argon beam plasma coagulation; endoscopic alcohol injection into the tumour.  Endoscopic photodynamic therapy (PDT) is used to destruct tumor and to relieve dysphagia. It is often used as a therapy in early cancer. Photosensitive haematoporphyrin agent is injected intravenously 48 hours before endoscopy. It is activated over tumour using laser. Visible infrared light also can be passed to tumour endoscopically to create tumour necrosis by released cytotoxic singlet oxygen through photosensitiser. Sunburn, fever, perforation, pleural effusions are complications. It is effective only to superficial cancers; effects will be seen only after 1 week; need to avoid direct sunlight exposure by the patient for one month is the drawback. xx Surgery  Transhiatal Orringer’s blind oesophagectomy is a palliative surgical procedure.  Kirschner palliative gastric bypass done in advanced carcinoma oesophagus wherein mobilised stomach is brought to neck via retrosternal or subcutaneous route and anastomosed to divided cervical oesophagus. Lower cut end of oesophagus is anastomosed to a jejunal loop. Here oesophagus is not addressed (left alone). Palliative procedures ™™ ™™ ™™ ™™ ™™ ™™

External or intraluminal RT (Brachytherapy) Traction tubes like Celestin or MB tubes through open surgery Pulsion tubes like self-expandable metal stents through endoscopes using C-arm Endoscopic laser Chemotherapy Transhiatal oesophagectomy—Orringer

Oesophagus

A

B

Figs 19.39A and B: (A) Mousseau-Barbin tube placed as a palliative method for carcinoma oesophagus; (B) Mousseau-Barbin tube. Complications of oesophagectomy 5–10% mortality Haemorrhage Respiratory infection, often severe Septicaemia Chylothorax, injury to thoracic duct Anastomotic leak—thoracic leak is most dangerous (5–10%) Hoarseness due to recurrent laryngeal nerve palsy Stricture formation (40%) Gastro-oesophageal reflux in gastric transfer Conduit necrosis due to ischaemia either stomach or colon ™™ Colonic dysmotility causing partial obstruction in colon transfer ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

xx Features may be asymptomatic (85%—identified incidentally during contrast X-ray/endoscopy); dysphagia/airway obstruction/ pneumonia/spluttering during swallowing; stridor/regurgitation. xx Leiomyoma (commonest—65%) is smooth, sessile, lobulated, firm, with grey-white whorled appearance.  Only when leiomyoma reaches 5 cm in size, it causes obstruction.  Multiple localised leiomyomas can occur which can be enucleated independently.  True diffuse leiomyomas can occur occasionally in females (4%) in lower oesophagus, as diffuse hyperplasia and thickening of both muscular layers; often as part of the Alport’s syndrome which needs total oeso-phagectomy with gastric pull up, even though benign.  Benign leiomyoma of oesophagus rarely turns into leiomyosarcoma.  90% of oesophageal leiomyomas occur in lower third of the oesophagus.  Leiomyomas are common in men in 5th decade.  Leiomyoma which expresses the c-kit oncogene (CD117) is considered as GIST. xx Investigations—barium swallow X-ray (smooth circular outline/ eccentric filling defect)/oesophagoscopy/endosonography/CT scan. xx Treatment—if tumour is more than 5 cm/symptomatic tumour/ intraluminal tumour/when diagnosis is doubtful surgical enucleation is indicated. Enucleation is the therapy of choice. Ideally it should be done through right-sided thoracotomy. Occasionally oesophageal resection is needed if tumour is very large/tumour with mucosal ulceration/if tumour is near OG junction. Thoracoscopic resection can be done. Leak, empyema, sepsis and stricture are the occasional complications.

Terminal Events in Carcinoma Oesophagus Cancer cachexia. Sepsis, mediastinitis. Immunosuppression. Malignant tracheo-oesophageal fistula (causes severe respiratory infection and death. Here expansile (self-expandable) endoluminal stents are used at the site of fistula to have temporary benefit). xx Erosion into major blood vessel—bleeding. xx xx xx xx

Prognosis xx Not good because of early spread, longitudinal lymp­ha­tics, aggressiveness, difficult approach, late presen­tation. xx Nodal involvement carries bad prognosis. xx 5-year survival rate is only 10%.

BENIGN TUMOURS OF THE OESOPHAGUS xx Benign tumours of the oesophagus are rare (0.5–1% of all oesophageal tumours). xx It grows slowly like a balloon by expansion, compressing surrounding structures. It never infiltrates or spreads. xx It can be solid, cystic, polypoid. xx It is usually in submucosal plane. xx It can cause obstruction/regurgitation/aspiration/ mediastinal compression. xx It can be squamous papilloma/polyp/inflammatory pseudo tumour/ leiomyoma (commonest benign tumour of oesophagus—65%)/ neurofibroma/rhabdomyoma/lipoma. True adenoma in oesophagus is very rare.

A

B Figs 19.40A and B: Oesophageal submucosal tumour— endoscopic view—leiomyoma.

Note: Unlike in the stomach and intestine (gastric leiomyoma more than 6 cm/intestinal leiomyoma more than 4 cm are potentially malignant) increased size of the oesophageal leiomyoma does not predispose the malignant transformation.

xx Oesophageal cysts  It is 2nd commonest benign tumour of oesophagus.  It can be congenital or acquired. Congenital is derived from foregut. It contains mucus. It is lined by ciliated columnar epithelium. In infants, it is common in upper third of oesophagus; often with a fistula into airway. It can cause obstruction.  Acquired cyst is from obstruction of the excretory ducts of oesophageal glands.  Treatment: Enucleation or resection. If fistula is present it should be ligated and divided.

Truth, like surgery, may hurt, but it cures.

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SRB's Manual of Surgery OESOPHAGEAL PERFORATION Causes xx Instrumental injuries—commonest cause, 75% commonest site is just above the level of crico­pharyngeus. xx Foreign bodies. xx Alkali injuries. xx Carcinoma oesophagus 1%. xx Boerhaave’s syndrome 15%. xx Trauma 9%. xx Surgical trauma (Vagotomy, thyroidectomy, Heller’s operation, pneumonectomy, spine surgery).

Treatment xx Conservative treatment: It is advocated in small perforations due to instrument where there is minimal air leak and contamination of mediastinum with less septic load. Crepitus should be absent; pleura should be clear and without any obstruction. Treatment is—antibiotics, nutrition (TPN/enteral through tube), fluid management, proper observation and monitoring the patient by repeated blood counts, and imaging. Biodegradable removable self-expanding stents also can be used. It may also act as a bridge therapy for eventual major surgical exploration. Stents which are used for carcinomas cannot be used as they cannot be removed. xx Thoracotomy, proper saline wash to pleura, mediastinum and repair with buttressing the area using pedicled intercostal musculopleural flap is done. Nasogastric tube for long duration, jejunostomy tube for feeding, ICT for drainage is essential. Often in late cases decortication of lung is needed to achieve full expansion of the lung. xx Repair over T-tube so as to create a controlled fistula along with feeding jejunostomy and ICT on both sides. xx Intraluminal stents/mediastinal irrigation and drainage. xx Resection of oesophagus with gastric pull up. As condition is an emergency situation and with sepsis it carries high mortality. xx Oesophageal exclusion with cervical oesophagostomy above and feeding jejunostomy below. xx Diversion surgeries using colon/stomach/jejunum.

Foreign body oesophagus

Fig. 19.41: Oesophageal perforation with mediastinitis and emyema; perforation is after eating large chicken bone.

Common foreign bodies: ™™ Coins, metals, plastics ™™ Dentures ™™ Pins, toothpicks, batteries ™™ Fish or meat bones—dangerous—40% ™™ Food (meat—common/vegetables) impaction—45%

Clinical Features

Sites of impaction in oesophagus:

Chest pain, vomiting, shock, subcutaneous emphysema.

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Investigations Chest X-ray—shows pneumomediastinum ™™ CT scan ™™

Complications Mediastinitis ™™ Septicaemia ™™ Empyema, ARDS ™™

Cervical constriction—C6 Broncho-aortic constriction—T4 ™™ Diaphragmatic constriction—T10 ™™ Pre-existing malignancy or inflammatory stricture site Features: ™™ ™™

Sudden dysphagia with chest pain and breathless­ness Later features of shock, sepsis, mediastinitis, empyema

Management: X-ray shows site and level of the foreign body (FB) Endoscopic removal can be tried. ™™ Impacted large FB should be removed by thoraco­tomy ™™ Antibiotics, jejunostomy, TPN, ICT are also required ™™ ™™

Oesophagus

Fig. 19.42: Foreign body in the oesophagus.

Fig. 19.43: Foreign body (COIN) in the lower oesophagus. Usually it can be removed by endoscope.

You can become strongest in your weakest place.

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Stomach CHAPTER OUTLINE ™™ Anatomy −− Blood Supply of Stomach −− Nerve Supply of Stomach −− Histology −− Lymphatic Drainage of Stomach −− Duodenum ™™ Gastric Physiology ™™ Gastric Function Tests ™™ Gastrin ™™ Barium Meal Study ™™ Gastroscopy ™™ Helicobacter pylori ™™ Congenital Hypertrophic Pyloric Stenosis ™™ Gastritis ™™ Acute Peptic Ulcer ™™ Gastric Ulcer ™™ Duodenal Ulcer ™™ P yloric Stenosis due to Chronic Duodenal Ulcer

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−− E lectrolyte Changes in Pyloric Stenosis Perforated Peptic Ulcer −− Perforated Duodenal Ulcer −− Perforated Gastric Ulcer −− Perforated Stomal Ulcer −− Dry Perforation Bleeding Peptic Ulcer −− Bleeding Duodenal Ulcer −− Bleeding Gastric Ulcer Haematemesis Complications of Gastric Surgery −− Duodenal Blow-out −− Recurrent Ulcer −− Dumping Syndrome −− Roux Stasis Syndrome −− Gastrojejunocolic Fistula Trichobezoar Chronic Duodenal Ileus

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Dunbar’s Syndrome Acute Gastric Dilatation Gastric Volvulus Gastric Polyp Menetrier’s Disease Duodenal Diverticula Carcinoma Stomach Gastric Lymphoma −− Primary Gastric Lymphoma −− Secondary Gastric Lymphoma Gastric Sarcomas Gastrointestinal Stromal Tumours Pyloroplasty Gastrostomy Gastrectomy Gastrojejunostomy R  etrograde Jejunogastric Intussusception Vagotomy

ANATOMY The stomach contains four anatomic regions: 1. Fundus. 2. Cardia. 3. Body. 4. Pyloric part contains pyloric antrum, pyloric canal. The duodenum is 20–30 cm in length. It extends from pyloric sphincter to ligament of Treitz. It is divided into four parts. Ninty per cent of duodenal ulcer occurs in the 1st part of duodenum (duodenal bulb/cap). CBD and pancreatic duct merges to form ampulla of Vater and enter the 2nd part of duodenum. The 3rd part of duodenum is wedged between aorta and superior mesenteric artery.

Fig. 20.1: Parts of stomach.

Stomach BLOOD SUPPLY OF STOMACH Arterial Supply xx Left gastric artery, a branch of coeliac artery (Smallest branch of coeliac axis). xx Right gastric artery, a branch of hepatic artery. xx Gastroduodenal artery, a (largest) branch of hepatic artery. xx Right gastroepiploic artery, a branch of gastro­duo­denal artery. xx Left gastroepiploic artery, a branch of splenic artery. xx Short gastric arteries, branches of splenic artery.

Fig. 20.3: Anatomy of nerve supply of stomach. xx In selective vagotomy splanchnic branches are retained but it is presently not done. xx Gastroduodenal pain is sensed via sympathetic fibres (T5 –T10).

HISTOLOGY Fig. 20.2: Blood supply of the stomach.

Venous Drainage xx Right and left gastric veins drain into portal vein. xx Right gastroepiploic vein drains into superior mesenteric vein. xx Left gastroepiploic vein and short gastric veins drain into splenic vein. xx Prepyloric vein of Mayo distinguishes pyloric canal from the first part of duodenum.

NERVE SUPPLY OF STOMACH xx Intrinsic innervation occurs through myenteric plexus of Auerbach and submucous plexus of Meissner. xx Right vagus is posterior and left vagus is anterior. xx Posterior vagus gives criminal nerves of Grassi, which supply lower oesophagus and fundus of stomach, which, if not cut properly during vago­tomy, may lead to recurrent ulcer. xx Vagus also gives splanchnic branches (hepatic and coeliac branches), ends as nerve of Latarjet which sup­plies the antrum and maintains the antral pump. xx Parietal branches help in HCl secretion, which is an important concept in vagotomy that is done as a treatment in duodenal ulcer. xx Truncal vagotomy with posterior gastrojejunostomy is done for chronic duodenal ulcer with pyloric stenosis. xx Highly selective vagotomy (HSV) is done in case of uncomplicated chronic duodenal ulcer which is not responding to available medical line of treatment. In HSV, nerve of Latarjet is retained so as to retain antral pump and no drainage is required. Here only the fibres entering the stomach are ligated close to the lesser curve to reduce the acid secretion.

xx The fundus and body contains parietal and chief cells. xx Parietal cells secrete acid and intrinsic factor. xx Chief cells produce pepsinogen. There are two types of pepsinogen secreted by chief cells—I and II. Pepsinogen I is produced only in stomach. In gastric atrophy pepsinogen I is decreased. xx In the antrum, endocrine cells produce gastrin (G cells) and somatostatin (D cells). xx 12% of epithelial cells of stomach are parietal (oxyntic) cells; 45% chief (zymogenic cells); 40% mucous cells; 3% endocrine cells. xx Pyloric sphincter is a thick circumferential layer of smooth muscle. xx Submucosa is strongest, collagen rich layer of gastric mucosa. xx Gastric mucus is a mucosal barrier containing mucopolysaccharides which maintains the integrity of gastric mucosa.

LYMPHATIC DRAINAGE OF STOMACH xx Lymphatics of proximal half of stomach drain into left gastric, splenic, and superior pancreatic lymph nodes. From antrum, it drains into right gastric, right gastroepiploic, and subpyloric lymph nodes. From pylorus, it drains into right gastric and subpyloric lymph nodes. xx Efferent lymphatics from suprapyloric region drain into para-aortic lymph nodes and so into left supraclavicular lymph nodes. Efferent lymphatics from subpyloric lymph nodes drain into superior mesenteric lymph nodes. Lymphatics near oesophagogastric (OG) junction communicate with oesophageal lymphatics. xx In carcinoma stomach if upper lymphatics are blocked, retrograde spread through lower lymphatics can occur. xx Presently in carcinoma stomach different resections are classified as R0, R1, R2, R3, or D1, D2 (dissection) based on levels of lymph nodes in the abdomen in relation to the stomach. R0 is no residual disease; R1 is microscopic residual disease; R2 is macroscopic residual disease; R3 is inoperable.

Goals and actions must meet.

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SRB's Manual of Surgery Lymphatic Drainage Drains mainly to pancreaticoduodenal nodes present along the inside of the curve of duodenum.

GASTRIC PHYSIOLOGY

Fig. 20.4: Lymphatic drainage of stomach.

DUODENUM Arterial Supply It is mainly supplied by superior and inferior pancreaticoduodenal arteries. First part also gets supply from right gastric artery, supraduodenal artery, a branch of hepatic artery.

Venous Drainage Drains into the splenic, superior mesenteric and portal veins.

Nerve Supply xx Sympathetic from spinal segments T8 and T10. xx Parasympathetic from vagus.

Fig. 20.5: After passing the Ryle’s tube to the stomach, air from the syringe should be infused through the tube. When auscultated gush of air into the stomach can be heard which confirms that tube tip is in the stomach.

xx Gastric function is regulated by hormonal and neural methods. Hormonal mediators control function through endocrine (through release into blood), paracrine (diffusion across interstitial space) and neurocrine (diffusion across synopsed target cell and receptor binding). xx Gastric acid secretion is regulated by acetylcholine, histamine and gastrin. Acetylcholine is the principal mediator of acid release through vagal parasympathetic ganglion cells. Vagus innervates parietal, G and enterochromaffin-like (ECL) cells. Basal acid secretion is 10% of maximal acid output (1-5 mmol/hour). It is reduced by 90% after vagotomy or H2 receptor blockage. Phases of acid secretion are—(1) Cephalic phase—through central meditation (smell/sight/taste → vagus → acetylcholine → muscarinic receptors. (2) Gastric phase—food enters the stomach → antral G cells → acid release though gastrin (gastric distension causes direct acid release). Gastric phase lasts until stomach is empty and releases 70% of total acid release. (3) Intestinal phase—it is 10% of acid release and is mediated by chyme entering the small bowel—nongastrin related. xx Receptors of acid secretions are—(1) Gastrin—CCK receptors: Two types are present in parietal cell; Gastrin CCK type A receptor has high affinity for CCK but less to gastrin; Gastrin CCK type B receptor has got high affinity for both CCK and gastrin. (2) Muscarinic receptor (parietal cell)—its M3 type is mediator for acetylcholine. (3) Histamine receptor (parietal cell)—H 2 subtype binds to histamine to cause effect. (4) Somatostatin receptor—these are 5 subtypes. Its inhibitory action is through parietal cell subtype. (5) Second messengers involved are intracellular cAMP and calcium. xx Luminal gastric pH is 2. The pH at surface epithelial cells is 7. These cells secrete bicarbonate continuously into the lining mucus gel to keep the pH of surface mucus at 5. Bicarbonate in mucus barrier reduces once luminal pH reduces below 1.4. xx Functions of gastric acid: Conversion of pepsinogen to pepsin which in turn hydrolyses proteins into polypeptides; promotes release of duodenal secretin; prevents bacterial colonisation of upper GIT; formation of food chyme which contains food particles of 1 mm size or less. xx Gastric juice contains HCl, mucus, swallowed saliva, reflux content from duodenum. Parietal cells secrete electrolytes of 160 mmol/L. They also secrete intrinsic factor, a mucoprotein which is essential for absorption of vitamin B12 in ileum; its secretion is independent of acid secretion from parietal cell and is not influenced by PPIs. Pepsinogen is a proteolytic proenzyme (42,000 mol wt). Type I is secreted from chief cells and mucous neck cells of only acid secreting part of the stomach (acid secreting mucosa). Type II is secreted from surface epithelial cells of entire stomach and proximal duodenum. Mucous is secreted by surface muocus cells and mucous neck cells from acid secreting area of stomach and antrum. Gel like viscous mucous contains 85% water and 15% glycoproteins. It contains bicarbonate secreted from surface epithelial cells. Mucous is strong gastric barrier. Mucous secretion is inhibited by anticholinergics and NSAIDs. H. pylori break the mucin and so barrier. xx Gastric motility begins from pacemaker cell of Cajal located at proximal stomach. Special myoelectric migrating complex slow

Stomach waves with electric spikes maintain gastric motility in three phases. Immediately after food intake resting tone of fundus and proximal stomach decrease causing receptive relaxation and gastric accommodation mediated by vagus. Vagotomy eliminates this causing early fullness, early satiety and rapid gastric emptying. Delayed gastric motility occurs in diabetes, H. pylori infection and after vagotomy. Many factors like stress, hormones increase the gastric motility. Prokinetics, erythromycin helps in gastroparesis. xx Mucosal defense factors are—mucous production, mucosal HCO3–, mucosal blood flow, growth factors, cell renewal, endogenous prostaglandins, epithelial barrier (hydrophobic phospholipids, restitution, NO, epidermal growth factor and microcirculation). Aggressive factors are—H. pylori, HCl secretion, pepsin, smoking, alcohol, duodenal bile reflux, ischaemia, NSAIDs.

GASTRIC FUNCTION TESTS Gastric function tests ™™ ™™ ™™ ™™ ™™

Pentagastrin test/Kay’s augmented histamine test Hollander’s insulin test Radioisotope labelled gastric emptying study 24 hours intragastric pH monitoring Gastrin level estimation

Peak Acid Output Test (Pentagastrin/ Augmented Histamine Test) Initially stomach is emptied completely. Basal acid level of aspirated stomach content (aspiration is done for 1 hour on empty stomach) is analysed. Pentagastrin—6 µg/kg or histamine 2 µg/kg is injected IV/SC/IM and 15 minutes samples for subsequent hours (usually 1 hour) are collected and analysed. Peak acid output level is calculated. Test is useful in Zollinger-Ellison (Z-E) syndrome, duodenal ulcer and gastric ulcer. Basal acid output (BAO) is 2–3 mEq/h. Peak acid output (PAO) is highest rate of secretion obtained in any of the 15 minutes samples following stimulation. Maximal acid output (MAO) is obtained by averaging the output of two final 15 minutes samples. In duodenal ulcer and Z-E syndrome basal and stimulated acid is increased; in pernicious anaemia, gastric atrophy and gastric cancer both are decreased. Basal

Peak

5 mmols

25–27

Gastric ulcer

2

15

Duodenal ulcer

6

35–38

Z-E syndrome

Very high

> than 60

Normal

Achlorhydria is defined as a condition in which stomach cannot produce secretions with a pH of less than 7.0 even after maximal stimulation. It is seen in 20% of carcinoma stomach. Note:

Achylia means—no pepsin in the gastric juice.

Insulin Test (Hollander) xx This test is useful postoperatively to confirm the completeness of vagotomy. 0.2 units/kg body weight of insulin is injected intra-

venously to a fasting patient so as to create hypoglycaemia of below 35 mg%, which in turn stimulates the parietal cells through hypothalamus and through vagus to cause inc­rea­sed acid secretion. Patient who had under­gone complete vagotomy does not show increase in acid secretion. xx Early response signifies incomplete vagotomy wherein there is increase in acid concentration in first hour of >20 mmols/L. xx Delayed response signifies an increase in acid concentration in between first and second hours, and is probably due to vagal gastrin release.

GASTRIN xx Gastrin is secreted by the G-cells from gastric antrum. xx Types of gastrin are—Big gastrin (G 34 ); little gastrin (G 17)—most common 90%; mini gastrin (G 14). Pentapeptide at the C terminal end of G 17 is active part which is identical to CCK. Luminal peptides and amino acids are most potent stimulator of gastrin release. Luminal acid is the most potent inhibitor of gastrin release. xx Gastrin promotes the release of acid and also regulates it. It also maintains mucosal defense, has trophic effects on parietal and ECL cells (enterochromaffin like cells). xx Number of G-cells are increased in duodenal ulcer, G-cell hyperplasia, but not in gastric ulcer. Normal plasma value is 50 ng/L of plasma (fasting). It is analysed by radioimmunoassay. xx It increases to many 1000’s in gastrinomas. xx Hypergastrinaemia can occur in ulcerogenic conditions like— antral G cell hyperplasia, retained excluded antrum, Z-E syndrome, short gut syndrome, gastric outlet obstruction; nonulcerogenic conditions are—PPIs, pernicious anaemia (–ve feedback), vagotomy, atrophic gastritis (hypochlorhydria), H. pylori, chronic renal failure. xx Gastrin is raised very high in gastrinomas.

Gastric hormones ™™ ™™

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Gastrin Somatostatin—2 types, 14 and 28. In stomach, type 14 is common; from D cells of gastric mucosa of fundus and antrum. Antral acidification is the main stimulus; vagal acetylcholine inhibits its release. It has paracrine effect inhibiting acid secretion from parietal cell, gastrin release from G cell and histamine release from ECL cell. H. pylori decrease antral D cells and so somatostatin, leading into increased gastrin release Gastrin releasing polypeptide (GRP, Bombesin)—it stimulates gastrin and somatostatin release by binding to receptors on G and D cells. It is released from sympathetic nerve terminals of the gastric mucosa of body and antrum. Its half-life is 1½ minutes Histamine is stored in ECL and mast cells. Its release is stimulated by gastrin, acetylcholine and epinephrine Ghrelin (28 amino acids) is mainly secreted from endocrine cells of gastric mucosa. It has mainly got growth hormone releasing action; prolactin, ACTH, cortisol, aldosterone release is also promoted. Its action on islet cells reduces insulin release. Ghrelin stimulates appetite. Gastric bypass, gastrectomy reduces the appetite.

Excellence is rarely found, more rarely valued.

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SRB's Manual of Surgery Investigations for gastroduodenal diseases ™™

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Gastroduodenoscopy is ideal and most common investigation used to visualise mucosa. Lesions if any biopsy is taken for H. pylori and carcinoma. Also often used for endotherapy Endosonography (EUS) is very sensitive method to assess tumours, visualise stomach layers (90% accuracy), lymph nodes (80%), and to detect early liver metastasis which may not be identified by CT especially from left lobe CT scan is good imaging method to detect the stage, spread, nodal status, liver secondaries, and status of lungs CT and PET scan (together) using FDG is better to assess early spread Laparoscopy is very good investigating tool to identify peritoneal secondaries, and to stage the disease. Laparoscopic US is very sensitive to detect the liver secondaries Barium meal studies are used to detect hiatus hernia Celiac angiography is useful in bleeding ulcers, both for diagnostic and therapeutic purpose (therapeutic embolisation)

BARIUM MEAL STUDY Indications 1. Gastric ulcer—shows a niche which is the ulcer crater, a notch which is due to spasm of circular muscle on the greater curvature. 2. Chronic duodenal ulcer—shows absence or defor­med duodenal cap (due to spasm of 1st part of duodenum, barium will not stay and so cap will not be formed). 3. Gastric outlet obstruction—the cause may be chronic duodenal ulcer with pyloric stenosis or carcinoma pylorus. Features are:  Enormous dilatation of stomach.  Greater curvature below the level of iliac crest.  Absence of duodenal cap.  No filling of dye in 2nd part of duodenum.  Mottled appearance of stomach because of retained food particles.  Evidence of gastritis. 4. Carcinoma stomach—irregular filling defect. 5. Pseudocyst of pancreas—widened vertebrogastric angle. 6. Stomal ulcer in previous gastrojejunostomy. 7. In chronic duodenal ileus (Wilkie’s syndrome)—shows dilatation of stomach, 1st and 2nd parts of duo­denum, proximal portion of 3rd part of duodenum. 8. Others—gastric volvulus, duodenal diverticula, trichobezoar, gastric fistulas, diaphragmatic hernias when stomach is the content. 9. Carcinoma of head of pancreas shows “pad sign”; in periampullary carcinoma—reverse “3’ sign. Frostberg’s reverse ‘3’ sign (inverted ‘3’ sign). Rose thorn duodenum in carcinoma head of pancreas. 10. Hiatus hernia.

B

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Figs 20.6A and B: Barium meal X-rays showing normal picture in one and dilated stomach with features of gastric outlet obstruction in another.

Complication It may precipitate intestinal obstruction.

GASTROSCOPY It is visualisation of interior of stomach, duodenum, oesophagus. It can be done as OP procedure.

Uses 1. For diagnosing any pathology, e.g.  Gastric ulcer.  Duodenal ulcer.  Gastritis.  Stomal ulcer.  Carcinoma stomach.  Oesophagitis.  Varices.  Biopsies from the suspected cases of malig­nancy or for Helicobacter pylori can be taken. –– Endosonography can be done to assess the staging, operability of carcinoma stomach or oesophagus. –– Presently fibreoptic, flexible, or video gastrod­uodeno­scopy is used.

Procedure xx Barium sulphate solution is used [Barium is neurotoxic, but in sulphate media it will not get absorbed and so barium sulphate is used (Barium phosphate is not used)]. xx About 300 ml solution is given to the patient to drink and its flow down to the stomach is observed under fluoroscopic guidance. Films are taken as required. Commonly oblique views are taken. xx Microcrystalised barium sulphate (Microbar solution) is better as it does not get precipitated.

Fig. 20.7: Technique of doing gastroscopy using videoendoscope.

Stomach

Fig. 20.8: Gastroscopic views of different parts—vocal cords; pyriform fossa; oesophagus; oesophagogastric (OG) junction; body, fundus and pylorus of stomach, duodenum with clearly visible duodenal papilla (Courtesy: Dr Tantry and Dr Sandeep Gopal, Gastroenterologists, KMC, Mangaluru).

2. Therapeutic  Videoendoscopy is used not only for diagnosis but also mainly for therapeutic procedures.  Both end viewing and side viewing gastroscopes are available.  For therapeutic procedures and ERCP, side viewing gastroscope is required. Therapeutic procedures done are: ™™ ™™ ™™ ™™ ™™ ™™

Variceal injection or ligation or glueing or banding Stenting of pseudocyst of pancreas through gastroscopy Polyp removal Submucosal resection For ERCP diagnostic and therapeutic proce­dures Percutaneous gastrostomy (PEG)

Procedure Gastroscopy is done following eight hours of fasting. After lignocaine spray into the oral cavity, gastroscope is passed gently down the oesophagus when the patient does the swallowing action. Once the scope is inside the stomach, air is inflated and different parts of the

stomach is visua­lised. Fundus is visualised by retropulsion. Scope is passed through the pylorus to see the 1st and 2nd parts of duodenum and looked for any pathology. If required biopsy is taken. Often sedation with midazolam is beneficial to have an easy passage. xx Buscopan is used to relax stomach wall. xx Z-line signifies squamocolumnar junction. xx Multi-byte biopsy forceps is used.

Complications xx Bleeding. xx Aspiration. xx Perforation (rarely). Perforation occurs mainly in therapeutic procedures like oesophageal dilatation, endoscopic mucosal resection (EMR). It is common in proximal and middle oesophagus but can occur anywhere. Patient presents with hypotension, tachycardia, sudden severe pain in chest, abdomen, neck and surgical emphysema.

HELICOBACTER PYLORI xx It is gram –ve spiral like flagellated organism, first studied

by Warren and Marshall (both got Nobel prize), which is commonly present in stomach. It is involved in pathogenesis of duodenal ulcer, gastric ulcer, gastritis (type B) and gastric cancer. H. pylori

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Fig. 20.9: Endosonography of stomach showing different layers with echogenicity.

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Duodenal ulcer—95% Gastric ulcer—70% Gastritis—70–90% Gastric cancer—No. 1 carcinogen Gastric MALTOMA (mucosa-associated lymphoid tissue lymphoma)

The stomach you can hear, the stomach you can see, the stomach you can feel.—Sir James Walton

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SRB's Manual of Surgery Control of H. pylori Infection It is treated with antibiotics and other drugs with different combinations Clarithromycin 500 mg BD

Metronidazole 400 mg BD

Omeprazole 20 mg BD

OR

OR

OR

Amoxycillin 500–750 mg BD

Tinidazole 600 mg BD

Lansoprazole 30 mg BD

OR

OR

Tetracyclines, or Bismuth.

Pantoprazole 40 mg BD

The above regime is given for 7–14 days and then only proton pump inhibitors are continued.

Pathogenesis xx It is the most common bacterial infection in the world.

Rhesus monkey is the only natural reservoir. Its incidence increases with age. xx It releases enzymes like urease that hydrolyses urea so as to release ammonia which through negative feedback mechanism increases the gastrin release from G-cells. xx Infection occurs in stomach, i.e. body, fundus, antrum, disrupts the mucosal barrier, causes chronic inflammatory response leading to gastritis, gastric ulcer. xx Other than urease it also secretes dehydrogenase (converts alcohol to aldehyde which is toxic to mucosa), endopeptidase (disrupts mucosal barrier). Urease creates alkaline environment around it in mucus layer of gastric epithelium. It can survive only in gastric epithelium or gastric metaplasia in duodenum or Barrett’s oesophagus or in heterotopic gastric mucosa in Meckel’s diverticulum or rectum. It is because receptors for organisms to adhere into mucosa are available only in gastric mucosa. xx H. pylori impair mucosal healing, cause degranulation of eosinophils. It releases various protease and lipases that break mucus and so strong protective mucus barrier. xx It also secretes cytotoxins (cagA and vacA) which may also be involved in inflammatory reaction or malignancy. xx Even though normal duodenum cannot harbour the Helicobacter, duodenum with gastric meta­plasia can very well get infected by Helicobacter which explains why Helicobacter is involved in duodenal ulcer. xx Helicobacter is normally not found in saliva. xx Infection is transmitted through faeco-oral route, with a infection rate of 80–90% in a population (common and high). xx It is more common in lower socioeconomic group. xx It is considered to be a carcinogen for stomach. It is not linked with carcinoma of OG junction. Enzymes and toxins released by H. pylori ™™ ™™ ™™ ™™ ™™ ™™

Urease Dehydrogenase Endopeptidase Vacuolising cytotoxin–Vac A exotoxin Haemolysin CagA–cytotoxin-associated gene A

It is identified by: a.  Rapid urease test (cod liver oil test/CLO test)— noninvasive. b. C13–C14 breath tests (labelled urea breath test)— noninvasive. c. Biopsy from the different parts of the stomach and staining to identify the organism—invasive. For H. pylori three biopsies are taken one each from antrum, body and fundus. Tests for H. pylori ™™ ™™

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Rapid urease test—90% sensitivity, 98% specificity C13/ C14 breath tests—95% sensitivity and specificity—'gold standard' –– C13 requires spectrometry and costly –– C14 uses radioactivity Serology to identify IgG antibody—ELISA test with 90% sensitivity and specificity Biopsy and culture—very costly Warthin’s starry silver stain, acridine orange are special stains used Newer methods—special fluorescent technique, PCR products of H. pylori—urease gene, 165 rRNA identified using specialised probes when organisms are in less number

Treatment Therapy consists of antimicrobials combined with suppression of gastrc acid. Various combinations like triple regimes are used to control and eradicate the infection. Clarithromycin, amoxicillin, tetracyclines, bismuth and metronidazole/tinidazole with omeprazole/lanzoprazole/pantoprazole (proton pump inhibitors) combinations–are used. Triple regime is given for 7–14 days. After that PPI should be continued for 6–12 weeks. Follow-up confirmation of the eradication of the infection is needed often. Quadruple therapy using PPI twice daily, bismuth 2 tablets 4 times daily, metronidazole 250–400 mg three times daily, tetracycline 500 mg 4 times daily is used for 7–14 days.

CONGENITAL (INFANTILE) HYPERTROPHIC PYLORIC STENOSIS It is hypertrophy of musculature of pyloric antrum, especially the circular muscle fibres, causing primary failure of pylorus to relax. Duodenum is normal. There is increased risk of developing the condition if newborn gets erythromycin or azithromycin in first 14 days after birth.

Stomach Clinical Features

Differential Diagnosis

Common in first born males (4:1). Incidence is 4 in 1000 births. It is familial. It is seen between 3rd and 6th weeks of age of an infant, the time taken by the hypertrophied muscle to cause complete obstruction. xx Vomiting—forcible, projectile and non-bilious. xx Visible gastric peristalsis (VGP).

xx Duodenal atresia (Bilious vomiting is present). xx High intestinal obstruction (e.g. volvulus neonato­rum). xx Intracranial haemorrhage.

xx xx xx xx

Treatment 1. Correction of dehydration and electrolyte imba­lance. 2. Surgery:  Ramstedt’s operation—After laparotomy, hypertrophied muscle is cut along the whole length adequately until the mucosa bulges out. Mucosa should not be opened (pyloromyotomy). If mucosa is injured, it should be sutured horizontally using interrupted vicryl or silk sutures.  Laparoscopic pyloromyotomy is becoming popular. 3. Endoscopic pyloromyotomy is also tried (alike POEM for achalasia cardia). 4. Balloon dilatation is tried but results are not optimum like surgery or myotomy.

Fig. 20.10: Visible gastric peristalsis. xx Palpable lump of hypertrophied pylorus which is better felt

from left side, as a mobile, smooth, firm, olive like mass, with all borders well made out, moves with res­piration, with impaired resonance on percus­sion. It is the most important clinical feature (95%). xx Constipation. xx Dehydration and loss of weight. xx Electrolyte imbalance—hypokalaemic metabolicalkalosis.

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Clinical features of congenital pyloric stenosis ™™ ™™ ™™ ™™

Vomiting VGP Palpable mass Constipation and dehydration

In premature infants: xx VGP and mass is better seen and felt. xx Vomiting is regurgitant. xx Anorexia is common. Diagnosis is established by: xx Clinical examination. xx Ultrasound abdomen (very useful)—Doughnut sign.  Pyloric muscle 4 mm or more in thickness.  Length of pyloric canal >14 mm.  Cervix sign on long axis, target sign on short axis. xx Barium meal shows obstruction. Contrast study is not commonly done; but when it is done, it shows ‘string sign’ or ‘railroad track sign’ or ‘double track sign’ with pyloric obstruction.

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Figs 20.11A to D: (A) Ramstedt operation for congenital hyper­ trophic pyloric stenosis. Note that here muscular layer is cut but not mucosal layer; (B to D) Ramstedt pyloromyotomy for congenital hypertrophic pyloric stenosis. Only muscular layer is cut to allow mucosa to bulge out. Complications of surgery ™™ ™™ ™™

Postoperative pyrexia (Hyperthermia). Gastroenteritis Electrolyte imbalance

Pleasure in the job puts perfection in the work.

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SRB's Manual of Surgery Note

•

Medical treatment: Not advisable as cure is not guaranteed. Atropine methyl nitrate orally is tried to relax the pylorus muscle.

GASTRITIS Types 1. 2. 3. 4. 5.

Type A gastritis. Type B gastritis. Reflux gastritis. Erosive gastritis. Others: Stress gastritis, lymphocytic gastritis, granulomatous gastritis, phlegmonous gastritis.

Type A Gastritis xx Autoimmune disease. xx There is formation of antiparietal cell antibodies. xx Parietal cell dysfunction occurs causing achlor­hydria and vitamin B12 deficiency. xx Antrum is not affected. xx ‘G’ cell hyperplasia occurs with raised serum gastrin level. xx There is formation of microadenoma of enterochromaffin like

cells (ECL cells) with pre­disposition to gastric carcinoma.

Type B Gastritis xx xx xx xx

Occurs due to Helicobacter pylori infection. Antrum is affected. Peptic ulcer is common. Helicobacter related pangastritis commonly occurs which may turn into gastric cancer.

Reflux Gastritis xx Usually occurs after gastric surgeries. xx Prokinetic drugs are useful—metochlopramide, domperidone, cisapride, mozapride.

Erosive Gastritis xx Occurs due to disturbed gastric mucosal barrier. xx Induced by NSAIDs/alcohol.

Stress Gastritis Treatment: xx IV ranitidine 50 mg 8th hourly. xx IV omeprazole/pantoprazole. xx Sucralfate orally.

xx Due to inhibition of cyclo-oxygenase type 1 (COX-1) receptor enzyme, resulting in decreased prostag­landin production (Prostaglandin is cytoprotective). xx COX-2 mediated NSAIDs will not cause erosive gastritis.

Lymphocytic Gastritis It is associated with H. pylori infection.

Granulomatous Gastritis It is seen in Crohn’s disease and tuberculosis.

Phlegmonous Gastritis It is due to severe bacterial infection of stomach. It is rare but dangerous. Nonulcer dyspepsia ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Symptom complex with pain and discomfort in the upper abdomen It is intermittent upper abdomen pain in the absence of peptic ulceration It occurs in 25% of population—large number Anatomical or biochemical abnormalities are not discovered in this condition H. pylori is not associated with this condition Often it lasts for long time decreasing the quality of life Differential diagnosis—GERD/acid peptic diseases/gallstones/ pancreatitis/carcinoma H. pylori eradication is not required and there is no surgical role

ACUTE PEPTIC ULCER (DUODENAL OR GASTRIC ULCER) They are usually multiple erosions due to disruption of the mucosal barrier.

Causes Stress, drugs like analgesics, steroids, surgeries.

Clinical Features xx Sudden onset of acute pain and tenderness in epigastric region. xx Vomiting with or without haematemesis. xx Often acute peptic ulcers can lead to perforations.  Acute ulcers after cerebral trauma or neurosur­geries are called as Cushing’s ulcers.  Acute ulcers after major burns are called as Curling’s ulcers. Diagnosis is by gastroscopy.

Treatment xx Intravenous ranitidine 50 mg, 8th hourly. xx IV fluids. IV pantoprazole/rabeprazole/omeprazole. xx Blood transfusions if there is bleeding. Most of the time surgery is not required for acute ulcers. During follow-up patients are advised to take antiulcer drugs for 4-6 weeks— ranitidine, omeprazole or lanso­prazole.

Curling’s Ulcers xx They are acute ulcers which develop after major burns, Fig. 20.12: Endoscopic view of erosive gastritis.

presenting as pain in epigastric region, vomiting or haemate-

Stomach mesis. Treatment is conservative—IV ranitidine. IV pantoprazole 80 mg in 100 ml DNS—slow, later 40 mg IV maintenance. xx Curling’s ulcer occurs when burn injury is more than 35%. It is observed in the body and fundus not in antrum and duodenum.

Cushing’s Ulcers

xx Microscopically, it shows ulcer crater with chronic inflammatory cells and granulation tissue, endarteritis obliterans and epithelial proliferation. (Ulcer to the right of the incisura is malignant unless proved otherwise).

They are acute ulcers which develop after cerebral trauma or after neurosurgical operations. It is commonly single, deeper ulcer more frequently perforates. It can occur in oesophagus and duodenum also. Treatment is conservative by IV ranitidine.

GASTRIC ULCER Aetiology It occurs due to imbalance between protective and damaging factors of gastric mucosa. xx Atrophic gastritis, duodenogastric bile reflux, gastric stasis, abnormalities in acid and pepsin secretion. Acid becomes ulcerogenic even to normal gastric mucosa. xx Smoking, alcohol, NSAIDs, steroids. xx Helicobacter pylori infection (70%). xx There is either normochlorhydria or hypochlor­hydria. xx Altered mucosal barrier mechanism. xx Lower socioeconomic group.

Factors Involved in Gastric Ulcer Formation xx Duodenogastric reflux—reflux containing bile salts and

lysolecithin break the mucosal barrier making it more vulnerable for injury, action of drugs and pepsin injury. xx Gastric stasis. xx Ischaemia of the gastric mucosa. xx Type II and III gastric ulcers show acid hypersecretion.

A

B

Figs 20.13A and B: (A) Barium meal showing Niche in the lesser curve as benign gastric ulcer; (B) Benign gastric ulcer endoscopic view. Biopsy is a must. Ideally 10 biopsies should be taken from the edge.

Fig. 20.14: Specimen of stomach (identified by the mucosal pattern and rugae) showing deep ulcer near lesser curvature. Margin of the ulcer is clear, not everted with gastric mucosal folds converging towards the base of the ulcer. 95% of benign gastric ulcer occurs towards lesser curve. Benign gastric ulcer is more common in lesser curvature, as it takes more burden of passage of food and so more of wear and tear. Benign gastric ulcer is rare in greater curvature, fundus and cardia. Histologically it shows destruction of epithelial lining; proliferation of margin; destruction of the part of the muscle layer; granulation tissue in the floor; infiltration with chronic inflammatory cells; endarteritis and fibrosis in the base. xx Gastric ulcer >3 cm is called as giant gastric ulcer. It has got 6–23% chances to turn into malignancy. Incidence of perforation and bleeding is also very high. Endoscopy and biopsy should be done to rule out malignancy. Follow-up endoscopy is a must if drug therapy is used for treatment to confirm the complete healing of the ulcer. If complete remission has not occurred then partial gastrectomy should be done. xx Grossly, margin of the benign gastric ulcer is clear; deep; near lesser curve; edge is not everted with gastric mucosal folds converging towards the base of the ulcer. xx Ninty-five per cent of benign gastric ulcer occurs towards lesser curve, as it takes more burden of passage of food and so more of wear and tear. Benign gastric ulcer is rare in greater curvature, fundus and cardia. xx Acute ulcer: It is confined to mucosa and submucosa. It is commonly due to NSAIDs. xx Chronic ulcer: It penetrates muscularis layer of stomach.

Clinical Features xx Equal in both sexes. It is becoming more common in

females.

Pathology xx Gastric ulcer is large in size, usually lies in the lesser curvature, its floor being formed by the muscular layer. xx Posteriorly it may penetrate into the pancreas; it may cause torrential bleeding by eroding left gastric (commonly) vessles or splenic vessels or vessels in the gastric ulcer wall. xx Anteriorly it may perforate or penetrate into the liver. It may lead into hour glass contracture, or tea-pot deformity.

xx Common after the age of 40 years. xx Pain in epigastric region after taking food, lasting up to

two hours. Pain is uncommon during night. It is relieved by vomiting or by inducing vomiting. xx Periodicity: Symptom free interval may be 2–6 months. Often with seasonal variation. xx Vomiting relieves pain and often it is induced by the patient for relief of pain.

Troubles waste the stomach like rust waste iron.—Croatian proverb

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SRB's Manual of Surgery Types of gastric ulcer (Daintree Johnson) Type

Location

Incidence

Acid level

Type I

In the antrum, near the lesser curve

55%

Normal

Type II

Combined gastric ulcer (in the body) with duodenal ulcer

25%

High

Type III

Prepyloric ulcer

15%

High

Type IV

Gastric ulcer in the proximal stomach or cardia

5%

Normal

xx Haematemesis and melaena: Haematemesis is more

common. xx Appetite is good but hesitant to eat, because eating induces pain and that results in loss of weight. But once complications occur, appetite decreases. Aversion to spicy, fried foods occurs. xx On deep palpation, tenderness is felt in epigastric region.

xx Gastroscopy is done to see the location, type of ulcer and

also to take biopsy (10 biopsies). xx Ultrasound abdomen mainly to rule out other diseases and

to confirm associated diseases.

Note: • Often in lesser curve, saddle-shaped ulcer can occur. • Type V gastric ulcer is – ulcer anywhere in the stomach associated with NSAIDs.

Fig. 20.16: Multiple ulcers visualised on gastroscopy.

Fig. 20.15: Types of gastric ulcer (Daintree Johnson). Differential diagnosis ™™ ™™ ™™ ™™ ™™ ™™

Hiatus hernia Cholecystitis Chronic pancreatitis Chronic gastritis Dyspepsia Carcinoma stomach.

Figs 20.17A and B: (A) Gastric ulcer in the body of the stomach; (B) Gastric ulcer in prepyloric region.

Investigations xx Barium meal X-ray to see niche and notch. Barium meal X-ray features of benign gastric ulcer Niche on the lesser curve with notch on the greater curvature Ulcer crater projects beyond the lumen of the ulcer Regular/round margin of the ulcer crater—stomach spoke wheel pattern ™™ Overhanging mucosa at the margins of a benign gastric ulcer— projects inwards towards the ulcer—Hamptom’s line ™™ Converging mucosal folds towards the base of the ulcer ™™ Symmetrical normal gastric mucosal folds ™™ ™™ ™™

A

B Fig. 20.18: Barium meal study showing niche and notch—gastric ulcer.

Stomach Treatment xx Drugs like H 2 blockers, proton-pump inhibitors,

–– Persistent pain. –– Vomiting. –– Loss of appetite and weight.

carbenoxolone (biogastrone, sucralfate, prostag­landins which coats the ulcer and so creates a mucosal barrier) helps in reducing or eliminating the symptoms. xx But asymptomatic ulcer may exist silently and may turn into malignancy. xx So surgery is the preferred line of treatment. Partial gastrectomy and Billroth I gastroduodenal anasto­mosis is done. xx Type IV proximal gastric ulcer is difficult to manage. It is treated by subtotal gastrectomy. Often distal gastrectomy with selective sleeve like extension cut along the lesser curve to remove the ulcer is done—Pauchet’s procedure. xx Other surgical procedures: 1. de Miguel’s antrectomy: Distal antrectomy, pylorectomy with excision of ulcer along with gastroduodenal anastomosis is done. It preserves gastric reservoir function, shows less recurrence rate and less operative morbidity. 2. Maki’s pylorus preserving gastrectomy: Hemigastrectomy with excision of pyloric ulcer but retaining 2 cm pre-pyloric stomach. It is only used in type I gastric ulcer. Even though it has got fewer incidences of postoperative diarrhoea and dumping, it has got high recurrence rate.

Fig. 20.20: Hour glass contracture.  Diagnosis –– Barium meal: It shows filling only in the proximal stomach

or double pouched stomach. –– Gastroscopy.  Treatment

Partial gastrectomy wherein gastric ulcer with lower compartment of the stomach is removed and Billroth I anastomosis is done.

2. Tea-pot deformity (Hand-bag stomach): It is due to cicatrisation and shortening of the lesser curvature.  They present with features of pyloric stenosis.  Treatment is partial gastrectomy with Billroth I anastomosis.

3. Perforation—most frequent. 4. Bleeding by erosion into the left gastric and rarely splenic vessels or to vessels in the wall of ulcer—35%. It is common in type II and III gastric ulcers.

Fig. 20.19: Diagram showing Pauchet’s, Kelling Madlener, Csendes operations for proximal Type IV benign gastric ulcer.

3. HSV with excision of ulcer. 4. Kelling Madlener procedure: It is antrectomy and excision of proximal gastric ulcer Type IV. 5. Csendes procedure: It is subtotal gastrectomy with sleeve extended resection along the lesser curve for type IV proximal gastric ulcer.

Complications of Gastric Ulcer 1. Hour glass contracture: It, occurs exclusively in women, is due to cicatricial contracture of lesser curve ulcer.  Here stomach is divided into two compartments.  Clinical features –– Loss of periodicity.

Fig. 20.21: Tea-pot deformity.

5. Penetration posteriorly into pancreas, anteriorly into liver. 6. Malignant transformation usually into adenocar­cinoma of stomach (5–10%).

DUODENAL ULCER Aetiology xx Common in people with blood group O +ve. xx Stress, anxiety—‘hurry, worry, curry’. xx Helicobacter pylori infection is an important aetiology for

duodenal ulcer (90%).

It is consequences which are more important than rewards or punishments.

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SRB's Manual of Surgery Mucosal folds Site Margin Floor Edge Surrounding area Size and extent

Benign gastric ulcer Converging mucosal folds up to the margin 95% lesser curve Regular margin Granulation tissue in floor Not everted; punched or sloping Surrounding area and rugae are normal Small, deep up to part of muscle layer

xx NSAIDs, steroids. xx Endocrine causes: Zollinger-Ellison syndrome, MEN

syndrome, hyperparathyroidism. xx Other causes: Alcohol, smoking, vitamin defi­ciency. xx Dragstedt dictum: “No acid – No ulcer”.

Malignant gastric ulcer Effacing mucosal folds Greater curvature Irregular margin Necrotic slough in floor Everted edge Surrounding area shows nodules, ulcers and irregularities Large and deep

xx Pain is more before food, in early morning and decreases

after taking food. It is classically called as hunger pain as it is relieved by taking food. Night pains are common. xx Common in males. xx Periodicity is more common than in chronic gastric ulcer with seasonal variation. xx Water-brash, heart burn, vomiting may be present. xx Melaena is more common, haematemesis also can occur. Differences between clinical features of gastric ulcer and duodenal ulcer Gastric ulcer

A

B

Figs 20.22A and B: (A) Anatomical location of chronic duodenal ulcer; (B) Serosal surface in a chronic duodenal ulcer. It appears like cayenne pepper.

Duodenal ulcer

Pain after food intake

Pain before food intake

Periodicity less common

Periodicity more common

Haematemesis more common

Malaena more common

Weight loss occurs

Weight gain occurs

Equal in both sexes

Common in males

xx Appetite is good and there is gain in weight. It decreases

once stenosis develops.

Pathology xx Ulcer occurs in the first part of duodenum, usually with in the first inch,involving the muscular layer. Sites: a.  In the bulb (bulbar)—95%. b.  Post-bulbar (5%). xx Eventually it shows cicatrisation causing pyloric stenosis. Serosa overlying the site of duodenal ulcer shows petechial haemorrhages with speckled red dots, appearing like sprinkled cayenne pepper. xx Microscopically, ulcer with chronic inflammation with granulation tissue, gastric metaplasia of duodenal mucosa, endarteritis obliterans are visualised. xx Sometimes two opposing ulcers, i.e. over anterior and posterior surfaces of duodenum are present and are called as kissing ulcers. xx An anterior ulcer perforates commonly, posterior ulcer bleeds or penetrates commonly.

Clinical Features xx In India, ratio of duodenal ulcer (DU) to gastric ulcer is 30

: 1. A very high incidence. xx It is common in all socioeconomic group, more with stressed professionals (Type A personality).

xx Eats more frequently without any restriction. xx Chronic duodenal ulcer can be uncomplicated or complicated.

Complications of Duodenal Ulcer 1. Pyloric stenosis: Due to scarring and cicatrisation of first part of the duodenum. 2. Bleeding (10%). 3. Perforation (5%). Both acute and chronic ulcers can perforate. Anterior ulcers perforate. 4. Residual abscess. 5. Penetration to pancreas. Note:

• Chronic duodenal ulcer will not turn into malignancy. • Ulcer which is more than 2 cm is called as giant duodenal ulcer.

Investigations xx Barium meal X-ray shows deformed or absence of duodenal

cap (because of spasm). Appearance of ‘trifoliate’ duodenum is due to secondary duodenal diverticula which occurs as a result of scarring of ulcer.

Stomach II. Specific measures:  Intragastric pH should be maintained above 5.

Drugs 1. H2 Blockers:  Promotes ulcer healing in 4–8 weeks, by reducing acid secre-

Fig. 20.23: Absence of duodenal cap—chronic duodenal ulcer. xx Gastroscopy reveals the type, location of ulcer, narrowing

if any. Biopsy also can be taken to look for the presence of Helicobacter pylori. Usually biopsies are taken from duodenum, pylorus, antrum, body, fundus, and confirmed by rapid urease test or C13 or C14 breath tests. xx Estimation of serum gastrin level, serum calcium level. Differential diagnosis ™™ ™™

Carcinoma stomach (pylorus) Dyspepsia due to other causes –– Hiatus hernia –– Oesophagitis –– Cholecystitis –– Chronic pancreatitis 

tion. –– Tab cimetidine. –– Tab ranitidine (300 mg HS or 150 mg BID), (IV preparation is available). –– Tab famotidine (IV is available) Most potent H2 blocker. Dose is 20–40 mg/day. –– Tab roxatidine. –– Tab nizatidine.

2. Proton-pump inhibitors:  Inhibit parietal cell H+, K+ ATPase enzyme responsible for

acid secretion. They are used for 6–12 weeks. They stop acid secretion completely. –– Omeprazole 20 mg OD 1 hour before food—IV preparation is available. –– Esomeprazole 40 mg. –– Lansoprazole 30 mg, Ilaprazole 10 mg –– Pantoprazole 40 mg—IV preparation available. –– Rabeprazole 20 mg—IV preparation available.

3. Antacids:  Neutralises the HCl to form water and salt and also inhibits

peptic activity.  Aluminium hydro­xide and magnesium trisilicate are com­monly

used.  Dose is 2 grams 2 hours after food.  Aluminium hydroxide causes constipation, magnesium trisili-

cate causes diarrhoea. Osteomalacia, milk alkali syndrome, rebound ulcer due to gastrin release are other complications.

4. Sucralfate  It is an aluminium salt of sulfated sucrose which provides a

protective coat to ulcer crater thereby promotes healing. It inhibits peptic activity.  It binds to ulcer bed and stays for 12 hours; prevents back diffusion of hydrogen ion; raises endogenous prostaglandin level in tissues; binds bile acid and pepsin; prevents colonisation of gastric mucosa by bacteria.  Dose is 1 g qid for 6 weeks (before food). It is an effective drug.

5. Anti-Helicobacter pylori regime:  It is very useful, given for 7–14 days—later the proton- pump

inhibitors are continued. Fig. 20.24: Endoscopic view of duodenal ulcer.

Treatment Aim of therapy: To relieve symptoms; to heal ulcer; to prevent recurrence. I. General measures:  Avoid alcohol, NSAIDs, smoking, spicy foods. Have more frequent food.

 Triple or quadruple (tetracycline, bismuth, tinidazole, panto-

prazole) regimes are used.

6. Colloid bismuth sulphate is a good drug for ulcer, but it stains the oral cavity and mucosa. 7. Misoprostol (200 mg tid) is the only prostaglandin agonist accepted.  PG E1 (mesoprostol) and E2 increase mucus and bicarbonate

secretion, improves mucosal blood flow, but reduces acid secretion.

Every man is the master of his own fortune.

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SRB's Manual of Surgery Anti-Helicobacter regime (Triple regime) Clarithromycin 500 mg BD

Metronidazole 400 mg BD

Omeprazole 20 mg BD

OR

OR

OR

Amoxycillin 500–750 mg BD

Tinidazole 600 mg BD

Lansoprazole 30 mg BD

OR

OR

Tetracyclines, or Bismuth, etc.

Pantoprazole 40 mg BD

Follow-up gastroscopy is a must, to confirm that ulcer has healed. Note:

Antacids and H2 blockers should not be used along with PPI as these drugs will reduce the action of PPIs by creating alkaline media.

Surgery for Uncomplicated Duodenal Ulcer Indications for surgical intervention for chronic DU (Uncomplicated DU): 1. Uncomplicated DU, not responding to drug therapy of 8–12 weeks—intractable duodenal ulcer 2. Repeated recurrences Presently most of the uncomplicated DU does not require surgery

xx Highly selective vagotomy (HSV).  In HSV, only fibres supplying the parietal cells are ligated. Nerve of Latarjet which supplies the antrum pump is retained and so no drainage procedure is required in HSV. HSV is also called as parietal cell vagotomy or superselective vagotomy. Here nerve fibres in last 6 cm of stomach, just proximal to pylorus are preserved (Crow’s foot). Vagotomy reduces acid secretion, hence ulcer heals. No acid, No ulcer.  HSV was first described by Amdrup and Johnston in 1969.  Distal 6 cm oesophageal nerve fiber clearance is essential. Fibers up to 6 cm proximal to pylorus in stomach are cleared; nerve of Latarjet is preserved; adequate distal greater curve clearance is essential.  Intraoperative test for completion of vagotomy should be done—Grassi test or insulin test.  It has got distinct advantages—low operative mortality (0.2%) and postoperative morbidity (0.5%); post-vagotomy diarrhoea and dumping syndrome is very low; chances of developing anaemia, weight loss, osteoporosis, tuberculosis, and carcinoma are very less.  Problems—lesser curve necrosis due to ischaemia; recurrent ulcer 10–15% in 10 years. xx Selective vagotomy with pyloroplasty (SV + P). xx Truncal vagotomy with gastrojejunostomy (TV + GJ). xx Posterior truncal vagotomy with anterior seromyo­tomy—Taylor’s operation. It can be done through laparoscopy. xx Vagotomy with antrectomy: Gastrin producing antrum, vagal cholinergic pathway from ulcer bearing area is removed with gastroduodenal anastomosis. Ulcer recurrence is very low but has got morbidity. xx Posterior truncal vagotomy with HSV without drainage procedure (Kim’s) often through laparoscopy is also done. xx Linear gastrectomy with posterior truncal vagotomy through laparoscopy.

xx Most of these procedures presently can be done through laparoscope. Note: • Presently, there is no role of gastrectomy or gastrojeju­nostomy (Just GJ) for uncomplicated DU.

• • •

A peptic ulcer is an excavated defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall. A refractory peptic ulcer is defined as an endoscopically proven ulcer greater than 5 mm in diameter that does not heal after 12 weeks of treatment with a proton-pump inhibitor. A recurrent peptic ulcer is defined as an endoscopically proven ulcer greater than 5 mm in diameter that develops following complete ulcer healing.

PYLORIC STENOSIS DUE TO CHRONIC DUODENAL ULCER

Pathology Chronic DU after many years undergoes scarring and cicatrisation causing total obstruction of the pylorus, leading to enormous dilatation of stomach.

Clinical Features xx Pain is severe, persistent, in epigastric region, and also with

feeling of fullness. xx Vomiting—large quantity, foul smelling and frothy, vomitus

contains food consumed on previous day (partially digested or undigested food). xx Loss of periodicity. xx Loss of appetite and weight. xx Visible gastric peristalsis (VGP)—may be elicited by asking the patient to drink a cup of water. xx Positive succussion splash which is done with 4 hours empty stomach, by placing a stethoscope over the epigastric region and shaking the patient adequately. xx Auscultopercussion test shows dilated stomach. Test is done by placing a stethoscope over the epigas­tric region. Skin is scratched from left side down­wards, at several points away from the epigastrium (towards left side) using finger and these points are joined. Normally greater curvature of stomach is above the level of umbilicus (midway between the umbilicus and epigastrium). In gastric outlet obstruction it lies below the level of the umbilicus (Stomach we see; stomach we feel; stomach we hear). xx Confused status because of alkalosis and electro­lyte changes.

Stomach xx Electrolyte changes: Because of vomiting, hypoch­lo­raemic,

hyponatraemic, hypokalaemic, hypocalcaemic, hypomagnesaemic alkalosis occurs. It causes para­doxical aciduria. xx Mass is never palpable. xx Goldstein saline load test—half an hour after installation of 750 ml of saline, if volume remained and if more than 250 ml, suggest obstruction.

Investigations 1. Barium meal study:  Absence of duodenal cap.  Dilated stomach where greater curvature is below the level of iliac crest.  Mottled stomach.  Barium will not pass into duodenum. 2. Gastroscopy to rule out carcinoma stomach and to visualise the stenosed area. 3. Electrolyte study for correction of electrolyte imbalance. 4. ECG to check for hypokalaemia.

Treatment xx Correction of dehydration and electrolytes by IV fluids—

normal saline or double strength saline, calcium, potassium, magnesium. xx Blood transfusion is given if there is anaemia. xx TPN support. xx Stomach wash to clean the stomach contents (using normal saline) is given using stomach tube like Eswald’s. It also reduces the oedema of stomach wall and improves gastric emptying time by increasing the gastric muscle tone. xx Surgery  HSV with gastrojejunostomy is present recommendation even

though it is technically difficult. HSV is better than TV as it maintains the nerve supply of the chronically obstructed antrum and so may eventually reduce the chronic emptying problems.  Truncal vagotomy along with gastroje­juno­stomy of Mayo (posterior, vertical/oblique, short loop, retrocolic, isoperistalsis) is done—ideal, commonly advocated procedure.  Vagotomy, antrectomy (acid secreting area) with Billorth I anastomosis along with feeding jejunostomy for nutrition is the other option.

Fig. 20.25: Pyloric stenosis with gastric dilatation.

Fig. 20.27: Gastric outlet obstruction showing dilated stomach on table.

A

B Figs 20.26A and B: Barium meal pictures showing gastric outlet obstruction.

Differential Diagnosis Carcinoma pylorus—here mass may be palpable. Pyloric stenosis—causes Congenital Chronic DU—fibrosed/cicatrised Carcinoma pylorus Adult pyloric stenosis—it is treated by pyloroplasty (not by pyloromyotomy) ™™ Pyloric mucosal diaphragm—it should be excised surgically or endoscopically   ™™ ™™ ™™ ™™

Fig. 20.28: Truncal vagotomy and gastrojejunostomy. It is posterior, vertical, short loop, retrocolic, isoperistaltic GJ of Mayo.

Patients with peptic ulcer were regularly “milked” for acid, which was used for patients suffering from hypochlorhydria.  — Albert E Coates

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SRB's Manual of Surgery drop, causing metabolic alkalosis. Alkalosis can lead to hypocalcaemia causing tetany. It is called as ‘gastric tetany’. To control alkalosis, kidney secretes excess bicarbo­n ate (In alkalosis without hyponatraemia, bicarbonate is secreted along with sodium). Here, due to hypo­natraemia, body conserves sodium and so bicarbonate is secreted along with hydrogen ion. So urine becomes acidic. It is called as paradoxical aciduria.

Clinical Features xx Irritability, confused status, dehydration. xx Often convulsions can occur. xx Features of alkalosis like rapid breathing—Cheyne-Stokes breathing and tetany.

Investigations Fig. 20.29: Gastrojejunostomy stoma view on endoscopy.

xx Serum electrolytes. xx Arterial blood gas analysis. xx Serum calcium level estimation.

Treatment xx xx xx xx

Double strength normal saline. IV potassium given slowly under ECG monitoring. The cause is treated. IV magnesium.

Note:

Metabolic changes are not severe in carcinoma pylorus as it is seen in pyloric stenosis due to chronic duodenal ulcer because in carcinoma stomach often there is hypochlorhydria or achlorhydria.

Fig. 20.30: Vagotomy and antrectomy. It is occasionally used for intractable resistant duodenal ulcer or chronic duodenal ulcer with obstruction. HSV is commonly used in intractable cases. GJ with vagotomy is commonly used in pyloric stenosis due to chronic duodenal ulcer. Note:

• O  ften gastric emptying may be delayed for 2–4 weeks after surgery in pyloric stenosis. It usually recovers in 7 days. • After recovery eradication of H. pylori infection is routinely done even though infection may not be evident in many of patients with outlet obstruction. • No role of pyloroplasty or only HSV in a scarred duodenum—as it can cause disruption and bile leak. • Gastrectomy and other procedures are usually not necessary in pyloric stenosis. • Endoscopic balloon dilatation of the stenosed area benefits only temporarily with high recurrence rate.

ELECTROLYTE CHANGES IN PYLORIC STENOSIS xx xx xx xx xx xx

Hyponatraemia. Hypokalaemia. Hypomagnesaemia. Hypochloraemia. Metabolic alkalosis. Paradoxical aciduria.

Because of severe vomiting which contains acid as well as undigested retained food, sodium, chloride, potassium, magnesium levels

PERFORATED PEPTIC ULCER xx It is the terminology used for perforation of duodenal ulcer or gastric ulcer or stomal ulcer. Otherwise all clinical features and management are similar. xx Perforation is common in duodenal ulcer (75% of perforated peptic ulcers). Mortality is more in gastric ulcer perforation and perforation in elderly.

A.  PERFORATED DUODENAL ULCER xx It is common in males (8:1) between 35–45 years of age

group, but can occur in any age group. xx Anterior ulcer perforates, commonly  In 80% of cases, there is a history of chronic DU.  In 20% cases, it is silent perforation.

xx Perforation can occur in acute ulcers or in acute presentation

of a pre-existing chronic ulcer. xx Perforation may be precipitated by steroids, analgesics

(NSAIDs), alcohol, antimalarials. xx Overall incidence is 5%. xx Active ulcers perforate commonly. xx Duodenal ulcer with H. pylori infection causes perforation

more commonly, especially in young individual; NSAIDinduced ulcer causes perforation in elderly. xx Mortality in perforated duodenal ulcer is 10% (in gastric ulcer it is more—20%).

Stomach Stages of Perforation xx Stage of chemical peritonitis:  Once perforation occurs, stomach contents escape into the perito­neal cavity. The acid from the stomach causes chemical peritonitis leading to severe pain in epigastric region, vomiting, tenderness, guarding, rigidity, tachycardia, sweating. xx Stage of reaction (Stage of illusion):  Peritoneum secretes lots of fluid to neutralise the escaped content and so temporarily the pain reduces, and the patient feels better. This phase lasts for about 6 hours. xx Stage of diffuse bacterial peritonitis:  After about six hours, bacteria from GIT (escape) migrate from the site of perforation causing diffuse peritonitis.

contact of expelled gastric contents with the parietal peritoneum. Pain often radiates to right scapular region. Pain becomes more on movements. xx Tenderness and rebound tenderness is seen (Blumberg sign) all over the abdomen. xx Fever, vomiting, dehydration, oliguria occurs. xx Patient is toxic, with tachycardia, hypotension, tachypnoea. xx Abdominal distension occurs. xx Guarding and rigidity, initially in the epigastrium but later all over the abdomen. xx Dullness over the flank because of fluid. xx Obliteration of liver dullness—as a result of collection of escaped gas under the diaphragm. xx Silent abdomen with absence of bowel sounds. xx Tenderness felt on per rectal examination. xx Sometimes fluid from supracolic region slowly trickles down along the right paracolic gutter and collects in right iliac region causing pain and tenderness in RIF mimicking appendicitis. xx Often slow, small perforation presents with subacute features, but diffuse peritonitis eventually sets in 24–48 hours. Terminal stage: Patient may have oliguria, septi­caemia, shock, Hippocratic facies (sunken eyes, cold periphery and shallow rapid breathing, ill look), with MODS (Multiorgan dysfunc­tion syndrome). Note:

Valentino’s syndrome is perforated peptic ulcer mimicking acute appendicitis. Rudolph Valentino, in 1926 died of appendicitis and peptic ulcer due to sepsis.

Fig. 20.31: Duodenal perforation—on table look.

Investigations xx Chest X-ray with abdomen in erect posture (plain X-ray):

Shows gas under diap­hragm in 70% of cases. In 30% of cases, there is no gas under diaphragm. It may be due to, either the gas leak is less than 1 ml or due to previous surgery causing adhesions between liver and diaphragm, or sealed peptic ulcer. (Chilaiditi’s syndrome is the interposition of the colon in front and above the liver. It is common in children and elderly. It may be mistaken for gas under diaphragm in plain X-ray abdomen).

Fig. 20.32: Spread in DU perforation.

Clinical Features xx Presents with severe persistent pain in the epi­gastrium

initially, later in the right side abdomen (as the inflammatory fluid spills along the right paracolic gutter) and finally becomes generalised. Pain is of sudden in onset, is due to

Fig. 20.33: Plain X-ray abdomen in erect position with ground-glass appearance and gas under diaphragm—perforation.

An inn has one entrance and three exist—to hospital, to asylum and to prison. —Croatian Proverb

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SRB's Manual of Surgery xx Surgery:  Emergency laparotomy through upper midline incision is done.  All infected fluid is sucked out.  Perforation is identified and closed with interrupted, horizontal sutures using either silk or vicryl. Omental patch is placed before suturing—it is called as Rosoe-Graham Operation. Because of its adhesion property it seals perforation; good vascularity and lymphatics promote the healing effectively.

Fig. 20.34: Lateral (Left) decubitus X-ray showing air under diaphragm. This is done when patient is critically ill and cannot make the patient stand in erect posture. xx Ultrasound abdomen shows free fluid and often gas. xx Blood urea, serum creatinine, total count, electro­lytes, are

helpful. xx CT scan abdomen is very sensitive investigation whenever

there is absence of gas under diaphragm. It rules out other conditions like pancreatitis. Gastrograffin upper GI study also confirms the perforation. Differential diagnosis ™™ ™™ ™™ ™™ ™™ ™™ ™™

Acute appendicitis Acute pancreatitis Acute cholecystitis Ruptured aortic aneurysm Myocardial infarction Mesenteric ischaemia Pneumonia

Fig. 20.36: Duodenal ulcer perforation closed horizontally using interrupted silk/vicryl sutures with omental patch over it.  Peritoneal wash (toilet) using 5–10 litres of saline is given.  Drain is placed and abdomen is closed, often if required with

tension sutures. Drain is removed in 3–5 days. During discharge, patient is advised to avoid alcohol and to take H2 blockers or proton pump inhibitors for 6–12 weeks.  After 12 weeks follow-up gastroscopy must be done.

Treatment xx xx xx xx xx

Patient is advised admission. IV fluids—Ringer lactate, normal saline, dextrose saline. Antibiotics—Cefotaxime, metronidazole, amikacin. Catheterisation. Ryle’s tube aspiration.

Fig. 20.37: Closure of duodenal ulcer perforation using interrupted silk/ vicryl sutures over a omental pedicle patch—Rosoe Graham’s operation. Note: Fig. 20.35: Approaches to manage duodenal ulcer perforation can be either open (upper midline incision) laparotomy incision or laparoscopic.

• V  ery rarely, in elderly people or in cases of subacute perforation which gets sealed on its own, conservative treatment is tried with careful observation, i.e. by giving IV fluids, antibiotics, Ryle’s tube aspi­ration, maintenance of urine output and electrolytes. It is called as Hermen-Taylor regime. But it should not be a standard treatment.

Stomach • L aparoscopy is beneficial for both diagnoses, as well as for therapy for perforation closure using omental patch. It is proposed and widely used for early duodenal perforation. It can be useful for most of the duodenal ulcer perforations. If it is problematic, conversion options should always be kept in mind. • Once perforation is closed, either by open or laparoscopic method, after recovery patient should be advised, anti-Helicobacter pylori therapy (triple regime for 14 days) with PPI for 3 months. It reduces rate of reperforation and ulcer recurrence in duodenal ulcer. • In patients with severe peritonitis and critically ill, after perforation closure it is better to insert a nasojejunal tube or feeding jejunostomy for nutrition in postoperative recovery period. Even if patient develops a temporary duodenal leak, this supports nutrition well until the leak stops. • Occasional large perforated duodenal ulcer with oedema which cannot be closed is managed by serosal patch/duodenal drainage and pyloric exclusion/gastrostomy, duodenostomy and jejunostomy/Roux-en-Y jejunal patch over the perforation. • Manheim peritonitis index or APACHE II scoring system is used to assess the patient properly. • Doing concomitant acid reducing surgical procedure like HSV is under debate and not used routinely (not advised) even though some centers advocate. HSV may be done if there is not much contamination of the peritoneal cavity or in early perforation of a chronic duodenal ulcer.

B.  PERFORATED GASTRIC ULCER

xx Commonly ulcer in the lesser curve near the antrum perforates. Amount of gas escaped is more than the perforated DU. Malignancy should always be suspected and so biopsy from the edge is a must. xx Mortality in gastric ulcer perforation is high (20%). xx Commonly they are prepyloric in position. xx Primary closure with an edge biopsy is commonly used. Distal gastrectomy, including ulcer area is better option if patient’s general condition is favourable. xx Posterior gastric ulcer perforation is often difficult to diagnose both clinically and radiologically.

A

D.  DRY PERFORATION

(Perforated Duodenal Ulcer Sealed by Omentum) xx Patient is ambulatory. xx Vomiting is absent. xx Rigidity confined to epigastrium and right hypo­chondrium. Different signs in X-ray in perforation Cupola sign—crescent shaped radiolucency under the diaphragm Riglers sign—visualisation of both aspects of the bowel wall being outlined by gas on either side ™™ Inverted V sign—gas on either sides of the falciform ligament ™™ Football sign—collection of gas in the center of the abdomen like a foot ball ™™ Triangle sign—gas between bowel loops ™™ ™™

Conditions which mimic pneumoperitoneum— pseudopneumoperitoneum Subpulmonary pneumothorax Chilladiti syndrome Subphrenic abscess due to infections by gas forming organism like Clostridium Welchii ™™ Subdiaphragmatic fat or omental fat under the diaphragm may rarely mimic gas under the diaphragm ™™ ™™ ™™

BLEEDING PEPTIC ULCER xx It is bleeding either from duodenal ulcer, or gastric ulcer or stomal ulcer. xx In bleeding from stomal ulcer, partial gastrectomy is required. xx Mortality in bleeding peptic ulcer is high (20–30%). Elderly age, associated systemic diseases increase the mortality. xx NSAIDs and H. pylori infection, coagulopathy, and anticoagulant drugs are common precipitating factors. Concomitant use of NSAID and steroids increase risk by 10-fold. xx Need of more than 5 units of blood transfusion during hospital stay is called as massive haemorrhage.

B

Figs 20.38A and B: (A) Gastric ulcer perforation on table finding; (B) Malignant gastric ulcer showing perforation.

C.  PERFORATED STOMAL ULCER

In perforation of stomal ulcer, often undoing of GJ or partial gastrectomy may be required.

Fig. 20.39: Sites of gastric ulcer and duodenal ulcer bleeding. Note GU can erode into the left gastric artery. DU can erode into the gastroduodenal artery.

There is something wrong if you are always right—Arnold Glasgow.

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SRB's Manual of Surgery A.  BLEEDING DUODENAL ULCER xx 10% common. xx Risk of bleeding in chronic duodenal ulcer increases to 35%

if patient has not taken specific anti-Helicobacter pylori therapy and PPI.

Fig. 20.40: In bleeding ulcer during endoscopy stomach should be inflated with air adequately so that bleeding ulcer is visualised well.

Fig. 20.41: Melaena—typical black, tarry coloured foul smelling stool. It signifies upper GI bleed. At least 50 ml bleeding should be there to cause melaena. Differential diagnosis

Precipitating causes ™™ ™™ ™™ ™™

Alcohol NSAIDs, steroids Excessive fibrosis Atherosclerotic disease

Forrest classification of bleeding or bled ulcer Ia Spurting and bleeding Ib Nonspurting but active bleeding IIa Visible vessel with red or blue protrusion or pulsatile pseudoaneurysm IIb Nonbleeding ulcer with clot overlying IIc Ulcer with haematin base III Clean ulcer—no clot, no vessel

™™ ™™ ™™ ™™ ™™ ™™ ™™

Erosive gastritis Oesophageal varices Carcinoma stomach Bleeding gastric ulcer Mallory-Weiss syndrome Gastric polyps Bleeding disorders

Investigations To look for in endoscopy, in bleeding ulcer ™™ ™™ ™™ ™™ ™™

Spurter Clot Visible vessel Aneurysmal dilatation of the arteriole in the wall of ulcer Ooze

xx Bleeding from DU is either from the small vessels in the wall

of ulcer crater or due to erosion into the gastroduodenal artery. xx Usually posterior duodenal ulcer bleeds. xx Bleeding from small vessels in the wall of ulcer is due to

sloughing of the ulcer. It is less severe, gra­dual and most often well-controlled by conser­vative treatment. xx Bleeding from erosion of gastroduodenal artery is severe, torrential and almost always needs early surgical intervention.

Clinical Features xx Haematemesis and melaena. xx Features of shock: Pallor, tachycardia, sweating, hypoten-

sion, tachypnoea, dry tongue, cold peri­phery. xx Past history of chronic DU may be present. But it is not always

necessary in every patient, as some may have a silent ulcer which may present as bleeding and haematemesis to begin with. xx History of pain and tenderness in epigastric region which has increased in intensity recently.

Fig. 20.42: Bleeding duodenal ulcer endoscopic view.

Stomach xx Gastroscopy is confirmative—it is a must. It identifies ulcer

bleed in 90% of cases clearly. Possibility of rebleed is also assessed by endoscopy. A flat clear based ulcer is less likely to rebleed. Active ulcer/fresh clot/visible vessel/pseudoaneurysm/large ulcer are more likely to rebleed. Rockall scoring system is used to predict rebleed. xx Coeliac angiogram to identify the bleeder may be helpful. xx Hb% and PCV—should be repeated at regular intervals (once in 2–3 hours). xx Blood group and cross-matching. xx Estimation of serum electrolytes, blood urea, serum creatinine, platelet count.

Treatment

Indications for surgical treatment ™™ ™™ ™™ ™™ ™™

In spite of conservative treatment condition of patient deterio­ rates Bleeding from gastroduodenal artery Recurrent bleeding Elderly patient If more than 4 units of blood required immediately

xx Surgery  After laparotomy, pyloric channel and first part of the

duodenum (gastroduodenum) is opened longitu­dinally, bleeder is identified. Underruning of the bleeding area with vicryl is done.

Seventy percent of bleeding duodenal ulcers are treated conser­ vatively. xx The shock is corrected initially by:  Foot end elevation.  IV fluids, plasma expanders (haemaccel, dextran, crystalloids). CVP line is better in these patients.  Sedation.  Catheterisation—to assess urine output.  Blood transfusion to replace the lost blood. xx Stomach wash is given—1 : 2,00,000 adrenaline in saline wash is given to the stomach through Ryle’s tube. xx IV ranitidine 50 mg 6th or 8th hourly. IV famotidine. xx IV pantoprazole 80 mg in 100 ml dextrose saline is given slow IV as starting dose and later 40 mg in dextrose saline IV OD/BD. Slow continuous infusion of pantoprazole 40 mg in dextrose saline, 500 ml IV can also be given. xx Endoscopic cauterisation of small vessel with either gastro­scopic bipolar cautery or through Laser (Nd: YAG) or through heater probe or through haemoclips can be tried to stop the bleeding. xx Sclerotherapy—ethanolamine oleate, distilled water. Epinephrine injection is also used commonly. Other agents used are absolute alcohol, polidocanol. xx Observation  Patients with bleeding from small vessels in the wall of DU will commonly respond to conservative treatment. xx Angiographic embolisation of gastroduodenal artery. xx Haemoclips placement over the bleeding point endoscopically.

Fig. 20.44: Gastroduodenal artery ligation is required in case of severe massive upper GI duodenal ulcer bleed.

Fig. 20.45: Underrunning of the bleeding duodenal ulcer at ulcer bed is done to control haemorrhage. After that duodenum is closed with Finney’s pyloroplasty.  If the bleed is from gastroduodenal artery, then it has to be

ligated to stop the bleeding. Opened gastro­duodenum is closed by Finney’s pyloroplasty.  Truncal vagotomy may be done together, if the general condition of the patient is good. Fig. 20.43: Sclerosants like ethanolamine oleate or distilled water are used through endoscopy to control bleeding ulcer. It causes tamponade, vasoconstriction, sclerosis. It is the best method to control the bleeding.

xx Further treatment  During discharge, patient is advised to take anti-Helicobacter pylori (triple) therapy, proton pump inhibitors for 6–12 weeks (Omeprazole, or Lanzoprazole).

65% of haematemesis is due to bleeding peptic ulcer. Among peptic ulcer, duodenal ulcer (35%) is the most common cause.

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SRB's Manual of Surgery  Healing of ulcer can be confirmed by doing a gastroscopy

after 6–12 weeks. Treatment schedule for bleeding duodenal ulcer Treatment of shock Blood transfusion Stomach wash with—1 : 2,00,000 adrenaline saline IV ranitidine, famotidine, pantoprazole, omeprazole Endoscopic sclerotherapy using ethanolamine oleate or distilled water ™™ Endoscopic bipolar cauterisation, laser therapy, heater probe, haemoclips ™™ Angiographic embolisation of gastroduodenal artery ™™ Open surgery and underrunning of the bleeding ulcer bed ™™ Ligation of gastroduodenal artery and then Finney’s pyloroplasty ™™ Proton pump inhibitors during discharge ™™ Follow-up gastroscopy after 3 months Sclerotherapy is the most popular endoscopic method used at present ™™ ™™ ™™ ™™ ™™

B.  BLEEDING GASTRIC ULCER

xx It is similar to bleeding DU. Bleeding may be either from the ulcer bed or from the erosion of gastric vessels commonly but occasionally splenic vessels. They commonly present with severe haematemesis and shock. xx Bleeding is much more severe than bleeding DU. xx Surgery is the main treatment: After initial resuscitation, blood transfusion and a trial of conservative management, laparotomy is done.

Fig. 20.46: Gastroscopy showing carcinoma stomach which is bleeding. Note the slough and everted edge.

On laparotomy one of the following procedures is done:

Underrunning of OR ligation of splenic vessels the ulcer bed. with splenectomy with or without partial gastrectomy and gastroduodenostomy. Postoperative management and follow-up is same like bleeding DU.

Treatment for bleeding gastric ulcer ™™ ™™ ™™ ™™

Underrunning of the ulcer bed Partial gastrectomy with Billroth I anastomosis Vagotomy with antrectomy Occasionally splenic vessel ligation with splenec­tomy may be required

HAEMATEMESIS Causes: xx Chronic peptic ulcer (duodenal + gastric) (65%). xx Acute peptic ulcer. xx Acute erosive gastritis (Steroids, NSAIDs). xx Oesophageal varices. xx Mallory-Weiss syndrome (5-15%) xx Carcinoma stomach (5%) xx Gastric polyps, lymphomas, leiomyomas. xx Portal gastropathy. xx Bleeding disorders. xx Pernicious anaemia. xx Thrombocytopenia.

Fig. 20.47: Various causes of haematemesis. xx Gastric antral vascular ectasia  It is a rare endoscopically confirmed condition which shows segmented dilated vessel meshes in the antral mucosa (watermelon/tiger stripe stomach).  It is often associated with achlorhydria and hypergastrinaemia.  It is common in middle aged females; common in liver diseases (25%) and autoimmune connective tissue disorders.  Pathologically it shows mucosal fibromuscular hyperplasia and hyalinisation.  After confirmation with gastroscopy, often antrectomy is needed. xx Osler-Weber-Rendu syndrome, aortoduodenal fistula, Crest syndrome are rare causes. xx Dieulafoy’s disease  A gastric arteriovenous malfor­mation which is covered by apparently normal mucosa.  It occurs in proximal stomach near OG junction (within 6 cm) along lesser curve (80% of cases).  Bleeding often may be severe and torrential.

Stomach  Vasculitis or atheroma are absent in the vessel.  It is 5% of nonvariceal upper GI bleed.  A large 1–3 mm tortuous abnormal submucosal artery (AVM)

is the cause, which due to its pulsation erodes the mucosa to expose itself to acid which further erodes the artery causing bleeding.  Endoscopy and endoscopic therapy or excision of the lesion is required.  Angiography can be done to confirm the disease and to do therapeutic embolisation using gel foam.  Failure of endoscopic or angiographic therapy needs gastrotomy and excision of the entire lesion—gastric wedge resection. It can be done by open/laparoscopic approach. Prior endoscopic tattooing is mandatory to identify the lesion during resection.

Management of Haematemesis xx Evaluation of patient by measuring BP, pulse, respiration looking for features of shock, oxygen saturation, investigating for Hb%, blood grouping, blood urea, serum creatinine, LFT, prothrombin time, platelet count, arterial blood gas analysis, gastroscopy. xx Initial treatment is central line insertion, fluid and blood replacement; catheterisation; IV PPI; nasogastric tube placement (controversial but now universally accepted); FFP, platelet transfusion if needed; gastroscopic sclerotherapy, banding, laser, haemoclip application; SB tube for varices; pharmacotherapy. xx Further treatment—critical care (ICU); antibiotics; treatment of complications like sepsis, DIC, ARDS. xx Specific treatment—open surgery for uncontrolled bleeding, ligation of gastroduodenal artery and underrunning of ulcer bed with pyloroplasty, gastrectomy, ligation of varices with devascularisation. xx Definitive surgery for underlying cause—shunt surgery; vagotomy and GJ; gastrectomy; TIPSS; splenectomy, etc.

Early postoperative—bleeding either intraluminal (from stomal site) or extraluminal; leak along anastomotic line; delayed opening of stoma; gastroparesis; duodenal stump blow out; lesser curve necrosis; fistula formation—gastric/duodenal/jejunal; omental infarction. Late postoperative—reflux gastritis, recurrence of ulcer; dumping syndrome; malnutrition; gastrojejunocolic fistula; motility disorders; small stomach syndrome; afferent or efferent loop obstruction; retrograde jejunogastric intussusception; remnant carcinoma; gallstones; pulmonary or GIT tuberculosis; bezoar formation. Stomal obstruction after gastric surgeries is due to: ™™ ™™ ™™ ™™ ™™

Mucosal oedema—usually subsides eventually Retrograde jejunogastric intussusception Hypertrophied stomal mucosa causing ball-valve mechanism Efferent loop obstruction Gastric atony eventhough there is wide patent stoma causing apparent stomal obstruction

™™ ™™ ™™ ™™ ™™ ™™

Iron deficiency anaemia Megaloblastic anaemia (after 5 years) (100 µg B12 is given IM weekly, later monthly) Vitamin B deficiency Calcium deficiency Calcium deficiency with bone changes (after 5 years)

Nutritional deficiencies following gastrectomy 40% 25% 10% 40% 5%

A.  DUODENAL BLOW-OUT

xx It is a very serious complication of Billroth II gastrectomy,

occurs usually on 4–5th day after surgery.

COMPLICATIONS OF GASTRIC SURGERY xx xx xx xx xx xx xx xx xx xx xx xx xx xx xx xx xx

Haemorrhage. Stomal obstruction. Biliary fistula. Injury to CBD. Duodenal blow out—on 4th postoperative day. Pancreatitis. Recurrent ulcer/stomal ulcer. Gastrojejunocolic fistula. Dumping syndrome (Postcibal syndrome). Nutritional disturbances, diarrhoea. Pulmonary tuberculosis. Carcinoma in gastric remnant (after 10–15 years). Gallstone formation. Alkaline gastritis. Afferent and efferent loop syndrome. Afferent loop obstruction—common. Efferent loop obstruction.

Complications may be classified as: Intraoperative—bleeding, injury to spleen, pancreas, CBD.

Fig. 20.48: Duodenal blow-out after Billroth II anastomosis usually occurs 4 days after the surgery. It is often life-threatening condition. xx Here contents in the afferent loop are not having free flow

which in turn increases the pressure in the duodenal ‘C’ loop leading to giving way of the closed duodenal stump. xx It is due to improper closure of duodenal stump, oedematous inflamed duodenum, afferent loop block, distal obstruction, ischaemia of least vascular duodenum and sepsis. Often there will be local pancreatitis which may cause disruption of the stump by its enzymes.

Choice, not chance, determines destiny.

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B.  RECURRENT ULCER

xx Sudden, severe pain abdomen postoperatively with features

It is a wide terminology which includes stomal ulcers, recurrence of ulcer in the original ulcer site or different parts of stomach/duodenum or jejunum after a therapeutic surgical procedure. Stomal ulcer can occur in gastrojejunostomy stoma or in gastroduodenostomy stoma. GJ stomal ulcer per se can occur after only gastrojejunostomy or after partial gastrectomy with Billroth II anastomosis. Recurrent ulcer at the original site is commonly referred to ulcer recurrence (after HSV commonly).

xx xx xx xx xx xx

of shock. Forming a duodenal fistula through the drain placed. May cause peritonitis. Severe electrolyte imbalance. Features of biliary peritonitis, septicaemia. Skin excoriation and its problems. CT scan is ideal to identify the leak.

Treatment xx Conservative therapy with nasogastric aspiration, IV fluids,

TPN, antibiotics. Usually, patient will recover in 40–60 days. xx Surgery is indicated when there is peritonitis, fistula not responding, when there is distal obstruction. xx Surgeries are—afferent and efferent loop connection, relieving the obstruction distally, serosal patch over the duodenal stump after excision of the fistula, creating a controlled fistula after placing a tube into the duodenum. (Duodenostomy). Duodenostomy reduces the intraluminal pressure; duodenostomy may be end, lateral, retrograde (tube) types. Duodenal fistula Causes ™™ Due to duodenal blow out—ischaemia, afferent loop obstruction, sepsis ™™ After closure of perforated DU ™™ Injury to duodenum by trauma, surgeries like hemicolectomy, renal surgeries, pancreatic surgeries, etc

Recurrent ulcer is 3–7%. It may be after: xx Gastrojejunostomy. xx Billroth I or Billroth II anastomosis. It may be: ™™ Gastrojejunostomy stomal ulcer ™™ Gastroduodenostomy stomal ulcer ™™ Jejunal ulcer ™™ Gastric ulcer ™™ Ulcer recurrence—10%

Causes xx xx xx xx xx xx xx

Incomplete vagotomy. Zollinger-Ellison syndrome, gastrinomas. Alcohol, smoking, NSAIDs. Hyperparathyroidism. H. pylori infection. Gastrojejunostomy when done without vagotomy—40%. After HSV—10%.

Types ™™ Low output - < 250 ml/24 hours ™™ Moderate output 250–500 ml/24 hours ™™ High output > 500 ml/24 hours Features ™™ Pain abdomen ™™ Bile leak through the drain site or fistula track ™™ Skin excoriation ™™ Electrolyte imbalance ™™ Malnutrition, anaemia ™™ Recurrent infection Investigations ™™ Electrolyte estimation, haematocrit ™™ CT fistulogram Treatment ™™ TPN, feeding through jejunostomy ™™ Management of anaemia, electrolytes ™™ Blood transfusion ™™ Antibiotics whenever sepsis is suspected ™™ Care of skin—zinc oxide cream application, controlled fistula by placing a Foley’s catheter into the fistula track ™™ Usually responds well by conservative therapy in 8–12 weeks ™™ If not improved then surgery is needed—anastomosis between afferent and efferent loops (jejuno-jejunostomy); serosal patch techniques; surgical closure of fistula, Roux-en-Y patch over fistula

Fig. 20.49: Stomal ulcer after GJ may be due to incomplete vagotomy, Zollinger-Ellison syndrome.

Clinical Features xx xx xx xx xx

Pain in the umbilical and left hypochondrium (severe, persistent). Back pain. Haematemesis. Anaemia, loss of weight.

Features of obstruction—10%.

Note:

Stomal ulcer may complicate to gastrojejunocolic fistula, perforation, bleeding, obstruction, penetration.

Stomach Investigations

Types

xx xx xx xx xx xx

Barium meal. Gastroscopy. Hollander’s insulin test. Pentagastrin test. Gastrin level estimation. Serum calcium and parathormone (PTH) to rule hyperparathyroidism. xx Visick grading is used to assess the response to therapy to various procedures (Grades 1, 2, 3, 4 and 5).

Treatment xx xx xx xx xx

Complete the vagotomy. Undoing of GJ. Conversion into another procedure, Roux-en-Y procedure. Treat hypergastrinaemia, hyperparathyroidism. Eradication of H. pylori infection using triple regime for 2 weeks and then continuation of therapy using PPI for 3 months. xx Subtotal gastrectomy in resistant recurrent ulcer cases. Stomal ulcer ™™ ™™ ™™

It is the ulcer in anastomotic site of GJ/GD Overall incidence is 10% in 10 years after surgery It is common on jejunal side but can occur on gastric side or both sides or at junction

Causes ™™ After only gastrojejunostomy procedure—40% ™™ After vagotomy and GJ—5–7% ™™ After partial gastrectomy and gastroduodenostomy—Billroth I—3% ™™ After partial gastrectomy and GJ—Billroth II—3% ™™ Other causes like gastrinomas, hyperparathyroidism, incomplete vagotomy, smoking, alcohol Features ™™ Pain and haematemesis/melaena is the main presentations ™™ Pain is persistent, severe over left upper abdomen often radiating to back ™™ Pain may be in the chest if it is antecolic anastomosis ™™ Weight loss and features of obstruction can occur Investigations ™™ Acid tests (Hollander’s), gastroscopy, tests specific for the cause ™™ Serum gastrin/calcium assay Complications ™™ Bleeding stomal obstruction ™™ Perforation ™™ Gastrojejunocolic fistula ™™ Nutritional deficiency Treatment ™™ Completion vagotomy ™™ Subtotal gastrectomy/revision gastrectomy ™™ Roux-en-Y anastomosis ™™ Treat the cause

1.  EARLY DUMPING SYNDROME: ™™ It is common and more severe type ™™ Incidence is 10% ™™ Vasomotor symptoms appear immediately after food, lasts for 30-40 minutes, aggravated by bulky food. It is relieved by lying down, aggravated by more food Clinical features: ™™ Sweating, tachycardia, colicky pain and diarrhoea ™™ Hypotension and features of hypovolaemia Pathogenesis: It is a primary disorder of carbohydrate metabolism wherein initial transient hyperglycae­mia, prevents further absorption of glucose, which in turn draws fluid from the bowel wall by high osmo­larity resulting in increased intestinal activity, resulting in diarrhoea and fall in blood volume Treatment: Small, dry, more frequent food, with avoidance of carbohydrates. Octreotide 100 µg given subcutaneously before meals is found to be beneficial Surgical treatment: ™™ Conversion of Billroth II to Billroth I ™™ Interposition of reversed jejunal loop (Henley's loop) Early dumping syndrome can last for long time (many years) 2.  LATE DUMPING SYNDROME: ™™ It is of less severe type ™™ Incidence is 5% ™™ It usually occurs 2 hours after meal ™™ It is relieved by glucose and aggravated by exercise Pathogenesis: Due to initial hyperglycaemia insulin secretion is stimulated which in turn leads to hypoglycaemia Clinical features: ™™ Tremor, fainting, nausea ™™ Features of hypoglycaemia Treatment: Symptoms are less severe and so treated conservatively, by giving glucose and food

D. ROUX STASIS SYNDROME (Matias, 1985)

xx It is occurrence of gastric atony after subtotal or partial gastrectomy if Roux-en gastrojejunostomy is done. xx They present with fullness, vomiting, loss of appetite and weight, early satiety, abdominal pain, bloating sensation after eating. xx It occurs in 25% of Roux-en-Y GJ. It is common in females. xx It is common in Roux-en-Y limb if more than 40 cm. It is late complication seen in months or year. xx Transection of the jejunum during the construction of the Roux limb separates the limb from the natural small intestinal pacemaker located in the duodenum causing appearance of ectopic pacemakers in the limb triggering retrograde contractions in its proximal portion. These contractions slow transit through the limb and result in Roux stasis. xx There may be dysfunction of both gastric remnant and Roux limb. It is due to ectopic pacemaker in Roux limb which delays the gastric emptying.

Treatment  Completion total gastrectomy is the choice.  Isolated jejunal loop interposition of 40 cm length— Henley’s

C. DUMPING SYNDROME

(Post-cibal Syndrome)

loop.

It is common in females, seen after Billroth II surgery.

 Intestinal pacing, OR usage of ‘uncut Roux’ limb.  Octreotide, tegaserod drugs are found useful.

Dream things that never were and make it true.

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SRB's Manual of Surgery E. GASTROJEJUNOCOLIC FISTULA

 A two staged procedure (Lahey’s procedure) can be done

in critical patients with triple resection and colostomy; later closure of colostomy after 3 months. But with the advent of proper fluid and nutrition therapy and antibiotics, single stage procedure is more popular. It has got high mortality.

It is a complication of gastrojejunal ulcer (stomal ulcer), wherein ulcer penetrates and erodes into the transverse colon leading to gastrojejunocolic fistula, a dreaded complication. Inadequate vagotomy or inadequate gastrectomy or inadequate therapy for H. pylori infection of development of carcinoma at stoma or formation of stomal ulcer, elderly malnourished people are the causes of developing GJC fistula.

Clinical Features xx Sudden onset of severe diarrhoea after every meal with past

history of GJ done and past history of gastrojejunal ulcer. xx Foul gas eructation. xx Dehydration. xx Rapid loss of weight, anaemia, cachexia, hypopro­teinaemia

(bacteria from colon enters the jejunum disrupting the absorptive mechanism). xx Steatorrhoea. xx Rarely faecal vomiting. xx Marshall and Knud-Hansen triad of GJC fistula are - diarrhea, weight loss and eructation of fecal-smelling gas. Often immediate diarrhea after oral intake may suggest GJC fistula with undigested food in the stool if the size of a GJC fistula is large.

Fig. 20.51: Resection of the gastrojejunocolic fistula (removal of involved parts of the stomach, jejunum and colon—triple resection) with maintaining the continuity.

TRICHOBEZOAR (Rapunzel Syndrome) xx It is a hair-ball commonly seen in stomach of females with psychiatric illness, who swallow hair regularly. xx It forms a ball like mass occupying the full stomach. xx When this hairball extends into the duodenum and jejunum it is called as Rapunzel syndrome.

Fig. 20.50: Gastrojejunocolic fistula.

Fig. 20.52: Trichobezoar—CT and hair ball mass (Courtesy: Dr (Professor) BM Nayak, KMC, Mangaluru)

Investigation Barium enema - 95% sensitivity (not barium meal). CT scan, endoscopy (upper and lower).

Treatment xx xx xx xx xx xx

IV fluids. Total parenteral nutrition (TPN). Blood transfusions. Antibiotics. Rehydration, electrolyte management. Surgery:  Single stage resection of the involved stomach, jejunum and colon is commonly done maintaining the corresponding anastomotic continuity—triple resection.

Clinical Features xx xx xx xx xx xx

Epigastric pain, early satiety. Haematemesis. Features of gastritis. Loss of appetite. Perforation. Epigastric mass.

Investigation xx Barium meal and endoscopy is confirmative. xx CT scan is very useful.

Stomach Treatment xx Gastrotomy and removal of hairball. Duodenum and small bowel should be examined on table for additional bezoars in these sites. xx Psychiatric counselling. xx Enzymatic digestion and endoscopic breaking of the bezoars is also tried. xx It can also be removed by laparoscopy.

Phytobezoar  It is due to solid ball formation in the stomach comprising

plant fibres and seeds.

 Phytobezoar is common in gastric remnant after partial

gastrectomy and in diabetics with autonomic neuropathy.  Enzymatic digestion can be tried using papain (found in

Adolph’s meat Tenderizer, as one tsp in 300 ml of water taken orally many times a day to fragment bezoar), cellulase substance. If fails, removal by gastrostomy.

CHRONIC DUODENAL ILEUS (WILKIE’S SYNDROME) xx It is also called as superior mesenteric artery (SMA)

A

B Figs 20.54A and B: (A) Wilkie’s syndrome; (B) Duodenojejunostomy, in case of chronic duodenal ileus.

xx Investigation  Barium meal is diagnostic.  CT scan abdomen.

xx Treatment  Duodenojejunostomy with division of the ligament of

syndrome. xx It is due to obstruction of the 3rd part of the duodenum due to decreased angle between SMA and aorta. xx There will be narrowing of aortomesenteric angle, becoming less than 15.2°; aortomesenteric distance becoming less than 10 mm with abnormally low origin of SMA. xx It can be congenital or due to low insertion of SMA or high insertion of duodenal end or due to traumatic aneurysm of SMA. xx It can be aggravated by plaster casts, lordosis, pancreatic tumour, enlarged lymph node in the 3rd part of duodenum (Cast syndrome).

Note:

Features

xx Condition is also called as median arcuate ligament syndrome (MALS) or coeliac artery syndrome or coeliac band syndrome. xx There is a connecting band between right and left crura which causes compression of celiac artery and SMA.

xx xx xx xx xx

Bilious vomiting. Upper abdominal fullness. Visible peristalsis. Dehydration.

Treitz is the most common and most successful procedure done.  Strong’s operation –division of ligament of Treitz and transposition of the SMA.  Anterior transposition of the 3rd part of the duodenum. Gastrojejunostomy should not be done.

DUNBAR ‘S (MALS) SYNDROME (Harjola—Marable Syndrome)

Differential Diagnosis  Pyloric stenosis with gastric outlet obstruction.  Annular pancreas.

A

B

Figs 20.53A and B: Superior mesenteric artery—SMA (Wilkie's) syndrome showing site of obstruction and dilated proximal gastroduodenum.

Fig. 20.55: CT scan showing coeliac artery syndrome.

What we need is cup of understanding, barrel of love and an ocean of patience.

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SRB's Manual of Surgery xx It may cause foregut ischaemia due to inadequate collaterals, or midgut ischaemia due to diversion of blood to foregut. xx Presentation—chronic abdominal pain after food, murmur in epigastric region, weight loss. xx It is often difficult to diagnosis. CT scan, CT angiogram may show poor perfusion. MRI may be useful. GDA clamp test and intra operative Doppler is very useful. xx Treatment—cutting/excising the fibrous band, with removal of the celiac ganglion through laparotomy or laparoscopy. Coeliac angioplasty, aortocoeliac bypass, coeliac endostenting and coeliac reimplantation are also tried.

ACUTE GASTRIC DILATATION xx It is an enormous acute dilatation of stomach with atonic gastric wall without peristalsis. xx Stomach distends enormously occupying most of the abdomen and pelvis causing sequestration of lots of fluid resulting in hypovolaemia.

Causes xx xx xx xx xx

After major surgery (abdomen, neurosurgery). Trauma, burns. Retroperitoneal haematoma. Electrolyte imbalance. Other causes: Anorexia nervosa, bulimia, polyphagia, drug abuse, diabetes, anaesthesia, debilitating diseases, spinal cord diseases, muscle dystrophy.

Clinical Features xx Features of hypovolaemia and shock. xx Vomiting, hiccough. Vomits large quantity of brownish black fluid like “the storm water of a peat-laden stream.” Vomitus when placed in a test tube and held in a strong light, myriads of small particles may be suspended in the fluid. xx Dilated stomach confirmed by ausculto percussion test. xx Positive succussion splash. xx Electrolyte imbalance is seen.

Fig. 20.56: Acute gastric dilatation showing dilated stomach occupying entire abdomen and also pelvis.

Investigations Plain X-ray abdomen, serum electrolytes, U/S abdomen.

Treatment xx Conservative treatment is given initially.  Large amount of intravenous fluids.  Ryle’s tube aspiration.  Electrolyte management, blood transfusion. xx The cause is treated. xx Rarely, surgical decompression is required. Condition has got high mortality.

Complications xx Aspiration pneumonia (Mendelson syndrome). xx Severe hypovolaemia and electrolyte imbalance. xx Raised intragastric pressure causes venous congestion, venous infarction, necrosis and perforation. Gastric ischaemia and perforation has got reportedly 80% mortality.

GASTRIC VOLVULUS It is twist in the axis of the stomach. xx Rotation occurs around the axis made by two fixed points—cardia and pylorus. xx It can be idiopathic (Type 1–65%) or secondary (Type 2–35%) to—hiatus hernia, left sided eventration, adhesions or pyloric obstruction with long-standing gastric dilatation. Twist may be: xx Organo-axial: Common in elderly—horizontal. xx Mesenterico-axial: Common in children—vertical. xx Combined.

Pathology xx Here stomach twists upwards between oesophagogastric junction and pyloroduodenal junction. Colon along with omentum also moves upwards initially. xx It is often associated with rolling hiatus hernia or diaphragmatic eventration.

Fig. 20.57: Types of gastric volvulus.

Stomach Clinical Features

2. Adenomatous polyp (10%)—neoplastic in origin. Size >2 cm is potentially malignant (25% chance). Borchardt’s triad

™™ ™™ ™™

Acute epigastric pain Violent ineffective vomiting-retching Inability to pass a nasogastric tube

Types xx Acute. xx Chronic recurrent. It is common type.

Complications xx Perforation. xx Gangrene of the stomach. xx Bleeding.

Investigations xx Plain X-ray chest and abdomen in erect posture will show retrocardiac gas filled viscous with dilated bowel loop in the abdomen. xx Barium meal X-ray. xx CT scan abdomen.

Treatment xx Untwisting of the volvulus and gastropexy by fixing the anterior wall of the stomach to anterior abdominal wall. xx Gastrojejunal fixation (gastrojejunostomy without a stoma). xx Gastrectomy when stomach is gangrenous. xx Treating hiatus hernia or eventration. xx Displacing colon downwards by dividing gastrocolic omentum— Tanner’s operation.

GASTRIC POLYP Gastric polyps are observed in 3% of total gastroscopies. 45% of them are found in fundus which does not show any malignant potential. These polyps are often associated with FAP or Gardener’s syndrome and colorectal neoplasms; but these gastric polyps perse are non-neoplastic.

A

B Figs 20.58A and B: (A) Gastric polyp in prepyloric region; (B) Polyp in the duodenum first part.

Types 1. Hyperplastic polyp—75% common, minimal risk of malignancy (2%). Size usually is 5 cm – open or laparoscopic sleeve resection. xx Partial gastrectomy of multiple polyps bearing area is needed in multiple polyps. xx Small polyps can undergo surveillance at regular intervals through endoscopy. xx All gastric adenomatous polyps should be resected due to their high potential for malignancy.

MENETRIER’S DISEASE xx It is an acquired condition with giant gastric mucosal folds (hyper­trophic gastropathy) in the fundus and body of the stomach‘cobblestone appearance’. Common in males. xx Histologically, it shows hyperplasia, mucosal thickening and gastric gland atrophy. xx Hypoalbuminaemia, anaemia and hypochlorhydria is common. xx Antrum is not involved. xx There is over expression of transforming growth factor alpha (TGFα) peptide which binds to epidermal growth factor (EGF). xx There is foveolar surface mucus cell hyperplasia with absence of parietal cells causing excessive mucus production, protein loss and achlor/hypochlorhydria. xx It is associated with CMV infection in children and H. pylori infection in adult.

Clinical Features xx Epigastric pain, anaemia and weight loss, melaena.

Carcinoma stomach is the commonest cause of Krukenberg’s tumour.

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SRB's Manual of Surgery Investigations xx Serum total proteins, albumin. xx Gastric function tests. xx Barium meal studies, gastroscopy. Menetrier’s disease ™™ ™™ ™™ ™™ ™™ ™™

Giant folds in fundus and body Gastric gland atrophy Hypochlorhydria Hypoalbuminaemia It may turn into malignancy Antral sparing

Treatment xx High protein diet, H2 blockers or PPIs, prednisolone, anticholinergics, antibiotics (for H. pylori), drugs for CMV infection, cetuximab – a EGFR blocker, a monoclonal antibody – are all tried. xx Total gastrectomy is the treatment if there is massive protein loss or dysplasia or carcinoma. Menetrier’s disease may turn into malignancy.

Fig. 20.59: Primary and secondary diverticula of the duodenum.

DUODENAL DIVERTICULA It is outpouching/prolapse of the duodenal mucosa. It may be mucosal outpouching of mucosa only through muscularis propria or of all layers. They are quiet common; 25% asymptomatic; only < 10% need surgical intervention. Duodenum is the 2nd most common site of diverticulum in the GIT after colon. It is common in periampullary region; common in females. Diverticulum can be congenital which is true one involving all layer diverticulum or acquired which is mucosal outpouching through muscular layer. But this classification is conflicting and confusing.

A

Figs 20.60A and B: Barium meal picture showing trifoliate duodenum as secondary diverticulum due to chronic duodenal ulcer.

It can be: Extramural diverticulum—protrudes outside; it can be – xx Primary—is usually mucosal; common on the medial wall of the 2nd (60%) or 3rd (30%) part of the duodenum. It is usually acquired one. It is diagnosed by barium fluoroscopic study / CT scan or MRI. It is treated with surgical excision of the diverticula from outside through laparotomy or laparoscopy - diverticulectomy. xx Secondary—always acquired; occurs in 1st part of the duodenum; is usually due to cicatrised chronic duodenal ulcer. Barium meal shows ‘trifoliate duodenum’. Endoscopy should be done. It is treated by truncal vagotomy and posterior gastrojejunostomy. Intramural diverticulum—protrudes inward into the lumen (Windsock diverticulum). Intramural diverticula are usually congenital. It shows ‘Windsock sign’ in barium study. When it is close to the ampulla of Vater, it can precipitate biliary stasis and stone formation with cholangitis, cholecystitis, pancreatitis and occasionally obstruction. It often can cause mechanical obstruction. It is diagnosed by contrast CT or MRI. It can be usually treated by endoscopy. Complications of diverticula—diverticulitis, haemorrhage (most usual), perforation, abscess formation, Lemmel syndrome (compression of the intrahepatic CBD by the diverticula causing intra- and extrahepatic biliary dilatation with no biliary calculi). Adenocarcinoma can occur within the diverticulum.

B

CARCINOMA STOMACH My kinsman, Antonio Bruno, retained the food he had eaten for too shor t a time, and then threw it up undigested…. His body wasted away through lack of nourishment till little more than skin and bone remained. At last, he was brought to his death. The body was cut open for reasons of public welfare. It was found that the opening of his stomach had closed up and it had hardened…with the result that nothing could pass through to the organs beyond, and death inevitably followed. —Antonio Benivieni, 1507

xx xx xx xx

‘It is the captain of men of death’. It is more common in Japan—70 per 1,00,000 population. It is more common in males 2:1. Decrease incidence in western world (Western Europe and US)—last four decades. But this decrease is confined to distal gastric cancers. Incidence of proximal gastric cancer is increasing. Carcinoma proximal stomach is not associated with H. pylori infection unlike cancers of body and distal stomach.

Stomach Risk Factors (Aetiology) xx Familial—10%. Napolean and many members of his family

died of carcinoma stomach. Familial gastric cancer in associated with mutation of e-cadherin gene (90% risk). It causes hereditary diffuse gastric cancer. Relatives of such family show mutation of this gene. Whether prophylactic total gastrectomy is needed or not in these high-risk individuals is a debate. xx Inactivation of p53, over expression of growth factors, bcl-2 gene mutations are other genetic causes. xx HNPCC, Li-Fraumen syndrome. xx Gastric mucosa of people with blood group ‘A’ is more susceptible for carcinogens—diffuse type. It is due to different mucopolysaccharide secretion in stomach of blood group A patients who are more susceptible for carcinogens. xx Gastric polyps, adenomatous polyp >2 cm. xx Pernicious anaemia—high-risk 6 times. xx Gastric remnant—15 years after gastrectomy and GJ.

xx Agammaglobulinaemia—high-risk (2–5%). xx Chronic benign gastric ulcer. Carcinoma arising from benign

gastric ulcer is called as ulcer cancer of stomach. xx Giant hyperplasia of gastric mucosal folds (Menetrier’s

disease). xx Carcinoma in proximal stomach is common in young and

upper socioeconomic group. xx Carcinoma in distal stomach is common in old and lower

socioeconomic groups. xx In western countries, carcinoma stomach is more common in

proximal, near OG junction. Obesity, young individual, white people, smoking, alcohol intake, gastro-oesophageal reflux, higher social status, high calorie diet and probably genetic factors are the causes for proximal gastric cancers. It is more aggressive, spreads early due to thin muscularis mucosa. It is often diagnosed late. Signet ring type is common. It carries poor prognosis. It needs oesophageal resection. xx In Asian countries, it is still common in distal stomach. xx In India, it is common in south India (4 times than North India). xx Epstein-Barr virus, radiation exposure. xx Occupational—Rubber workers, coal workers. xx Zinc, lead, talc, asbestos all can cause carcinoma stomach.

Precursor Lesions of Carcinoma Stomach

Fig. 20.61: Gastrectomy specimen showing ulcerative gastric carcinoma. xx Diet—high salt diet, food with more nitrosamines increases

the risk. Smoked salmon fish increases the risk. They release polycyclic hydrocarbons. Ingested nitrates and nitrites from preserved food are converted to nitrosamines by GI bacteria. xx Fruits and vegetables rich in vitamin ‘C’ protect from carcinoma stomach. xx Chronic gastritis (atrophic, autoimmune), intestinal metaplasia. Type A causes proximal gastric cancer. Type B causes distal gastric cancer. xx Gastric dysplasia: Chronic gastritis → gastric atrophy → intestinal metaplasia → dysplasia → carcinoma in situ → carcinoma—this cycle occurs in body and distal stomach and is often called as Correa cycle. xx Smoking, alcohol. xx Helicobacter pylori infection—high-risk (Cag A strain) 6-fold increase in incidence. It causes intestinal type of gastric cancer.

xx Chronic atrophic gastritis: It is the most common precursor lesion mainly intestinal subtype. In Japan 95% of atrophic gastritis develop early gastric cancer. Incidence is higher in elderly and in those associated with H. pylori infection. xx Adenomatous gastric polyps. xx Intestinal metaplasia: Risk of carcinoma depends on extent of metaplasia in mucosa. H. pylori eradication is important here. Based on histological and biochemical nature, two types are found:  Complete: Glands are completely lined with goblet cells and intestinal absorptive cells indis­tinguishable histologically and biochemically from their small bowel counterparts.  Incomplete: It contains columnar cells, goblet cells but without intestinal absorptive cells. It also can be:  Type I—Mature; goblet cells secret sialomucin.  Type II—Cells in different levels of dedifferentiation. Cells secrete sialomucin and an abnormal sialomucin (sulphomucin)—a small quantity.  Type III—Marked dedifferentiation of cells, secreting mainly sulphomucin. xx Menetrier’s disease. xx Benign gastric ulcer: Here risk is 2-5%. But it is related to the size, extent and duration of the benign gastric ulcer. Giant gastric ulcer has got as high as 6–23% risk. Cancer developing in a pre-existing benign gastric ulcer is called as ulcer cancer. xx Stomach remnant (stump carcinoma): It can occur after Billroth II gastrojejunostomy (common) or vagotomy GJ. It takes around 15 years or more to develop cancer. Common site is close to the stoma. Atrophic gastritis—metaplasia—dysplasia and carcinoma develops. Altered acid level, enterogastric bile refluxes are the pathogenesis which increases the peptic activity causing mucosal metaplasia and dysplasia. Earlier history of gastric surgery, recent history of loss

Many very skillful operators are not good surgeons.— William J Mayo

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SRB's Manual of Surgery of appetite and decreased weight with often a palpable mass are the features. Liver secondaries, ascites may develop in late cases. Gastroscopy with biopsy and CT scan confirms the diagnosis. Treatment is gastrectomy with nodal clearance. Aetiology for gastric cancer Environmental/ occupational/diet/habits

Genetic and familial

• E-cadherin gene mutation in diffuse cancers • Mutation in APC gene for β-catenin in intestinal cancers—50% • Inactivation tumour suppressor gene p53 in 30% cases • Loss of heterozygosity in the BCL2 gene, an inhibitor of apoptosis (intestinal type) • Amplification/over expression of different growth factor receptors • HNPCC—carries 5–10% risk of gastric cancer • Li Fraumen syndrome • Blood group A Precancerous lesions: • First degree relative carries 3–6 • H. pylori infection, chronic folds increased risk of gastric gastritis cancer. • Pernicious anaemia • Monozygotic twins carry more • Intestinal metaplasia risk than dizygotic • Adenomatous polyps • When both parents have gastric more than 2 cm cancer, the siblings are at risk of • Agammaglobulinaemia diffuse proximal gastric cancer • Benign gastric ulcer • FAP—10-folds more risk of gastric • Previous gastric surgery cancer • Menetrier’s disease • Mutation of H-ras oncogene and over expression of c-erb B2 gene • Smoking/alcohol/obesity • Low vegetables, diet with low vitamin A and C • Consuming red meat, smoked salmon fish, cabbage, diet rich in nitrosamines, lead • Viral infections like EB virus • Occupational—rubber/ coal workers • Lower social status— distal cancers • Higher social status— proximal cancers

Pathology I. Gross types:

Fig. 20.62: Endoscopic view of carcinoma of stomach. –– It is usually poorly differentiated/signet type with

early gastric wall penetration and both submucosal and subserosal lymphatic spread. –– Linitis plastica, ulcerative growth without glandular formation is common in this type. –– It shows decreased E-cadherin with p53, p16 inactivation. c. Others—Unclassified (14%). III. Depending on the depth of invasion: a. Early gastric cancer is defined as involvement of mucosa and/or submucosa only with or without involvement of lymph nodes – T1 + any N. It is being classified as: (Japanese’s classifi­cation) 1. Protruded. 2. Superficial—elevated (a), flat (b), depressed (c). 3. Excavated.

Cauliflower type Ulcerative type Leather-bottle (Linitis plastica)

II. Lauren’s classification (DIO classification): a. Intestinal type (53%): –– Has got favourable prognosis. –– Polypoid and superficial types are intestinal varieties—common in H. pylori induced. Gland formation and definite cellular architecture are the features. –– Synchronous/polypoid/superficial types are common. –– Gastric mucosa is replaced with epithelium that resembles small bowel mucosa. –– It is common in men and aged individuals, probably has environmental factors, commonly shows haematogenous spread, microsatellite instability, APC gene mutations, p53, p16 inactivation. b. Diffuse type (33%): –– It has got poor prognosis. Common in blood group A, familial type, young people and females.

Fig. 20.63: Japanese’s classification for early gastric cancer.

Stomach Type 2: Tumour within 2 cm of squamocolumnar junction. Here total gastrectomy with Roux-en-Y oesophagojejunostomy is needed. Type 3: Tumour in subcardial region. Here total gastrectomy with Roux-en-Y oesophagojejunal anastomosis is done.

It is:

–– More common in Japan—50% of gastric cancers

treated are early gastric cancers. In USA—20%. –– 10% of early gastric cancers will have nodal

metastases. 3% in only mucosal lesions. 20% in submucosal lesions. –– Nodal spread in early gastric cancer depends on tumour size (>2 cm) and differentiation. –– About 70% are well-differentiated. –– Endoscopic mucosal resection (EMR) is possible in cancer of only mucosal lesions. –– Overall cure rate with adequate gastric resection and lymphadenectomy—95%. b. Advanced gastric cancer is defined as involve­ment of muscularis and/or serosa with or without involvement of lymph nodes. It is classified as: (Borrmann’s classification): I. Single, polypoid carcinoma. II. Ulcerated carcinoma with clear cut margin. III. Ulcerated carcinoma without clear cut margin. IV. Diffuse carcinoma—linitis plastica. V. Unclassified.

Note: Not commonly used are:

VII. Morphovolumetric classification: It is based on ratio of invasion into muscle to mucosa in advanced carcinoma as:  Funnel type—mucosa involvement is more compared to muscle with a ratio of 15 mitoses per 30 high power field), mixed pathology (spindle + epithelioid). xx Liver spread. xx KIT exon 9 mutation which is more aggressive than KIT exon 11 mutations—carries poor prognosis. xx Ruptured GIST—nearly all ruptured GISTs show abdominal metastases.

PYLOROPLASTY xx Indications  Bleeding duodenal ulcer.  As a drainage procedure after vagotomy in uncomplicated‑ DU which is not responding to medical line of treatment.  As a part of procedure like Ivor-Lewis operation and SiguiraFutagawa operation. xx Contraindications  Duodenal ulcer with cicatrisation and scarring. xx Types  Finney’s pyloroplasty.  Heineke-Mikulicz pyloroplasty. xx Complications  Duodenal leak—very dangerous one.  Later reflux.

A

B

Figs 20.88A and B: Types of pyloroplasty. (A) Finney’s pyloroplasty; (B) Heineke-Mikulicz pyloroplasty.

GASTROSTOMY xx It is the procedure wherein a tube is passed into the stomach per abdominally for the purpose of enteral feeding. xx It can be temporary or permanent.

Types A. Serous lined—for temporary gastrostomy. B. Mucosa lined—for permanent one.

Stomach Complications ™™ ™™ ™™ ™™ ™™

Infection Trauma to other organ, e.g. colon Leak from gastrostomy site Aspiration pneumonia Blockage.

GASTRECTOMY A

B

Figs 20.89A and B: Types of gastrostomy. (A) Temporary gastrostomy; (B) Permanent gastrostomy. After minilaparotomy, gastrotomy is done. Foley’s or Malecot’s catheter is placed in the stomach. It is fixed to parietal peritoneum through two circular purse string sutures.

Types 1. Billroth I is done for benign condition. Here along with partial gastrectomy, gastroduodenostomy is done. 2. Billroth II is done for carcinoma stomach. After partial gastrectomy, gastrojejunostomy is done and duo­denal stump is closed.

Other Types xx xx xx xx

Stamm’s temporary gastrostomy. Kader-Senn temporary gastrostomy. Janeway’s permanent gastrostomy. Endoscopic percutaneous gastrostomy—becoming popular (PEG). Indications

Oesophageal strictures. ™™ Any conditions where tube feeding is required for more than 4 weeks (e.g. burns, severe sepsis). ™™ Major neck surgeries. ™™

A

Contraindications xx Previous gastrectomy. xx Gastric diseases with impaired gastric emptying. xx Intestinal obstruction.

B Figs 20.91A and B: Types of gastrectomy. (A) Billroth I anastomosis; (B) Billroth II anastomosis. 3. Lower radical gastrectomy is done in early carcinoma pylorus. Here along with the growth and proximal 5 cm of stomach, omentum, lymph nodes, spleen with tail of pancreas are removed and Billroth II anastomosis is done. 4. In growth of upper part or OG junction, upper radical gastrectomy is done along with oesophagogastric anastomosis. 5. In some cases like linitis plastica, total gastrectomy along with oesophagojejunal anastomosis is done.

B

A

Indications

C Figs 20.90A to C: Percutaneous endoscopic gastrostomy (PEG). It is easier and acceptable method and less invasive.

™™ ™™ ™™ ™™ ™™ ™™ ™™

Chronic benign gastric ulcer Benign tumours of stomach (Leiomyoma) Carcinoma stomach Stomal ulcer Bleeding ulcer Leimyosarcoma, gastric lymphoma Menetrier’s disease.

Goodness is the permanent investment.

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SRB's Manual of Surgery Complications ™™ ™™ ™™ ™™ ™™ ™™

Bleeding Bile leak Duodenal blow-out Gastric fistula Dumping syndrome Anaemia.

Problems with GJ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Stomal obstruction Afferent or efferent loop obstruction Dumping syndrome Duodenal blow-out Retrograde intussusception Reflux gastritis. It is a rare entity occurs after gastrojejunostomy It can occur immediately, in weeks or in months.

RETROGRADE JEJUNOGASTRIC INTUSSUSCEPTION

Fig. 20.92: Different types of gastrectomy. Subtotal—more than 80% of stomach is removed; partial—60–75% removed.

GASTROJEJUNOSTOMY (GJ) Types 1. Anterior GJ. 2. Posterior GJ. Anterior gastrojejunostomy is done as a palliative procedure in case of advanced inoperable (adherent posteriorly) carcinoma pylorus to palliate vomiting. It is anastomosis between jejunum and anterior surface of stomach, in front of transverse colon (antecolic). Posterior GJ is done along with truncal vagotomy, in pyloric stenosis due to chronic duodenal ulcer. It is posterior, vertical, retrocolic, short loop, isoperistaltic (of Mayo). GJ is also done as part of the Billroth II gastrectomy.

Fig. 20.94: Retrograde jejunogastric intussusception with gangrene—resected specimen. xx Jejunogastric intussusception is rare but definitive complication which occurs in loop (omega) gastrojejunostomy only; not in Roux en Y type. 80% cases efferent limb intussusception occurs; 20% cases afferent; rarely both. It can present as acute with features of obstruction or strangulation or intermittent with repeated episodes of symptoms. xx Presents with pain above and left of the umbilicus, haematemesis, firm, tender mass above and towards the left side. Patient becomes better in erect posture. xx Condition causes stomal obstruction. xx Barium meal shows coiled spring look within the stomach remnant. Gastroscopy is diagnostic. xx It is treated by open reduction of the intussusception with anchoring stitch to the bowel or enteroanas­tomosis. When gangrenous, resection and Roux-en-Y anastomosis is done.

VAGOTOMY In an inquiry which I had formerly instituted, respecting the functions of the stomach, I divided these nerves (the vagi) in the neck of a dog, for the purpose of ascertaining the influence which they possess on the secretion of the gastric juice…. We may conclude that the suppression of the secretions…sufficiently demonstrate, that the secretions of the stomach and intestines are very much under the control of the nervous system.

Fig. 20.93: Gastrojejunostomy stoma view on endoscopy.

—Benjamin Collins Brodie, 1814

Stomach Types

Contd...

1. Truncal vagotomy along with GJ as drainage procedure, is done in case of pyloric stenosis due to chronic DU.

A

B

Pneumothorax Oesophagogastric disconnection Early postoperative Gastric atony Lesser curve necrosis in HSV Transient dysphagia

–– Alteration in intestinal villi and enzyme content, altered small bowel motility due denervation –– Altered biliary and pancreatic exocrine function –– Cholestyramine 4 gram tid/ reverse jejunal loop is the treatment for intractable case • Reflux oesophagitis • Oesophageal stricture • Gallstones—due to bile stasis and gastric atony—15%

C

Figs 20.95A to C: Types of vagotomy. (A) Highly selective vagotomy; (B) Selective vagotomy with pyloroplasty; (C) Truncal vagotomy with gastrojejunostomy. Complications of vagotomy Intraoperative

Late complications

Injury to spleen/ oesophagus/liver/ pancreas/thoracic duct stomach Bleeding from phrenic veins/gastric vessels/ perioesophageal vessels

• Vagotomy diarrhoea—20% –– Most common complication of vagotomy –– Gastric stasis –– Hypoacidity with fermen-tation with bacterial over- growth causing enteritis Contd...

  In uncomplicated DU, with failure of medical treatment and when HSV cannot be done, then truncal vagotomy with pyloroplasty is done. 2. HSV (Highly selective vagotomy) or Parietal cell vagotomy or Super selective vagotomy is done in case of uncomplicated DU where medical treat­ment fails. Here only fibres entering the stomach is divided both anteriorly as well as posteriorly. Nerve of Latarjet is retained to supply antrum and so no drainage proce­dure is required (Amdrup). It has got 10% recurrence rate. 3. Selective vagotomy is at present not done often. Here along with a drainage procedure, either GJ or pyloroplasty, vagotomy is done with retaining of coeliac and hepatic branches. It has got 10% recurrence rate.

Success is the better way of dealing with failures.

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Small Intestine CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™

Anatomy Meckel’s Diverticulum Regional Enteritis Surgical Complications of Typhoid Surgical Complications of Roundworm ™™ Pneumatosis Cystoides Intestinalis

™™ ™™ ™™ ™™ ™™ ™™ ™™

Mesenteric Vessel Ischaemia Necrotising Enterocolitis Small Bowel Tumours Benign Tumours of Small Bowel Malignant Tumours of Small Bowel Carcinoid Tumour Short Bowel Syndrome

ANATOMY The small intestine is 6 m in length. This includes upper fixed (duodenum, 25 cm), lower mobile part (proximal 2/5th is jejunum and distal 3/5th is ileum).

Differences between the Features of Jejunum and Ileum Jejunum 1. Long and few vasa rectae 2. 3. 4. 5.

6. 7.

Ileum Short and numerous vasa rectae Long plicae Small plicae Thick wall, wider—4 cm Thin wall—3 cm Mesentery transparent Mesentery contains fat Peyer’s patches are scanty Peyer’s patches are abundant, located in the antimesenteric border Villi, leaf like and more abundant Villi, finger like and less abundant. Proximal 40% of small bowel— Distal 60%—pale pink deep red

Mesentery attaches the small intestine to the posterior abdominal wall, contains blood vessels, lymphatics, fat. Mesentery at its root is attached to L2 vertebra on the left side at duodenojejunal junction, running obliquely downwards and right towards right sacroiliac joint at ileocaecal junction. Mesentery is 25 cm in length at its root and spreads life a wide fan when it reaches to small bowel wall becoming 5–6 meters in length. It crosses the

™™ ™™ ™™ ™™ ™™

Massive Bowel Resection Small Bowel Enema Capsule Endoscopy Small Bowel Enteroscopy Enteric/Gastrointestinal Fistula

duodenum, aorta, IVC, right ureter, right psoas major muscle, right gonadal vein. Mesenteric cyst, mesenteric lymph nodes, mesenteric tear, mesenteric inflammations are of surgical importance. SMA, SMV and their branches and tributaries pass through it. During small bowel resection, mesentery should be ligated using surgical ligatures or energy sources and later anastomosis is done.

Nerve Supply Sympathetic supply is from T9-T11 and parasympathetic supply is from vagus. Both pass through coeliac and superior mesenteric plexus. Bowel wall contains the myenteric plexus of Auerbach which lies between the circular and longitudinal muscle coats; and submucous plexus of Meissner. Sympathetic nerves are motor to sphincter, inhib­itory to peristalsis; parasympathetic nerves are inhibitory to sphincter and stimulates peristalsis.

A

B Figs 21.1A and B: Vascular pattern in (A) jejunum, (B) ileum.

Small Intestine MECKEL’S DIVERTICULUM It appears at a specific site in the ileum and the wall contains each of the several layers of the intestinal tract…. The proof that the diverticulum is a residuum of the communication between the intestinal canal and the umbilical stalk rests in the findings which I have observed in three stillborn, full-term fetuses. —Johann Friedrich Meckel, 1809

It is a congenital diverticulum arising from the terminal ileum and is part of the unobliterated proximal portion of the vitellointestinal duct. It is: ™™ 2% common. ™™ 2 feet from the ileocaecal valve. ™™ 2 inch in length. ™™ 2% of Meckel’s diverticulum only will be symptomatic. ™™ 50% of symptomatic are below 2 years of age. ™™ 20% heterotopic epithelium. ™™ 2:1 female preponderance is seen.

Fig. 21.2: Blood supply of the small bowel.

xx It is congenital, results from incomplete closure of vitello-

intestinal duct. Normal GIT secretions Saliva—1000 ml Gastric­—1500 ml Intestinal—4000 ml Bile—1000 ml Pancreas—1500 ml

Cell type

Function

Goblet cells

Mucous

Paneth cells

Lysozyme, tumour necrosis factor, cryptidins

Enterocytes

Absorption

Enteroendocrine cells

Different hormones

xx It is the most common congenital anomaly of small intestine. xx Arises from the antimesenteric border of the ileum,

containing all three layers of the bowel with independent blood supply. xx In 20% of cases mucosa contains heterotopic epithelium like gastric (commonest—50%), colonic and pancreatic tissues (5%). xx It may be connected to or communicated with the umbilicus through a band or fistula. xx It may be associated with oesophageal atresia, exomphalos, and anorectal malformations.

Investigations for small bowel diseases ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Barium meal follow through Small bowel enema (Enteroclysis) Plain X-ray abdomen to see intestinal obstruction Selective splanchnic angiography to see vascular bleed or malformation (DSA) Isotope scintigraphy to see Meckel’s diverticulum Estimation of faecal fat in 24 hours—normal is less than 7 gram Schilling test to find out the absorption of vitamin B 12 from terminal ileum SeHCAT bile acid absorption test (selenium labelled) to find out the absorption of bile acids from the terminal ileum Many different breath tests are used to find out malabsorption, bacterial overgrowth and transit time Jejunal biopsy CT scans to see fistula, tumour, and spread Capsule endoscopy is very useful

A

B Figs 21.3A and B: (A) Anatomy of Meckel’s diverticulum; (B) Meckel’s diverticulum.

Presentations in Meckel’s Diverticulum xx Asymptomatic—in majority cases. xx Severe haemorrhage most common, seen in children aged 2 years or younger (Maroon-coloured blood). xx Intestinal obstruction due to bands/adhesions/ intussusception. xx Perforation. xx Intussusception, volvulus of small bowel. xx Peptic ulceration. xx Diverticulitis (20%)—features mimic acute appen­dicitis. xx Littre‘s hernia—it is presence of Meckel’s diverticulum in hernial sac as content. It is observed in inguinal/femoral hernia.

One cannot love what he cannot respect, whether it be himself or another.

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SRB's Manual of Surgery xx Silent Meckel’s diverticulum found during laparotomy or laparo­ scopy or by radioisotope study. xx Carcinoid or GIST can occur in Meckel’s diverticulum. Note:

“Meckel’s diverticulum frequently suspected; often sought; seldom found”—Charles Mayo.

Diagnosis xx Technetium (Tc99) radioisotope scan is very useful (90–95% accuracy). 90% of heterotrophic gastric mucosa can be identified in Meckel’s diverticulum by radioisotope study. It can detect Meckel’s diverticulum with minimal bleeding also (0.1 ml/ minute). So it is very useful investigation in children presenting with bleeding. xx X-ray abdomen to see complications like obstruction, perforation. xx Laparoscopy is very useful. xx Enteroclysis/small bowel enema under fluoroscopy may show the Meckel’s diverticulum. It is probably the most accurate investigation.

Treatment xx Asymptomatic Meckel’s diverticulum can be left alone when identified during laparotomy. xx Resection of a short segment of ileum containing Meckel’s diverticulum and end-to-end anastomosis is done. xx Meckelian diverticulectomy with closure of enterotomy also can be done, but chances of retaining heterotopic tissues and stenosis are higher.

Fig. 21.5: Meckel‘s diverticulum—surgical treatment. Meckelian diverticulectomy is done by obliquely clamping beyond the base of the Meckel‘s diverticulum. Care should be taken not to retain heterotopic gastric (or other) epithelium which can be felt-like indurated area. Enough precaution should be taken so that stricture will not form later. When heterotopic tissues extend beyond the Meckel‘s diverticulum into the ileum, then resection of ileum with Meckel‘s and anastomosis is done. Clamping distal to the base of the Meckel‘s diverticulum like appendicectomy should not be done. It will cause stricture, leak or retaining heterotopic tissues in the part.

Indications for surgery Surgery is done whenever the base is narrow, and in lengthy diverticulum. ™™ Presence of adhesions or band which may precipitate obstruction, intussusception or volvulus. ™™ Symptomatic patients or presence of complications. ™™ If it is found in children below 2 years. ™™

Fig. 21.4: Laparoscopic view of Meckel’s diverticulum. Patient presented with features of acute appendicitis. On laparoscopy, Meckel‘s diverticulum which was adherent to umbilicus by a cord was found. Appendix was identified separately. Appendicectomy and Meckelian diverticulectomy was done.

Duodenal diverticulum is the most common acquired diverticulum of small bowel. ™™ Meckel’s is the most common true congenital diverticulum of small bowel. ™™ Duodenal diverticulum: It is common in females; 65% occur within 2 cm of ampulla. Commonly they are asymptomatic; < 5% need surgery. It can be congenital/acquired; true/false; intra- or extraluminal. Biliary obstruction, pancreatitis, cholangitis, haemo­r rhage are complications. Diverticulectomy; duodenotomy and invagination of diverticulum when it is very close to ampulla embedded in pancreas; sphincteroplasty are the treatment. Perforated diverticulum is treated with serosal jejunal patch/ duodenal diversion/duodeno- or gastrojejunostomy. Trifoliate diverticula is an acquired one, occurs in chronic duodenal ulcer. ™™ Jejunoileal diverticula: It is rare (0.1%). It is false type, common in elderly. They are common in jejunum, often multiple, protrudes from mesenteric border. Chronic pseudo-obstruction, vague pain, malabsorption, haemorrhage, perforation can occur occasionally. Diverticulitis leads into perforation and peritonitis or abscess. Bile salt deconjugation with steatorrhoea, megaloblastic anaemia (vitamin B12 deficiency) can occur. Treatment—enterotomy with removal of enterolith or resection and anastomosis. ™™

Small Intestine involved (60%). In 75% cases perianal is involved (fissure in ano). xx Incidence is 5/1,00,000; prevalence is 50/1,00,000. It is common in North America and north Europe.

Aetiology xx xx xx xx xx

Fig. 21.6: Jejunal diverticula are rare. Often can cause obstruction, haemorrhage. It needs surgical resection.

Unknown, but a familial and infective nature is thought of. Increased autoantibodies. Diet and food allergy. It is slightly more common in females. DNA of Mycobacterium paratuberculosis was found in intestines of 60% of patient’s with Crohn‘s disease but antituberculous drug therapy has not helped them. xx Focal ischaemia as a vasculitis may be the cause. xx 10% of first degree relatives; 50% of monozygotic twins develop Crohn‘s disease. Genes NOD2/CARD15 in chromosome 16q12 has got strong association with Crohn‘s disease. CARD15 is expressed in Paneth cells of the ileum. xx Smoking is related to Crohn‘s disease as aetiology, as for relapse and for exacerbations. Causes for Crohn’s ™™ ™™ ™™ ™™ ™™ ™™

Infectious—Mycobacterium paratuberculosis and atypical mycobacteria. It causes Johne’s disease in cattle Immunologic Genetic—chromosome 16q—IBDI with CARD15/NOD2 gene (40 fold risk) Environmental Jews are more prone Smoking, diet, OCPs (controversial), psychosocial factors

Fig. 21.7: Jejunal diverticula—multiple.

REGIONAL ENTERITIS (Crohn’s Disease) We propose to describe, in its pathologic and clinical details, a disease of the terminal ileum, affecting mainly young adults, characterised by a subcutate or chronic necrotising and cicatrising inflammation. The ulceration of the mucosa is accomplished by a disproportionate connective tissue reaction…a process which frequently leads to stenosis of the lumen of the intestine, associated with the formation of multiple fistulas. —Burrill Bernard Crohn, Leon Ginzburg, Gordon D Oppenheimer, 1932

xx It is a granulomatous, noncaseating (transmural) inflamma-

tory condition of the ileum commonly and of the colon often. xx It is independent of age, sex, socioeconomic status and

geographic areas. xx Rarely other parts of the GIT like colon, jejunum, stomach,

duodenum, oesophagus can get involved. Small bowel alone is involved in 30% cases; in 50% cases both small and large bowels are involved. Terminal ileum is most commonly

Fig. 21.8: Multiple ulcers in the jejunum—Crohn’s or tuberculosis.

Pathology Transmural inflammation ↓ Granuloma formation with linear snake like ulcers ↓ Cicatrisation ↓ Thickening of the bowel wall (Hose pipe pattern) ↓ Adhesions ↓ Fistula formation

Happiest people are not only happy in themselves; they are the cause of happiness to others.

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SRB's Manual of Surgery xx There is increased mucous membrane permeability → antigeninduced cell-mediated inflammatory response → release of cytokines like TNF, interleukin 2 → defect in suppressor T cell → granuloma and other pathology. xx Fibrosis, stricture formation, deep ulcers, oedema of mucosa between ulcer areas which looks like ‘cobble stone’, skipped normal areas in between, serosal opacity, mesenteric fat stranding, enlarged mesenteric lymph nodes, abscesses in the mesentery, fistula are the pathology. Small mucosal aphthous ulcers are earliest gross feature. xx Disease may be inflammatory, stricturing or perforating types. xx Noncaseating giant cell granuloma with chronic inflammation of all layers; focal arterial blocks in muscularis propria are the microscopic features. xx Extensive fat wrapping around bowel which is been thickened, firm, rubbery, incompressible, segmental is typical.

xx Mild fever, weight loss, lethargy. xx Crohn’s disease may present as tender, firm, resonant mass

in right iliac fossa xx Obstruction, fistula formation, often perforation. xx Bleeding which is usually chronic but occasionally massive

can occur. xx Perianal disease with fissure, fistula, and abscess can occur

in 25% of patients with small bowel Crohn’s. It can be the only presentation of Crohn’s in 5% of cases. 50% of colonic Crohn’s will have perianal disease. xx Extraintestinal manifestations occur in 30% of Crohn’s disease.

Main features of Crohn’s disease ™™ ™™ ™™ ™™ ™™ ™™

Ileum—most common site of occurrence—60% Rectal sparing is usual and common Skip lesion Hose-pipe pattern Linear ulcers and cobblestone appearance of mucosa Transmural

xx Mesentery is thickened, oedematous, with enlar­ged lymph glands which will neither break nor calcify. xx Rarely jejunum, stomach and other parts of GIT like oral cavity, oesophagus are involved. xx In colon (30%), it is commonly observed in caecum and ascending colon. xx Toxic megacolon with acute colitis even though rare, can occur in Crohn‘s disease. Note:

• •

Anal fissure is most common anal problem in Crohn’s disease. It may lead into perianal abscess and fistula. Cytokine response in Crohn’s disease is associated with Th17.

Vienna classification of Crohn’s disease Age in years: –– A1: < 40; A2: ≥ 40 ™™ Behaviour: –– B1: Nonstricturing, nonpenetrating –– B2: Stricturing –– B3: Penetrating ™™ Location: –– L1: Terminal ileum –– L2: Colon –– L3:Ileocolon –– L4: Upper GIT ™™

Fig. 21.9: Crohn’s disease in small bowel. It is transmural full thickness disease. In 30% cases colon is involved. Skip lesion, stricture, fistula are common. It can involve any part of GIT occasionally.

Presentations a. Acute presentations (5%): It mimics acute appen­dicitis with severe diarrhoea. Often there will be localised or diffuse peritonitis. b. Chronic Crohn’s: First stage—Mild diarrhoea, colicky pain, fever, anaemia, mass in right iliac fossa which is tender, firm, nonmobile along with recurrent perianal abscess. Second stage is either acute or chronic intestinal obstruction due to cicatrisation with narrowing. Third stage—Fistula formation—enterocolic, enteroenteric, enterovesical, enterocutaneous, etc. It is precancerous condition but not as much as ulcerative colitis. Extraintestinal manifestations of Crohn’s disease

Clinical Features

™™

xx It is common in young age group. xx Abdominal pain and diarrhoea is the initial slow insid-

™™ ™™ ™™ ™™ ™™ ™™ ™™

ious presentation. There is also asymptomatic period in between. xx Diarrhoea is usually less severe without blood, pus or mucous.

Skin: Erythema nodosum, pyoderma gangre­n osum—most common Eyes: Iritis, uveitis Joints: Arthritis, ankylosing spondylitis, sacroiliitis Sclerosing cholangitis, gallstones Nephrotic syndrome, renal stones Pancreatitis, chronic active hepatitis Amyloidosis, aphthous ulcers Blood: Anaemia, thrombocytosis, DVT, arterial thrombosis.

Small Intestine Investigations xx Plain X-ray abdomen, ultrasound abdomen. xx Barium meal follow through or small bowel enema shows:     

Straightening of valvulae conniventes. Multiple defects (cobblestone appearance). Cicatrisation of ileum (string sign of Kantor). Rose-thorn appearance of the bowel wall. Radiologically Crohn’s disease is classified as nonstenosing type or stenosing type.

xx CT scan and CT fistulogram is useful method. xx Colonoscopy usually shows normal rectum; with colon

showing aphthoid like ulcers and reddened mucosal margin. Deep ulcers, stricture and fistula will be evident in late cases. Colonoscopy also shows segmental, deep, cobblestone look. xx Blood tests for anaemia, protein loss, mineral and trace element loss like magnesium, zinc, and selenium. There will be raised C reactive protein and orosomucoid in active disease. xx Capsule endoscopy is useful investigation, but when stricture is present capsule may get stuck in the narrow part. xx MRI to diagnose anal disease. MR enteroclysis is very useful to demonstrate fistula. xx Serum markers: 90% of patients with Crohn’s disease show ASCA (anti-saccharomyces cerevisiae antibody)positive and pANCA (perineural antineutrophil cytoplasmic antibody)-negative, whereas in 98% of patients with ulcerative colitis, ASCA is negative but pANCA positive.

xx

xx xx

xx

xx

xx

Complications of Crohn’s ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Intestinal obstruction Stricture Bleeding Fistula formation Carcinoma small and large bowel Perianal abscess Peritonitis Pericolic abscess

Differential Diagnosis xx xx xx xx xx

Radiation enteritis and Yersinia enteritis. Ulcerative colitis, acute appendicitis. Intestinal tuberculosis, Salmonella, Shigella, CMV Carcinoma ileum or caecum. Differential diagnosis for mass in the right iliac fossa (carcinoma caecum, actinomycosis, appen­dicular mass, ileocaecal TB, ectopic kidney, mesenteric lymphadenitis).

Treatment Medical xx Cessation of smoking xx Bed rest, protein and vitamin supplementations. Often nasogastric tube nutrition or TPN is required. xx Steroids are mainly used to induce remission of the disease in initial phase. It is less useful for maintenance. Dose is 20–40 mg/

xx

day of perdnisolone (0.5 mg/kg/day) for 3–6 weeks. Methylprednisolone infusion IV 60 mg/day for 5–7 days can be given initially. Budesonide, a newer steroid shows high first phase metabolism in liver and so in high dose achieves targeted delivery into the intestine. It is often combined with mesalamine or used as an alternate first line therapy. Azathioprine is used for maintenance therapy. It inhibits the cellmediated immunity. 6-mercaptopurine and cyclosporine are also used. Tacrolimus (FK-506) inhibits production of IL2 and is effective in improving fistula. Short course intravenous cyclosporin can also be used to induce remission. Salazopyrines are mainly used in acute ileitis and colitis. It is not useful in inducing remission. 5-aminosalicylic acid (5-ASA) and sulfasalazine are also used. 5-ASA inhibits leukotriene, TNF, interleukin production. It acts mainly on colonic and partly on small bowel mucosa. Mesalamine which causes slow release of 5ASA is better with a dosage of 4 gram/day. It is released throughout its passage along the small and large bowel. Mesalamine remains the first line therapy for Crohn’s disease. Metronidazole is useful in reducing the anal and colonic pathology by suppressing the cell-mediated immunity and also as antibacterial. It is not beneficial for small bowel disease. Monoclonal antibody like infliximab (Murine chimaeric monoclonal antibody) is used in severe refractory cases which act against tumour necrosis factor alpha (TNFα). Single dose is used for induction. Later given after 2nd week, 6th week and then once in 8 weeks at a dose of 5 mg/kg. It is also useful in promoting closure of fistula in 60– 80% cases. But its long-term side effects are not confirmed. Anti-IL1, anti-IL12, anti-IL18, anti-interferon-γ antibodies are tried. Natalizumab is recombinant human monoclonal antibodies against α integrin. Adalimumab, a human monoclonal antibody is also effective. Monoclonal antibodies cannot be used in patients with tuberculosis or associated malignancy. They are expensive; relapse can occur after cessation of the therapy. Antibiotics (Ciprofloxacin) are useful in controlling sepsis in fistula, colitis. Medical therapy

To induce remission—steroids For maintenance—immunomodulating drugs like azathioprine Antibiotics, metronidazole (as immunomodulator) Monoclonal antibody—infliximab Nutritional support Note: Patients with Crohn‘s disease should avoid NSAIDs. ™™ ™™ ™™ ™™ ™™

Surgery Indications xx Failure of medical treatment. xx If patient cannot be weaned off systemic steroid after 6 months. xx Intestinal obstruction—most common indication. xx Fistula formation, bleeding, malignant change. xx Perforation, fulminant colitis. xx Perianal problems. xx Crohn’s disease children with growth retardation. Note:

Surgery is not to cure the disease, but to correct complications. Recurrence of complications and relapse of disease can occur even after surgery. Patient should be on postoperative azathioprine/6 MP/5ASA.

The successful man is the average man, but focused.

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SRB's Manual of Surgery Surgeries xx Ileocaecal resection (common procedure done because commonly ileocaecal region is involved). xx Segmental resection—conservative resection is better. xx Total colectomy and ileorectal anastomosis. It is only done in extensive colonic Crohn’s. Ileoanal anastomosis with pouch is not done after total proctocolectomy or continent ileal pouch is not done as disease may later recur in the pouch itself. xx Stricturoplasty. xx Temporary ileostomy. xx Right hemicolectomy is done occasionally. xx Emergency colectomy may be needed in 8% of patients with extensive severe colitis but with rectal sparing. xx Laparoscopic resection is good alternative. xx Occasionally if rectum is diseased or anal disease is severe then total proctocolectomy with ileostomy is done. xx Corrective surgery for anal diseases like fissure, abscess and fistula. xx Definitive procedures for internal fistulas like ileovesical, ileocolic with faecal and urinary diversions. xx Bypass and exclusion procedures are not commonly used at present. xx In free perforation and peritonitis ileostomy is needed. But later, it is difficult to decide the timing of closure of ileostomy as disease is extensive; it is wiser to do right ileocolic resection or right hemicolectomy in these patients. xx Enterocutaneous fistula is treated with excision of fistula with resection and anastomosis of that particular segment. Organ fistulas are also treated with resection of adherent bowel and closure of organ like urinary bladder wall. xx Small bowel Crohn’s causes chronic bleeding; colonic Crohn’s often may cause massive bleed. In massive bleed, angiographic control or colonoscopy is needed.

Typhoid S typhi, S paratyphi A, B and C Gram-negative flagellated bacilli ™™ Faeco-oral route is commonest mode of spread ™™ Asymptomatic human carriers are most important reservoirs (Typhoid Mary) ™™ Peyer’s patches, mesenteric lymph nodes, gallbladder, spleen, liver and bone marrow are commonly involved ™™

™™

Complications of typhoid ™™ ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Paralytic ileus is the most common complication Intestinal haemorrhage—as the Peyer’s patches in terminal ileum are enlarged and ulcerated—20%. Usually blood transfusion and antityphoid therapy is sufficient to control bleeding. Rarely in massive bleed resection anastomosis is needed Perforation Cholecystitis and carrier stage Venous thrombosis particularly of common iliac vein is known Typhoid cystitis, bacilluria, epididymo-orchitis Arthritis Typhoid osteomyelitis (granular sequestrum) Typhoid perichondritis and laryngitis leading to airway obstruction Typhoid abscess in liver, spleen, brain and parotid Myositis, myocarditis, meningitis

Typhoid (Enteric) Perforation Perforation usually occurs in 3rd week of the infection: xx Ulcers are multiple, arranged in parallel and in antimesen-

teric border of the ileum. xx One or more ulcers might perforate and many ulcers may

be on impending perforation. xx Patient is toxic, presents with: Severe diarrhoea Relative bradycardia Soft abdomen Obliterated liver dullness Abdomen without guarding and rigidity (because of Zenker’s degeneration) ™™ Initial history of fever for few days then pain abdomen and tenderness, which is progressive ™™ ™™ ™™ ™™ ™™

Fig. 21.10: Stricturoplasty can be done in Crohn’s disease in case of short strictures in the absence of active inflammation.

Associated features

Note: Appendicectomy should not be done in acute phase of Crohn’s disease as it may lead to external faecal fistula; if there is no acute inflammation, elective appendicectomy can be/should be done as it eliminates appendix as a source of future abdominal pain.

SURGICAL COMPLICATIONS OF TYPHOID xx Typhoid (Enteric fever) is caused by organism—Salmonella

typhi. xx Mode of transmission is faecooral route. xx Presents initially with fever, chills, abdominal pain.

™™ ™™ ™™

Splenomegaly Fever, headache Rose spots in the skin

Investigations xx xx xx xx xx

Possibility of missing typhoid perforation is very high. X-ray in erect posture shows gas under diaph­ragm. Widal test is positive. Neutropenia is seen in blood. Blood culture (90% + ve) and stool cultures are often required. Marrow culture is useful.

Small Intestine xx Identification of specific and sensitive markers (to detect Ig G/ IgM). These tests are positive even when blood culture is negative. xx PCR assay for typhoid infection is also useful. Note:

• • • • •

Incidence of typhoid perforation is 2% of total cases. 75–80% of perforations are single which needs simple closure after taking biopsy from the edge of ulcer. 20–25% of perforations are multiple which requires either resection or exteriorisation as ileostomy. In paratyphoid B fever colon perforation can occur. CT scan abdomen is ideal investigation to detect early pneumoperitoneum and fluid collection.

Fig. 21.12: Roundworm removed from peritoneal cavity. Note the faecal contamination.

Treatment xx Antityphoid drugs (Quinolones, chloramphenicol, ceftriaxone sodium) are started. xx Later laparotomy is done to close the perforation. xx Ulcers which are on impending perforation should be sutured with serosa. xx Presently, resection and anastomosis is also accep­ted as treatment when multiple perforated ulcers are present. xx ZIP technique (laparostomy) to reopen the abdomen whenever required is also beneficial. xx Exteriorisation of ileum is ideal in a critically ill patient. Once patient recovers properly after 6–12 weeks closure and continuity is maintained. xx Closure of perforation with ileotransverse anastomosis is the other option, but not ideal. xx ICU care, TPN/enteral feeding/monitoring/blood transfusion/fluid and electrolyte management/ prevention or management of other complications like DVT/DIC/ARDS/septicaemia.

Fig. 21.13: Specimen of ileum showing roundworm bolus. Bolus causes intestinal obstruction, commonly near terminal ileum.

A Fig. 21.11: Enteric perforation is often severe causing faecal peritonitis. Resection/exteriorisation may be needed in severe cases.

SURGICAL COMPLICATIONS OF ROUNDWORM (Ascaris lumbricoides) Life Cycle Eggs → faeco-oral route → larvae → portal circulation → liver → hepatic veins → IVC, heart, pulmonary artery → lungs → maturation of larvae (8 weeks) → alveoli, tracheobronchial tree → coughed out or swallowed to intestine → adult roundworms → male + female worms union → release of eggs → stool → reinfection.

B

Figs 21.14A and B: Gastroduodenoscopy view of roundworm. It was removed through endoscopy. Roundworm in proximal bowel can cause pancreatitis, cholangitis. Vomiting of roundworms signifies intestinal obstruction. It need not be due to roundworm obstruction. Because of the obstruction and proximal bowel irritation, worms move proximally into stomach and come out through the mouth (Courtesy: Dr Tantry and Dr Sandeep Gopal, Gastroenterologists, KMC, Mangaluru).

Features xx Worm colic. xx Toxicity—fever, tachycardia.

When you get to the end of your rope, tie a knot and hang on.

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SRB's Manual of Surgery xx Subacute intestinal obstruction. xx Acute intestinal obstruction with palpable roundworm bolus per abdomen. xx Perforation—common in the ileum. Note:

Perforation usually occurs at the site of pre-existing disease like nonspecific ileal ulcer, amoebic ulcer, typhoid ulcer, and suture line.

xx Intraperitoneal abscess. xx Dyspepsia, malabsorption, iron deficiency anaemia. xx Due to migration of worm into the CBD/pancreatic duct causes ascending cholangitis with fever, jaundice and upper abdominal pain or features of pancreatitis. xx Loeffler’s syndrome is due to larvae in the alveoli causing

colon, hypertonic saline wash per anum makes them to disperse and pass outside. xx Removal of worms by enterotomy is rarely done. Enterotomy should be securely sutured using silk otherwise reperforation from sutured site can occur by worm toxins or by worm activity and migration. xx If there is perforation (common site is ileum) or gangrene with peritonitis, peritoneal worms should be essentially removed. Ideally ileum should be exteriorised to prevent suture line breakdown after closure due to worms. Once patient recovers bowel ends are sutured to maintain the continuity and abdomen is closed. Even though it is ideal method, it is not commonly performed. xx ERCP, worm extraction and stenting is done for worm in CBD/ pancreatic duct.

fever, dry cough, chest pain, dyspnoea.

Treatment of roundworm obstruction Drugs—piperazine citrate, mebendazole, alben­dazole Most often by conservative treatment, worms get dispersed and passed per anally. But patient requires nasogastric aspiration, IV fluids, antibiotics, and observation ™™ If patient is not responding then laparotomy is done. Worm bolus in the distal ileum is milked into the caecum. Often enterotomy and removal of worms is required ™™ Perforation due to worm requires immediate lapa­r otomy, removal of worms and closure of perforation ™™ Only rarely, resection and exteriorisation is required ™™ ™™

PNEUMATOSIS CYSTOIDES INTESTINALIS A

B

Figs 21.15A and B: (A) Plain X-ray abdomen in a child showing features of intestinal obstruction due to roundworms in the bowel; (B) Roundworm obstruction. Worms removed through an enterotomy.

Investigations xx Small bowel enema/barium meal follow through may show roundworms in the ileum. xx US can demonstrate the worms/worm bolus/worm in CBD or pancreatic duct. xx Blood may show eosinophilia, anaemia, hypoalbuminaemia. LFT for worm in CBD. xx Chest X-ray may show bronchitis. xx Sputum or bronchial wash may show larvae or Charcot-Leyden crystals. xx Stool examination may show ova. xx CT/MRI will show worms/obstruction/worm in CBD or pancreatic duct.

xx It is transient, thin cysts containing nitrogen in submucosa and subserosa of ileum. xx It is due to increased intraluminal pressure, which forces N2 through the layers of the bowel due to hyperperistalsis. xx It is associated with chronic duodenal ulcer, chronic pulmonary disease, bowel obstruction. xx It can be associated with connective tissue disorder like scleroderma. xx In neonates it is associated with necrotising enteritis. xx It is common in subserosal and submucosal planes. Cysts contain nitrogen and hydrogen. xx They can occur anywhere in GIT but commonly seen in jejunum. Later in ileocaecal and colon region.

Treatment xx Antihelminthic drugs like piperazine citrate 60 ml is given immediately if there are features of obstruction, otherwise at night time. Albendazole, mebendazole are other drugs used. Proper nutrition is important. xx Nasogastric aspiration; IV fluids; observation is sufficient in most of the situations. In 48 hours, obstruction will be relieved and child passes worm bolus per anally. xx Occasionally laparotomy and milking of the worm bolus into the caecum without enterotomy is needed. Once worms are in the

Fig. 21.16: Pneumatosis cystoides intestinalis.

Small Intestine xx Mesentery and peritoneum may also be involved. xx It is equal in both sexes. xx These gas-filled cysts in small bowel may rupture into peritoneal cavity to cause sterile pneumoperitoneum. Peritonitis is unusual. xx Abdominal pain, distension, bowel disturbances, vomiting are the presentations. xx Intestinal obstruction, haemorrhage, perforations are complications.

B

A

Figs 21.17A and B: Ischaemic bowel necrosis. It will lead to perforation and peritonitis. So always requires surgical resection.

Treatment xx Oxygen therapy by 70% oxygen for 5 days or hyperbaric oxygen 2.5 atmospheres for 2 hours daily for 3 days. xx Metronidazole therapy. xx Treating the cause; resection only in refractory cases. Small bowel strictures Causes ™™ Tuberculosis of ileum/jejunum ™™ Crohn‘s disease ™™ Radiation enteritis ™™ Ischaemic strictures—after bowel ischaemia, necrotising enterocolitis ™™ Nonspecific causes ™™ Garrey’s stricture following long standing irreducible hernia occurs after reduction and surgery (due to constriction band causing ischaemia at the site) Management ™™ Small bowel enema/capsule endoscopy/CT scan—investigations ™™ Treatment: Treating the cause; resection anastomosis, and stricturoplasty

MESENTERIC VESSEL ISCHAEMIA Superior mesenteric artery is commonly involved than inferior mesenteric artery. Often superior mesenteric vein can also get involved.

Causes xx Embolism (50%)—Sources

From left auricle, as seen in atrial fibrillation. A mural infarct. Atheroma from aorta or aneurysm. Endocarditis vegetations. Left atrial myxoma. xx Thrombosis  It may block the origin of the superior mesenteric artery and can cause ischaemia of full length of small bowel. It is life-threatening.  It may be due to atherosclerosis or occasionally TAO.  Often all main splanchnic vessels—coeliac, superior and inferior mesenteric arteries may be involved by atherosclerosis. xx Nonocclusive  It is due to hypotension/hypoperfusion.  It is due to vasospasm due to shock—nonocclusive mesenteric ischaemia (NOMI). xx Superior mesenteric vein thrombosis, occurs in patients with portal hypertension, portal pyaemia, sickle cell disease, women with contraceptive pills (OCP).     

A

C

B

Figs 21.18A to C: Acute extensive mesenteric ischaemia causing small bowel gangrene. Patient will develop short gut syndrome.

Pathology xx Bowel and mesentery will be oedematous, friable, discoloured, and collected with fluid and blood. xx Once gan­grene sets in, perforation can occur leading to peritonitis.

Clinical features In acute xx Abdominal pain that is out of proportion in relation to tender-

ness; pain is around umbilicus to begin with later diffuse. xx Persistent vomiting, bloody diarrhoea; later shock and toxicity. xx Initially abdomen will be soft but later develops tenderness,

rebound tenderness, distension, guarding and rigidity. xx Rectal examination shows bloody stool.

In chronic xx Post-prandial abdominal pain is the most important

symptom with aversion to food and weight loss. xx Abdominal angina—recurrent colicky pain, diffuse in nature

occurs with or without food intake. xx Bloody diarrhoea—it is a feature of both acute and chronic

and is confirmed by rectal examination.

xx Later, once severe infarction of bowel occurs; it may present

with acute features.

Courage is grace under pressure.

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SRB's Manual of Surgery Types It can be: xx Acute type, sloughing of intestinal mucosa occurs in 3 hours; infarction of entire thickness of bowel occurs in 6 hours. xx Chronic type, it is slow and gradual process. It can also be: xx Extensive involving large segment of bowel, small or large. xx Localized:  Colonic localised ischaemia at splenic flexure—the most common.  Focal segmental ischaemia often with necrosis in small bowel.  Chronic mucosal infarction.

Specific Features of Mesenteric Ischaemia xx It is often considered as intestinal failure. xx It can be thrombotic; embolic; and nonocclusive (low flow status—is due to reduced SMA perfusion by underlying causes like cardiogenic shock, mesenteric vasoconstriction or part of systemic disease. There is no documented thrombosis or embolus). xx It is rapidly progressive causing early mortality. xx Clostridium, anaerobic and streptococci infections are evident. xx Gas bubble in the mesenteric vein is pathognomonic sign of irreversible mesenteric ischaemia. xx CT/CT angiogram is very useful. An occlusion at the ostium of SMA signifies thrombosis. Embolic occlusion is smooth filling defect, usually distal to origin of middle colic artery sparing proximal small bowel, right side colon and transverse colon. Emboli can be fragments causing multiple patchy necrosis of bowel at different sites. xx Decreased blood volume; poor tissue perfusion; metabolic acidosis; myocardial depression by depressant factor; endotoxaemia; ARDS; renal failure; septicaemia and MODS are the pathological events. xx On laparotomy—musty smell and dusky look of extensive gangrenous bowel is typical. When in doubt, ischaemia should be confirmed by oxygen support; warming; on table Doppler.

Investigations xx Plain X-ray in erect posture and US of abdomen. xx CT scan is the investigation of choice. xx Angiogram or CT angiogram is the most reliable investi­

gation especially in NOMI. It is also ideal for chronic ischaemia. xx Angiogram—on-table angiogram xx Doppler study—on table. xx Blood tests: Total count is raised with drop in haemoglobin. Raise in blood urea and serum creatinine is common. Serum phosphate level is increased very early in 4 hours as small bowel is rich in phosphate. Arterial blood gas analysis is often essential. Blood culture may be needed.

Treatment xx Emergency laparotomy is done. With the help of Doppler

the block is identified and the vessel is opened. The block is removed and the bowel is reperfused. xx If patient has presented after 24–48 hours, gangrene might have already occurred, then resection and anastomosis is done.

xx If patient presents within 6 hours, it is possible to prevent

gangrene and to salvage the bowel. Emergency SMA angiography is done. Papaverine is injected for vasodilatation (by many studies its benefit is not confirmed). Often heparin (20,000 units loading dose and then maintenance dose of 5000–10000 units 6th hourly) or thrombolytics are injected. Immediate laparotomy is done. SMA is opened (arteriotomy) over the obstruction and thrombus/embolus is removed using Fogarty catheter. Perfusion is maintained. Close monitoring is essential for possibility of formation of bowel gangrene and if it is so relaparotomy should be done for bowel resection. xx In acute condition, thrombolysis using streptokinase, urokinase and recombinant tissue plasminogen activator can be tried. It should be done within 8 hours of onset of pain. xx NOMI is often treated with selective infusion of vasodilator papaverine into SMA. It is also used in all types of mesenteric ischaemia. Catheter is placed into SMA under guidance; 45 mg of papaverine given as a bolus initially, later 30 mg/hour continuous infusion with 1 mg/ml concentration. Catheter is usually kept for 2 weeks and repositioning with regular angiographic confirmation is needed. Papaverine being a vasodilator increases the bowel perfusion through end arteries as well as collaterals. xx Chronic mesenteric arterial ischaemia is treated with surgical revascularisation using aortomesenteric bypass graft and mesenteric endarterectomy. It also can be treated with PTA with or without stenting. PTA should not be done if there is bowel infarction. It is done through transfemoral or transaxillary route; balloon should be longer than the lesion and 10% wider than the arterial diameter. xx Chronic mesenteric vein thrombosis is treated with anticoagulation or propranolol or oesophageal variceal banding or portocaval shunt. xx Eventually patient requires oral anticoagulant therapy using warfarin for 12 months. xx Repeated post-therapy angiography is needed in all patients. xx Steroids are given to reduce lysosomal membrane destruction and effects of endotoxins; to maintain arterial resistance and complement activity. High dose hydrocortisone is used. xx Higher generation antibiotics; critical care; ventilator, fluid, electrolytes and nutritional support (TPN) are essential. Note:

• • • •

Minimum bowel length required to be retained is 1.2 meters, other­wise the patient will have high mortality (due to short bowel syndrome). Small bowel transplantation is under trial for the same. Mesenteric bowel ischaemia has got very high mortality. Development of septicaemia, ARDS, DIC, postoperative leak are common.

NECROTISING ENTEROCOLITIS xx Necrotising enterocolitis is an acquired inflammatory disease commonly seen in infants and newborn but occasionally can occur in children and adults. It is more commonly seen in premature babies. It is more common in formula fed babies than breastfed babies. Reduced gut flora make virulent pathogens to act and cause sepsis.

Small Intestine xx Common site is terminal ileum, caecum and ascending colon. Often it can involve entire small bowel. xx Gas in the bowel wall and often in portal vein is typical.

Incidence xx Often associated with low birth weight babies. xx Preterm babies 90%. xx Term babies 10%. Pathogenesis Hypoxia Umbilical artery cannulation Hypothermia Exchange transfusion Hypotension Hyperosmolar feeds Packed cell transfusion Hyperviscosity Acidosis Over dosage with calcium antagonists     Mesenteric ischaemia.

↓

A

B

Figs 21.20A and B: Necrotising enterocolitis. Skin necrotic lesions are typical. It is common in infants and children but can be seen in adolescents occasionally (Courtesy: Dr Rupen, MS, KMC, Mangaluru).

Investigations xx Plain X-ray abdomen:  Linear gas shadow in bowel wall.  Free intraperitoneal air implies perforation. xx Blood examination—leukocytosis, anaemia, hyper­kalemia, metabolic acidosis.

Bacterial invasion of mucosa and bowel wall.

↓

Necrosis—skip lesions are common.

↓

Necrotising enterocolitis.

Complications Stricture—small bowel. Perforation—peritonitis. ™™ Colonic stricture can develop lately after healing of ischaemic area. It is seen in 10% of cases. ™™ ™™

Sites

Management

xx Common in small bowel. xx Terminal ileum and caecum.

I. Medical therapy  Nasogastric aspiration.  Broad spectrum IV antibiotics.  TPN for 10–14 days.  Oxygen supplement is required. II. Surgery Indications 1. Pneumoperitoneum. 2. An abdominal mass. 3. Dilated intestinal loops.

Fig. 21.19: Necrotising enteritis. Note the segmental involvement of the disease.

Clinical Features Most babies present with: xx Bilious vomiting. xx Abdominal distension, guarding and rigidity. xx Bradycardia. xx Apnoea, lethargy. xx Gross or occult blood in stool (75%). xx Erythema and oedema of anterior abdominal wall—late feature. xx DIC. xx Mortality is 20%.

Procedures done xx Bowel necrosis and perforation—resection with stoma. xx Localised disease—resection and primary anasto­mosis. Complication: Extensive bowel resection—short bowel syndrome.

SMALL BOWEL TUMOURS xx They are rare neoplasms—3% of all GI tumours (Even though 80% total length and 90% of mucosal surface area of the GIT is small bowel). xx Common in elderly men. xx Common in New Zealand and Hawaii. xx It can be benign or malignant. xx Early diagnosis is difficult. xx Presentations are vague initially.

A man who does nothing never has time to do any thing.

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SRB's Manual of Surgery Patients with chronic immunosuppression have very high-risk of developing NHL (PTLD—post-transplant lymphoproliferative disorder, HIV) or sarcoma ™™ Patient with von Recklinghausen’s disease of neurofibromatosis is prone to develop GI neurofibroma or neurofibrosarcoma ™™ Smoking, red meat, alcohol, salt food ™™

Fig. 21.21: Jejunal haemangioma. Surgical resection cured the condition.

B

A

Figs 21.23A and B: Jejunal tumour coming out of serosa.

Presentations xx Asymptomatic initially. xx Features of obstruction/intussusception/bleeding. xx Vague abdominal discomfort.

Investigations

Fig. 21.22: Jejunal tumour. Reasons why malignancy is uncommon in the small bowel (even though it comprises 75% of length and 90% of GI mucosa): xx Rapid transit time, 30 minute to 2 hours. So exposure of mucosa to toxins and metabolites is less. xx Alkaline mucus rich luminal content is protective. xx Cells of small bowel produce the enzyme benzopyrene hydroxylase which detoxifies the carcinogen—benzopyrone. xx High levels luminal IgA provides immunity. xx Plenty of lymphoid tissue in the wall provides immunity. xx Healthy small bowel has got less bacterial load and so their toxic metabolites (as compared to colon). Risk factors implicated are: ™™ ™™ ™™

™™ ™™ ™™

Bile acids and their metabolites Post-cholecystectomy status Familial adenomatous polyposis (FAP) especially with duodenal adenomas has got very high chance of developing adenocarcinoma Crohn‘s disease has got 100 times increase in incidence of adenocarcinoma Celiac disease increases the risk of lymphoma Peutz-Jegher’s syndrome has got increased risk of small bowel adenocarcinoma

xx Often it is very difficult to assess small bowel. It may be on table finding during surgery, while presenting as complication like obstruction. xx Small bowel enteroclysis. xx CT abdomen is better investigation to assess bowel/ nodes/organs. CT enteroclysis shows 90% accuracy. xx Video capsule endoscopy enables to visualise small bowel mucosa properly. xx CT angiography is useful in identifying vascular tumours. xx Enteroscopes (push type or Sonde pull enteroscopes) are technically difficult. xx Intraoperative enteroscopes are useful.

BENIGN TUMOuRS OF SMALL BOWEL xx Benign tumors of small bowel are 50% of primary small bowel tumours. xx Adenoma can be potentially malignant.

Types Leiomyoma or GIST xx It is the most common symptomatic benign tumour of small bowel. xx It arises from interstitial cell of Cajal. It can be spindle cell type (70%) or epithelioid type. xx Commonly they are benign in small bowel. xx GIST express CD117 (90%), the c-kit proto-oncogene protein membrane receptor for stem cell growth factor and CD34 (80%), a human progenitor cell antigen.

Small Intestine Spigelman classification of duodenal adenomatosis Parameter about polyps

A

Figs 21.24A and B: Leiomyoma of jejunum.

Adenomas xx It is 15% of all benign small bowel tumours. xx 50% are in ileum; 30% in jejunum; 20% in duodenum. xx Commonly single but can be multiple when familial or associated with FAP. xx Commonly presents as bleeding and obstruction.

Adenomas can be: xx Brunner gland adenoma  It occurs as benign hyperplastic tumour in proximal duodenal submucosa which secretes alkaline bicarbonate rich fluid.  Bleeding is the usual problem.  It is treated by endoscopic resection.  It never turns into malignancy. xx Villous adenoma  It can occur anywhere in small bowel presenting as intestinal obstruction or haemorrhage.  But commonly seen in periampullary region presenting as obstructive jaundice, upper abdominal pain.  Size more than 3 cm can lead into adenocarcinoma with an adenoma—carcinoma sequence.  EUS is ideal tool to assess size and depth.  ERCP is done to relieve obstruction, to biopsy and to remove if it is small in size.  Malignant potentiality is very high—50%.  Transduodenal excision/pancreaticoduodenectomy are the surgical options. Small bowel adenomas are treated by reception. xx True adenomas  It can be tubular or tubulovillous.  It is usually single.  Endoscopic excision is the treatment; resection/pancreaticoduodenectomy is done if there is invasive lesion. xx Familial adenomas  It is associated with FAP with 5% risk for adenocarcinoma in duodenum.  It is diffuse throughout the duodenum.  Spigelman classification is used for assessment of FAP related duodenal adenomas. Villous adenomas larger than 3 cm or suspicious lesions identified on endoscopy are biopsied.  Screening endoscopy to be done every year.  Endoscopic or open polypectomy; argon beam or photodynamic therapy is tried in benign lesions.  Pancreaticoduodenectomy is done in high grade, carcinoma in situ, Spigelman IV classification.

Point 2

Point 3

Number

1–4

5–20

More than 20

Size

1–4 mm

5–10 mm

More than 10

Histology

Tubular

Tubulovillous

Villous

Mild

Moderate

Severe

Dysplasia

B

Point 1

Stage 0 1 2 3 4

Points 0 1–4 5–6 7–8 9–12

Lipoma xx xx xx xx

It mainly causes intussusception. It is common in elderly men. It is usually single intramural submucosal lesion. Lipoma does not have malignant potential.

Peutz-Jegher's Syndrome xx Autosomal dominant condition with melanotic pigment patches and GI polyps. xx Brown black pigments of 1–2 mm diameter in circumoral face, cheek, forearms, palms, soles, digits, perianal region. xx Hamartomas are located in entire jejunum and ileum; 50% of colorectum; 25% of stomach. xx Intussusception, bleeding, anaemia—presentations. xx Cancer of small intestine, stomach, pancreas, ovary, lung, uterus and breast can occur. xx Cure is not possible. Segment which is causing complication is resected.

Haemangioma It is 4% of all small bowel benign tumours. They are multiple in 60% of patients. They are usually submucosal abnormal proliferative vessels. Jejunum is the commonest site. They are often seen in association with Osler Weber Rendu disease, Turner’s syndrome. xx It presents as small bowel bleed. xx It can be diagnosed by angiography, 99mTc RBC scanning or capsule endoscopy. xx Treatment: Endoscopic sclerotherapy or angiographic embolisation or resection of bowel segment. xx xx xx xx xx

General Features xx They cause haemorrhage, colicky pain, and intussusception. xx Diagnosis is by suspicion. Small bowel enema, capsule endoscopy, radioisotope study, CT scan or MRI may help in identifying the disease. Laparoscopy and proceed may be useful. xx Commonly it is on table finding during exploration for acute presentations. xx Adenomas are potentially malignant depending on the size (> 3 cm).

A fault once denied is twice committed.

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SRB's Manual of Surgery Treatment xx It depends on type, number, nature, size of the tumour. xx Resection and anastomosis cures the condition. xx Surgery is not done for Peutz-Jegher’s syndrome unless it presents with complications.

MALIGNANT TUMOURS OF SMALL BOWEL 1. Adenocarcinoma xx Its incidence is 40% of small bowel tumours. xx It is most common primary malignant small bowel tumour.

Fig. 21.25: Resected small bowel specimen showing small bowel adenocarcinoma.

Fig. 21.26: Carcinoma ileum near ileocaecal junction. It (adenocarcinoma of ileum) carries poor prognosis. It is often on table diagnosis. xx In 80% cases it is in the duodenum and jejunum. xx FAP, adenoma, Crohn’s, coeliac diseases are the causes. xx Adenocarcinoma in Crohn’s disease occurs in younger age

group and commonly in ileum (70%). xx Nonspecific features, anorexia, crampy pain abdomen, bleeding and diarrhoea, obstruction or features of metastases (liver).

xx xx xx xx

CT scan, capsule endoscopy are the investigations. TNM system is used for staging. Nodal spread is the important prognostic factor. Surgical resection is the choice of therapy. Pancreaticoduodenectomy is done for duodenal tumour; for ileal/jejunal site tumours radical resection with 10 cm margin with adjacent mesenteric clearance is done. Adenocarcinoma of terminal ileum is treated with right hemicolectomy. xx RT and chemotherapy are less beneficial. xx It carries a poor prognosis.

Fig. 21.27: Jejunal adenocarcinoma presenting as stricture with features of proximal small bowel obstruction.

2. Non-Hodgkin’s lymphoma (NHL)—25% xx GI is the commonest extranodal site of NHL (20%), with small bowel (primary intestinal NHL) as second common site (30%) for extranodal site of NHL (First common site is stomach—60%). xx Lymphadenopathy/mediastinal lymph node enlargement are absent. Normal spleen, liver, blood peripheral smear are observed. xx B cell type is the commonest type 75%. It is common in ileum. xx T cell type (25%) carries poor prognosis. xx Presentations are malabsorption, obstruction, perforation, haemorrhage or palpable mass. xx In children lymphomas are the most common intestinal neoplasm. xx 25% of patients develop perforation. xx Fever when present suggests systemic spread. xx CT scan with CT guided biopsy or laparoscopic biopsy is needed. xx Surgical resection and chemotherapy are the treatment. xx Prognosis is poor. 3. Carcinoid tumour—30%. 4. GIST (gastrointestinal stromal tumour) xx It is rare but most common nonepithelial small bowel

tumours.

Small Intestine 6. Secondaries in small bowel They are very rare—if it is present, primary being commonly melanoma. Malignant tumours of small bowel ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Adenocarcinoma is commonest—40%. Order of occurrence— duodenum, jejunum and ileum GIST is new entity comprising smooth muscle tumours also Carcinoid and lymphoma has got better prognosis Adenocarcinoma and GIST has got poor prognosis Presentations are pain, diarrhoea, weight loss, anaemia, melaena, palpable mass, intestinal obstruction and metastatic features Bleeding and perforation are common in lymphoma and sarcoma Enteroclysis/capsule endoscopy/CT scan/histochemistry are needed to diagnose Surgery is the main therapy Imatinib is used in GIST with favourable results

Fig. 21.28: Gross look of small bowel lymphoma. xx 25% of GIST occurs in small bowel (stomach—50 to 60%).

It is 0.2% of all GI tumours. xx It is equal in both sexes. xx It arises from interstitial cell of Cajal. xx More than 95% show c-kit (transmembrane receptor tyrosine kinase) mutation. xx Many mesenchymal tumours of small bowel are now classified as GIST. GIST attains massive size when presenting clinically. xx Palpable mass, compression, haemorrhage are the features; has less affinity for lymphatics. xx CT is diagnostic. Histochemistry and tumour markers are needed. xx GIST can be low risk or high-risk group based on tumour size and mitotic index. xx Surgical wide resection is the treatment. xx Imatinib mesylate a KIT kinase inhibitor is used successfully. SU11248 with similar effect is also used.

Fig. 21.29: GIST of small bowel (Courtesy: Dr Chinivalar, MS, Surgeon).

5. Liposarcoma and myxoliposarcoma.

CARCINOID TUMOUR xx The term ‘Karzinoids’ was coined by Oberndarger in 1907. xx They arise from the enterochromaffin cells (Kulchitsky cells)

found in the crypts of Lieberkuhn.

xx These cells are capable of APUD (Amine precursor

uptake and decarboxylation) and can secrete vasoactive peptides. xx It commonly occurs in appendix (45%), ileum (25%) and rectum (15%). Other (15%) sites are—other parts of GIT (including pancreas and biliary tract), bronchus and testis. In the ileum it is almost always in the terminal 2 feet. xx Metastasis occurs in 3% of appendiceal carcinoid; 35% of ileum. xx 75% of carcinoids are less than 1 cm and 2% of them will spread; carcinoid of 1–2 cm shows 50% chances of spread; more than 2 cm shows 85% chances to spread. xx 75% of carcinoids are asymptomatic and found incidentally. xx It secretes amines (5 HT, 5 HIAA, 5 HTP—85%, histamine, and dopamine), tachykinins (kallikrein, substance P, neuropeptide k), peptides (chromogranins—100%, pancreatic polypeptide—40%, neurotensin, HCG α, HCG β, motilin), prostaglandins. xx 10% of cases are associated with MEN syndrome type I. xx Pathologically it is smooth, firm, yellowish submucosal nodule seen in antimesenteric border of bowel with mesenteric nodal mass having desmoplastic reaction. xx Carcinoid in appendix is usually single. But commonly it causes luminal obstruction and so presents with features of appendicitis. Common site is at tip/distal 2/3rd. xx Small bowel carcinoids are multiple in 40% cases. In 50% of cases other primary malignancy is observed like of breast and colon. xx Small bowel carcinoids (jejunoileal) < 1 cm incidence, of nodal and liver spread is 20–30%. If it is 1–2 cm, nodal spread is 60–80% and spread to liver is 20%. If it is >2 cm, nodal spread is more than 80% and spread to liver is 50%.

Man is a creation of desire; not a creation of need to this world.

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SRB's Manual of Surgery Types of Carcinoids

Investigations

1. Foregut carcinoids (Bronchial, thymic, gastro­duo­denal, pancreatic): Produce low levels of serotonin, but may secrete 5 HPT (5 hydroxy tryptophan) and ACTH. 2. Midgut carcinoids (Jejunal, ileal, appendiceal, right colic): Secretes high levels of serotonin. 3. Hindgut carcinoids (Distal colon, rectum): Rarely produce serotonin, but produce somatostatin and peptide YY. They present as submucosal nodules without ulcer. Hormonally inactive.

xx Urine shows increased 5-hydroxyindoleacetic acid (5HIAA)

Foregut carcinoids—argyrophillic (cells can be stained with metallic silver only in the presence of reducing agent) Midgut carcinoids—argentaffin (stained with metallic silver without a reducing agent) and argyrophillic both Hindgut carcinoids—do not stain with silver 

Features of small bowel carcinoids Primary tumour is usually small < 1 cm Age: Seen in 50–60 years May be multicentric in small bowel—40% May coexist with synchronous adenocarcinoma of small or large bowel (10%) ™™ Highest propensity to metastasise to liver to produce carcinoid syndrome ™™ ™™ ™™ ™™

Clinical Features xx Most often asymptomatic—an incidental finding. xx May present with abdominal pain, features of intestinal

levels (Normal value—2–8 mg/24 hours). xx 111In-octreotide scintigraphy to detect the tumour. xx CT scan is very useful for evaluation. xx I131 MIBG scan is also done. xx Plasma level of chromogranin A will be elevated in 80%

of patients. xx Provocative tests using pentagastrin, calcium or epinephrine

may be used.

xx PET scan using 1C 5 HTP and 18 F L DOPA isotopes when

fused with CT scan will give the best image; with urine 5 HIAA and serum chromogranin A, diagnosis will be accurate.

Treatment xx If it is in the tip of the appendix (tip is common), appendicec-

tomy and regular follow up with urine 5HIAA is sufficient.

xx If it is in the base of appendix or appendicular lesion

>2 cm size or terminal ileum, right hemicolec­tomy is required. xx In small bowel, if the primary tumour is 500 ml/day—usually small bowel; 50% mortality; less chance of spontaneous closure. • Moderate output—200–500 ml/day—colonic and small bowel mixed. • Low output—< 200 ml/day—colonic; mortality is 15%; more chance of spontaneous closure.

Favourable: • Site—oropharyngeal, oesophsgeal, duodenal stump, pancreaticobiliary, jejunal, colonic. • Cause—postoperative, appendicitis, diverticulitis. • Low output, absence of sepsis, transferrin level more than 200 mg/dl. • Healthy adjacent tissues with intestinal continuity, without distal obstruction. • Fistula track more than 2 cm; bowel wall defect less than 1 cm2. Unfavourable: • Site—gastric, lateral duodenal, ileal. • Cause—malignancy, inflammatory bowel disease. • High output, poor nutrition, sepsis, transferrin < 200 mg/dl. • Diseased adjacent bowel, presence of distal obstruction, large abscess, complete bowel disruption, radiation. • Track < 1 cm; bowel wall defect > 1 cm2. Track epithelialisation, presence of foreign body.

Complete disruption of anastomotic site Partial disruption Lateral fistula with distal obstruction Fistula in stricture bowel

Fistula stoma categories: Category 1: A single orifice fistula through an intact abdominal wall or healed scar with normal skin adjacent Fistula may be: Category 2: Single or multiple fistulas passing • Single through abdominal wall close to bony part or • Multiple umbilicus or surgical scar Category 3: Fistula through a small dehiscence Fistula may be: through the main wound • Simple Category 4: Fistula through a large dehiscence • Complicated—if multiple tracks, track with an abscess, communication to more through main wound or dehiscence at the bottom of wound sites or more than one viscus. Note: Fistula of duration of more than 3 months is called as chronic fistula Fistula may be: • End fistula • Lateral fistula

A Fig. 21.39: Fistula can have multiple tracks even though it is opening at one point in the skin.

B

C

Figs 21.38A to C: Multiple enterocutaneous fistulas can occur from same site or from different sites.

Factors Precipitating the Fistula Formation xx Patient factors: Anaemia, malnutrition, sepsis, hypotension, hypothermia, poor oxygen saturation, associated respiratory diseases/ failure, emergency surgeries, specific diseases like malignancy, Crohn’s, tuberculosis, adhesions. xx Technical factors: To reduce the chances of fistula formation technical care is essential like—proper mobilisation, meticulous dissection, tension free anastomosis, proper secure anastomosis, most important is proper blood supply at the bowel cut edges, care to avoid cautery injury as bowel is very sensitive to heat/cautery injury, proper prior preparation of patient and bowel.

Problems with enterocutaneous fistulas

Factors which prevents spontaneous closure of fistula

• • • •

• • • •

Skin excoriation Electrolyte imbalance Severe malnutrition Recurrent sepsis— locally and systemic like pneumonia, candida, varicella • Pellagra, osteomalacia, zinc deficiency

Distal obstruction Foreign body in the track Abscess in the track, infection Definitive disease like carcinoma, Crohn’s, tuberculosis • Epithelialisation of the track • Anaemia, hypoalbuminaemia (2.5 g/dl) • Complete disruption of anastomotic site

Management of Fistula Phase 1 xx Resuscitation and restoration of volume with crystalloids and colloids, blood transfusion to achieve haematocrit of 30%, maintenance of albumin level at 3.0 gm/dl with albumin infusion.

You cannot bring about prosperity by discouraging thrift. You cannot strengthen the weak by weakening the strong. You cannot help the poor by destroying the rich.

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SRB's Manual of Surgery xx Sepsis control with antibiotics, percutaneous drainage of abscess under guidance or open drainage. xx Skin care to prevent excoriation using Karya powder, zinc oxide cream/powder, ion exchange resins, stoma adhesive and controlled fistula drainage using sump constructed suction catheter drain system or vacuum assisted closure (VAC) system or silicone barrier or created inverted cone system. xx Reduction of output of fistula—proton-pump inhibitors, histamine antagonists, sucralfate, octreotide, infliximab (in fistula in Crohn’s patients). Long-term nasogastric aspiration should be avoided. xx Nutrition: Nutritional status should be assessed by clinical (weight, anthropometry), biochemical methods. 30 Kcalories/kg/day; 1.5 g/kg/day of protein is the basic need. Initially TPN is used. Once patient tolerates oral, enteral feeding should be started ideally. Enteral feeding (oral/gastrostomy/jejunostomy) is contraindicated in presence of distal obstruction. Enteral feeding reduces the sepsis, improves the bowel activity, caliber, thickness and ability to hold sutures. It also avoids TPN related problems.

Phase 2 xx Investigations are done to assess fistula and its causes. It is done in 7–10 days of fistula formation. xx Fistulogram using water soluble contrast, CT fistulogram to see the pathological anatomy of fistula—site, number, length, status of bowel, distal obstruction, presence of abscess cavity. xx Biochemical analysis (electrolytes, haematocrit and albumin) and renal, hepatic, respiratory, cardiac status should be assessed carefully.

Phase 3

xx Decision by observation and assessment, whether fistula will close spontaneously or not. Favorable fistulas are likely to close spontaneously but not unfavorable. xx Definitive procedure is done for fistula only after 6 weeks. Mortality and recurrence is higher if operated prior to 6 weeks due to obliterative peritonitis.  Definitive surgical procedure is lengthy, complex and team work. Optimum nutrition, proper planning, prophylactic antibiotics are needed.  Reopening should be done through a new distant often transverse incision.  Bowel refunctionalisation by freeing entire bowel from ligament of Treitz to rectum should be done to clear adhesions and obstructions and all areas of sepsis and abscesses. Sharp dissection using scissor should be done to clear adhesions. As much as possible bowel injury should be avoided; if occurs it should be closed transversely using interrupted 3 zero silk sutures.  Resection of the bowel adjacent to fistula with track is the ideal procedure with end-to-end meticulous two layered closure using interrupted 3 zero silk sutures.  When it is not possible, fistula area bypass, Roux-en-Y drainage, serosal patch technique is used. Duodenal fistula is better managed by bypass using gastrojejunostomy and vagotomy without intervening the fistula.  Proper irrigation of abdominal cavity with saline and antibiotics during procedure, omental flap around the anastomosis, various solutions to prevent repeat adhesions are also often

done. Supportive jejunostomy may be added for enteral feeding.  Abdominal wall closure is important by primary closure or by using myocutaneous flap. Mesh should not be used for closure as recurrent fistula may occur.

Phase 4 xx Treatment during recovery and healing time also should be adequate and optimum. xx Supplementing of nutrition, protein, vitamins and essential element are important. xx Physical, psychological therapy is needed.

Important Measures in Enterocutaneous Fistula Sepsis control is a absolute need in all fistulas. Sepsis is the commonest cause of death in fistulas. Prevention or treatment of abdominal compartment syndrome should be remembered. Assessing the fistula type and anatomy, nutrition, skin care, fluid and electrolyte therapy are essential. Normally 7 litres of fluid is secreted into the GIT lumen in one day; it is absorbed in distal ileum and colon. Fistula output more than 1000 ml will need TPN and is unlikely to close spontaneously. Fistula output less than 500 ml is more likely to close spontaneously. Fluid should be restricted to 1500 ml/24 hours with 1000 ml should be hypertonic content. PPI decreases gastric secretion; loperamide (4 mg qid) and codeine phosphate (60 mg qid) is useful drug to reduce the output. Octreotide 200 ug tid subcutaneously for 48 hours is shown to decrease the pancreatic and small bowel secretion. Monitoring should be done by urine output (>1 litre/day), urinary sodium more than 20 mmol/litre, serum magnesium > 0.7m mol/ litre. Proper nutrition, avoiding weight loss is important. Liver, renal functions, haematocrit should be assessed. Assessing the fistula as favorable and unfavorable is important. (on page 883). Decision for surgical intervention and timing of surgery should be judicial. Usually surgical intervention when needed is done after 12 weeks.

Surgery xx Surgery is done if fistula is not healing spontaneously or in high out or unfavourable fistula. It is resection of fistula tract with adjacent bowel and anastomosis or creation of stomas like ileostomy, gastrostomy, colostomy, depending on anatomical location of the fistula. In small bowel fistula, after excising the fistula track with its adjacent skin, entire small bowel along its length should be mobilized after adhesiolysis. Restoration of normal continuity is the goal at a later period. xx Reconstruction of the abdominal defect is also equally important. Reconstruction of the abdominal wall is done by primary closure, or compartment separation technique (Ramirez) with use of biological mesh like decellularised collagen mesh as inlay or onlay. Initial vacuum-assisted dressings, packing are other options. Recurrence of fistula after proper therapy is 15–20%. Disruption, distal obstruction, specific causes, malnutrition, old age, immunosuppression are different causes.

Chapter

22

Large Intestine CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™

Anatomy Hirschsprung’s Disease Diverticular Disease of the Colon Ulcerative Colitis Ischaemic Colitis Pseudomembranous Colitis Surgical Complications of Intestinal Amoebiasis ™™ Tumours of Colon

–– B  enign Tumours/Polyp of the Colon –– Juvenile Polyps –– Metaplastic/Hyperplastic Polyp –– Peutz-Jegher’s Polyp –– Adenoma of Colon –– Familial Adenomatous Polyp –– Gardner’s Syndrome ™™ Carcinoma Colon

™™ ™™ ™™ ™™ ™™ ™™ ™™

Angiodysplasia of Colon Ogilvie’s Syndrome Colostomy Stoma Care Stoma Appliances Faecal Fistula Preparation of Large Bowel for Surgery ™™ Surgical Pouches ™™ Barium Enema

ANATOMY xx The colon (large intestine) is 135 cm long, and is divided into caecum, ascending colon, transverse colon, descending colon and sigmoid colon. xx The wall of the colon is composed of mucosa, submucosa, innercircular muscle layer and outer longitudinal muscle layer which, in turn, is concen­trated into 3 separate longitudinal strips—taeniae coli. xx Small pockets of fat filled peritoneum—appendices epiploicae is scattered all over the colon except appendix, caecum and rectum. xx Haustra are sacculations between the taeniae. xx All the 3 above are important features of colon. xx Ileocaecal valve serves as a sphincter to prevent the back reflux to terminal ileum.

Fig. 22.1: Arterial supply and lymphatic drainage of colon.

Blood Supply

Lymphatic Drainage

xx Ileocolic, right colic, and middle colic arteries which are branches of superior mesenteric artery supply the colon from caecum to splenic flexure. xx Left colic, sigmoid, superior rectal arteries which are branches of inferior mesenteric artery supply the descending and sigmoid colon. xx The anastamotic arcade formed between the branches of superior and inferior mesenteric arteries is called ‘arc of Riolan’. xx Venous drainage occurs into superior mesenteric vein (which joins the splenic vein to form the portal vein) and inferior mesenteric vein (drains into the splenic vein).

xx Mucosa contains no lymph channels, so mucosal cancers rarely metastasize. xx Nodes are epicolic (located in the colonic wall), paracolic (located along the inner margin), intermediate (located near mesenteric vessels), principal (located near main mesenteric vessels).

Nerve Supply xx Colonic motility is under control of autonomic nervous system; parasympathetic via vagi and pelvic nerves, sympathetic via superior and inferior mesenteric ganglia.

Once you learn to quit, it becomes a habit.

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SRB's Manual of Surgery xx The effect of meal on colonic activity is termed as gastrocolic reflex.

HIRSCHSPRUNG’S DISEASE (CONGENITAL MEGACOLON) My first specimen is a colon, but a colon of such a size that it will no doubt surprise you to learn that it comes from a child only 11 months old when it died…. Only (the) rectum was not dilated, nor indeed subject to any obstruction. —Harald Hirschsprung, 1888

Fig. 22.3: Zones in Hirschsprung’s disease.

xx It is a congenital, familial condition, occurring in newborn

due to the absence of ganglion cells—Auerbach’s and Meissner’s plexus in anorectum, which may extend proximally either a part or full length of the colon. xx It always involves the anus, internal sphincter and rectum (partly or entirely). xx There is narrow, spasmodic, non-relaxing pathological segment. xx Transitional zone proximal to it contains only few ganglion cells with formation of cone. xx Still proximal to it, colon is dilated enormously with hyper­ aemia, multiple ulcers and hypertrophied circular muscle fibres. xx It is one of the causes of neonatal intestinal obstruction. xx Severe enterocolitis can occur which may be fatal. Perforation, peritonitis and septicaemia can occur. xx Often there will be a chronic course of the disease with malnutrition, abdominal distension.

Fig. 22.4: Congenital megacolon showing spasmodic aganglionic segment, coning (transitional zone), and proximal dilated normal ganglionic segment.

Types 1. Ultrashort segment HD—only anal canal and terminal rectum is aganglionic. 2. Short-segment HD—anal canal and rectum is completely involved (80%). 3. Long-segment HD—anal canal, rectum and part of the colon is involved (10%). 4. Total colonic HD—anal canal, rectum and full length of the colon is involved—10%.

Fig. 22.2: Types of Hirschsprung’s disease.

Fig. 22.5: Newborn with Hirschsprung’s disease with intestinal obstruction (Courtesy: Dr Vivek Prabhu, MCh, Mangaluru).

Large Intestine xx In children, there is passage of goat pellet like stools,

malnutrition, abdominal distention—chronic type. Constipation, with history of passing stools once in 3–4 days with straining is seen throughout the child­hood and also in adolescent period. Occasionally, condition can cause intestinal obstruction. xx 10% familial. xx Gene mutation can occur in chromosome no. 10 commonly; occasionally in chromosome no. 13. xx Rectal examination shows tight sphincter with empty rectum. Child passes lot of gas and meconium.

Diagnosis xx History of failure of passing meconium. xx Plain X-ray abdomen—shows intestinal obs­truction. Useful

in case of perforation. Fig. 22.6: Barium enema X-ray showing parts of congenital megacolon—spasmodic area, cone, proximal dilated segment.

It has got three zones: I. Distal immobile spastic segment, i.e. aganglionic zone. II. Proximal, middle transitional zone of about 1–5 cm length with less, sparse number of ganglions (cone). III. A still more proximal, hypertrophied dilated segment is actually the normal ganglionic area.

Clinical Features

xx Biopsy from all three zones to study the ganglions and

hypertrophic nerve terminals in spasmodic segment. Starting from 2 cm above the dentate line, a full thickness rectal biopsy is ideal. xx Barium enema is done to look for the extent of disease and three zones. Foley’s catheter should not be used while doing barium enema in case of Hirschsprung’s disease. xx Anorectal manometry—shows the absence of rectoanal reflex in Hirschsprung’s disease, which is diagnostic. xx Acetylcholine esterase staining shows hypertrophied nerve bundles.

Fig. 22.8: Barium enema X-ray showing features of Hirschsprung’s disease in a newborn. Fig. 22.7: Child suffering from Hirschpurung’s disease undergone initial sigmoid colostomy.

Complications ™™

Presentations: Acute, recurrent, chronic. xx It is common in males (80%). xx Its incidence is 1 in 5000 live births. xx It is common in infants and children, occasionally it occurs in adults also. xx Often it is associated with Down’s syndrome (10%). (Commonest association). xx In 90% of cases, symptoms appear in early neonatal period, i.e within three days of birth. The child fails to pass meconium. After introducing finger into the rectum, child passes toothpaste like stool, with evidence of straining. Distension of the abdomen with features of intestinal obstruction is seen.

™™ ™™ ™™ ™™

Colitis (Intramucosal gas in plain X-ray). Enterocolitis may be fulminant and fatal. Intestinal obstruction. Growth retardation. Constipation. Perforation, peritonitis, septicaemia.

Differential diagnosis ™™ ™™ ™™ ™™ ™™

Total neuronal dysplasia Acquired megacolon—rectum is loaded with stool Anorectal malformations (ARM) Hypothyroidism Meconium plug syndrome

Much wisdom often goes with fewer words.

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SRB's Manual of Surgery Treatment xx Initially, colostomy is done either transverse or transi­tional,

so to have normal bowel function. xx Nutritional supplementation. xx Once the child attains 10 kg of weight, definitive procedure is done, i.e. a. Excision of aganglionic segment (spasmodic segment). b. Maintenance of continuity by doing coloanal anastomosis. c. Closure of colostomy later. Common procedures done are: xx Modified Duhamel operation—resection of upper part of the rectum and a part of colon; anastomosis of colon to posterior part of the lower rectum and crushing the spurs to create the rectal pouch. It is technically easier and a retro-rectal pull through. New pouch is created by anterior part of the aganglionic rectum and by ganglionic proximal pulled down colon. Biopsy should be taken from proximal pulled down colon to look for evidence of ganglions. Pulled down proximal colon is sutured to full thickness posterior anal canal just above the dentate line. Spur between these two segments is crushed by Kocher’s forceps or specialized instrument to create a single pouch. xx Soave’s mucosectomy and pull through operation. xx Coloanal anastomosis after proctocolectomy. xx Total proctocolectomy with ileo-anal anastomosis in case of total colonic HD. xx Swenson’s operation—through abdomino-anal approach, aganglionic segment is resected and colo-anal anastomosis is done. xx Anorectal myectomy is found to be very useful for ultrashort segment and short-segment Hirschsprung’s disease. Mucosa in incised horizontally 1 cm proximal to mucocutaneous junction. A strip of muscularis with part of internal sphincter is excised with both muscle layers of the rectum for about 6–10 cm length. Mucosa is sutured back. Complications are abscess formation and failure.

Fig. 22.9: Modified Duhamel operation. Normal colon is brought behind the aganglionic rectum and anastomosed just above the dentate line. Complications of surgery ™™ ™™ ™™ ™™

Severe colitis Faecal fistula Stenosis Stunted growth

Acquired megacolon ™™ ™™ ™™ ™™ ™™ ™™ ™™

No contracted segment in rectum Seen in children with faulty toilet training Rectum and sigmoid colon are dilated Normal ganglions in all levels Improper bowel habit causing chronic bowel dilatation Repeated enemas, manual evacuation, toilet training, educating the parents are required Should be differentiated from Hirschsprung’s disease

DIVERTICULAR DISEASE OF THE COLON xx They are acquired herniations of colonic mucosa through

circular muscles at the points where blood vessels penetrate (points of least resistance). xx It is more commonly localised to sigmoid colon (90%) but occasionally seen in full length of the colon. Rectum is not affected. Saint’s triad (5%) ™™

Diverticulitis, hiatus hernia, gallstones

xx It is rare in Asian and African countries because of the high

fibre diet. It is common in western countries.

xx Colonic diverticulosis is usually of false type with only

mucosal herniation.

Fig. 22.10: Diverticular disease of colon.

Aetiology xx Diet—it is the main factor. Low fibre diet increases the stool

transit time, reduces the stool weight, reduces the bulkiness of stool which increases the intraluminal pressure and muscle hypertrophy. High fibre diet prevents this. xx Disease is more common in females. It is more common in aged.

Large Intestine xx It is more common in non-vegetarian than in vegetarian. xx NSAID intake by inhibiting prostaglandin synthesis may

cause diverticular disease. It is more common in individuals with steroid therapy or immunocompromised people. xx Smoking and alcohol. xx Long-standing constipation increases the stool transit time and causes diverticulosis.

Diverticula-associated Colitis (DAC) It is distinct entity herein diverticula is associated with colitis. It presents tenesmus, diarrhoea, haematochezia. There is segmental colitis.

Pathology There is hypertrophy and thickening of the muscle layer with progressive colonic narrowing and segmentation with raised intraluminal pressure causing pulsion diverticula of only mucosa adjacent to taenia in antimesenteric region. Pathology is common in sigmoid colon.

Features of Diverticular Disease

Fig. 22.11: Diagram showing the formation of diverticula. Note the difference between congenital and acquired diverticula.

Types Diverticulosis These false diverticula occur at the site where arteriole perforates the muscular wall; so they occur on the mesenteric side of the antimesenteric taenia; they do not occur on the antimesenteric border. Diverticula are common in sigmoid colon (50%), descending colon (40%), rarely in the other parts of the colon; muscular wall thickening with hypertrophy limits to sigmoid colon only. Sigmoid gets narrowed due to spasm with mucosal false diverticula adjacent to lateral taenia with raise in intraluminal pressure 90 mmHg or more. There will be muscular incoordination, segmentation, causing episodic spasmodic left iliac fossa pain—painful diverticular disease. Here luminal perforation with peridiverticulitis is not observed.

xx In western countries, 50% risk to develop diverticular disease for an individual is at the age of 60 years. Only 15% of patients with diverticulosis develop diverticulitis. 75% of patients with diverticulitis have uncomplicated course with features of only diverticulitis. 25% of patients with diverticulitis develop complications like abscess, stenosis and fistula. Abscess can be commonly pericolic and pelvic, rarely in buttock and ischiorectal fossa. xx Features of diverticulosis—fullness of abdomen, bloating, flatulence, vague discomfort. xx Features of diverticulitis—pain in left iliac fossa which is constant radiates to back and groin, tenderness, bloody stool, often massive haemorrhage, fever, rigidity and mass in left iliac fossa. Mass is usually tender, firm, resonant, non-mobile. xx Features of fistula—colovesical is the commonest type of fistula. It causes passage of gas in the urine (pneumaturia) commonly and occasionally faeces. Complications of diverticulitis ™™ ™™ ™™ ™™

Perforation with pericolic abscess or peritonitis Progressive stenosis and intestinal obstruction Profuse colonic haemorrhage (17–20%) Fistula formation (5%)—vesicocolic, vaginocolic, enterocolic, colocutaneous

Peridiverticulitis (Diverticulitis) Diverticulitis is a misnomer; actually it is perforation through the diverticula with peridiverticulitis; if extraluminal extraperitoneal perforation with only pericolic infection it is called as uncomplicated; if there is pericolic abscess or fistula or intraperitoneal perforation with peritonitis it is called as complicated. xx Uncomplicated type (75%) is—actually peridiverticulitis with extraluminal pericolic infection caused by luminal perforation into pericolic area without formation of fistula ore abscess or intraperitoneal perforation. Presentations are—pain in the left iliac fossa and left groin persistent or recurrent, fever, loose stool, tender palpable thickened colon, urinary urgency, radiating pain towards back and suprapubic region. xx Complicated type (25%) shows—abscess or fistula into urinary bladder (commonly) or small bowel (occasionally), intraluminal perforation and peritonitis, haemorrhage (it is common due to close proximity of diverticula to perforating arterioles).

Fig. 22.12: Sigmoid diverticula causing pericolic abscess as a known complication.

The eyes see only what the mind is prepared to comprehend.

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SRB's Manual of Surgery  CT scan shows thickening of muscle layer, abscess, perfora-

tion, fistula, involvement of organs like urinary bladder and associated pathology. CT scan is the ideal investigation. xx Cystoscopy and colonoscopy in case of fistula. Ureteric stenting is needed to make eventual surgery easier. Differential diagnosis Carcinoma sigmoid colon Amoebic colitis, ulcerative colitis, ischaemic colitis and Crohn’s disease ™™ Tuberculosis   Coexistence of carcinoma and diverticulitis can occur in 12% of cases ™™ ™™

Treatment Fig. 22.13: Diverticular disease causing colovesical fistula. Patient will have urine stained with faecal matter and severe urinary infection. Contrast dye study, CT scan is required. Initial colostomy as diversion is required before definitive procedure. Note:

Diverticulitis is not a precancerous condition. It may coexist with malignancy, irritable bowel syndrome, Crohn’s disease.

Hinchey’s classification of diverticulitis ™™ ™™ ™™ ™™

Stage I: Pericolic or mesenteric abscess Stage II: Walled off pelvic abscess Stage III: Generalised purulent peritonitis Stage IV: Generalised faecal peritonitis

Investigations xx Barium enema (best method to diagnose) shows ’saw-

Medical treatment High fibre diet Antibiotics Bulk purgatives Avoid constipation Regular follow-up of the progress of disease and onset of complications ™™ Abscess can be drained by CT guided aspiration or percutaneous drainage tube ™™ ™™ ™™ ™™ ™™

xx In acute stages, conservative treatment like bowel rest, antispasmodics, antibiotics are advised. xx Guided aspiration of the abscess is sufficient if abscess is small. Proper antibiotics are needed. xx Later, surgery is required. Resection of sigmoid colon and anastomosis (colorectal) is done. Indications for surgery ™™ ™™

Recurrent diverticulitis Diverticulitis with complications

teeth’ appearance. Champagne glass sign—partial filling of diverticula by barium with stercolith inside—seen in sigmoid diverticula. xx Sigmoidoscopy is useful but should not be done in acute stage. Once acute stage subsides, barium enema, sigmoidoscopy, colonoscopy can be done (To rule out associated malignancy). xx CT scan in acute phase to see pericolic abscess.

Fig. 22.14: Colonoscopic view of sigmoid diverticula.

Fig. 22.15: Resection and primary anastomosis can be done in sigmoid diverticula after proper bowel preparation electively.

Large Intestine xx If colon is loaded with faecal matter, initially a trans­verse

colostomy is done. Then resection and anastomosis; later colostomy closure is done as a staged procedure.

Fig. 22.18: Hartmann’s operation for acute diverticulitis with sepsis/ perforation/peritonitis. Here after resection proximal colon is exteriorised as end colostomy. Distal rectal stump is closed. Fig. 22.16: Resection of sigmoid colon for sigmoid diverticula with primary anastomosis and defunctioning diversion colostomy. xx In case of perforation, proximal colostomy and exteriorisation of the affected bowel with later resection and anastomosis is done as it has high mortality.

Note:

• • •

It is basically a benign condition, therefore the prognosis is good. High fibre diet is advised. Complications like perforations, fistulas are dangerous and life threatening. Right-sided diverticulum in the caecum and ascending colon is usually solitary and congenital.

Myotomy ™™ ™™ ™™

Heller’s myotomy—achalasia cardia Ramstedt’s myotomy—congenital pyloric stenosis Reilly’s myotomy—diverticulosis

ULCERATIVE COLITIS

xx It is an inflammatory condition of rectum and colon of

unknown aetiology perhaps related to stress, wes­ternized diet, autoimmune factor, familial tendency, allergic factor. xx Disease commonly starts in the rectum, spreads proximally to the colon and often into the ileum as back wash ileitis (5%).

Aetiological Factors Fig. 22.17: Resection and formation of end colostomy and mucous fistula for acute sigmoid diverticulitis. xx Occasionally, Hartmann’s procedure (combination of sigmoidectomy, end colostomy and closure of rectal stump) is better and life saving. xx Fistulas are treated by resection of the diseased bowel and closure of the fistula along with diversion procedures like colostomy, cystostomy, ureterostomy. xx In certain cases of diverticulosis, a longitudinal incision through the taenia and muscular layer without opening the mucosa is sufficient (like Heller’s/Ramstedt’s myotomy)—Reilly’s sigmoid myotomy.

xx Westernized diet, red meat; less common in vegetarians. xx Defective mucin production in the colonic mucosa and

mucosal immunological reaction. xx Autoimmune factors—cytotoxic T lymphocytes against

colonic epithelial cells and presence of anticolon antibodies. Association with HLA DR2 is observed in ulcerative colitis. DR 1501 is associated with less severe type’ DR 1502 is associated with more severe form. xx Appendicectomy and smoking protects ulcerative colitis especially from extraintestinal features and from postoperative complications. xx Familial in nature.

The best doctors in the world are—Doctor Diet, Doctor Quiet and Doctor Merryman.—Jonathan Swift

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SRB's Manual of Surgery xx Allergy to milk (cow milk) and other dietary factors. xx Excess reactive oxidative metabolism in ulcerative colitis. xx Psychological aspects, stress, lifestyle, personality disorders.

Pathology To begin with, multiple minute ulcers (pin point ulcers) occur with proctitis and colitis ↓ These ulcers extend into the deeper layer ↓ Spasm of the bowel ↓ Stricture of the colon ↓ Permanently contracted colon (pipe stem colon) ↓ In between ulcers, epithelial thickening occurs which appears like polyps ↓ Pseudopolyposis.

      

Multiple crypt abscesses Sparing of the deeper layers of the colonic wall Inflammatory pseudopolyps Multiple pinpoint ulcers Increase in substance p containing nerve fibres Lymphoid hyperplasia in mucosa and submucosa (25%) Presence of anti neutrophil cytoplasmic antibodies with a perinuclear staining pattern (86%)  Decreased goblet cell mucin xx Only in toxic megacolon (1.5–2.5%) there is acute inflammation extending to entire thickness of the colonic wall including the serosa. It is not the colon that is toxic but it is the patient who is toxic, hence the name. It is precipitated by non specific causes, during barium enema study, due to drugs like opiates, antidiarrhoeal drugs and anticholinergics. Toxic megacolon commonly affects the transverse colon which will be more than 6 cm in diameter. Left colon or entire colon also may be involved. Caecum when rarely involved; becomes more than 10 cm in diameter. Colon will be like wet blotting paper. It is prone for perforation, peritonitis which carries high mortality (25-50%). C-reactive protein will be increased. It needs emergency laparotomy with total colectomy/proctocolectomy with ileostomy. Occasionally toxic megacolon can occur in pseudomembranous colitis, amoebic colitis or typhoid colitis. xx Carcinoma in ulcerative colitis is more prevalent than in Crohn‘s disease. Factors involved are:  Extent of involvement (more in total colonic).  Duration of the disease; continuous active disease than inter-

mittent disease.  Incidence is 5% when duration is 15 years; 25% in 25 years;

35% in 30 years; 45% in 35 years; 65% in 40 years.  Incidence of developing cancer in left sided colitis is 10 years

later than universal ulcerative colitis.  Incidence of carcinoma developing in ulcerative colitis is equal

in both sexes.  Carcinoma in ulcerative colitis is commonly aggressive and

Fig. 22.19: Operated specimen showing colon with features of ulcerative colitis. xx It is a disease confined to mucosa and submucosa. xx There is no bowel wall thickening and no granuloma formation. xx There are no skip lesions. Rectum is always involved. Distal bowel is involved to begin with, then spreads proximally. Distal involvement is more severe. Entire colon including caecum and appendix may be involved. xx Only rectum involvement, as proctitis occurs in 25% cases. Such patients will have 5% risk of developing rectal cancer. In 15% cases, it is left sided ulcerative colitis presenting with severe recurrent diarrhoea. In 25% patients, total proctocolitis is the presentation. Bloody diarrhoea, malnutrition, complications like toxic megacolon, perforation (steroid may mask the features) and carcinoma are common here. xx Pseudopolyps are of inflammatory in nature. Absence of normal mucosa between these pseudopolyps is important to differentiate it from neoplastic polyps. xx Intense inflammation in the mucosa and submucosa with typical feature like:

poorly differentiated, multicentric, synchronous, infiltrative and scirrhous; half the patients will have colloid carcinoma (signet ring), more advanced at the time of presentation, dysplasia developing into cancer is common.  Ulcerative colitis with primary sclerosing cholangitis has still increased risk of developing cancer.  In ulcerative colitis, dysplasia is very important factor to transform into carcinoma. It may be mild, moderate or marked. It is often called as dysplasia associated lesion or mass (DALM).

Fig. 22.20: Multiple pseudopolyposis involving entire colon in ulcerative colitis. Disease involves only mucosa and submucosa.

Large Intestine Clinical Features Disease usually begins in rectum as proctitis later becomes left sided colitis and eventually causes severe total proctocolitis. xx More common in females (2:1), begins in 3rd decade. xx Watery diarrhoea, mucus or blood stained dis­charge per rectum. xx Colicky pain, spasms. xx Decreased appetite and loss of weight. xx Relapses and remissions at regular intervals.

•

Clinical grading of ulcerative colitis Mild

Moderate

Severe

Stool frequency

6

Pulse

< 90

90–100

>100

Haematocrit

Normal

30–40

10%

Temperature

Normal

99–100

>100

ESR

30

Albumin

Normal

3–3.5

6 cm. It has high mortality and requires emergency surgery, i.e. either colostomy or resection with ileostomy and later ileo-anal anastomosis. Here colon is like wet blotting paper. b. Chronic type (95%):  Lasts for months to years with diarrhoea, blood loss, anaemia, invalidism, abdominal discomfort and pain.  Severe malnutrition and hypoproteinaemia. Note:

• • • • • •

•

•

5 times more in these patients compared with ulcerative colitis without PSC. It causes pain abdomen, obstructive jaundice, later liver cirrhosis and failure. Total colectomy will not resolve PSC. Surveillance colonoscopy to identify transformation to carcinoma in ulcerative colitis is done as follows – Every year from 8 years after the onset of pancolitis and 15 years after the onset of left sided colitis. 10–30 random biopsies should be done. No dysplasia (less chance of carcinoma)/low grade dysplasia (10% chance)/high grade dysplasia (40% chance)/DALM (50% chance). All dysplasia types need proctocolectomy. Flow cytometry of biopsy specimens to study DNA aneuploidy or polyploidy is needed for further confirmation. 30% of high grade dysplasias show invasive carcinomas. Sacroiliitis and ankylosing spondylitis are 20 times more common in patients with ulcerative colitis and is associated with HLA B27.

Prevalence is 40–100/1,00,000. It is common before 30 years. Smoking increases Crohn’s but protects ulcerative colitis. Incidence of colonic stricture is 10% in ulcerative colitis and is due to muscular hypertrophy. Strictures are usually benign. But 60% stricture appear after 20 years; 80% of stricture occur proximal to splenic flexure; stricture causing obstruction are likely to be malignant. Perinuclear staining antinuclear cytoplasmic antibodies (pANCA) are seen in 85% of patients with ulcerative colitis and is diagnostic test to differentiate from Crohn’s. Arthritis (20%), ankylosing spondylitis (5%), erythema nodosum (15%), pyoderma gangrenosum are extraintestinal features which resolve after total colectomy. Primary sclerosing cholangitis (PSC, 5%) is common in ulcerative colitis before 40 years of age; common in males; related to HLA B8 and HLA DR3 (10 times). Malignant transformation in colon is

Investigations xx Barium enema—shows loss of haustrations, narrow

contracted colon (hose pipe colon), mucosal changes, pseudo-polyps. It is avoided in fulminant cases. xx Sigmoidoscopy and biopsy. xx Colonoscopy is also required. Due to very high incidence of malignant transformation in ulcerative colitis (10–20%), multiple biopsies should be taken from suspected areas of the colon. Risk increases with age of the patient and duration of the disease (20%).

A

B Figs 22.21A and B: Colonoscopic view of ulcerative colitis and multiple ulcers. Sigmoidoscopic grading of ulcerative colitis

0—Normal mucosa 1—Loss of vascular pattern 2—Granular, non-friable mucosa 3—Friability on rubbing 4—Spontaneous bleeding, ulcerations

xx Plain X-ray abdomen is useful in obstruction, toxic mega-

colon, perforation. xx C-reactive protein will be very high in acute phase. Differential diagnosis ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Crohn’s disease Ischaemic colitis Irritable bowel syndrome Amoebic colitis Bacillary dysentery Carcinoma colon Collageous colitis in females Infectious colitis by Clostridium difficile, Campylobacter jejuni

Hard work doesn’t guarentee success, but improves its chances.

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SRB's Manual of Surgery Differences between Crohn‘s disease and ulcerative colitis Crohn‘s disease

Ulcerative colitis

• It affects ileum and often colon but can involve any part of GIT—rectal sparing is common

• It affects rectum and colon from distal to proximal

• Full thickness—transmural disease

• It affects mucosa and submucosa—not deeper

• Skip lesions are typical

• Skip lesions are not observed

• Granulomatous lesion on histology—deep ulcers; pseudopolyps are not found

• Not a granulomatous lesion—superficial ulcers, pseudopolyps are present

• Stricture and fistula are common

• Narrowing can occur but not very common

• Anal fissure and perianal abscess are more common

• Fissure and perianal disease can occur but not as common as in Crohn’s disease

• May mimic appendicitis

• Will not mimic appendicitis

• Bleeding is not common

• Bleeding is common

• Fever is common

• Fever is uncommon

• Mass in RIF is common

• Mass is not a common feature

• Anal pathology very common • Anal pathology is rare • Discontinuous segmental asymmetrical colitis

• Continuous mucosal disease—colitis

• Toxic megacolon is rare

• Toxic megacolon is common

• Normal vascular pattern

• Distorted vascular pattern

• Fistula is very common

• Fistula is uncommon

• Recurrence is common after resection

• Total proctocolectomy cures the disease

Complications GIT ™™ Pseudopolyposis ™™ Turning into malignancy ™™ Stricture formation, commonly in recto sigmoid and anal canal—10% ™™ Toxic megacolon in transverse colon ™™ Massive haemorrhage—1% ™™ Fistula in ano—20% ™™ Perforation—10-20% Extraintestinal ™™ Severe malnutrition ™™ Liver cirrhosis (50%) ™™ Skin lesions—pyoderma, erythema nodosum ™™ Arthritis, iritis, ankylosing spondylitis—common ™™ Sclerosing cholangitis, carcinoma of bile duct

Drugs In active disease, drugs are used to induce remission. Later drugs also should be given for maintenance of remission and to prevent relapses. xx Salazopyrine/sulfasalazine splits into 5 amino-salicylic acid and sulphapyridine in colon. It is used as first line therapy. Its dose is 2–4 gm/day. It is mainly used to induce remission. It suppresses PG E1 and PG E2 to reduce the inflammation, inhibits proteolytic enzymes and also causes immunosuppression. 5 ASA is the most active ingredient. Side effects are skin rashes, bone marrow suppression, folic acid deficiency, haemolysis in glucose 6 phosphate dehydrogenase deficiency patients, temporary fertility problems in men. xx 5 ASA (Mesalamine) is also used in active disease as first line therapy. It is used with an azo bond to prevent its absorption in small bowel. Its induction of remission is same as sulfasalazine. Idiosyncrasy and temporary infertility is not present in mesalamine. Its oral dose is 2–4 gm/day. It is also used as retention enema which is better than steroid enema in left sided ulcerative colitis/proctitis. But mesalamine enema (4 gm in 100 ml saline) is costly. Enema is combined with oral mesalamine or oral steroid in acute cases. Mesalamine 500 mg suppository is also used in BID doses. Daily oral (1.6 gm) and topical 4 gm enema, twice weekly is often used for maintenance therapy. Headache, dyspepsia and myocarditis are the complications. xx Steroids are used in cases where salazopyrine fail to induce remission. It is a drug for refractory cases. Oral prednisolone 60 mg/ day tapering in 4 weeks is the dose. Intravenous hydrocortisone 100 mg 8th hourly is used in acute cases. 100 mg hydrocortisone enema/40 mg methylprednisolone enema (steroid retention enema) are used for 2 weeks in acute active diseases. Most patients with moderate to severe disease need steroid therapy. Budesonide is a newer steroid hydrocortisone analogue is also equally effective with lesser side effects and less adrenal suppression. xx Immunomodulators are used often to induce remission and for maintenance. Azathioprine and 6-mercaptopurine are used. They act at DNA level (purine ribonucleotide) and inhibit lymphocyte function (of T cells). But this action is slow. xx Cyclosporin is used in refractory, fulminant severe ulcerative colitis as a reserve drug. Dose is 4 mg/kg/day IV. xx Mebeverine HCl and Tegaserod (6 mg) are the other drugs used in ulcerative colitis. Other measures are using sucralfate, short chain fatty acids, probiotics, antidiarrhoeal drugs (diphenoxylate, loperamide, codeine), avoiding milk products, fibre, fruits. xx Antitumour necrosis factor alpha—Infliximab is also used selectively (in some studies). It is given intravenously at interval of 6 weeks. It shows 70% remission in ulcerative colitis. xx Newer drugs with a targeted delivery into the colon is used nowadays, e.g. Olsalazine (azobond); Balsalazine (4 aminobenzoyl carrier). Management of severe ulcerative colitis

Treatment

™™

General Correction of anaemia Fluid and electrolyte supplimentation Nutrition (high protein, carbohydrate, vitamin, but low fat diet), TPN ™™ Sedatives and tranquillisers ™™ Psychological counselling ™™ ™™ ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™

It is more than 6 stools per day, with cramping pain, toxicity, fever, raised ESR, anaemia, tachycardia, more than 10% weight loss, hypoalbuminaemia less than 3.5 gm% It always needs hospitalisation IV corticosteroids [hydrocortisone] 300 mg/day/oral prednisolone/5 ASA orally or as enema IV cyclosporine with azathioprine or 6 mercaptopurine Fluid and electrolyte management TPN/enteral nutrition Proper monitoring of the patient for complications Surgery

Large Intestine Indications for Surgery—30% Cases ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Intractability—commonest indication Toxic dilatation Perforation Haemorrhage Risk of malignant transformation, dysplasia (DALM) Onset at early age Chronic invalidism Progressive disease with stricture, abscess, fistulae Steroid dependency, persistent active disease Malignancy Severe extraintestinal manifestations Growth retardation in children

Toxic megacolon ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

1.5% incidence Common in transverse colon Colon is more than 6 cm in diameter Colon is like wet blotting paper Commonly seen in ulcerative colitis Can occur in bacterial colitis, pseudomembranous colitis, fulminant amoebic colitis May be precipitated by antidiarrhoeal drugs IV fluids, blood transfusion, antibiotics, steroids are also needed Can be life threatening Plain X-ray is very useful Emergency surgery, colectomy, colostomy/ileostomy may be required In olden days blow hole procedure was advocated for toxic megacolon, may be still useful in severe cases. Skin level transverse colostomy, sigmoid colostomy and a loop ileostomy is done to decompress entire small and large bowel. After many months (6–8 months) once patient recovers from acute illness, total proctocolectomy with ileal pouch anal anastomosis is done

Surgeries xx Total proctocolectomy with ileo-anal anastomosis with

pouches as reservoir (“J’, ’S’, or “W’ pouches). It is called as restorative proctocolectomy with ileal pouch anal anastomosis (IPAA). It is ideal curative procedure for ulcerative colitis. Anal sphincter complex is preserved. 30 cm ileal pouch is created either hand sewn or with stapler. Created ileal pouch reservoir is anastomosed just above the anal canal using end to end stapler. Diameter of the pouch should be twice the diameter of the ileum. Obstruction (25%), diarrhoea, pouchitis (25%), leak, sepsis, incontinence are the complications. xx Total proctocolectomy with ileostomy (perma­nent, continent Kock’s ileostomy, with one way valve is done). It is used at present only in revision surgery when needed after restorative proctocolectomy. xx Total proctocolectomy with end non continent ileostomy was the earliest operation done for ulcerative colitis. It is now reserved only for ulcerative colitis complicated with carcinoma of rectum. Ileostomy site should be marked in standing and sitting position. Stoma should be within the right rectus abdominis muscle at the summit of infraumbilical fat, away from midline incision, bony prominences and umbilicus.

Fig. 22.22: Different pouches are used after restorative proctocolectomy and during ileoanal anastomosis. Pouch acts as reservoir and reduces the frequency of stool. It avoids ileostomy with natural stool passage with continence. Pouchitis can occur with diarrhoea, blood in stool, perianal pain. Occasionally, redoing or conversion may be required. J type is commonly used. xx Total colectomy with ileorectal anastomosis. Proper follow-up at regular intervals by regular sigmoido­scopy evaluation should be done as rectum is also diseased and vulnerable for complications. It is not commonly practiced now. xx Total colectomy with rectal mucosectomy and anastomosis above the dentate line on posterior aspect is also occasionally used. Ileostomy It is usually end ileostomy. But often loop ileostomy is also done Indications: ™™ After total proctocolectomy for ulcerative colitis, total colonic Hirschsprung’s diseases, Crohn’s disease (occasionally), and total colectomy for carcinomas ™™ Loop ileostomy is done in critically ill patient with acute ileal conditions like multiple ileal perfora­tions, ileal gangrene or distal fistulas or sepsis. It is temporary ileostomy ™™ Ileostomy is placed in right iliac fossa through the right rectus muscle. ™™ Ileostomy may be temporary (loop) or permanent (end) ™™ Brooke’s classic end non continent ileostomy or Kock’s continent ileostomy (with continent intra-abdominal pouch) are used ™™ Ileum should project as a spout at least 4 cm above the skin surface, which facilitates the effluent to pass directly into the bag ™™ Ileostomy usually acts in 48 hours ™™ Ileostomy bag, ileostomy care, nutrition and electrolyte management are important ™™ Complications like prolapse, stenosis, haemorrhage, retraction can occur

Complications of Surgery for Ulcerative Colitis xx Pouchitis (20%) with pain, diarrhoea, fever, bleeding, toxicity, pouch—vaginal fistula, fecal incontinence (5%). Pouchitis disease activity scoring index is at present used which is based on clinical, endoscopic and histological inflammatory features. xx Stenosis, pelvic abscess formation. xx Leak, fistula formation. xx Problems with ileostomy—psychological trauma, skin excoriation, retraction, stenosis (25%), prolapse, bleeding, enteritis, ileal

God gives every bird its food, but he does not throw it into the nest.

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ISCHAEMIC COLITIS It occurs in splenic flexure where blood supply is precarious. Splenic flexure is the water shed area of colon, receiving blood supply from terminal branches of superior and inferior mesenteric arteries. xx Ischaemic colitis is common in females; common in aged. xx It is related to atherosclerosis, emboli, vasculitis, diabetes, chronic renal failure, autoimmune diseases, polycythaemia, haemodialysis, etc. xx Water shed point—Griffith’s point in artery of Riolan gets poor perfusion by arterial disease/low perfusion pressure/altered viscosity causing ischaemic colitis.

Types (Marston’s Classification) 1. Gangrenous type—ischaemia of full thickness colon causing peritonitis. 2. Stricture type— ischaemia of muscularis layer causing scarring. 3. Transient type—most vulnerable layer, mucosal involvement usually recovers completely.

Clinical Features xx Pain in left iliac fossa and left hypochondrium. xx Vomiting, diarrhoea. xx Passing blood in the stool. Differential diagnosis ™™ ™™ ™™ ™™

Carcinoma colon Ulcerative colitis Crohn’s disease Tuberculosis

xx CT scan shows colonic wall thickening with posterior fat shadowing. Angiography is not helpful. xx In acute stage, barium enema or contrast study or sigmoidoscopy or colonoscopy is avoided due to risk of perforation. xx In chronic stage, colonoscopy and contrast study is a must.

Treatment xx 80% of patients will recover from conservative treatment— bowel rest, fluids, antibiotics, adequate perfusion. xx Surgery is indicated in gangrene and peritonitis, stricture (15%), segmental ischaemia (20%). xx Laparotomy, resection and anastomosis (splenic flexure) is done. xx In acute phase with peritonitis (covering), diversion colostomy is needed. Colonic ischaemia Colon is the commonest site of intestinal ischaemia Most of colonic ischaemia results from small vessel occlusion or low flow ischaemia. ™™ Vascular diseases, vasculitis, diabetes, hypotension, aortic surgery with ligation of inferior mesenteric artery, aortic atherosclerosis blocking opening of IMA, OCP intake, cocaine abuse, coagulopathies, CMV, E. coli infections, long distance running—are the causes ™™ Splenic flexure is the most common site; but any segment like sigmoid colon can be involved ™™ Rectum is spared due to rich collaterals ™™ ™™

PSEUDOMEMBRANOUS COLITIS xx It is an acute diarrhoea due to toxins produced by the overgrowth of Clostridium difficile after antibiotic therapy (usually after clindamycin). xx Clostridium difficile is a Gram positive, anaerobic, spore forming bacillus. It produces toxin A (enterotoxin) and toxin B (cytotoxin, more potent). xx It is also often seen in immunocompromised patients and patients who are on cancer chemotherapy. xx Incidence is 2%. Mortality is 30%. xx Stool cytotoxin assay is highly sensitive and specific. ELISA test for toxins is also useful. xx Colonoscopy is ideal as right side involvement is more common. xx It can occur up to 6 weeks after stopping the drug. xx Diarrhoea, toxaemia, perforation, haemorrhage also can occur. xx Treatment  IV vancomycin 500 mg 8th hourly.  IV metronidazole 8th hourly.

SURGICAL COMPLICATIONS OF INTESTINAL AMOEBIASIS

Fig. 22.23: Ischaemic colitis in splenic flexure.

Investigation xx Plain X-ray reveals ‘thumb printing sign’ due to mucosal oedema and submucosal haemorrhage. Perforation is also diagnosed.

Trophozoites of Entamoeba histolytica by digesting mucosa, submucosa of rectosigmoid (75%) region commonly or ileocaecal region of the colon, causes retort shaped amoebic ulcers which exudes blood, pus and necrotic material. xx Cyst is the infective agent. It enters through faeco oral route. It forms trophozoite which multiplies and causes inflammation and flask shaped ulcers in the rectosigmoid, caecal and often in the terminal ileal region. xx It causes blood with mucus diarrhoea, toxaemia, secondary bacterial infection, fulminant colitis, perforation and peritonitis, rarely toxic megacolon, extraintestinal amoebiasis.

Large Intestine xx Amoebic liver abscess is the commonest form of extra- intestinal amoebiasis. Others are cutaneous amoebiasis, amoebic empyema, and very rarely amoebic brain abscess, amoebic pericarditis. xx Chronic amoebiasis causes vague abdominal pain, decreased appetite, intestinal colic and psychological trauma to the patient.

Complications of amoebic colitis ™™ ™™ ™™ ™™ ™™ ™™

Amoeboma—right side common Perforation in rectosigmoid/caecal region bleeding, peritonitis Stricture rectum and colon Intestinal obstruction Pericolic, paracolic, ischiorectal abscess and fistula formation Amoebic typhlitis, amoebic liver abscess

Treatment xx In acute cases, hospitalization and proper rehydra­tion is done. xx Antispasmodics to alleviate pain is given. xx Metronidazole IV or metronidazole retention enema is

given. It is very effective in both intestinal and extraintestinal amoebiasis. xx In less severe disease, tab metronidazole (400–800 mg) 3 times daily is given for 10 days or tab tinidazole 2 gm daily for 3 days. xx Diloxanide furoate is very effective in chronic amoebiasis and cyst passers. Dose is 500 mg, 3 times daily for 10 days. xx Other drugs used are—paromomycin, iodoquinol. Fig. 22.24: Amoebic ulcer is common in left side (sigmoid colon). Amoeboma can occur in caecal region where it forms granuloma in pericolic area presenting as mass abdomen. Amoebic ulcers are classically flask/retort shaped.

Presentations 1. Amoebic dysentery with diarrhoea, colicky pain, tenderness in left iliac fossa (in“ Sir Philip Manson-Bahr amoebic point’). 2. Amoebic typhlitis (inflammation of caecum) presen­tation with pain and tenderness in right iliac fossa and often also as a mass in the right iliac fossa mimicking carcinoma caecum called as amoeboma (amoebic granuloma) (1.5%). Differential diagnosis for amoeboma ™™ ™™ ™™ ™™ ™™

Appendicular mass Ileocaecal tuberculosis Carcinoma colon Retroperitoneal tumour Lymph node mass

TUMOURS OF COLON

BENIGN TUMOURS/POLYP OF THE COLON xx Polyp is a tumour/swelling arising from mucosal surface

with a pedicle/stalk. ‘Poly’ means many; ‘pous’ means foot in Greek. xx Polyp is a mass projecting into the bowel lumen beyond the surface epithelium.

Classification Inflammatory xx xx xx xx xx

Ulcerative colitis. Segmental colitis. Crohn’s disease. Diverticulitis. Dysenteric colitis.

Hyperplastic (Metaplastic) xx Also called as metaplastic mucosal polyps.

Hamartomatous 3. Acute fulminant amoebic colitis is a severe type with sloughing of colonic and rectal mucosa causing torrential bleeding, toxicity which can be life-threatening. Investigations for intestinal amoebiasis ™™ ™™ ™™ ™™

Saline wet mount of fresh stool—trophozoites in 90% cases Serology—indirect haemagglutination test PCR P/R and proctoscopy

xx Peutz-Jegher’s syndrome. xx Juvenile polyp. xx Cronkhite—Canada syndrome.

Neoplastic xx xx xx xx

Tubular—pedunculated. Villous—sessile. Tubulo—villous. FAP—familial adenomatous polyposis.

Perpetual optimism is a force multiplier.

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Hyperplastic

Hamartomatous

Neoplastic

Ulcerative colitis

(Metaplastic)

Peutz-Jegher syndrome

Adenomatous

Segmental colitis

Juvenile polyp

– Tubular

Dysenteric colitis

Cronkhite-Canada syndrome

– Tubulovillous

Crohn’s disease

– Villous

Diverticulitis

Malignant (carcinomatous)

Others xx Lipoma, haemangioma, leiomyoma.

xx It also can be solitary or multiple, sessile or pedun­culated. xx Tubular is commonly 1–2 mm sized and sessile is 3–4 mm

sized.

JUVENILE POLYPS xx Commonest polyp of colorectum in infants and children. xx Can cause intussusception, prolapse through rectum,

bleeding. xx Colonoscopic polypectomy is done. xx Not a premalignant condition.

METAPLASTIC/HYPERPLASTIC POLYP xx Metaplastic—indicates a difference in appearance from

normal mucosa. xx Very minute in size—1–2 mm. Multiple. xx Common in rectum. Also occurs in other parts of colon. It

is most common colonic polyp. xx Contains columnar epithelium, cystic dilatation, goblet cells,

and lymphocytes. xx Not a pre-malignant entity.

PEUTZ-JEGHERS POLYP xx It is common in small intestine (jejunum) but can also occur

in large intestine. xx Features are multiple, familial, hamartomatous intestinal

polyps. xx Asssociated with melanosis of the oral mucosa, lips (lower

lip) and occasionally digits (not in tongue).

xx Microscopically it contains tree like branching filaments of

Fig. 22.25: Colonoscopic view of colonic polyp. xx It has malignant potential.

Potentiality increase with:  Size, is an important factor in causing carcinoma. If size of adenoma is >2 cm—30–50% chances of developing carcinoma; 1–2 cm —10% chances of carcinoma; 7.5 ng/ml signifies poor prognosis. b. If postoperative level does not fall, it indicates either incomplete resection, or occult metastasis elsewhere. c. Increase CEA during follow-up indicates recur­rence or secondaries.

Fig. 22.41: Barium enema X-ray showing irregular filling defect in caecum—feature of carcinoma colon.

Fig. 22.42: CT scan picture showing growth in the right side colon.

Treatment

A

B

C

D

Figs 22.43A to D: (A to C) Levels of resection in growths in different portions of the colon; (D) Diagram showing extended right hemicolectomy.

Large Intestine  Left-sided stenosing type of growth can present with acute

Fig. 22.44: Ileotransverse anastomosis in case of inoperable hepatic flexure growth. Colosigmoid bypass in case of inoperable growth in splenic flexure.

Mainly Surgical xx Right-sided early growth:  Right radical hemicolec­tomy with ileo-transverse anastomosis is done. Structures removed are terminal 6 cm of ileum, caecum and appendix, ascending colon, 1/3 of transverse colon, lymph nodes (epicolic, paracolic, intermediate).  In inoperable right sided growth, ileotransverse anastomosis is done as a by-pass procedure.

Fig. 22.45: Specimen of hemicolectomy done for carcinoma caecum. Note the different parts—terminal ileum, ascending colon, hepatic flexure and omentum. xx Transverse colon growth:  An extended right hemicolectomy is the procedure done for transverse colon growth which includes division of right colic, middle colic arteries at their origin, with removal of terminal 6 cm ileum, ascending and transverse colon; anastomosing terminal ileum and proximal part of the descending colon— ileocolic.  Alternatively, in mid-transverse colon growth, transverse colon with both flexures can be removed; anastomosing cut ends of ascending and descending colon—colocolic. xx Left-sided early growth:  Left radical hemicolectomy is done, where in left ½ of transverse colon and des­cending colon is removed along with lymph nodes.

intestinal obstruction, in which case initially colostomy is done. Later, after 3–6 weeks, following proper preparation, required formal procedure is done, followed by colostomy closure after 8 weeks (3 stage operation).  Often growth in the transverse or left sided colon, which is stenosing or obstructive type, can cause closed loop obstruction because of the competent ileocaecal valve. As a result, pressure increases in the caecum eventually leading to its perforation. Perforation can also occur occasionally at the site of tumour. They need emergency intervention—caeco­stomy or colostomy, or ileostomy with resection and anastomosis. If severe peritonitis sets in, it may be life-threatening.  Left-sided colon growth with obstruction can be treated with resection of tumour, saline lavage and cleaning the rest of the colon by passing a catheter through the appendix into the caecum followed by primary anastomosis thus avoiding colostomy.  In severely obstructed sigmoid growths are often alternatively treated as tumour resection with removal of entire proximal colon and continuity is maintained with ileo sigmoid/ileorectal anastomosis. It also avoids diversion.  During exploration, presence of any synchro­nous growths has to be looked for. Now it is found that carcinoma colon can be associated with tuberculosis or lymphoma of colon. So this association is also looked for.  In acute left sided growths, trans anal self-expanding metal stents can be used instead of defunctioning colostomy.  Turnball’s ‘No touch technique’: Here the vessels are ligated at its origin, at the beginning, in order to prevent the tumour spread—due to tumour handling. xx Multiple synchronous primaries in the colon:  Total abdominal colectomy with ileorectal anastomosis is done if there are multiple primary tumours or in HNPCC. Significant chronic diarrhoea is the problem due to defective water absorption. xx Surgical treatment of liver secondaries:  In solitary liver secondary, segmental hepatic resection is useful.  In case of multiple secondaries confined to one lobe of the liver, hemihepatectomy can be tried.  Metastasectomy—it is done in one secondary/one lobe secondaries/less than 3 metastases in both lobes/without any extrahepatic spread. xx ‘A second look operation’ is most often helpful in carcinoma of colon, to resect the residual or recurrent tumours (Owen Wangensteen’s Second look surgery). xx If there are synchronous growths or growth with other area having multiple potential polyps, then total colectomy with colorectal anastomosis is done. xx Recurrent tumour should be treated by re-exploration and resection with adjuvant chemotherapy of different regime. xx Laparoscopic evaluation and resection is becoming popular. Laparoscopic assisted colonic resection is also done [Hand assisted laparoscopic surgery (HALS)]. Note:

•

Caecum and ascending colon—right radical hemicolectomy (terminal ileum to mid transverse colon); hepatic flexure and transverse colon—extended right radical hemicolectomy (terminal ileum to

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• • • • • • • • •

• • • • •

proximal descending colon); splenic flexure—extended left radical hemicolectomy (hepatic flexure to rectosigmoid); descending colon and sigmoid—left radical hemicolectomy ( splenic flexure to rectosigmoid). Minimum 5 cm margin clearance at colonic side/sides is needed; 6 cm terminal ileum clearance is sufficient in case of right sided growth. Duodenum, ureter, IVC, superior mesenteric vein should be taken care of during dissection in right hemicolectomy; spleen, stomach, tail of the pancreas should be taken care of in left hemicolectomy. It is ideal to mobilize both flexures adequately in all colonic surgeries to reduce the anastomotic tension. Bleeding at anastomotic site edges should be adequate; in emergency obstructive situation, better to do temporary covering colostomy or ileostomy to prevent anastomotic leak. On table and postoperative hypoxia and hypotension should be prevented to minimize anastomotic leak. Preoperative mechanical bowel preparation earlier once said to be important is questioned now; it was practiced in elective colonic resection using polyethylene glycol, mannitol, oral bowel antiseptics like neomycin / streptomycin / gentamicin and metronidazole. Infiltration into adjacent local structures is not a contraindication for surgical resection. At least 12 nodes should be examined during histology after resection. Blood transfusion before or during surgery for colonic cancer may alter the immunological aspect of the colonic cancer and may increase the recurrence rate and so may alter the prognosis. It is presently not very well-proved. Reason thought is—blood transfusion raises the suppressor T cells leading into immunosuppression. So autologous blood transfusion is better when in case of need. Antibiotic prophylaxis; DVT prophylaxis by crepe bandage or stockings bandage, heparin or low molecular weight heparin. Pulmonary function tests and pulmonary exercise preoperatively as well as postoperatively. Urinary catheterisation, nasogastric tube placement. Postoperative proper care with fluid, electrolyte, drain care, early mobilisation, monitoring. Complications of surgery are leak (fecal fistula), bleeding, infection like intraperitoneal/pelvic abscess, respiratory problems, DVT, wound infection, burst abdomen.

xx 5 FU infusions into the portal vein during and immediately after surgery have shown benefits in terms of outcome and recurrence. EGFR and VEGF blockers (EGFR is epithelial growth factor receptor; VEGF is vascular endothelial growth factor): xx They are used as single agent and also in combination with chemotherapy drugs in phase II and III trial. xx Drugs are monoclonal antibody, cetuximab which blocks EGFR, bevacizumab which binds VEGF. Dose of 5 FU is 400 mg/m2/day IV × 5 days once in 3-4 weeks for 6-12 months ™™ Dose of leucoverin is 20 mg/m2/day × 5 days once in 3-4 weeks for 6 months ™™ Dose of levamisole is 150 mg/day × 3 days once in 2 weeks for one year ™™ Capecitabine is given orally 1250 mg/m2 twice daily ™™

Radiotherapy (RT) xx Usually there is no role for RT as tumour is radioresistant. xx It is often used in locally advanced tumour, infiltrating the psoas major muscle or lateral abdominal wall, left sided colonic growth. xx It is also used in inoperable recurrent tumour.

Follow-up of Carcinoma Colon xx For 3 years at regular intervals, once in 3–6 months.

Adjuvant Therapy Chemotherapy Indications for chemotherapy xx Positive nodes. xx T4 lesions. xx Venous (microscopic) spread. xx Signet cell type. xx Poorly differentiated tumour/aneuploidy. xx Changes in CEA level. Postoperative chemotherapy is used commonly. Occasionally also given preoperatively. Regimes are: xx 5 fluorouracil (5 FU) with folinic acid (leucoverin/ LV) is the most commonly used regime for 6 months as monthly cycles. Folinic acid potentiates the action of 5 FU. xx Levamisole 150 mg/day for 3 days given once in 15 days for one year with intravenous 5 FU monthly for one year. xx Irinotecan/5 FU/LV—IFL regime is also used. xx Folinic acid (LV)/5 FU/oxaliplatin—FOLFOX regime is also used. It is becoming treatment of choice. xx Irinotecan/oxaliplatin—IROX regime is used in previously untreated metastatic colonic cancer. xx Capecitabine (xeloda) an oral drug which generates 5 FU at tumour tissue, shows significantly greater response than 5 FU/LV regime. xx Phase II trials are going on for capecitabine/oxaliplatin and capecitabine/irinotecan combination regimes.

Fig. 22.46: Patient has undergone left hemicolectomy earlier for sigmoid growth with a colostomy; now presenting as recurrence at colostomy site. It could be recurrence of original disease or could be new metachronous disease in the mucosa of the colostomy site. CT scan/CEA/PET scan will help to differentiate. Re-excision can be done if it is metachronous local growth. This is by: ™™ Regular CEA analysis ™™ Ultrasound abdomen ™™ Barium enema X-ray ™™ Colonoscopy Rise in CEA is a definite indicator of recurrence or secondaries In patients with raised CEA, radioisotope antibody study will show the site of recurrence or secondaries ™™ Serum alkaline phosphatase

Note:

•

Local recurrence: Incidence of local recurrence after radical resection is 15%. 85% of recurrence is detected in 2 years. It is more in colocolic

Large Intestine

• • •

and colorectal anastomosis than ileocolic. Recurrence may be—local/ locoregional/regional/metastatic. Recurrence may be—true recurrence at anastomotic site, probably mucosal; adjacent and close to anastomotic site, at the original primary tumour bed; peritoneal recurrence; recurrence in adjacent organ. It is due to implantation of spilled tumour cells during easier surgery, incomplete resection, metachronous new lesion, retrograde lymphatic spread. It is identified by CEA, CT scan, radioisotope/radioimmuno assay, colonoscopy. It is treated by curative surgery with clearance, chemotherapy, RT. Colonoscopy after 1 year to see anastomotic site, new / missed polyp/metachronous growth. Later colonoscopy is done once in 3-5 years unless there is a family history (here yearly colonoscopy is needed). CEA estimation once in 3 months for 2 years. If there is a raise any time, further screening is done for recurrent/metastatic disease by CT/MRI/PET scan.

Prognosis

xx Also called as colonic pseudo-obstruction caecum more than 10 cm in diameter. Splenic flexure and descending colon goes for functional atony. xx Severe colonic ileus occurs without any mechanical obstruction. xx Tympanic, nontender, distended abdomen and bowel sounds will be normally present—are the clinical features. Features of causative etiology may be present. xx Occurs in critically ill patients. xx Due to sacral parasympathetic nerve dysfunction. xx Commonly seen in right and transverse colon. xx Due to sacral parasympathetic malfunctioning, there is atony of descending colon causing functional obstruction. Splenic flexure will be the junction of dilated and collapsed parts of the colon wherein parasympathetic supply of vagus ends and of sacral parasympathetic begins. Increased sympathetic activity causes colonic dilatation. ™™

Depends on: xx Site—left sided tumours has got better prognosis as they present early. xx Type—colloid carcinoma has got poorer prognosis. xx Size of the tumour. xx Lymph nodes status: Number of lymph nodes involved decides the prognosis. xx Liver secondaries has poor prognosis. xx Age of the patient. xx Associated diseases like HIV. xx Stage of the tumour. xx Presence of complications, perforation, peritonitis. On the whole, it is a curable malignancy with proper surgery and adjuvant therapy. 5 year survival is: Stage I – 90%. Stage II – 75%. Stage III – 50%. Stage IV – less than 5%.

ANGIODYSPLASIA OF COLON xx It is a vascular ectasia seen commonly in right side colon. xx It is uncommon in healthy individual. xx It is commonly seen in elderly of 70 years age. It is acquired malformation of aging. xx It is not common in left side colon. It is often associated with calcified aortic stenosis; and ectasia bleeding if present, stops once aortic stenosis is corrected. xx Common cause of rectal bleed in adults and elderly. xx An acquired condition seen in caecum and ascen­ding colon due to degeneration of the mucosal and submucosal vessels of the colon. xx Diagnosis is by mesenteric angiography. Angiographic criteria in angiodysplasia—early and prolonged filling of draining veins; cluster of small arteries; visualisation of vascular tuft. xx Colonoscopic fulguration or resection is the treatment. xx Therapeutic embolisation is useful in 85% of cases.

OGILVIE’S SYNDROME xx Described by Sir William Heneage Ogilvie in 1948.

It is seen in: –– Scleroderma, SLE, dermatomyositis –– Chaga’s disease –– Myotonic dystrophy, multiple sclerosis –– Neuropathies –– Myopathies –– Hypothyroidism, diabetes mellitus –– CRF, renal transplantation –– Poisoning, sepsis, hypoxia –– Radiotherapy, orthopedic procedures –– Psychiatric disorders, drug abuse –– Retroperitoneal irritation by blood, urine, pancreatic enzymes –– Lumbar spine and pelvic trauma, shock, stroke –– Septicaemia, burns, MI –– Can be idiopathic also

xx It is often seen as reactivation of Varicella zoster infection in the enteric ganglia causing dilatation of the colon. xx Investigations:  Plain X-ray abdomen shows dilatation of colon.  Barium enema will be normal.  Careful gentle colonoscopy is useful as therapeutic also.  CT abdomen to rule out mechanical obstruction of large bowel.

Treatment xx Mainly conservative. xx Motility enhancing drugs like neostigmine and erythromycin are used. Neostigmine is given 2.5 mg IV for 3 minutes, showing response in 10 minutes in 90% of patients. But bradycardia should be watched for and atropine should be kept ready. xx Prokinetic drugs like cisapride/mosapride are used. xx Ceruletide decapeptide 0.3 µg/kg IM is used to stimulate intestinal motility. xx Ryle’s tube aspiration. xx Flatus tube insertion. It is not very useful as disease is common in proximal colon. xx Epidural anaesthesia causes sympathetic blockade relieving pseudo-obstruction. xx Colonoscopic decompression is also useful. xx Correction of electrolyte imbalance. xx Sodium enema.

Art is long, life short, judgement difficult, opportunity transient.

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stools. But it is time consuming with chance of water intoxication due to excess water absorption during irrigation.

COLOSTOMY It is an artificial opening made in the colon to the exterior (skin) to divert faeces and flatus.

Types

A

1. Temporary: Is done in conditions wherein diversion is required to facilitate healing distally in the rectum or distal colon. And this is closed once the purpose is over.   Site of temporary colostomy is usually right hypochondrium and left iliac fossa.   It can be loop colostomy or Devine’s double-barrel colostomy (wherein there is a gap between the two openings of colostomy which prevents spillage into the distal loop). 2. Permanent colostomy is always end colostomy placed in left iliac fossa, 6 cm above and medial to the anterior superior iliac spine.

B

C

D

Figs 22.47A to D: Types of colostomy. (A) Temporary colostomy; (B) Loop colostomy; (C) Devine’s double barrel colostomy; (D) Permanent colostomy.

Indications Temporary

Permanent

Congenital megacolon

AP-Resection.

Anorectal malformations

Carcinoma anal canal.

Sigmoid volvulus

After Hartmann’s operation

Perforation of left sided colon Left sided colonic growth

Fig. 22.48: Different types of stomas used in colostomy.

High anal fistula Trauma to left sided growth

Colostomy can be: xx Loop, end, double barrel. It can be: xx Diversion colostomy: It is done when there is breach in bowel wall, trauma, destruction, sphincter injuries, Crohn’s, carcinoma rectosigmoid. It is usually brought out as an end colostomy with a mucus fistula or with a Hartmann’s resection. It can be at sigmoid, descending and transverse colon.

A

xx Decompression colostomy: It is done for obstructive lesions

in rectosigmoid, toxic megacolon. Types—(1) Blow hole procedure is done as a single or multiple small stomas onto the skin to decompress colon in acutely ill patients with massively dilated or impending perforation of colon. Problems are—remaining possible ischaemic parts of the colon is not identified still risking perforation; peristomal skin complications and mucosal prolapse is common. (2) Tube caecostomy—It is technically easier without much complications; but tube getting blocked limits its use regularly. (3) Loop transverse colostomy—It serves as decompressing and diverting long stoma without getting blocked. It is done only in mobile colon. xx Irrigation colostomy: It avoids need for appliance wear; reduces the passage of uncontrolled gas with less leak of

B Figs 22.49A and B: Diagram of colostomy in a patient with colostomy bag.

Large Intestine Complications of colostomy ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Prolapse of mucosa (prolapse of distal loop mucosa is common)— commonest complication Retraction Necrosis Stenosis Herniation Bleeding Diarrhoea Enteritis Skin excoriation

skin is resected and anastomosed using silk/vicryl. Sutured bowel is placed into the peritoneal cavity. Drain is placed into the peritoneal cavity. Abdomen is closed in layers. xx Closure of colostomy is done after proper bowel preparation, under general or spinal anaesthesia. xx Proper postoperative care is important. xx Patient should perform anal sphincter exercises to prevent sphincter atrophy and to maintain sphincter tone.

Educating the patient regarding the proper usage of colostomy bags and proper care of the colostomy is very essential.

Colostomy Care  Similar to stoma care.  Initially stoma bag should be transparent as content is liquid

stool but later it can be opaque.  Regular consultation with stoma therapist.  Care of the skin.  Training for managing colostomy, its care to prevent leak,

odour, and discomfort.

Closure of Colostomy Criteria for temporary colostomy closure: xx Integrity of distal colon should be normal and adequate. xx Anorectal sphincter should be normal. xx Cause for construction of colostomy is cured completely without any suspicious of recurrence of same disease distally. xx When temporary colostomy is done, it is closed usually after 3 months. xx Two types of closure are present—extraperitoneal and intraperitoneal type. Now intraperitoneal closure is done. Earlier extraperitoneal closure was done in loop colostomy by placing a spur in between and closing the antimesentric part of the colon. It prevents the peritoneal contamination. But inadequate closure, leak, adhesions are the problems. Intraperitoneal closure—commonly advocated technique now, is done by placing a circumferential incision over the margin with skin edge. Incision is deepened to enter the peritoneum and pull out the colostomy stoma. Part adjacent to the

Fig. 22.50: Patient with colostomy bag. He has undergone abdominoperineal resection (APR) for carcinoma rectum.

A

B Figs 22.51A and B: Prolapse of colostomy is a common complication.

Fig. 22.52: Caecostomy is often done in acute colonic conditions as diversion procedure after surgery distally like perforation closure and resection. But it is not as popular as colostomy because it may not function adequately, may get displaced or blocked. But it is technically easier and usually done by doing appendicectomy and passing Malecot’s tube through appendicular stump. Removal is easier without any surgical intervention.

The most vital test of a man’s character is not how he behaves after success, but how he sustains defeat.

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SRB's Manual of Surgery STOMA CARE Definition of Stoma Stoma is an artificial opening or ‘mouth like’ to the exterior, the abdominal wall so as to drain the content from the tubular structures inside, like bowel or ureter. It is done for diversion of urine or faecal matter in case of malignancy, trauma, and sepsis or after surgery.

Types xx Ileostomy—terminal 5 cm ileum is projected out, on to the skin of abdominal wall to drain semi-liquid, faecal matter. xx Colostomy—colon at different levels, can be brought out to the skin as required as colostomy, to divert faecal matter. xx Cutaneous ureterostomy—cut ends of one or both ureters are apposed to the skin of abdominal wall. xx Ileal urinary conduit—segment of isolated ileum can be used to drain urine from the ureter as urinary ileal conduit. Ureters are anastomosed to a closed ileal conduit. Ileal stoma is brought out as stoma. Different types of continent ileostomies are in use to prevent leak, soakage and discomfort. xx Vesicostomy—it is done in children. Here anterior wall of bladder is brought out and bladder mucosa is sutured to the skin of abdominal wall. Stoma created may be round (commonly) or square in shape.

xx Dressing should be done first over the stoma and after placement of appliance, laparotomy wound is dressed otherwise stoma appliance will not sit properly. xx Patient should be observed for any complications. xx Once wound has healed patient can take bath by removing the appliances. After bath skin is dried up and stoma appliances can be fit again. xx Patient should be taught about the stoma care and its appliances. xx Care and prevention of skin excoriation due to leak is also looked into. xx Psychotherapy is given for the patient. xx Skin should be absolutely dry prior to placing the stoma appliances.

Preparation and Counselling of the Patient for Stoma xx To certain extent stoma of any type causes psychological and physical trauma to the patient, as it is nonphysiological, distressing and socially not acceptable. xx Patient should be explained about the procedure and should be convinced and consoled about the stoma. xx Detailed meaning, explanation and after care of the stoma should be discussed. xx Indication for the stoma and consent for the same should be taken. xx Reassurance about the stoma, its care, and its position should be diagrammatically explained to the patient and his close relative. xx In case of obstructive disease, stoma is done as an inevitable procedure to relieve the obstruction, often it may be temporary. xx Proper bowel preparation by bowel wash, gut irrigation is required before surgery. xx The surgeon selects the site of the stoma.  Stoma is usually sited midway between anterior superior iliac spine and umbilicus.  It should be away from the belt line.  It should be away from the scar, creases, and bony points.  Patient should be assessed for proper size, adequacy for stoma in lying down, sitting, and standing positions.  Proper stoma appliances should be decided after thorough checkup and discussion with patient and patient’s relative.  Stoma site should be marked properly before surgery.  Ileostomy is usually sited in the right iliac fossa, colostomy in left iliac fossa.  Allergy for the particular appliances should be checked for.  The patient should consult stoma therapist.

Postoperative Care for the Stoma xx Stitches are removed in 6–10 days.

Fig. 22.53: Right sided temporary loop colostomy. Note the tube kept in between.

Complications of Stoma xx Skin excoriation. xx Mucosal prolapse—common complication.

Fig. 22.54: Colostomy prolapse is the common complication. xx xx xx xx

Stenosis and block. Infection either bacterial or candidial. Diarrhoea due to irritation. Leak due to improper fitting of the appliances, scar, irregularity of stoma, prolapse.

Large Intestine xx Bleeding from the stoma edge. xx Herniation of the abdominal contents adjacent to stoma.

xx Opaque, in which fluid cannot be visualised. It is used eventually later.

Skin Excoriation

General Care and Advice to Patients with Stoma

It is a major problem in stoma patients. It is basically due to leak adjacent to appliances.

Causes for Excoriation xx xx xx xx xx xx xx xx

Leak due to improper appliances. Wet skin before placing the appliance. Inadequate stoma hole. Improper and inadequate adhesive sheet usage. Allergy. Infection like of bacteria and candida. Altered weight of the patient. Stoma bag is overfilled or kinked or air in the stoma bag.

Treatment of Excoriation xx Control of infection by antibiotics and control of moniliasis. xx Allergy has to be confirmed, and if it is the cause, the agent is found out and treated as required. xx Zinc oxide cream application. xx Change of the type of appliance. xx Refashioning of the stoma.

xx Patient can have normal diet. Diet, which regulates the bowel action, is better. Plenty of water is advisable. xx Patient can go for normal work, exercise like sports, swimming, tennis. Stoma appliances suitable for these works are available. xx Antidepressants, anticholinergics might cause constipation. So these drugs should be taken carefully. xx Using irritant solutions near stoma should be avoided. It may lead to dangerous complications. xx Patient can have normal sexual activity. xx Patient should have additional stoma bags in hand so as to use if required urgently. xx Patient should be aware of different appliances available and should be well-versed with its use. He can take the help of the stoma societies.

FAECAL FISTULA

Stoma appliances are devices, which are used to collect and dispose the effluent materials which come out of the stoma.

xx This is a dangerous entity. xx It commonly occurs after appendicectomy (gan­gre­no­ us), ileal resection, colonic surgery, malignancy, ileocaecal TB, actinomycosis and Crohn’s disease. xx It may be from the ileum or the colon. xx It may be single or multiple openings. xx More proximal the fistula, more is the severity in fluid and electrolyte imbalance. xx It may be from the main incision wound or from the drain

Ideal stoma appliance is:

xx If there is no distal obstruction, the fistula will heal sponta-

STOMA APPLIANCES

wound.

™™ ™™ ™™ ™™ ™™

Leak proof Should not damage the stoma and surrounding skin Should prevent odour Should be available Easier to use

neously, but may take a longer time. xx Fistulogram often delineates the track. xx CT fistulogram with CT scan abdomen is essential. xx Often gastrograffin study is also useful to study the fistulous

track in detail.

Types of Appliances

Factors preventing closure (FRIENDS)

It can be: xx Closed type is discarded when full and is used in patients with well-formed stool. xx Drainable type is used in patients with loose liquid stool. It can be emptied and retained and reused. Immediately after colostomy, drainable appliance is used. Later, it can be changed over to closed type. It can also be: xx One-piece stoma appliance as a bag with adhesive system attached which adheres to skin around the stoma. xx Two-piece stoma appliance has got a flange with adhesive system and a bag over it, which can be removed and replaced with a new one without disturbing the flange underneath. Bag can be: xx Transparent, in which fluid can be visualised. It is used in initial period of the stoma.

™™ ™™ ™™ ™™ ™™ ™™ ™™

F : Foreign body in fistula tract R : Radiation enteritis I : Inflammatory bowel disease E : Epithelialisation of tract N : Neoplasm D : Distal obstruction S : Sepsis

Factors preventing spontaneous closure of faecal fistulas ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

High output > 500 ml/24 hr Distal bowel obstruction Sepsis, inflammatory bowel disease Tuberculosis Cancer Radiation enteritis Foreign body in fistula tract Epithelialisation of tract

Better alone than in bad company.

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SRB's Manual of Surgery PREPARATION OF LARGE BOWEL FOR SURGERY Principle Behind Bowel Preparation Colon contains large amount of bacteria up to 109 / ml of faeces. Most common anaerobe is bacteroides; commonest aerobe is Escherichia coli; Pseudomonas, Enterococcus, Proteus, Klebsiella, Streptococcus are other organisms. Bowel preparation is done to clear this bacterial load to reduce postoperative complications.

Methods Used

Fig. 22.55: Multiple faecal fistulous openings in the abdominal wall. Patient has undergone laparotomy for acute peritonitis. Investigations for faecal fistula ™™ ™™ ™™

Fistulogram using gastrograffin CT scan and CT fistulogram Barium enema study

1. Mechanical bowel preparation  Polyethylene glycol (PEG) is a non-absorbed sodium sulphate solution, 2–3 litres of which is asked to drink by the patient along with plenty of additional fluids orally. It cleans the bowel by passing loose stool for 10–15 times in 12 hours. It acts by its hygroscopic action. Side effects are—nausea, vomiting, and abdominal cramps. Antiemetics are often needed. It is ideal in renal failure, ascites, cirrhosis, CCF.  Sodium phosphate is an alternative to PEG as smaller volume is sufficient to take. But it causes electrolyte imbalance. Its efficacy is similar to PEG. But patient compliance is better with sodium phosphate. It can cause hyponatraemia, hypocalaemia, hypocalcaemia and hypophosphataemia in case of renal dysfunction. In such patients it is contraindicated.  Other methods—(1) Total gut irrigation daily using 200 ml of oral mannitol or through nasogastric tube for 3 days prior to surgery. (2) Bowel wash daily for 3 days prior to surgery using 2 litres of normal saline (not water as it will cause water intoxication); it cleans entire large bowel. (3) Senna, castor oil, bisacodyl. (4) Repeated enemas. PEG or sodium phosphate has taken over all this methods. Contraindications for mechanical bowel preparation: Complete bowel obstruction and perforation. 2. Antibiotics—parenteral and as bowel antiseptics  Oral neomycin (gentamycin, streptomycin were used in olden days) 1 gram, erythromycin 1 gram, is used 3 days prior to surgery. Alternatively ciprofloxacillin and metronidazole are used. IV fluids should be given in addition to these patients to maintain adequate hydration.  IV antibiotics 4 hours before making incision, reduces the incidence of sepsis. Usually cephalosporins are given.

Fig. 22.56: Gastrointestinal faecal fistula after an emergency surgery for ileal perforation with severe peritonitis. Patient recovered after long-term stay in the hospital.

Treatment xx TPN and blood transfusion may be required to improve the nutritional status of the patient. xx Sepsis is controlled with proper antibiotics. xx Management of fluid and electrolyte loss. xx Skin is protected from excoriation by using zinc oxide cream. xx If it persists, later exploration and resection is done. xx The cause is treated. xx Bypass may be required. (Most of the time, the decision is, taken on table during surgery).

Controversies xx There is doubt about the advantages of preoperative mechanical bowel preparation even though it is practiced universally. xx Oral antibiotics to reduce the bacterial load in the colon is also controversial. However, preoperative single dose parenteral antibiotic improves the result and reduces the sepsis.

Indications for Large Bowel Preparation xx xx xx xx xx

Carcinoma colon (especially left sided). Anorectal malformations. Megacolon. Carcinoma rectum. Surgery for ulcerative colitis.

Large Intestine Pathological pouches

Experimental physiological pouches

Natural pouches

• Zenker’s diverticulum causing pharyngeal pouch • Physick’s pouch in the rectal wall in between rectal valves • Hartmann’s pouch is protruded pathological gallbladder infundibulum

• Heidenhein pouch: To study gastric physiology done in stomach • Pavlov pouch: Gastric pouch created with retaining vagii to study gastric physiology

• • • •

xx xx xx xx

Rathke’s pouch in pituitary Seessel’s pouch in pharynx Morrison’s hepatorenal pouch Rectouterine pouch of Douglas

Note:

FAP. Diverticulitis. High pelvirectal fistulas. Before colonoscopy.

Pouch is contraindicated in Crohn’s disease.

BARIUM ENEMA

SURGICAL POUCHES Pouches are created as reservoir whenever needed as a replacement for the existing reservoir like stomach, rectum, and urinary bladder.

Types xx Jejunal pouches: It is used for stomach. Hunt Lawrence pouch, omega loop, Roux en loop are the examples. It is commonly used after total gastrectomy. Hunt Lawrence pouch is 15 cm in length. xx Ileal pouch: It is used as rectal reservoir, urinary reservoir, ileostomy reservoir. Examples are—J, S, W, H pouches after proctocolectomy with ileo anal anastomosis; Koch’s pouch for ileostomy; Ileal pouch for bladder replacement or cutaneous ureterostomy. xx Colonic: Sigmoid reservoir or caecal/ileocaecal reservoir is often used to replace urinary bladder.

Principles xx Blood supply should be preserved. xx Mesentery should extend adequately. xx Bowel is opened on the antimesenteric border and sutured using vicryl posterior and anteriorly. xx Created pouch is anastomosed to the required area from its summit or from open end.

xx It is the contrast X-ray done to visualise large bowel. xx Therapeutic barium enema is done in intussus­ception in

children. Barium enema Indications

Finding

Carcinoma colon

Irregular filling defect

Ileocaecal tuberculosis

Pulled up caecum, obtuse ileocaecal angle Filling defect, incompetent ileocaecal valve

Ulcerative colitis

Loss of haustrations, lead pipe appearance

Colonic polyps

Smooth, regular filling defect

Congenital mega colon

Narrow zone, zone of cone, dilated proximal segment

Diaphragmatic hernia

Colonic shadow in the left thoracic cavity

Gastrojejunocolic fistula

Leak into the stomach from colon

Complications xx Obstruction (25%) is the common complication. It may be due to stomal stricture, internal hernia, volvulus and adhesions. xx Pouch disruption and leak can occur which is usually treated conservatively. xx Pelvic abscess formation in ileoanal pouch is confirmed by clinical features of fever, back pain, raised total count, CT scan. It is treated with antibiotics, drainage per abdomen or reservoir excision and ileostomy. xx Pouchitis: It is the common problem (20%). Tenesmus, bloody diarrhoea, spasm, back pain, fever, cramps, dehydration are the presentations. It is treated conservatively with antibiotics, hydration, probiotics. xx Vaginal fistula formation. xx Anal canal stricture formation. xx Faecal incontinence. xx In urinary conduits, sepsis, acidosis, electrolyte imbalance, stone formation, urine leak are the complications.

Fig. 22.57: Barium enema showing normal peristaltic movement.

Liberty means responsibility; that is why most men dread it.

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A

B

C

Figs 22.58A to C: Barium enema X-ray in different indications should be taken with complete filling, postevacuation and after air-contrast.

Procedure Laxative is given previous evening. Enema is given on same day before doing the procedure. About one litre of barium sulphate solution is infused into the colorectum per anally through enema tube. In children 12F Foley’s catheter is used. Once complete filling occurs, X-ray is taken. Patient is asked to evacuate the

barium and postevacuation film is taken. After that, air is inflated into the colon which gives a better contrast to visualise thin mucosa of the colon (air-contrast barium enema).

Contraindications Acute colonic conditions.

Chapter

23

Intestinal Obstruction CHAPTER OUTLINE ™™ ™™ ™™ ™™

Intestinal Obstruction Dynamic Obstruction Duodenal Atresia Small Intestine Atresia

™™ ™™ ™™ ™™

Malrotation Meconium Ileus Intussusception Volvulus

INTESTINAL OBSTRUCTION: TYPES Classification I: Depending on Aetiopathology A. Dynamic. B. Adynamic.

™™ ™™ ™™ ™™

Sigmoid Volvulus Paralytic Ileus Adhesions and Bands Internal Hernias

Classification II: Depending on Type of Obstruction 1. Acute: Common in small bowel. 2. Chronic. 3. Acute on chronic: Common in large bowel. 4. Closed loop obstruction.

Dynamic

Adynamic

Outside the wall

In the wall

In the lumen

Hernia—25% Adhesions—40% Volvulus Intussusception

Tuberculous stricture Crohn’s disease Malignancy

Gallstones Roundworm Inspissated faeces Meconium ileus

Cessation of peristalsis Postoperative period Electrolyte imbalance Spinal injuries Uraemia Diabetes mellitus Retroperitoneal—haematomas and surgeries Renal surgeries Mesenteric ischaemia Pseudo-obstruction

Classification III: Depending on Site of Obstruction Proximal small bowel

Distal small bowel

Large bowel

Site of obstruction

Duodenum and jejunum

Ileum

Anywhere in large intestine

Causes:

Congenital Lipomas Leiomyomas Malignancy Bands and adhesions

Tuberculosis strictures Malignancy Crohn’s Gallstones Hernias—common cause Roundworm Congenital

Malignancy Tuberculosis stricture Anorectal malformation Volvulus Congenital megacolon Bands Contd...

Today’s friction is tomorrow’s destruction.

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Clinical features:

Proximal small bowel

Distal small bowel

Large bowel

Severe vomiting, dehydration, no or less distension, colicky pain

Central distension, vomiting, dehydration Central abdominal pain

Constipation, distension— early; Late vomiting less pain

Valvulae conniventes

Characterless Central fluid level

Dilatation and haustration

Special features: Plain X-ray

Classification IV

DYNAMIC OBSTRUCTION

A. Congenital. B. Acquired.

xx It is mechanical blockage of normal propulsion and passage

of intestinal contents. xx Obstruction may be external/internal; partial (incomplete

Congenital

Acquired

Anorectal malformations

Hernia (commonest)

Congenital megacolon

Postoperative

Adhesions

Intussusception

Duodenal atresia

Roundworm

Intestinal atresia (ileal)

Gallstones

Bands and adhesions

Tuberculosis

Malrotation

Malignancy

Volvulus neonatorum

Internal hernias

Bolus obstruction ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Worms Gallstones Trichobezoars Phytobezoars Meconium pellets Foreign body Food bolus Stercoliths

or subacute)/complete; acute/acute on chronic/or chronic; simple/closed loop/strangulation; congenital/acquired; proximal/distal. xx Earlier, hernia was the commonest cause of intestinal obstruction. Now adhesions (40%) are the commonest cause especially in developed countries and hernia being 15–25% common. In developing countries both adhesions and hernia are the common causes of intestinal obstruction. xx Adhesions commonly cause small bowel obstruction than large bowel. xx Eighty per cent of intestinal obstruction occurs in small bowel; 20% in colon. 70% of colonic obstruction is due to malignancy. Other 30% is due to volvulus; diverticulitis, inflammatory cause like tuberculosis, etc. xx Mortality is 3% in obstruction without strangulation; 30% in obstruction with strangulation. xx Recurrent obstruction is more common in adhesions.

Pathology and Pathogenesis xx Changes proximal to the bowel obstruction:

Intestinal obstruction still is a challenging, commonly acute condition in surgical practice. Adhesions are becoming the more common cause of intestinal obstruction than hernia nowadays. Common causes for adhesions are gynaecologic surgeries, appendicectomy, colonic and pelvic surgeries. 20% cases of intestinal obstruction are due to malignancy or its peritoneal carcinomatosis spread. More than 50% of intestinal obstruction in Western countries are due to adhesions; 20% due to malignancies; 10–15% due to hernias. Crohn’s disease is also becoming a common cause of obstruction. Note:

• • • •

Adhesions and hernias are most common causes of intestinal obstruction Depending on degree of block intestinal obstruction can be complete, partial or partial circumferential. Subacute obstruction implies incomplete obstruction. Depending on the vascular compromise it can be – simple obstruction with intact blood supply or strangulated with compromised blood supply. 80% of intestinal obstruction is in small bowel; 80% of small bowel obstructions are due to benign cause. 70-80% of large intestine obstruction is due to malignancy, others being volvulus and tuberculosis.

Fig. 23.1: Step ladder peristalsis with visible dilated bowel loop in intestinal obstruction due to adhesions – post-laparotomy patient.

Intestinal Obstruction Intestinal obstruction ↓ Increased peristalsis ↓ Becomes vigorous ↓ Obstruction not relieved ↓ Peristalsis ceases ↓ Flaccid, paralysed, dilated bowel  Fluid collects just proximal to the obstruction which is derived

from saliva, stomach, pancreas and intestine. Because of oedema and inflammation absorption decreases, sequestration of fluid from the circulation into the lumen occurs and bacteria (E. coli, Klebsiella, anaerobes, bacteroides and other organisms) multiply, toxins are released—toxaemia occurs. This leads to severe dehydration, electrolyte imbalance.

 Defective absorption, decreased fluid intake, loss of fluid by



 

 





vomiting, sequestration of fluid into the bowel lumen—leads into severe dehydration, fluid and electrolyte imbalance. Inflammatory response in the bowel wall (intramural inflammation) causes accumulation of activated neutrophils and macrophages in the muscle wall which release reactive enzymes and cytokines. These substances damage secretory and motor process of muscle leading into dilatation of the bowel. Increased release of nitric oxide in muscle wall and production of intramural reactive oxygen metabolites alter gut motility and permeability. Intestinal wall hypoxia is also the cause for dilatation. In first 12 hours of obstruction, there is only decreased absorption which causes accumulation of fluid and electrolytes in the lumen. After 12 hours, there is also increased intestinal secretion causing further accumulation of the fluid. Accumulation of bacterial toxins, bile salts, prostaglandins, and mucosa-derived free radicals, VIP—all increase the luminal secretion of fluid in obstructed bowel. Dilatation of bowel wall increases intraluminal pressure which exceeds the bowel wall venous pressure causing ischaemia which causes further dilatation and ischaemic injury. This leads into eventual blockage of arterial perfusion causing bowel wall necrosis/gangrene. Increased bacterial colony in the bowel (Normal flora is less than 106 colonies/ml in jejunum and 108 colonies /ml in the ileum) due to altered luminal content and environment → multiplication → toxins → further mucosa damage → disrupted mucosal defense/barrier/integrity → translocation of bacteria across mucosa into submucosa and also absorption of bacterial and other toxins into the circulation → bacteraemia/toxaemia/ septicaemia/SIRS/MODS.

Fig. 23.2: Intestinal obstruction due to band. Note the ischaemic bowel under the band.

Fig. 23.4: Multiple strictures in the small bowel with dilated bowel – intestinal obstruction probably due to tuberculosis.

Fig. 23.3: Postoperative internal hernia with obstruction.  Proximal to the collected fluid, air accumulates (derived from

swallowed air (70%), diffusion from blood into the lumen (20%), from digested product and bacterial action (10%)), in which, main component is nitrogen (90%) and also hydrogen sulphide. During vigorous peristalsis, air enters the distal fluid, results in churning, is the reason to cause multiple air-fluid levels in plain X-ray abdomen.

Factors causing systemic problems in intestinal obstruction ™™ ™™ ™™ ™™ ™™ ™™ ™™

Dilatation of the bowel Decreased absorption across mucosa Increased secretion into the lumen Intramural inflammation and hypoxia Increased intraluminal pressure Venous congestion and increased venous pressure Disrupted mucosal barrier → bacterial translocation

The coexistence of intestinal colic and borborygmi, establishes the diagnosis of obstruction of the small intestine in more than 9 out of 10 cases. —Clarence Dennis

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SRB's Manual of Surgery  Perforation also can occur at the site of obstruction due

xx Changes at the site of the obstruction:

to the malignant growth.

Initially venous return is impaired ↓ Congestion, oedema of bowel wall occurs which turns purple. ↓ Later this jeopardizes the arterial supply. ↓ Loss of shineness, blackish discolouration, loss of peristalsis. ↓ Gangrene. ↓ Perforation occurs. ↓ Bacteria and toxins migrate into the peritoneum. ↓ Peritonitis. A

B

Figs 23.6A and B: (A) Closed loop obstruction. Here loop of the bowel is obstructed at its point of entry and exit creating closed loop; (B) Closed loop obstruction of ileo-caecal region.  Closed loop obstruction also can occur when bowel get

obstructed at both proximal and distal parts of the loop of the bowel. It can occur in external or internal hernias, volvulus, etc. Necrosis and perforation are both common at obstructed site and over the convex summit of the bowel content. xx Bowel distal to the obstruction is inactive and collapsed. Changes in intestinal obstruction Fig. 23.5: Gangrenous bowel with proximal dilated and distal collapsed bowel segments. Note:

• • • • •

Causes for strangulations are—external like hernia (by constriction ring of the sac), adhesions, bands; compression in the wall causing mechanical block and compromised blood supply like in volvulus, intussusception; increased intraluminal pressure like closed loop obstruction; mesenteric ischaemia. Morbidity, poor outcome and mortality are more common in intraperitoneal strangulation than in strangulation of hernia as it is localised with less fluid loss. Outcome also depends on age of the patient, extent of the disease and time at which patient reaches for therapy. Massive 3rd space fluid loss, dehydration, hypovolaemia, hypotension, hypochloraemia, hypokalaemia, metabolic alkalosis, oliguria, azotemia, haemoconcentration (after fluid therapy haematocrit falls indicating the need for blood transfusion). Translocation of bacteria across oedematous small bowel wall causes septicaemia.

xx Closed loop obstruction:

Proximal to obstruction ™™ Distension of bowel – –– By gas due to swallowed air (70%), from blood in the lumen (20%), from bacterial action and digestion (10%); mainly N2 and H2S. –– Due to fluid mainly of digestive juices which normally get absorbed, but in obstruction absorption ceases and accumulated fluid causes bowel distension (1500 ml saliva, 2000 ml gastric juice, 1000 ml bile, 1500 ml pancreatic juice and 3000 ml from small intestine [succus entericus]); often oedematous bowel wall further secretes more fluid into the lumen aggravating the distension. This fluid is toxic with high bacterial load. ™™ Peristalsis initially increases (borborygmi) to overcome obstruction; but later fatigue develops and peristalsis ceases. Distal to the obstruction – bowel initially empties the content and become collapsed and contracted remaining silent. At the level obstruction depends on cause strangulation, perforation, peritonitis can occur. Systemic features – Toxaemia, septicaemia, renal failure, ARDS, SIRS, MODS can occur.

 When there is obstruction in the large bowel, with ileocaecal

valve competence (40%), pressure increases in the caecum. ↓ Stercoral ulcer in the caecum. ↓ Gangrene. ↓ Perforation. ↓ Peritonitis (Faecal).

Clinical Features xx Abdominal pain:  Initially colicky and intermittent: later continuous and

severe.

 Pain is the first symptom to develop which is sudden and

severe. Initial colicky pain suggests obstruction and eventual diffuse persistent pain suggests strangulation. Pain begins usually around umbilicus in small bowel obstruction.

Intestinal Obstruction  In case of strangulated hernia, a swelling which is

Fig. 23.7: Step ladder peristalsis seen in small bowel obstruction. Note the previous laparotomy scar signifies obstruction is due to adhesions. Laparoscopy and proceed—is the needed management.  In small bowel obstruction, it is crampy, recurrent

paroxysms occurring as short crescendo/decrescendo episodes (of 30 seconds).  In large bowel obstruction, it is of longer episodes of minutes (In paralytic/adynamic ileus, pain is diffuse and mild). xx Vomiting:  In jejunal obstruction, it is early and persistent.  In ileal obstruction, it is recurrent occurring at an interval; initially bilious later faeculent.  In large bowel obstruction, vomiting is a late feature. xx Distension:  It is absent or minimal in case of jejunal obstruction  Obvious with visible intestinal peristalsis (VIP) and borborygmi sounds in case of ileal obstruction—Step ladder peristalsis.  It is enormous in case of large bowel obstruction. xx Constipation:  It is absolute, i.e. neither faeces nor flatus is passed. Exceptions ™™ ™™ ™™ ™™

Richter’s hernia obstruction Gallstone obstruction Mesenteric vascular occlusion Intestinal obstruction with a pelvic abscess

tense, tender, rigid, irreducible, no expansile impulse on coughing and history of recent increase in size is seen. xx Temperature:  Fever signifies inflammation in the bowel wall/ ischaemia/perforation.  Hypothermia can occur when septicaemia develops due to lack of pyrogenic response. It suggests poor prognosis. xx Bowel sounds: They are increased—high-pitched metallic (rushes and groans) sounds followed by metallic tinkling sounds of dilated bowel. Eventually once fatigue occurs or gangrene develops, bowel sounds are not heard—silent abdomen of peritonitis develops (in paralytic ileus, there are only continuous metallic sounds of dilated bowel). xx Per-rectal examination:  Shows empty, dilated rectum, often with tenderness. If rectal growth is the cause for obstruction, it may be palpable. Cardinal features of intestinal obstruction Colicky abdominal pain; vomiting; distension; constipation later. In high jejunal obstruction—no distension (scaphoid abdomen), severe bilious vomiting, no peristalsis, without constipation initially. In ileal obstruction—central moderate distension, bilious and faeculent vomiting, intermittent crescendo colicky pain, step ladder peristalsis, constipation at a later period. In low/colonic obstruction—variable colicky pain, right to left peristalsis, marked enormous distension, constipation to begin with, late feculent vomiting.

Investigations xx Plain X-ray abdomen: (initially supine abdominal X-ray is taken; later if needed, X-ray in erect posture is taken if perforation is suspected).  Multiple air-fluid levels.  Proximal the obstruction → Lesser the air fluid level.  Distal the obstruction → More the air fluid level.

xx Dehydration:

 Leads to oliguria → renal failure.

xx Features of toxaemia and septicaemia:  Tachycardia, tachypnoea, fever, sunken eyes, cold

periphery. xx Abdominal tenderness:  It is initially localised but later becomes diffuse—is a

feature of intestinal obstruction. Rebound tenderness and guarding will not be present in simple obstructions which are features of strangulation. xx Features of strangulation:  Continuous severe pain, shock, tenderness, rebound tenderness (Blumberg’s sign).  Guarding and rigidity, absence of bowel sounds.

Fig. 23.8: Plain X-ray abdomen in erect posture showing dilated bowel and colon—a feature of intestinal obstruction.

Never insult an alligator unless and until you have crossed the river.

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SRB's Manual of Surgery xx CT scan is very reliable investigation for intestinal obstruc-

tion. It has got 93% sensitivity; 94% accuracy and 100% specificity. In CT scan, small bowel loop >2.5 cm suggests dilatation. It can show dilated loop, transition zone and collapsed part which are definitive features of intestinal obstruction. It can also give idea of changes in the bowel wall, ischaemia, strangulation, mesenteric oedema and thickening. It also shows bowel wall gas, portal venous gas and mass lesion.

Fig. 23.9: Plain X-ray abdomen showing multiple air fluid levels due to bowel obstruction.

xx Barium (micro bar solution) enema or gastrografin contrast enema X-ray is useful in intussusception. [Barium meal is usually contraindicated in acute intestinal obstruction. However dilute (micro bar) barium meal/gastrografin meal follow through X-ray may be done with caution in suspected subacute/partial intestinal obstruction under fluoroscopy, otherwise it may precipitate complete obstruction or may cause perforation and barium peritonitis which is very dangerous]. xx Haematocrit, blood urea and serum creatinine; arterial blood gas analysis (acidosis is common), LFT, platelet count (in severe sepsis, there will be altered LFT with thrombocytopenia). xx Serum electrolytes estimation. Hypokalaemia is common. xx Total count is increased. But can be significantly low in severe stage of sepsis. xx Estimation of serum D lactate, CPK-BB isoenzyme, intestinal fatty acid binding proteins are different investigations may be useful to predict bowel ischaemia/gangrene. xx US abdomen is useful to see dilated bowel and fluid in the peritoneal cavity. It is better than X-ray but not as good as CT scan. It has got 95% sensitivity; 80% specificity; 80% accuracy. Doppler US is useful in detecting strangulation. xx Basic electrical rhythm of small bowel will be changed in ischaemia. It can be determined by noninvasive method using superconducting quantum interference device (SQUID).

Fig. 23.10: Plain X-ray showing valvulae conniventes with intestinal obstruction.

Normally, three fluid levels can be seen in plain X-ray film—at fundus of stomach, at duodenum and often at caecum.  Jejunum shows concertina effect due to valvulae conniventes (Herring bone pattern)—by the valves of Kerckring.  Ileum is smooth and characterless (by Wangen­steen).  Large bowel shows haustration.  Pneumobilia (gas in biliary tree) may be due to gall- stone ileus.  Distended caecum is shown as round gas shadow in the right iliac fossa. Dilated caecum signifies large bowel obstruction.  Small bowel >3 cm diameter; proximal large bowel >9 cm; transverse colon >5.5 cm; sigmoid colon >5 cm are suggestive of intestinal dilatation. But this increased diameter need not suggest intestinal obstruction everytime. Triad of small bowel obstruction in plain X-ray 1. Dilated small bowel loops > 3 cm 2. Multiple air fluid levels in erect X-ray 3. Paucity of air in the colon

Fig. 23.11: CT abdomen showing dilated bowel loop; CT is ideal investigation for intestinal obstruction.

Complications of intestinal obstruction ™™ ™™ ™™ ™™ ™™ ™™

Peritonitis Hypovolaemic and septic shock Renal failure ARDS Intra-abdominal abscess formation Moribund status

Intestinal Obstruction  Warm-saline soaked mop is placed over the doubtful area with

Differential diagnosis ™™ ™™ ™™

Paralytic obstruction Pseudo-obstruction Ascites

Treatment xx Nasogastric aspiration: To reduce toxic effects, to reduce

bowel distension which indirectly improves pulmonary ventilation and to reduce possibility of aspiration pneumonia. xx Replacement of fluid and electrolytes. xx Antibiotics: Ampicillin, gentamicin, metronidazole, cephalosporins. xx Blood transfusion: FFP or platelet transfusions are often needed in critical patient. xx ICU critical care: Systemic management of complications like ARDS, DIC, SIRS are important. If there is hypotension, dopamine/dobutamine are also needed. xx CVP for fluid and monitoring: PCWP (pulmonary capillary wedge pressure) monitoring are often needed in haemodynamically unstable patient. xx Surgery:

100% oxygen inhalation for 20 minutes; if colour becomes normal with peristalsis then bowel is viable.  On table Doppler study may be useful.  Fluorescein fluorescence study may be helpful on table to check the viability. 1000 mg of fluorescein is injected into the peripheral vein and bowel is inspected under Wood’s UV light; nonviable loops are identified which requires resection and anastomosis.  If bowel is not viable, resection and anastomosis is done. A

good peritoneal wash is given and the abdominal cavity is drained.

 Immediate laparotomy is done and the site (by finding the junc-

tion of dilated proximal and collapsed distal bowel) and cause of the obstruction is identified. The obstruction is relieved. To check for viability of bowel, look for: ™™ ™™ ™™ ™™ ™™ ™™

Peristalsis Pulsations Bleeding in mesentery and bowel wall Friability—friable, flabby muscle is seen in ischaemia Colour (black/pink)—dull and lusterless serosa is seen in ischaemia Serosal shining

Fig. 23.12: Bowel resection and anastomosis for gangrene in case of intestinal obstruction. Cheatle’s cut on the antimesenteric margin of the collapsed distal segment is often needed to avoid discrepancy in luminal width. Single layer interrupted (silk/vicryl) or two layered continuous sutures can be used. Single layer is better in acute conditions.

Fig. 23.13: Gangrenous bowel-resected specimen in a case of mesenteric ischaemia.

 Abdomen is closed in layers using nonabsorbable sutures

(polyethylene, polypropylene, nylon). Often tension sutures are required.  Small bowel can be decompressed using Savage’s decompressor.  In case of right-sided colonic obstruction, right hemicolectomy with ileocolic anastomosis is done.

Fig. 23.14: Colonic obstruction due to stricture/growth in the transverse colon; right hemicolectomy is done.

An unspoken word never does harm.

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SRB's Manual of Surgery  In case of left-sided colonic obstruction, left hemicolec­tomy



 



(resection) and colo-colic anastomosis is done with a defunctioning colostomy (right-sided transverse) which is closed after 6 weeks. Obstruction due to rectosigmoid growth with patient being severely ill—Hartmann’s operation can be done to save the life of the patient wherein distal stump after removal of the growth is closed, proximal colon is brought out as end colostomy. Second look operation may be needed in doubtful cases or multiple segment obstructions in 24–48 hours to confirm viability. Laparoscopic approach may be useful in partial obstruction, proximal obstruction, obstruction due to band. Conversion when needed, should be done without hesitation. Acute postoperative obstruction is difficult to identify and manage. CT is very useful. Initially it is treated conservatively (90%), but suspected ischaemic cases or persistent obstruction becomes an indication for surgery. Resection with exteriorization may be the choice. Postsurgery complications

™™ ™™ ™™ ™™ ™™ ™™

Pelvic abscess Subphrenic abscess Biliary or faecal fistulas Burst abdomen Bands and adhesions Incisional hernias.

DUODENAL ATRESIA xx It is the commonest site of intestinal atresia. xx It is usually a complete stenosis of the second part of

duodenum at the level of ampulla of Vater. xx It is defective fusion of foregut and midgut with failure of

recanalisation. xx Incidence is 1 in 10,000 live births.

Types

Type 1: Duodenal complete atresia: It is the commonest type (50%). It is usually complete separation with intact wall. In 25% cases, complete separation with wall also occurs. ™™ Type 2: Fibrous cord. ™™ Type 3: Incomplete or partial obstruction. It can be stenosis or web with an aperture. ™™

xx Duodenal diaphragm/web can present as complete; incom-

plete with a fenestra; incomplete diaphragm with central aperture which causes ‘windsock’ deformity due to proximal dilatation. Here actual diaphragm will be proximal to the site of obstruction. xx Duodenal atresia may be preampullary (nonbilious vomiting) or postampullary (bilious vomiting). Postampullary is common (80–90%).

Associations xx Duodenal stenosis is often associated with annular pancreas. xx It can be isolated duodenal atresia or in association with Down’s syndrome (30%)/incomplete rotation of gut (20%)/congenital heart diseases (30%)/trisomy (30%)/anorectal malformations (10%), etc. xx It is commonly associated with maternal polyhydramnios (50%). Antenatal US can confirm it. 50% infants are premature.

Features xx xx xx xx xx

Jaundice. Bilious/nonbilious vomiting immediately after birth. Features of gastric outlet obstruction. Dehydration. Electrolyte changes are common. Growth retardation of newborn due to deprived nutrition (by swallowed amniotic fluid in fetus).

Investigations xx Plain X-ray shows classic double-bubble sign with absence of air in the distal part.

Fig. 23.16: Double-bubble sign in duodenal atresia. Fig. 23.15: Types of duodenal atresia—complete; fibrous cord; duodenal stenosis and windsock deformity.

xx In partial obstruction, air may be present in distal loop and so contrast study has to be done. Risk of aspiration in newborn infant should be remembered.

Intestinal Obstruction xx US will show distended stomach and proximal duodenum, rail road track duodenum and features of associated anomalies. Maternal and fetal ultrasound in pregnancy may identify the pathology and also maternal polyhydramnios.

Treatment xx Proper preoperative preparation like correction of fluid and electrolytes; gastric decompression; TPN; injection vitamin K; evaluation for associated anomalies. xx Duodenoduodenostomy is done. Associated malrotation should be corrected in these patients (Ladd’s operation). Side-side duodenoduodenostomy may cause dilated duodenum (megaduodenum—30%); anastomotic dysfunction; and delayed transit of the content. xx Kimura’s diamond-shaped anastomosis between transversely opened proximal pouch and longitudinally opened distal pouch reduces the problems of anastomosis. Presence of bile in the duodenum and proximal and distal patency should be confirmed by saline irrigation. xx Transanastomotic nasojejunal or gastrostomy tube for feeding purpose is needed as prolonged postoperative ileus is the usual problem.

Fig. 23.18: Typical intestinal atresia. Griesfield modification of martin’s classification of intestinal atresia Type I: Membranous/mucosal with normal mesentery— 20%. Type II: The lumen is atretic—fibrous cord between proximal and distal parts of the segment involved (only one atretic segment) but mesentery is normal—40%. ™™ Type III (a): Atresia with complete separation of proximal and distal ends and V-shaped defect of mesentery—35%. ™™ Type III (b): Atresia with Christmas tree-shaped defect in mesentery with distal bowel being supplied by single artery—right colic/ileocolic/superior mesenteric—apple peel atresia. ™™ Type IV: Multiple atresias—5%. ™™ ™™

Fig. 23.17: Duodenoduodenostomy is ideal in duodenal atresia. Kimura’s modification has got lesser chance of developing side effects like gastroparesis. Note:

•

Duodenojejunostomy may cause blind loop problems. Gastrojejunostomy should not be done due to high incidence of marginal ulceration and bleeding.

SMALL INTESTINE ATRESIA (INTESTINAL ATRESIA) xx It is jejunoileal atresia. xx It is due to intrauterine mesenteric vascular accidents (occlusion) of the segments affected. V-shaped mesentery; presence of bile pigments in the distal segments suggesting earlier period of patency—are supportive for the above theory. xx It is often associated with malrotation, gastroschisis, volvulus— 20%. xx Common site is proximal jejunum; next common is distal ileum. xx Maternal polyhydramnios occurs in 35% of jejunal atresia. xx Proximal bowel wall is dilated with hypertrophy but villi are normal. Distal bowel is collapsed but with hypertrophied villi. Narrow collapsed large intestine (microcolon) is seen in proximal atresia.

Fig. 23.19: Types of intestinal atresia.

If the hand is kept flat upon the abdomen the underlying coil may be felt to harden and soften alternately much like in a pregnant uterus, in a case of intestinal obstruction. — Arthur H Burgess

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SRB's Manual of Surgery Clinical Features xx Equal in both sexes. xx Commonly infant is of low birth weight. xx Bilious vomiting with features of intestinal obstruction like

distension. xx Features of associated anomalies. xx Respiratory distress. xx Jaundice.

Investigations xx Plain X-ray abdomen shows—triple-bubble appearance in

Stages of normal rotation of midgut Stage 1: In 4th-8th week of intrauterine period, midgut supplied by superior mesenteric artery (SMA) grows rapidly. As coelomic cavity cannot accommodate growing midgut during that period, it protrudes into the umbilical cord as physiological hernia. ™™ Stage 2: In 10th-12th week, midgut migrates into coelomic cavity. First, small bowel returns towards the left side of the abdomen. Then caecocolic loop returns to left lower abdomen. It rapidly rotates 270° counterclockwise to reach right iliac fossa. Then duodenojejunal segment rotates 270° counterclockwise to reach left of SMA and behind the colon. ™™ Stage 3: Fusion of different parts of mesentery and posterior peritoneum. ™™

jejunal atresia; multiple air fluid levels in ileal atresia.

xx Barium enema may show narrow microcolon. Calcification

suggests antenatal fetal bowel perforation. xx US abdomen to confirm associated anomalies.

Differential Diagnosis xx Other causes of neonatal intestinal obstruction like duodenal

atresia, malrotation, volvulus of midgut.

Fig. 23.20: X-ray abdomen of a patient with intestinal obstruction in a newborn as neonatal intestinal obstruction.

Treatment xx Resection and anastomosis is the choice of therapy. xx Treatment of associated anomalies. xx Tapering proximal jejunoplasty is done if extensive length

of jejunum is involved. xx Prognosis depends on length of atretic bowel; multiple atresias; associated anomalies.

Different Errors of Rotation xx Stage 1: Exomphalos major/minor or gastroschisis. xx Stage 2: Errors of rotation in this stage is important and is usually considered under malrotation.  Nonrotation: Causing small bowel in right side; colon in left side; caecum in midline as suspension.  Incomplete rotation: It is the most common type of malrotation. Caecum is located in subhepatic right hypochondrium. Ladd’s peritoneal band connects from caecocolic loop to posterior abdominal wall compressing the 2nd part of the duodenum. Entire midgut is hanging down along with SMA with a narrowbased mesentery causing midgut volvulus.

Fig. 23.21: Diagram showing incomplete gut rotation and small bowel volvulus.  Reverse rotation: Final 180° rotation occurs clockwise bringing

colon posterior to duodenum and SMA.  Hyper-rotation: Rotation up to 360° or 450° causing caecum

on left side of the abdomen.  Encapsulated small bowel occurs while fetal midgut returns

into coelomic cavity. xx Stage 3: Final defect in fixation causes mobile caecum and ascending colon leading into caecal volvulus. Associated anomalies (20%)

MALROTATION It is interference in the process of normal rotation of midgut in fetus and its mesenteric fixation.

™™ ™™ ™™ ™™

Congenital diaphragmatic hernia of Bochdalek Prune belly syndrome Duodenal atresia Oesophageal atresia

Intestinal Obstruction Presentations xx Acute/recurrent/subacute intestinal obstruction. xx Midgut volvulus (30%) (usually clockwise rotation) with features of strangulation, perforation, peritonitis. xx Shock, septicaemia, passage of dark blood per rectum, oedema and erythema of anterior abdominal wall. xx In children—failure to thrive, recurrent abdominal pain, cyclical vomiting, constipation and diarrhoea.

Investigations xx Plain X-ray abdomen shows air fluid levels. xx Barium meal (dilute/microbarium) and follow through X-ray is the investigation of choice. xx US abdomen/CT abdomen, if needed. xx Haematocrit, serum electrolytes estimation.

Treatment

inspissation it forms a firm bolus leading to obstruction of the ileum. xx Neonates present with features of ileal obstruction as well as respiratory dysfunction, exocrine pancreatic insufficiency, and – high salt in the sweat (Na+ and Cl more than 90 mmol/L). xx Meconium ileus occurs in 15% of patients with cystic fibrosis. Cystic fibrosis is an autosomal recessive disease involving bronchioles, exocrine pancreas and sweat glands. Condition is common in Caucasians. Exocrine pancreatic insufficiency and malabsorption is seen in 90% of patients with cystic fibrosis. xx There is hypertrophy and dilatation of the proximal ileum containing thick, viscid, tenacious dark green meconium. Distal ileum and colon are narrow and contracted having grayish meconium pellets. Meconium gets calcified very rapidly. Gangrene, perforation, volvulus can occur in 50% of cases. xx Intrauterine perforation causes fetal meconium peritonitis which leads to dense adhesions and calcification in peritoneum. Fetal meconium peritonitis is sterile.

xx Resuscitation, antibiotics, fluid and electrolytes, blood

transfusion.

Fig. 23.22: Ladd’s operation for incomplete gut rotation. Ladd’s band is released. Duodenum is straightened. Appendicectomy is done. xx Laparotomy through horizontal incision is done. Clockwise rotated midgut which is congested and cyanotic is identified. Untwisting of the midgut in counterclockwise direction is done. Viability of bowel is confirmed (colour, vessels in mesentery, peristalsis, on table Doppler). Ladd’s band is divided large bowel is repositioned in left side. The entire duodenum is Kocherised and the ligament of Treitz is divided so that duodenum becomes straight towards right iliac fossa. This achieves wide root of the mesentery and places the small bowel in the right side of the abdomen thus preventing further volvulus. A complementary appendicectomy is done—Ladd’s operation. xx After laparotomy, if bowel is gangrenous, it is resected and remaining parts of the bowel are exteriorised as enterostomies. A second look operation is done to look for viability of remaining bowel and also to maintain the continuity. Often it will be extensive bowel resection leading into poor prognosis.

MECONIUM ILEUS xx It is neonatal manifestation of fibrocystic disease of the

pancreas wherein thick meconium, which is viscid and paste-like, gets collected in the terminal ileum. Because of

Fig. 23.23: Pathology of meconium ileus. Note the meconium pellets in the distal ileum and colon; thick viscid meconium in proximal ileum. xx Plain X-ray shows calcified meconium pellets with multiple air

fluid levels which appear as ‘soap-bubbles’ (Neuhauser sign).

xx Vomitus of the patient which does not contain trypsin, when

poured on the exposed X-ray film, will not digest the gelatin of the film whereas the vomitus of individual with normal pancreas will digest the gelatin of X-ray film—very useful test. xx Pilocarpine, a cholinergic drug is injected into skin to stimulate the sweating and collected sweat (100 µg sweat) is analysed for sodium and chloride. xx Elevated albumin level in meconium, sodium level assay in nail clipping and serum immune active trypsin assay are other investigations. Meconium ileus ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Commonly associated with cystic disease of pancreas but not necessarily always Respiratory dysfunction Exocrine pancreatic insufficiency High salt in the sweat >90 mmol/L Ileal obstruction Soap-bubble appearance in X-ray Gelatin in X-ray film will not get digested by patient’s vomitus Bishop-Koop operation, ileostomy, dissolving ileal meconium pellets are required

The remedy for injuries is not to remember them.

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SRB's Manual of Surgery Complications of meconium ileus ™™ ™™ ™™

Intestinal bolus obstruction Perforation and peritonitis Gangrene, volvulus formation

Treatment

Management of meconium ileus Nonoperative wash per rectally using acetyl-cysteine or gastrografin through Foley’s catheter passed per anally. Acetyl cysteine can also be passed for irrigation per orally through a Ryle’s tube as 10 ml 6th hourly. ™™ Bishop-Koop and Santulli operations done in very sick neonates. ™™ Resection and anastomosis is ideal when child is adequately fit. ™™

Nonoperative measures xx Dissolution through enema can be tried using gastrografin which is hyperosmolar and contains Tween 80 as dissolving agent. Gastrografin is diatrizoate meglamine with Tween 80 (polysorbate 80) as dissolving agent. N acetylcysteine 10% also can be used for irrigation per-anally. xx N acetylcysteine 10% wash through nasogastric tube also can be used—5–10 ml 6th hourly. xx Treatment for cystic fibrosis.

Operative Measures Present standard surgical approach—Enterotomy with irrigation using warm normal saline or 4% N acetylcysteine and complete evacuation of all meconium pellets (or can be pushed down into large bowel manually) closure of the enterotomy is present standard method. N acetylcysteine, by breaking the disulphide bonds of the meconium, separates it from intestinal mucosa allowing its retrieval. A T tube can be placed in the small bowel through which N acetylcysteine wash can be given repeatedly if further meconium needs dissolution.

Other Methods xx When patient’s condition is critical with obstruction, BishopKoop operation is done. Proximal dilated segment is resected and resected end is anastomosed to the side of the distal collapsed ileum. End of the distal ileum is brought out as ileostomy. Through the ileostomy gastrografin or acetyl cystine wash is given regularly to dissolve meconium pellets. This ileostomy can be kept for long time. Continuity is maintained at later period. xx Santulli operation is done where proximal ileum is brought as ileostomy for irrigation using a fine tube and distal ileum is sutured to proximal ileum as end to side anastomosis. xx Resection and anastomosis is ideal if patient is fit and if proximal bowel is suitable for anastomosis.

Fig. 23.25: Santulli operation done for meconium ileus wherein proximal ileum is brought out as ileostomy. Distal ileum is sutured to proximal. Causes of neonatal intestinal obstruction ™™ ™™ ™™ ™™ ™™ ™™ ™™

Hirschsprung’s disease Duodenal atresia Intestinal atresia Malrotation Midgut volvulus/volvulus neonatorum Meconium ileus Anorectal malformation

INTUSSUSCEPTION (ISS) Definition It is telescoping or invagination of one portion (segment) of bowel into the adjacent segment.

Types 1. Antegrade: Most common. 2. Retrograde: Rare (jejunogastric in gastrojejunostomy stoma). In elderly intussusception: ™™ Colocolic is most common type ™™ Apex is formed usually by growth ™™ No role of hydrostatic reduction

xx It can be single or multiple (rare). xx It can be ileo-colic (most common type, 75%), colocolic,

ileoileocolic, colocolic. xx It is common in weaning period of a child (common in male),

between the period of 6–9 months. Fig. 23.24: Bishop-Koop operation. Here distal ileum is brought as ileostomy and proximal part sutured to distal bowel.

xx It is the commonest cause of intestinal obstruction in chil-

dren of 6–18 months age.

Intestinal Obstruction Pathology xx Apex is the one which advances; xx Intussuscipiens is the one which receives (outer sheath); xx Intussusceptum are the tubes which advance (middle and inner sheath).  Apex and inner tubes will have compromised blood supply which leads to gangrene.  Because of ischaemia, apex sloughs off and bleeds, which mixes with the mucus to produce the classic red-currant jelly that is passed per anum.  Gangrene which sets in leads to perforation and peritonitis.  Red currant jelly is not commonly observed in ISS in adult, but it can occur.

A

B

Figs 23.26A and B: (A) Typical intussusception—on table look; (B) Parts of intussusception.

Aetiology

xx Common in males (3:2). xx Common in 6–9 months. But can also occur at later age-

grouped children.

xx Idiopathic ISS is common in children, occurs in terminal

50 cm of ileum.

xx During weaning, change in diet causes inflam­mation and

oedema of Peyer’s patches—may stimulate ISS. xx Upper respiratory tract viral infection which causes oedema

of Peyer’s patches is also thought as an aetiology for intussusception in children. xx Other causes in adolescents and adults are sub­mucous lipoma, leiomyoma, polyps in jejunum (Peutz-Jegher syndrome), other polyps and carcinomas with papillary projections. Causes ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Clinical Features

Change in diet during weaning Upper respiratory tract viral infection Intestinal polyps Submucous lipoma Leiomyoma of intestine Meckel’s diverticulum Carcinoma Purpuric submucosal haemorrhages

xx Common in spring and winter, coinciding with the gastro-

enteritis and respiratory infections in respective periods. xx Commonest cause of intestinal obstruction in infancy. xx Initial colicky abdominal pain (75%) which eventually

becomes severe and persistent. xx Sudden onset of pain in a male child, with progressive

distension of the abdomen, vomiting, with passage of “redcurrant-jelly” stool. It is usually not found in adult ISS. xx Often ISS is recurrent, when it gets reduced, child automatically becomes asymptomatic (Mother often complains “Bachha rotha he, Bachha sotha he”. It means child cries during an episode and sleeps peacefully once it gets reduced).

Fig. 23.28: Sausage-shaped mass of intussusception. xx On examination, a mass is felt either on the left or right

Fig. 23.27: Intussusception. Different parts and apex point is also clearly seen.

of the umbilicus which is sausage shaped with concavity towards umbilicus, smooth, firm, resonant, not moving with respiration, mobile, contracts under the palpating fingers. Often mass appears and disappears.

In the field of observation, chance favours only the prepared mind.

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SRB's Manual of Surgery xx Right iliac fossa is empty (Sign of Dance). xx After 24–48 hours, abdominal distension appears and

increases progressively with features of intestinal obstruction. xx Features of intestinal obstruction with step-ladder peristalsis. xx Blood-stained stool is often obvious on digital examination of the rectum. Occasionally ISS can be seen per anally and felt with a long mesentery. xx Eventually, gangrene and perforation occurs with features of the peritonitis.

Investigations xx Barium enema shows typical claw sign or coiled spring

sign (Pincer end). xx Ultrasound shows target sign or pseudokidney sign or bull’s

eye sign, which is diagnostic. xx Doppler may show mass with doughnut sign and is useful

to check blood supply of bowel.

xx Plain X-ray abdomen shows multiple air fluid levels. xx CT abdomen is needed. Treatment

Abdominal palpatory findings in ISS Palpable mass (85%) –– Sausage-shaped smooth, firm mass –– Mass does not move with respiration –– Mobile in all directions –– Resonant –– Mass contracts under the palpating fingers –– Mass appears and disappears ™™ Empty right iliac fossa ™™ Features of intestinal obstruction/peritonitis—later ™™

Fig. 23.29: A rare condition where colonic intussuscep­tion has occurred through rectum, coming out per anally. Part is already gangrenous.

Initial management ™™ Ryle’s tube aspiration ™™ IV fluids ™™ Antibiotics ™™ Catheterisation.

Later management Nonoperative management xx Reduction by hydrostatic pressure using either warm saline or microbarium sulphate solution or air (popular in China). Barium or saline is infused into the rectum through a catheter (Foley’s catheter). Under fluoroscopy, reduction can be observed. Child will pass large quantity of air and faeces; distension reduces; child shows recovery and stops crying. Air or contrast enters the proximal bowel freely. Palpable abdominal mass disappears. Rare complication is perforation of colon. It is done in early stage within 24 hours of presentation. 70% cases of ISS will respond to nonoperative method. It is contraindicated in complete obstruction; perforation and peritonitis.

A

Complications ™™ ™™ ™™

Intestinal obstruction Perforation Peritonitis

Differential Diagnosis In children: Acute gastroenteritis. Purpura with intestinal symptoms. In adults: Carcinoma colon. Mesenteric mass.

B Figs 23.30A and B: Barium enema showing the typical ‘Claw sign’ of intussusception.

Intestinal Obstruction SIGMOID VOLVULUS (Volvulus of Pelvic Colon)

Indications for surgery in ISS ISS more than 48 hours Features of perforation, strangulation, peritonitis ™™ Recurrent ISS ™™ In adult commonly, resection is required ™™ ™™

Surgery xx Cope’s method: If reduction does not occur, laparotomy is done under G/A. By gently milking out the intussusception with warm packs, it is reduced. After reduction, viability of the bowel is checked carefully. If manual reduction is not possible, it is understood that the bowel is likely to be gangrenous which requires resection and anastomosis. In case of viable bowel, often terminal ileum is anchored to the ascending colon and Jackson veil band is cut. Patient also requires nasogastric tube aspiration, IV fluids, antibiotics. Appendicectomy should be done after reduction of the intussusception. xx Laparoscopic approach may be used to reduce the intussusception. xx If intussusception persists for more than 48 hours or intussusception in adult requires resection.  Ileocolic resection is sufficient.

xx It is common in Asia, common in India (7% of intestinal

obstruction) and especially South India because of high fibre diet. xx It is very common cause of large bowel obstruction in Peru and Bolivia due to high altitude. xx More common in males and old age. xx It is common in patients with chronic constipation with laxative abuse. It is common in: ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Ogilvie’s syndrome Mentally-retarded individuals Chaga’s disease Hypothyroidism Anticholinergic drugs Multiple sclerosis Scleroderma Parkinson’s disease

Recurrence rate In hydrostatic reduction—10% In open manual reduction—2% ™™ In resection—very less 6 mm AP diameter,

hyperechoic thickened appendix wall > 2 mm—target sign.

xx Appendicolith. xx Interruption of submucosal continuity. xx Periappendicular fluid.

xx Contrast CT scan is very much useful when diagnosis is difficult especially in old people. Dilated appendix; dilated lumen; thickened wall; nonfilling of the lumen by contrast or air; periappendicular fluid collection; presence of mass/abscess/ associated pathology like carcinoma can be identified. It has 95% sensitivity and specificity with 95% accuracy. Dirty fat thickened mesoappendix, appendicular phlegmon, appendicular faecolith and thickened caecum funneling contrast into the orifice of the appendix as arrowhead sign—are all relevant features in CT scan. xx C-reactive protein, even though nonspecific increases in acute phase. 99mTc HMPAO labeled leukocyte imaging may give guidance in deciding the management. xx MRI is very useful tool in pregnancy. xx Plain X-ray may show lumbar scoliosis towards right due to psoas spasm which is not uncommon; faecolith on the right side; obliteration of preperitoneal fat line due to retrocaecal appendicitis; segmental ileus in caecum and terminal ileum; speckled extraluminal gas in right iliac fossa, gas in appendix, pneumoperitoneum (very rare); intestinal obstruction (occasionally only); soft tissue mass in mass or abscess of appendix—all these features are very much nonspecific. X-ray is useful to rule out DU perforation, intestinal obstruction, ureteric stone.

Different Scoring Systems Used Alvarado scoring for appendicitis (1986):

1

Anorexia

1

Nausea and vomiting

1

Tenderness in right iliac fossa

2

Rebound tenderness

1

Elevated temperature

1

Leucocytosis with count more than 10,000

2

Shift to left with neutrophilia in peripheral smear

1

Total score

10

Score less than 5: Not sure. Score between 5–6: Compatible. Score between 6–9: Probable.

A Fig. 24.13A

Score

Migrating pain

Score more than 9: Confirmed.

Appendix xx Kalam modified Alvarado scoring system (1994) where shift to left is removed. xx Tzanakis scoring system 2005—lower abdominal tenderness—4; rebound tenderness—3; total count > 12,000/cm—2; USG features—6. xx RIPASA scoring system (2010)—with 15 parameters. xx Anderson scoring system—8 parameters.

xx In difficult cases—Retrograde appendicectomy can be done. In presence of pus or burst appendix, the peritoneal cavity is drained. xx Postoperatively, IV fluids, antibiotics are given. Once bowel sounds are heard, oral diet is started.

Treatment Surgery-Appendicectomy:

Approaches 1. Gridiron incision: Incision is placed perpendicular to the right spinoumbilical line at the McBurney’s point (i.e. at the junction of lateral one-third and medial two-third of spinoumbilical line). (Gridiron is a frame of cross beams to support a ship during repairs. This incision was first described by McArthur). 2. Rutherford Morison’s muscle cutting incision (Muscles are cut upwards and laterally). 3. Lanz crease incision centering at McBurney’s point— cosmetically better. 4. Right lower paramedian incision/lower midline incision— when in doubt or when there is diffuse peritonitis. 5. Laparoscopic approach: Becoming popular and better. 6. Fowler-Weir approach by cutting muscle medially over the rectus.

Fig. 24.15: Appendix, on table during appendicectomy.

A

Fig. 24.14: Approaches for appendicectomy.

Procedure xx Under general anaesthesia, skin is incised. Two layers of superficial fascia are cut. External oblique apo­neurosis is opened in the line of incision. Internal oblique and transverse muscles are split in the line of fibres. Peritoneum is opened in the line of incision. Caecum is identified by taeniae, and ileocaecal junction. Omentum when adherent is separated. Appendix is held with Babcock’s forceps. Meso­appendix with appendicular artery is ligated. Using thread or silk, a purse—string suture is placed around the base of the appendix. Base of the appendix is crushed with artery forceps and transfixed using vicryl (absorbable). Appendix is cut distal to the suture ligature and removed. Stump is cleaned with anti­septics. Purse string suture is tightened so as to bury the stump.

B Figs 24.16A and B: Burst appendicitis showing pus. Tip of appendix is burst causing collection of pus adjacent. Usually proximal site of appendix just distal to the site obstruction will burst.

Perforated appendix rarely causes pneumoperitoneum.

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Fig. 24.17: Steps in open appendicectomy. Note the base of appendix, mesoappendix; its ligation; transfixation of the base using 2 zero vicryl; cutting of appendix and closure of the wound. Burying is not essential; it is optional. Burying is done using silk/vicryl using purse string suture.

Complications after appendicectomy ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Paralytic ileus Reactionary haemorrhage due to slipping of ligature of the appendicular artery Residual abscess (pelvic, paracolic, local, sub­diaphragmatic) Pylephlebitis (portal pyaemia) Adhesions, kinking and intestinal obstruction Right inguinal hernia (direct)—due to injury to ilioinguinal nerve Wound sepsis 10% Faecal fistula Respiratory problems and DVT

Fig. 24.19: Transfixation of the base of appendix using 2 zero vicryl is an important step after secured ligation of appendicular artery.

Fig. 24.18: Gangrenous appendix. It is gently ligated at the base using 2 zero vicryl. It is not buried as stump will be friable (burying is not necessary to any appendicectomy). Portal pyaemia It is rare nowadays It is septic portal system thrombosis Commonly seen in immunosuppressed individuals Infection spreads to liver through portal vein causing rapid multiplication of virulent organisms leading into septicaemia (toxaemia with hypotension, tachycardia), jaundice, tender palpable liver. Patient will be drowsy ™™ Treatment—antibiotics like cefoperazone, amikacin, metronidazole, meropenem; fluid management; ventilator support ™™ It carries poor prognosis ™™ ™™ ™™ ™™

Fig. 24.20: Faecal fistula after appendicectomy. Most of the time faecal fistula subsides by conservative treatment unless there is distal obstruction or specific causes like Crohn’s, tuberculosis or malignancy.

Appendix Contd... ™™ ™™ ™™ ™™ ™™ ™™

Fig. 24.21: Wound infection after appendicectomy in patient with burst appendicitis.

™™

Troubles in Appendicectomy xx During surgery if appendix is found normal, other cause for symptoms should always be looked for like Meckel‘s diverticulum, Crohn‘s disease, ovarian/pelvic causes in females, malignancy, etc. xx Appendicular tumour may be found. If it is in the tip, appendicectomy is sufficient. It could be carcinoid tumour. If it is in the base right hemicolectomy is done. xx Absence of appendix—a rare occasion can occur. Caecum and taeniae should be traced properly before finalising it. xx Appendicular abscess/pelvic abscess formation. xx Malignancy in the caecum is identified on table—right hemicolectomy should be done. xx If Crohn‘s disease is identified during surgery, appendicectomy can be done with care, if base of the appendix is normal. But in rare occasion where appendix is involved by Crohn‘s disease, appendicectomy should not be done but treated only with antibiotics and steroids, otherwise fistula can develop.

™™ ™™ ™™ ™™

™™ ™™

™™

™™

INCIDENTAL APPENDICECTOMY xx Here removal of normal appendix is done at laparotomy for other conditions, e.g. hysterec­tomy. xx It is done in vague lower abdominal pain of doubtful severity. xx It is a useful procedure to tackle ‘Munchausen syndrome, i.e. the patient is always worried of pain abdomen and gets relieved after the procedure (psychological benefit). Baron Hieronymus Munchausen (1797) was a German officer who fought with Russians against Turks and returned to tell tall stories. Patient presents with various stories of pain, bleeding, earlier medical or surgical therapies. xx It is done along with Ladd’s procedure for malrotation. xx It is also done during on table colonic lavage (Doodleys lavage). xx It is not done in Crohn’s disease (during acute phase), post-radiation, immunosuppression, aortoiliac grafts. Remember

™™

™™ ™™ ™™

™™

™™

Appendicitis is common in white races, young males and in those who are on westernised diet ™™ It most commonly affects individuals of age group 10-20 years. 2/3rd will develop perforation due to rapid progression and poor localisation ™™ Gangrene, perforation and peritonitis are rare in nonobstructive type; but recurrent appendicitis of nonobstructive origin can cause perforation ™™

™™

™™

Pneumoperitoneum is not common in appendicular perforation Appendicular artery which is an end artery can undergo infective thrombosis and can cause gangrene and perforation In retrocaecal appendicitis rigidity is not common; psoas spasm is known to occur Pelvic and post-ileal appendicitis can cause diarrhoea. Post ileal appendicitis is difficult to diagnose It is difficult to remove subhepatic appendix through McBurney’s incision Pain will be above and lateral in appendicitis in pregnant women. Appendicitis is the most common acute abdominal condition in pregnancy (1:1500 pregnancies). Incidence of foetal loss is 5% without perforation and it becomes 20% if there is perforation. It is better to do laparotomy to remove the appendix in pregnancy In elderly atypical features are more common and so diagnosis is often missed. Gangrene and perforation are common in elderly. Often it mimics subacute obstruction In obese patients diagnosis is often difficult Appendicitis is rare before 2 years. But when it occurs perforation and peritonitis are common carrying poor prognosis Negative appendicectomy—incidence is 30% Reginald Fitz of Boston coined the term appendicitis. McBurney described clinical features; Claudius Amyand (1736) did first appendicectomy Appendix is found on the left side in situs inversus patient. Situs inversus may be both thoracic and abdominal or only abdominal Acute pancreatitis (straw/haemorrhagic chicken broth fluid), DU perforation (bile fluid), perforated Meckel’s diverticulum, twisted ovarian cyst/ectopic pregnancy (bloody fluid) are important lifethreatening conditions which may be missed for appendicitis and patient might undergo appendicectomy as a wrong procedure in these patients Simple appendicitis is one where the symptoms are of less than 48 hours duration with imaging studies showing appendicitis without abscess or phlegmon Chronic appendicitis’ earlier this term was not used, but is presently accepted terminology; few attacks of recurrent appendicitis will lead into chronic appendicitis. It presents with episodic often vague discomfort with colicky pain in RIF, anorexia, malaise, pain with movement and is often called as grumbling appendicitis. TC, US, CT scan may be normal in these patients Perforation rate in appendicitis is 25% in general; in children and elderly it becomes 45-50%. High fever more than 102°F, TC > 18,000/- are suspected features of rupture Mortality rate of appendicectomy is less than 1%. Morbidity and complications are more after surgery for perforated appendicitis Surgical site infection is 5% in uncomplicated appendicitis; 20% in perforated appendix after surgery Small bowel obstruction postoperatively is 1% with simple appendicitis; 3–5% in perforated appendicitis after surgery. More than 50% of obstruction occurs in first year of postoperative period In children with appendicitis, there is poor localisation and so peritonitis is common. So conservative therapy should be avoided. Surgery is the only choice of treatment otherwise early peritonitis is the danger. Appendicular mass is initially treated with Ochsner Sherren regime. After 6 weeks, interval appendicectomy is done. Children, old age, faecolith, laxative abuse, diabetes mellitus, immunosuppression and pelvic appendix are high-risk factors for perforation in appendicitis In pelvic and retrocaecal appendicitis, adjacent ureteral inflammation can occur in which urine on analysis shows blood cells and pus cells

Contd... Poverty knows how extremely expensive it is to be poor.

Contd...

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SRB's Manual of Surgery Contd... Incidence of removal of normal appendix is 30% Stump appendicitis is inflammation and infection in the remaining portion of the appendix in the stump after appendicectomy. It is a rare entity ™™ On table during surgery, normal appendix if found, it is called as ‘Lily white appendix’. Then other pathology like Meckel’s, ileal/ mesenteric lymph node/ovarian disease has to be looked for ™™ ™™

APPENDICULAR MASS (Periappendicular Phlegmon) xx It is the localisation of infection occurring 3 to 5 days after

an attack of acute appendicitis.

Fig. 24.23: Appendicular mass is formed by dilated ileum; greater omentum; inflamed appendix and caecum. It is resonant, smooth, firm, and tender with well defined borders which does not move with respiration and does not have mobility.

Fig. 24.22: Appendicular mass—a well localised one. xx Inflamed appendix, greater omentum, oedematous caecum,

parietal peritoneum and dilated ileum (ileus) forms a mass in the right iliac fossa. xx This mass is tender, smooth, firm, well localised, not moving with respiration, not mobile, all borders well made out (well localised) and resonant on percussion. Patient may have fever and features of toxicity.

xx Marking the mass to identify the progression/regression. xx Antibiotics (ampicillin, metronidazole, genta­micin, or other drugs given depending on severity and requirement). xx IV fluids. xx Analgesics. xx Initial nasogastric aspiration.  Patient usually shows response by 48 to 72 hours and mass reduces in size, temperature and pulse becomes normal. Appetite is regained. 90% of patients respond to conservative therapy.  Patient is discharged and advised to come for interval appendicectomy after 6 weeks.

Contraindications for Ochsner-Sherren regimen 1. 2. 3. 4.

When diagnosis is in doubt. In acute appendicitis in children and elderly. In burst, gangrenous appendicitis. In patients in whom diffuse peritonitis sets in. Criteria to discontinue Ochsner-Sherren regimen

Differential diagnosis ™™ ™™ ™™ ™™

Carcinoma caecum Crohn’s disease Ovarian disease Twisted ovarian cyst

 Actinomycosis  Mesenteric lymphadenitis  Ruptured ectopic pregnancy  Ileocaecal tuberculosis

Investigations xx TC is increased. xx Ultrasound confirms the mass.

Treatment Conservative (Ochsner-Sherren Regimen), as nature has already localised the infection, if now disturbed will cause faecal fistula. Includes observation: xx Temp, BP, pulse chart.

Patient becomes more toxic (tachycardia, high fever) Persistent vomiting Increase or spread of pain abdomen (means onset of diffuse peritonitis) ™™ Increased size of the mass ™™ Suppuration (abscess formation) in the mass In these patients the regimen is discontinued. The patient is taken for immediate surgery, either through laparotomy or through classic approaches ™™ ™™ ™™

APPENDICULAR ABSCESS xx It occurs due to suppuration in an acute appendicitis or

suppuration in an already formed appendicular mass.

xx Abscess commonly occurs in retrocaecal region but

often can occur in subcaecal, preileal lumbar or postileal regions.

Appendix xx Pelvic abscess is also common after an attack of acute

appendicitis.

peritoneally, which is sent for culture and sensitivity. Wound is closed. A drain is placed through a separate incision. Antibiotics are continued. xx Interval appendicectomy is done after 3 months. Pelvic abscess is drained per-rectally or through posterior colpotomy (in females).

FAECAL FISTULA AFTER APPENDICECTOMY Causes xx It can occur when appendicectomy is done in gangrenous/perforated/friable base appendix. xx It can occur after drainage of appendicular abscess. xx It can occur if appendicectomy is done/attempted in appendicular mass. xx If there is underlying additional pathology like Crohn‘s disease/ carcinoma/ileocaecal tuberculosis/actinomycosis during appendicectomy, fistula can occur. Fig. 24.24: Appendicular abscess. Swelling with ill-defined lower border.

Features xx Faeculent, foul smelling discharge from either main wound or drain site.

Clinical Features xx High fever, features of toxicity, tender, smooth, dull (to percuss), soft swelling in right iliac fossa which lies towards right lateral and lower side with clear upper margin but indistinct lower margin. xx Ultrasound confirms the diagnosis.

Treatment xx Antibiotics are started. xx CT-guided aspiration or catheter drainage is done often as initial therapy. xx Under G/A, incision is made in the lower lateral aspect of the swelling above the inguinal ligament. Skin, external oblique muscle is cut. Abscess cavity is opened and pus is drained extra-

Fig. 24.26: After appendicectomy fistula can occur. Note the faecal discharge. xx Features of infection. xx Skin excoriation. xx Features suggestive of cause.

Investigations xx CT fistulogram to delineate the track. xx CT scan abdomen to find out the other pathology. xx Other relevant investigations, Hb%, albumin level, etc.

Treatment Fig. 24.25: Different sites where abscess can occur after appendicitis retrocaecal, appendicular; pelvic; subphrenic; preileal and lumbar. Portal pyaemia can occur with multiple pyaemic abscesses in the liver.

xx Conservative—antibiotics, IV fluids, dressing, zinc oxide cream over the skin, observation. xx Most of the time fistula subsides provided there is no distal obstruction by adhesions or kinking or specific causes like carcinoma or tuberculosis.

Those who can’t hear the music think the dancer’s mad.

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SRB's Manual of Surgery xx If persists even after 6 weeks, resection of ileocaecal segment and anastomosis is done.

MUCOCELE OF APPENDIX xx It can be neoplastic or non-neoplastic. xx It occurs when proximal end of the lumen of appendix gets slowly and completely occluded, usually by a fibrous stricture causing collection of sterile fluid (mucus) in the lumen. It is a retention cyst. xx Appendix is grossly enlarged with features of sub-acute appendicitis. xx Mucocele can get infected leading to empyema of appendix. xx Rupture of mucocele can lead to pseudomyxoma peritonei. Neoplastic type causes generalised pseudomyxoma peritonei; non-neoplastic type causes localised pseudomyxoma peritonei. (Other cause for pseudomyxoma peritonei is ruptured mucinous carcinoma of ovary). xx Often mucocele of appendix is also caused by a mucus secreting adenocarcinoma and if it is so right hemicolectomy is done. xx Clinical features: Colicky pain in right iliac fossa, Tenderness in the right iliac fossa. xx Investigations: Ultrasound abdomen. xx Treatment: Appendicectomy.

in crypts of Lieberkuhn (argentaffin tissue). It is ten times more common than other types (One in 400 appendices). Commonly its location is in the tip. 75% are less than 1 cm; 15% are 1–2 cm; 10% are > 2 cm in size. It stains chromograninB immunohistochemically. Distant and nodal spread occurs if tumour is more than 2 cm. Carcinoid of appendix may be goblet cell type or classical type histologically. Goblet cell has got more mortality than classic type. Treatment is appendicectomy. Right hemicolectomy is done if base is involved or size is more than 2 cm or nodes are involved. 5-year survival is 90%. xx Primary adenocarcinoma of the appendix is rare. It can be mucinous (common) or colonic (less common) type. Acute presentation as appendicitis is common in colonic type. It is staged as Duke’s staging A, B, C and D. 5-year survival rate for each is 100%; 65%; 50% and 5% respectively. Mucinous type has got better prognosis. 5-year survival for mucinous type is 70% and colonic type is 40%. Mucinous type can rupture into the peritoneal cavity and can cause pseudomyxoma peritonei. Tumours of the appendix ™™ ™™ ™™

Carcinoid tumour—most common site is appendix Primary adenocarcinoma of appendix Mucocele of appendix leading into pseudomyxoma peritonei

Pseudomyxoma peritonei ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Jelly like mucoid yellowish-brown substance accumulates in peritoneal cavity Due to ruptured adenocarcinoma appendix/mucocele or mucinous carcinoma of ovary Common in females Painless progressive distension of abdomen with intestinal obstruction occurs eventually Shifting dullness is absent Surgical debulking, oophorectomy, appendicec­tomy, omentectomy are often done Chemotherapy is useful—cisplatin Carries poor prognosis

Note:

Pseudomyxoma peritonei is presently consi­d ered to be due to neoplastic adenocarcinoma of appendix with gelatinous fluid collection in the peritoneal cavity. It is also seen in cystadenocarcinoma of ovary. Treatment is surgery and chemotherapy.

A

NEOPLASMS OF THE APPENDIX xx It is rare. xx It is often postappendicectomy histological diagnosis. xx Cystic neoplasms of appendix: Simple cyst (non-neoplastic mucocele); mucinous cystadenoma; mucinous cystadenocarcinoma (most common form of cystic neoplasms); pseudomyxoma peritonei. Simple cyst is non-neoplastic obstruction of the lumen and is less than 2 cm in size which contains mucin. Mucinous cystadenoma attains progressively large size of up to 8 cm with CT showing calcification of the wall. Laparoscopic appendicectomy is not used in mucinous cystadenoma. Hemicolectomy is done in mucinous cystadenocarcinoma and cystadenoma of large size and if base is involved. xx Carcinoid tumour is the most common type. It is less aggressive. It is often incidentally found. It is arising from Kulchitsky cells

B Figs 24.27A and B: Carcinoid tumour in two different patients. If it is in the tip or away from the base, then appendicectomy is sufficient. If it is in the base or extending into the caecum then right hemicolectomy is needed.

Appendix LAPAROSCOPIC APPENDICECTOMY This is newer, popular and ideal method of appendicectomy. It has become gold standard method of treatment.

Advantages xx xx xx xx xx xx

Diagnosis is confirmed. Other parts of the abdomen are visualised. In females pelvic structures are assessed properly. Trauma of access is less. Faster recovery. Laparoscopic appendicectomy is definitely better whenever there is vague abdominal pain; atypical pain; situs inversus; in women; subhepatic appendix and as interval appendicectomy.

left side. Scrub nurse on the right side. Monitor is kept on the foot end right side. xx 10 mm camera port is placed at the umbilicus. Working ports are two 5 mm, one on each side of lower abdomen or one on left side and another on the lower midline. One of the working ports can be 10 mm in difficult appendectomies. xx Pneumoperitoneum is created using CO2. xx Appendix is held with grasper or Babcock’s forceps. Mesoappendix is cauterised by bipolar or unipolar cautery. xx Appendix is dissected up to the base of the appendix. xx Base of the appendix is ligated with loop ligature. Intracorporeal ligature also can be placed using vicryl 2 zero suture material. Appendix is removed through 10 mm working port along with reducer. Often retrieval bag can be used to remove the appendix.

Disadvantages xx Technical difficulties especially in burst appendix. xx Cost factor and availability. Note:

Consent for conversion should be taken.

Technique xx Procedure is done under general anaesthesia. Head down position with right tilt is needed. Surgeon and camera man stands on the

Fig. 24.28: Different possible port placements for appendicectomy.

A

B Figs 24.29A and B: Laparoscopic appendicectomy. Note the mesoappendix is being cauterised. Ligation of the appendix is done using vicryl (Courtesy: Dr Keshava Prasad, MS, KMC, Mangaluru).

An essential aspect of creativity is not being afraid to fail.

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SRB's Manual of Surgery Laparoscopic assisted appendicectomy can be done if caecum is mobile without much adhesions and mobilised appendix can be delivered through the 10 mm umbilical port. As in regular laparoscopic procedure, appendix is identified and mobilised. Appendix which is not friable and not turgid can be delivered through umbilical port gently. During this procedure gas flow should be stopped so that all gas in the cavity will be empty. Mesoappendix is ligated. Appendix is transfixed like in open method and removed. Stump is pushed back into the place. Telescope is passed again to confirm the position and security of the stump. Advantage is that it is faster.

Complications Fig. 24.30: Laparoscopic assisted appendicectomy. xx Umbilical port is closed in two layers. Other ports are closed by skin sutures. If gangrenous or burst appendix drain can be placed through one of the ports. xx Oral food is started in 12 hours.

xx Injury to bowel, vessels while passing the ports. xx Complications of pneumoperitoneum. xx Accidental cautery injury to bowel, vessels and other vital structures. xx Bleeding. xx Bowel perforation, peritonitis. xx Ligature slipping, leak, peritonitis, fistula formation.

Chapter

25

Rectum and Anal Canal CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Anatomy P  er-rectal Examination Proctoscopy (Kelly’s) Sigmoidoscopy Colonoscopy Carcinoma Rectum Solitary Ulcer Syndrome Rectal Prolapse Anorectal Malformations Pilonidal Sinus Piles/Haemorrhoids – External Piles

™™ Anal Fissure

™™ Proctitis

– Sentinel Pile

™™ Proctalgia Fugax

™™ Anorectal Abscess ™™ Fistula-in-Ano

™™ H  idradenitis Suppurativa of Anal Region

™™ Anorectal Strictures

™™ Pruritus Ani

™™ Condyloma Acuminata

™™ Gastrointestinal Haemorrhage

™™ Anal Intraepithelial Neoplasia

– Upper GI Bleed

™™ Malignant Tumours of Anal Area

– Lower GI Bleed

™™ Sacrococcygeal Teratoma

– Obscure GI Bleed

™™ Anal Incontinence ™™ Descending Perineal Syndrome

ANATOMY

pathetic (S234) is motor to musculature and inhibitory to sphincter. Sensation of distension is carried through parasympathetic; pain sensation is carried by both.

Rectum xx It is the distal portion of the large gut, placed between the sigmoid colon above and anal canal below; in front of last three pieces of sacrum and coccyx (From S3). xx The three cardinal features of large intestine (saccu­lation, appendices epiploicae and taeniae) are absent. xx The upper third of rectum is covered by peritoneum on front and sides, mid third only on the front, lower third is infraperitoneal. xx The rectum is pulled forward by the puborectalis muscle forming the anorectal sling which is primarily responsible for rectal continence. xx It has got three lateral flexions left, right and left from below upwards (Valves of Houston). xx Rectum is supplied by rich network of vessels that originates from superior and middle rectal arteries and median sacral artery. xx Lymphatic drainage from upper half of rectum is to inferior mesenteric nodes; from lower half to internal iliac nodes. xx It is innervated by autonomic nervous system; sympathetic (L1, L2) is motor to sphincter and inhibitory to musculature; parasym-

Rectosigmoid Junction xx Implies a segment of bowel comprising the last seven centimetre of sigmoid colon and upper five centimetre of rectum. xx On sigmoidoscopic examination it is taken as a point 15 cm from the anal verge.

Supports of Rectum xx Pelvic floor. xx Fascia of Waldeyer: It is the condensation of pelvic fascia behind rectum, contains superior rectal vessels and lymphatics. xx Lateral ligaments of rectum: It is the condensation of pelvic fascia, attaches rectum to the posterolateral wall of lesser pelvis. xx Denonvillier’s fascia: It is the fascial condensation which separates rectum from prostate in males and vagina in females.

The drops of rain make a hole in the stone not by violence, but by oft falling.

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SRB's Manual of Surgery Venous drainage: Internal rectal venous plexus lies in the submucosa of the anal canal. It drains mainly into the superior rectal vein but communicates freely with external plexus. It is an important site of portasystemic communication. They are situated in anal column at 3,7,11 o’clock. Their saccular dilatation forms ‘primary internal piles’.

Fig. 25.1: Interior of the anal canal.

Fig. 25.3: Blood supply of rectum.

PER-RECTAL EXAMINATION (Digital Examination of the Rectum Refer Chapter 16) We had almost come to the conclusion that the case (of vasovesiculitis) was one of acute appendicitis, but decided to make a rectal examination for the sake of completeness. —Ulysses Grant Dailey, WS Grant, 1924

Fig. 25.2: Sphincters of anal canal.

Anal Canal xx It is 4 cm long, extends from levator ani muscle to anal verge. xx The dentate line represents the former site of the embryonic anal membrane. xx The lining of the canal above this line is columnar epithelium and below is skin. xx The mucosa above this line has an autonomic nerve supply, below is by pudendal nerve. xx The venous drainage above this line is by inferior mesenteric and portal circulation, whereas below to systemic venous circulation. xx Internal haemorrhoids develop above this line.

No abdominal examination is complete without a per-rectal examination. a. It is done to palpate. 1. Carcinoma rectum. 2. Stricture rectum. 3. Polyps. 4. Thrombosed piles. 5. BPH and carcinoma prostate. 6. Secondaries in the rectovesical pouch (Blumer shelf). 7. Sphincter tone. 8. Pelvic abscess (is felt as boggy swelling). b. To feel the internal opening of anal fistulas. c. In bimanual palpation of the bladder or pelvic tumours. d. In acute abdominal conditions—it reveals dilated empty rectum with tenderness. Positions for Per-rectal Examination

Sphincters of Anal Canal Internal sphincter: Downward extension of circular muscle of rectum, under control of autonomic nervous system. External sphincter: Surrounds the internal and continuous with the levator muscle. Blood supply is from inferior rectal artery.

™™ ™™ ™™ ™™ ™™

Right lateral position. Left lateral position. Dorsal position in ill-patients. Lithotomy position. Knee-elbow position.

Contd...

Rectum and Anal Canal SIGMOIDOSCOPY

Contd... Picker position: Patient in standing position leans forward by grasping a chair or stool. This method is used to palpate seminal vesicles which is involved by tuberculous seminal vesiculitis (as craggy feeling) or in trichomonas vaginalis infestation of seminal vesicle. Per-rectal examination is contraindicated in acute fissure-in-ano. ™™

Annual sigmoidoscopy for all, after their fortieth birthday: something to look forward to. — Henry George Miller, 1968

PROCTOSCOPY (KELLY’S) Indications a. Diagnostic—piles, fissure in ano, polyps, stricture, etc. b. Therapeutic—injection therapy for partial prolapse or piles, cryotherapy for piles, polypectomy, biopsy for carcinoma rectum or anorectum.

A

B Figs 25.4A and B: Types of proctoscopes: (A) Non-illuminating; (B) Illuminating.

Types a. Illuminating. b. Nonilluminating.

Parts (10 cm) Proctoscope is conical shape, with proximal diameter more than the distal, so as to illuminate the light at the required site properly. Obturator is the inner part which allows the easy insertion of the proctoscope.

Positions for Proctoscopy xx xx xx xx

Left lateral position (common). Right lateral. Lithotomy. Knee-elbow position.

Fig. 25.5: Rigid sigmoidoscope with inflation balloon and biopsy forceps. xx It is used to visualize rectum and sigmoid colon, take biopsies from suspected lesions and do therapeutic procedures (polypectomy, control of bleeding, etc.). xx There are two types: 1. Rigid—25 cm long, with illumination. 2. Flexible—60 cm long. xx In lateral position as in P/R examination or proctoscopy, sigmoidoscope with obturator is passed into the rectum and obturator is removed. Rectosigmoid is inflated with air and scope is negotiated into the sigmoid through Alpha (a) manoeu­vre. Looked for any disease, biopsies are taken and also any required procedure is done. Precaution: Care should be taken in acutely inflamed sigmoid colon, because chance of perforation is high.

COLONOSCOPY xx It is 160 cm long, flexible. xx Technique is same as sigmoidoscopy, but is passed up to the caecum.

Technique of Proctoscopy

Technique

After doing digital examination, proctoscope with the obturator is introduced inside, through the anal canal in the direction towards the umbilicus.The obturator is removed. Proctoscope is withdrawn and during the course of withdrawal, any pathology has to be looked for. Acute anal fissure is contraindication for proctoscopy.

It is often done under GA using propofol or with laryngeal mask airway (LMA). It can be also done under high sedation. But patient finds difficult to tolerate pain and distension. Passage by elongation; looping with a manoeuvre; dither-torquing (clockwise-anticlockwise rotations) methods are used. Difficulty is encountered while passing through

Use your imagination not to scare yourself to death, but to inspire yourself to life.

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SRB's Manual of Surgery sigmoid colon, splenic flexure, and hepatic flexures. Continuous air inflation is important. It is better to visualise the lumen and then pass the colonoscope. Often it can also be negotiated into the terminal ileum. Changing position, abdominal pressure is required for better negotiation of the colonoscope. Technique differs in patients after haemicolectomy or through colostomy.

Indication xx xx xx xx xx xx

Bleeding per rectum, resistant anaemia. To take biopsies from different parts of the bowel. To identify synchronous growths, ulcerative colitis. To remove polyps. When barium enema shows irregularity. For therapy—colonoscopic polypectomy, dilatation of stricture colon, fulgaration.

xx In 3% of cases, it occurs in multiple sites (syn­chronous). xx Usually originates from a pre-existing adenoma or papilloma

(tubular polyp). xx Any tumour within 15 cm proximal to the anal margin is

called as rectal tumour/cancer. More than 95% are adenocarcinoma. It is characterized by chromosomal instability. Microsatellite instability (MSI) is rare in rectal cancer.

Aetiology xx xx xx xx

Red meat and saturated fatty acids increase the risk. High fibre diet reduces the risk. Alcohol and smoking increases the risk. FAP and adenomas are more prone to carcinomas.

Contraindication ™™

Acute ulcerative colitis.

™™

It helps to visualise full length of the colon. GA is not used, except in children.

™™

Takes a long time and requires expertise to do the same.

™™ ™™ ™™ ™™ ™™

Perforation of bowel, splenic flexure is the commonest site. Trauma to anorectum. Sepsis. Haemorrhage. Problems of incomplete therapeutic procedures.

Advantage

Disadvantage Hazards

CARCINOMA RECTUM

Fig. 25.7: Large rectal polyp which has come out of the anal canal. It is potentially malignant.

Bubo is an apostem breeding within the anus in the rectum with great hardness but little aching. This I say, before it ulcerates, is nothing else than a hidden cancer…. Out of bubo (cancer) goes hard excretions and sometime they may not pass, because of the constriction caused by the bubo, and they are retained firmly within the rectum…. I never saw nor heard of any man that was cured…but I have known many that died of the foresaid sickness. —John of Arderne, 1414

xx It is common in females.

Fig. 25.8: Pathological specimens of anal canal, rectum and sigmoid colon after abdominoperineal resection for low rectal carcinoma and midrectal carcinoma. xx Villous adenoma has 40% chance of turning malignancy,

size more than 2 cm is at high-risk. Fig. 25.6: Rectal polyp—it is premalignant condition.

xx Ulcerative colitis; Crohn‘s disease; HNPCC carries higher

incidence of carcinoma of rectum.

Rectum and Anal Canal xx Family history of rectal cancer—any first degree relative of

a person with rectal cancer will show two times increased risk of carcinoma rectum. xx Risk of developing other cancers like of endometrium (40%); stomach (20%); biliary tree (20%); ovary (10%) in the same patient also increases. xx ‘Adenoma—carcinoma sequence’ like in carcinoma of colon is known common method of occurrence.

Modified Duke’s staging A. Growth limited to rectal wall (15%) B. Growth extending into extra-rectal tissues but no lymph node spread (35%)    B1: Invading muscularis mucosa    B2: Invading in to or through the serosa C.  Lymph node secondaries (50%) D.  Distant spread to liver, lungs, bone, brain

Gross: It can be: ™™ Ulcerative ™™ Papilliferous ™™ Infiltrative ™™ Annular: It is common in rectosigmoid junction. ™™ Diffuse type: Often observed in patients with ulcerative colitis which carries poor prognosis

Note: • Astler-Coller's grading (Refer Chapter 22).

Histologically: It is adenocarcinoma which may be:

•

™™ ™™ ™™

Well-differentiated—10% Moderately differentiated—65% Undifferentiated—25%

Colloid carcinoma of the rectum It is 12% common in young people Types ™™ Primary and secondary ™™ Secondary colloid carcinoma is common type and is due to mucoid degeneration of adenocarcinoma itself.  Primary is mucus within the cell with displaced nucleus (signet ring).   Primary type has got poorer prognosis compared to secondary.

• •

• •

Primary rectal cancers are divided into 4 groups – very early; early; intermediate; locally advanced. For sessile adenoma, Kikuchi sm (submucosal invasion) classification is used (in T1) depends on depth of submucosal invasion: sm1—upper (inner) 1/3rd; sm2—middle 1/3rd; sm3—lower 1/3rd.

Lymphatic spread: Above the peritoneal reflection, spread occurs upwards along the colonic lymph nodes. In mid-rectum, into the para-rectal and mid-rectal lymph nodes. Downward spread is rare occurs wh en growth is close to the anal canal into the inguinal lymph nodes. Obturator nodes may be involved in 8% of lower rectal growths. Venous spread occurs to the liver 35%, lungs 20%, adrenals 10% and other areas. Perineural spread carries poor prognosis.

Clinical Features xx Bleeding per rectum/anum (may mimic haemor­rhoids)—

earliest symptom. xx Spurious diarrhoea: It occurs in early morning due to over-

Spread xx Local spread: Initially, it spreads, locally circumferen­tially

(takes 12–18 months to complete the circum­ference of the bowel). Later spreads out to the muscular coat and peri-rectal tissue. Then to prostate, bladder, seminal vesicles in males, and uterus and vagina in females. Posteriorly into the sacrum and sacral plexus, laterally into the ureters. Haggitt’s invasion of malignant polyp (Similar to carcinoma colon) In pedunculated polyp Level 0—noninvasive carcinoma over the summit Level 1—invasion to head of pedunculated polyp Level 2—invasion to neck of the pedunculated polyp Level 3—invasion to stalk of the pedunculated polyp Level 4—invasion to base of pedunculated polyp In sessile polyp—all lesions are level 4

Duke’s staging of carcinoma rectum A.  Confined to bowel wall, mucosa and submucosa B. Extends across the bowel wall to the muscularis propria with no lymph nodes involved C.  Lymph nodes are involved

night mucus accumulation in the rectum causing urgency for defecation, but results in spurious diarrhoea with incomplete evacuation.

TNM Classification of rectal cancer—7th edition, 2010 Tumour: Tx—Primary not assessed T0—No primary tumour Tis—Carcinoma in situ: intraepithelial or invasion of lamina propria T1—Submucosa T2—Muscularis propria T3—Subserosa/perirectal tissue; T3a 50% of the external sphincter, anterior in females, multiple tracks, recurrent, or the patient has preexisting incontinence, local irradiation, or Crohn’s disease.

A

B Figs 25.77A and B: Fistula-in-ano (simple type)— typical look and site. xx Often it may heal superficially but pus may collect beneath Fig. 25.75: Fistula in ano both anterior and posterior (Multiple).

forming an abscess which again discharges through same or new opening.

Rectum and Anal Canal xx Ischiorectal fossa on each side, most often com­municates

with each other behind the anus causing horseshoe fistula. Goodsall’s (1900) Rule

Fistulas with an external opening in relation to the anterior half of the anus is of direct type. ™™ Fistulas with external openings in relation to posterior half of the anus, has a curved track may be of horse-shoe type, opens in the midline posteriorly and may present with multiple external opening all connected to a single internal opening. ™™

A

Tuberculous fistulas do not have induration, will have pale granulation tissue with watery discharge and they are most often multiple. Here, the infection occurs in lymphoid tissue over the lower part of anal canal, around anal gland opening.

Investigations xx xx xx xx

Chest X-ray, ESR and barium enema X‑ray. If required fistulogram is done only under anaesthesia. MRI/MRI fistulogram ideal. Endorectal ultrasound (US perineum) is useful to assess deeper plane. xx Discharge study, methylene blue dye study, biopsy. xx Colonoscopy often when ulcerative colitis/Crohn’s is suspected. xx Specific blood test.

B

Fig. 25.78A and B: (A) Goodsall’s rule. Anterior fistulas are having straight track. Posterior fistulas are having curved track with internal opening in the posterior midline; (B) Complex fistula-in-ano. xx P/R examination shows indurated internal open­ing usually in the midline posteriorly. xx Most of the fistulas are on posterior half of anus. xx Probing in the ward and fistulogram in the ward before surgery using Lipiodol is not advisable as it may cause recrudescence of inflammation. It can be done with adequate precaution. Probing is done under general anaesthesia gently with care without creating extensions.

Fig. 25.79: Anterior fistula-in-ano with probe in place. Anterior low fistula has got straight track. Both internal and external openings are seen.

Fig. 25.80: Fistulogram X-ray showing track.

Fig. 25.81: MR fistulogram.

Our senses don’t deceive us; our judgement does.

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Fig. 25.82: Multiple fistulas-in-ano. It may be Crohn‘s disease; carcinoma or HIV. Biopsy should be done prior to formal therapy. MRI of perineum is of great help in such patients to anatomically evaluate the fistula-in-ano.

Fig. 25.83: Methylene blue injection to delineate track on table in fistula-in-ano.

Differential diagnosis for fistula-in-ano ™™ ™™ ™™ ™™ ™™ ™™

Urethral fistula in male Chronically infected Bartholin’s gland Pilonidal sinus Hidradenitis suppurativa Carcinoma Crohn’s tuberculosis, ulcerative colitis

Treatment xx Fistulectomy  Under G/A or spinal anaesthesia, probe is passed through external opening up to the internal opening which is felt as an induration. Fistula is opened along the probe using a knife. Fibrous track along with unhealthy granulation tissue and additional external open­ings are excised. Specimen is always sent for histopathology. Principles in management

Procedures

• Identify the cause— cryptoglandular or other • Delineate exactly the fistula anatomy — MRI/EUS • Identify relation of fistula to anal sphincter • Drain all sites of infection • Eradicate track and secondary extensions • Preserve anal continence function

• Laying open the fistula— fistulotomy with curetting • Fistulectomy • Gluing of fistula—not much useful • Mucosal flap procedure • Fistulectomy with primary repair • Fistulectomy with primary repair with episiorectopexy • Fistulectomy with secondary repair • Anal fistula plug repair (AFP) • LIFT Technique (Ligation of intersphincteric fistula track) • Seton technique (Latin—seta—a bristle) • Colostomy—lay open, fistulectomy, later closure of colostomy—for high type • VAAFT procedure (Video assisted anal fistula track ligation)

The primary objectives are to eradicate the tract and drain all associated sites of infection while simultaneously preserving anal continence

 Postoperatively—sitz bath, antibiotics, analgesics, laxatives

are given.

 Fistulectomy for low level fistulas do not cause rectal incon-

tinence.  Proper curetting of the infected anal gland area is essential.

xx Fistulotomy It is done in low anal fistula. It is technically easier. After passing the probe through the entire fistulous track, incision is made over the probe to cut and lay open the fistulous track. It is allowed to granulate and heal from the floor/surface. Technique is safer, easier and can be done on outpatient basis. xx Advancement flaps are used occasionally to get better result— mucosal flap procedure. xx Gluing of the fistula track is tried but success rate is not good. Fibrin glue is a multicomponent system containing mainly human plasma fibrinogen and thrombin. Once prepared it is injected into the fistula track which hardens in few minutes and fills the entire track. Success rate is 70%. xx Anal fistula plug (AFP) repair: Surgisis anal fistula plug (porcine small intestine submucosa, SIS) is used with 85% success rate in simple fistula. It contains naturally derived extracellular matrix which acts as scaffolding, ingrowth of tissue, remodeling. xx LIFT technique (Ligation of intersphincteric fistula track): Under anaesthesia in lithotomy position, intersphincteric space is reached through a transverse incision. Fistula running across is identified and ligated using vicryl on either side. Part is excised; outer part is curetted through external opening. xx VAAFT procedure (Video assisted anal fistula track ligation): Fine specialized endoscope is passed through the outer opening into the fistula track; with continuous irrigation fistula track is cleaned and wall is cauterized. Inner opening is ligated through vicryl from luminal side. xx Fistula clip closure—closure of the internal fistula opening with a superelastic clip made of nitinol (over-the-scope clip - OTSC) – by German surgeon Ruediger Prosst.

HIGH-LEVEL FISTULAS xx Its upper opening is at or above the anorectal ring. It is

difficult to treat.

Rectum and Anal Canal  Loose setons are used mainly to drain for long period in

Common causes are: ™™ ™™ ™™ ™™ ™™

recurrent/postoperative fistulas and due to specific causes like Crohn‘s. There is no tension in seton.  Cutting setons are used when enclosed muscle is needed to cut (cheese wiring through ice effect). It is placed tight.

Crohn’s disease Ulcerative colitis Trauma Carcinomas Foreign body

ANORECTAL STRICTURES

xx Incontinence may follow after lay opening of these fistulas.

Investigations xx Barium enema X-ray, colonoscopy, chest X-ray, biopsy.

Treatment

Causes ™™ ™™ ™™ ™™ ™™

Congenital  LGV (in females) Fibrotic anal fissure  Ulcerative colitis Irradiation  Crohn’s disease Senility  Carcinomas Postoperative (surgery for piles, coloanal anastomosis)

xx Requires staged procedure—initial colostomy is done

followed by definitive procedure. This prevents sepsis and promotes faster healing. xx Later closure of colostomy is done.

Seton Technique

Features xx Progressive constipation. xx On P/R examination, stricture can be felt as a tight ring. xx Features relevant of specific cause.

xx A silk or linen ligature is passed across the fistula and left in place with a tie. xx Striated muscle superficial to fistula track is encircled with Seton material and tied securely and left in situ to create ischaemic necrosis, dividing the muscle slowly without allowing it to spring apart avoiding gutter deformity. Even though internal sphincter is divided in this, causing adequate laying open of entire fistula track, it will well-preserve the sphincter function and pressure. xx This allows the fistula to granulate and heal from above and to close completely. Usually takes longer duration to heal. xx It is done for intermediate and intersphincteric fistula. It is used prior to definitive procedures like fistulectomy or advancement flap. It is staged fistulotomy.

A

B Fig. 25.84: Seton technique for intersphincteric fistula-in-ano. It is kept for 3 months. It can be tight or loose seton depending on the indications. It promotes formation of granulation tissue, healing by fibrosis and track recedes downwards. xx Seton can be kept for 3 months. It can be regularly replaced by new silk or any material by rail road technique without anaesthesia. xx Two types of setons are present.

Figs 25.85A and B: Anal dilator. Many proctology surgeries require regular anal dilatation postoperatively. Note how to hold the dilator to pass into the anus after applying lubricant. xx Investigations: Barium enema X-ray, biopsy, colonoscopy.

Treatment xx The cause is treated. xx Dilatation of the anal canal under general anaes­thesia. xx Resection in severe recurrent cases.

Two types of mankind are there; Hosts and Guests; on either way you are in trouble.

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SRB's Manual of Surgery xx Anal reconstruction—anoplasty is technically demanding with preservation of continence along with prevention of restenosis is important.

CONDYLOMA ACUMINATA xx It is most common sexually transmitted anal disease. It is

common in homosexual men. Penile warts or female genital warts may be present. It is caused by Human Papilloma Virus (HPV). Pruritus, discharge, pain and bleeding are the features. Large wart may block the anal canal orifice. Whitening occurs on applying acetic acid on it. Biopsy confirms the diagnosis. Treatment is local application of 25% podophyllin cream; surgical excision of the wart; intralesional injection of interferon a 2b. xx Malignancy should be ruled out by histology. xx xx xx xx xx xx xx

xx Causes may be HPV infection; HIV infection; AIN (Anal intraepithelial neoplasia); organ transplant recipients; immunosuppression. xx Anal canal tumours arise from the anorectal ring proximally to the anal verge distally, and include the anal transition zone and the nonhair or gland-bearing squamous tissue comprising the anoderm. The anal margin is defined as the hair and gland-bearing skin lateral and up to 5 cm away from the anal verge. This distinction between anal canal and anal margin malignancies is important as anal canal lesions are more aggressive and are treated differently. The incidence of anal canal lesions is significantly higher (5 times) than that of anal margin lesions. xx Epidermoid carcinoma is the most common type of anal canal malignancy—85% of all lesions. This includes squamous cell carcinoma and its variants—cloacogenic, basaloid, and transitional carcinomas. xx Twenty to twenty five per cent cases metastases occur to inguinal lymph node. xx Anal canal tumours are common in females.

Note:

•

• • • •

Buschke – Lowenstein disease (1925, giant condyloma acuminata) is a slow-growing, locally destructive verrucous plaque but seldom metastasizes that typically appears on the penis but may occur elsewhere in the anogenital region. It is commonly considered to be a regional variant of verrucous carcinoma. It is common in the penis but can also occur in anal region, vagina and scrotum. It is common in males. HPV 6, 11 and HIV infections may commonly coexist. Biopsy and MRI confirms the diagnosis. Giant condyloma acuminatum is differentiated histologically from ordinary condyloma acuminata by its thicker stratum corneum and the presence of an endophytic downgrowth, along with a tendency to invade deeper. Treatment—surgical wide excision, topical podophyllin, 5 FU, interferon, cidofevir gel, bleomycin are different treatment modalities. HPV vaccine (Gardasil) may prevent the disease. A combination of radiofrequency surgical dissection and oral acitretin is used in perianal Buschke-Lowenstein tumor with good success. The use of acitretin may eliminate the residual disease that was not removed by surgery.

ANAL INTRAEPITHELIAL NEOPLASIA (AIN) xx It is dysplasia of anal or perianal epidermis. xx It is seen in individuals with HIV infection; HPV infection (16, 18); individual who do anorectal intercourse. Classification: AIN I—absence of keratocyte maturation and cellular atypia observed in outer 1/3rd of epithelium—low grade. AIN II—cellular atypia observed in middle 1/3rd—low grade squamous intraepithelial neoplasia. AIN III—cellular atypia full thickness—high grade squamous intraepithelial neoplasia. xx Thirty per cent of anal warts will show AIN. xx It is raised scaly white/pigmented/cracked lesion. xx Biopsy confirms the disease. xx Treatment: Excision; topical imiquimod, 80% tricholoroacetic acid and oral retinoids.

MALIGNANT TUMOURS OF ANAL AREA xx Anal malignant tumours are < 2% of large bowel tumours. It can be below the dentate line (SCC, 80% of anal tumours); above the dentate line (Basaloid/transitional/cloacogenic).

A

B

Fig. 25.86A and B: (A) Anal canal carcinoma. Squamous cell carcinoma is commonest type—80%; (B) Carcinoma anal region—looks like anal margin tumour;

Classification of tumours of anal area It can be: ™™ Benign ™™ Malignant It also can be: ™™ Tumour of the anal canal (proximal to dentate line)—SCC, adenocarcinoma, melanoma ™™ Anal margin tumour (distal to dentate line)—ANI, Bowen’s disease, Paget’s disease, BCC, anal margin SCC

Types 1. Squamous cell carcinoma is the commonest type. Predisposing causes: Papilloma, irradiation, derma­titis, long standing fistula-in-ano. 2. Basaloid carcinoma—it is rare, non-keratinising squamous cell carcinoma. Highly malignant. 3. Muco-epidermoid carcinoma—arises near squamo– columnar junction. 4. Basal cell carcinoma. 5. Melanoma—blue/black in colour mistaken for thrombosed pile—poor prognosis (5 years—10%). 6. Adenocarcinoma from the anal glands in a pre-existing fistula-in-ano.

Rectum and Anal Canal Features

Investigations

• Ulceration

• Biopsy from anal region

• Bleeding

• FNAC of inguinal node

• Pain, pruritus and discharge

• US abdomen

• Irregular indurated mass

• MRI perineum is very useful

• Anovaginal fistula in females

• P/R is a must to assess upper extent of the growth

• Faecal incontinence in late cases

AJCC staging Tis—carcinoma in situ

• Inguinal node—hard, nontender

T1—tumour 5 cm T4—invasion into adjacent organs like vagina/urethra N1—perirectal nodes + N2—unilateral internal iliac/ inguinal nodes N3—perirectal + inguinal/iliac or bilateral nodes M 0—no distant spread M1—distant spread present

• Iliac nodes • Later—late constipation— obstruction

xx Squamous cell carcinoma of anal canal, usually present as

a fungating or ulcerative growth, which spreads to inguinal lymph nodes.  Biopsy and FNAC of lymph nodes are the essential investigations.  Treatment: Wide excision of the lesion with 3 to 5 cm clearance and ilioinguinal block dissection for lymph nodes are done. Follow-up radiotherapy is also often given.  Nigro regime

xx All other tumours: Abdominoperineal resection with permanent colostomy is done. Paget’s ™™ ™™ ™™ ™™ ™™

Paget’s disease of breast Paget’s disease of anal margin—of apocrine glands Paget’s disease of penis Paget’s test Paget’s disease of bone

SACROCOCCYGEAL TERATOMA xx It is an uncommon tumour, but most common of the large tumours in first 3 months of life. xx More common in females. xx Retention of large amount of primitive toti-potential cell in this region may be the reason for this tumour. xx It occurs between coccyx and rectum xx It is attached to coccyx, extends commonly downwards as a huge mass, occasionally upwards into the pelvis. xx It is a congenital condition arising from totipotent cells. xx X-ray and CT scan are must. xx Treatment: Excision soon after birth. Complications

Differential diagnosis

Ulceration

Sacral meningocele

Infection

Sacral chordoma

Urinary obstruction

Postanal dermoid

Malignant changes

Nigro Regime Nigro Regime for Anal Carcinoma (Norman Nigro, et al. 1974) ™™ Initial radiotherapy for 3 weeks 3000 rads (30 Gy total) to perineum and pelvis ™™ Then chemotherapy—5 FU, for 4–5 days; is a radiosensitizer, started on 1st day of RT as 1000 mg/m2 continuous infusion. Mitomycin C is 15 mg/m2 as single dose on 1st day of RT ™™ Later after 3 weeks abdominoperineal resection (APR)

A

 Chemoradiation is becoming popular for carcinoma of anal

canal.  Drugs used for chemotherapy are 5 FU, bleomycin, vincristine,

adriamycin.  If persistent or recurring disease presents following combined

modality therapy (CMT—chemoradiotherapy), APR with colostomy is indicated.  Neoadjuvant chemotherapy using 5 FU, cisplatin and mitomycin C is also commonly used.  In advanced growths radiotherapy is the only treatment.

B Figs 25.87A and B: Sacrococcygeal teratoma, typical site (Courtesy: Professer Suresh Kamath, MS, Mangaluru).

You never get the second chance to make the first impression.

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SRB's Manual of Surgery Causes Causes of anal incontinence ™™ ™™ ™™ ™™ ™™ ™™ ™™

xx xx xx xx xx xx xx xx

Denervation—spinal injury, spina bifida Damage—childbirth, wounds, surgeries Descent—rectal prolapse, perineal descent Debility—old age, diseases Destruction—RT, malignancy Dementia—senility, psychosis Deficiency—congenital anomalies

Irritable bowel syndrome, severe diarrhoea. Prolapsed piles, rectal prolapse. Old age, malnutrition, debilitating illness. Congenital anomalies. Trauma, surgeries, injury during childbirth in females. Spina bifida, spinal tumours, spinal injuries and surgeries. Malignancy, postirradiation. Psychological causes. Evaluation of the patient

Fig. 25.88: X-ray of a patient with sacrococcygeal tumour (Courtesy: Professor Suresh Kamath, MS, Mangaluru).

™™ ™™ ™™ ™™ ™™ ™™ ™™

For specific causes Anorectal manometry Per-rectal examination Sigmoidoscopy Electromyography Defaecography Perineometer to assess level and angle of anorectal junction

Treatment xx Suturing of the torn sphincter. xx Repair of puborectalis muscle and plication of external sphincter. xx Encircling operations around anal canal to give support using gracilis sling or mersiline sutures. xx Electrical stimulation of the puborectalis. xx Secca therapy: Temperature controlled radiofrequency energy in the anal canal and distal rectum to create scarring and fibrosis of internal sphincter and adjacent tissues.

DESCENDING PERINEAL SYNDROME Fig. 25.89: Recurrent chordoma of sacrum.

ANAL INCONTINENCE Continence of anal canal is maintained by two factors: xx Normal rectal and colonic pressure and activity. xx Normal pelvic floor function.

Types xx Urge incontinence—here rectal and colonic pressure and activity is increased but normal pelvic floor. xx True incontinence—here rectal and colonic pressure and activity is normal but defective pelvic floor function. xx Full incontinence—here rectal and colonic pressure and activity is reduced and also defective pelvic floor function. xx Temporary—treated by reassurance. Often seen after Lord’s dilatation. xx Permanent—needs definitive therapy.

xx When a healthy person increases the intra-abdominal pressure and relaxes the pelvic floor muscles, there will not be any changes in the concavity of the perineum. xx In chronic ill-patients, malnourished, and people with preprolapse, perineal descent can occur with obliteration of the normal concavity of the perineum. It is called as descending perineal syndrome. xx Levators got injured directly or indirectly causing weakening of pelvic floor. xx Anal canal is situated many centimeters below the pubo coccygeal line. Usually 3–4 cm low during straining. xx Defecography is ideal to evaluate such patients. Perineometer is also used. xx Presentations are tenesmus; incomplete evacuation; incontinence. xx Treatment is diet, laxatives, avoiding straining, and suppositories. xx Restoration of pelvic floor by various surgical methods may be needed often with rectal resection and suspension. xx Total pelvic marlex mesh repair; transcoccygeal posterior hitching of the rectum (Kraske); correction of cystocele, rectocele and enterocele. xx Results are not very good as recurrence or residual problems may persist.

Rectum and Anal Canal PROCTITIS

xx Occasionally, only cutting of puborectalis muscle is required

but with danger of developing incontinence.

It is inflammation of rectal mucosa often with the inflammation of colon and anal canal.

Types xx xx xx xx xx

Acute. Chronic. Nonspecific—common. Ulcerative proctocolitis as part of ulcerative colitis. Specific  Bacillary dysentery.  Amebic proctitis—common.  Combined amoebic and bacillary.  Gonococcal proctitis.  Lymphogranuloma inguinale (LGV).  Tuberculous proctitis.  Bilharzial proctitis due to schistosoma haema­tobium.  Enema induced proctitis especially of herbal enemas. Clinical features

™™ ™™ ™™ ™™ ™™ ™™ ™™

Pain per rectum and anum Tenesmus Passage of mucus and blood Frequent urge to pass stool Fever, loss of appetite Pain and tenderness in left lower abdomen P/R is tender

xx It is a chronic suppurativa condition of apocrine glands of the skin in axilla/perineum/mons pubis/ thighs/scrotum, etc. xx Apocrine gland duct obstruction → bacterial infection → multiple glands involvement → secondary infection (Staphylococcus aureus, streptococci) → skin oedema, multiple raised pustules → multiple communicating fistulae formation. xx Disease does not extend above dentate line or into sphincter. xx It is common in young obese females. xx Sinus; scarred areas; discharge; skin changes; pain and tenderness; foul smelling fluid are the presentations. xx Differential diagnosis are—Crohn‘s disease; fistula-in-ano; pilonidal sinus; tuberculosis; actinomycosis; LGV. xx Treatment:  Weight reduction; proper hygiene.  Antibiotics; analgesics.  Incision and drainage of abscess.  Laying open of all communicating tracks and regular dressing.  Radical local excision of entire apocrine bearing perineal skin with reconstruction using flap.  Recurrence is known to occur.

PRURITUS ANI xx It is intractable itching in and around anal canal. xx Skin is reddened, hyperkeratotic, cracked and moist.

Investigations xx xx xx xx xx

HIDRADENITIS SUPPURATIVA OF ANAL REGION

Sigmoidoscopy is more relevant than just proctoscopy. Stool study, stool culture. Mucosal biopsy. Serological tests. Relevant investigations like ESR, blood smear, and chest X-ray.

Treatment xx Antibiotics, antiamoebic drugs like metronidazole. xx In severe cases, retention enema using metronidazole, prednisolone, salazopyrin. xx IV fluids, IV antibiotics and IV metronidazole are often required. xx Treating the specific causes like tuberculosis, gonococcal infection and bilharzial infection.

PROCTALGIA FUGAX

Causes xx xx xx xx xx xx xx xx xx

Poor hygiene. Anal discharge due to fissure/fistula/piles/warts/ polyp. Trichomonas vaginalis infection of vagina in females. Parasites. Epidermophytosis. Allergic cause. Dermatitis/psoriasis. Intertrigo/erythrasma (Corynebacterium minutissimum). Diabetes mellitus; psychological cause.

Treatment Proper cause should be assessed and treated. Good hygiene; local steroid application; topical xylocaine; strapping of the buttocks are needed.

xx It is sudden severe recurring pain in the rectum of unknown

cause with segmental pubococcygeal spasm.

Features xx It is common in young people may be due to stress, straining. xx Common at night, starts suddenly, lasts for few minutes and

then subsides spontaneously. xx Pain is unbearable and severe with often constipation. xx Gradually subsides on its own.

GASTROINTESTINAL HAEMORRHAGE (GI BLEED) GI bleed is classified as upper GI and lower GI bleed. xx Upper GI bleed is bleeding above the level of ligament of Treitz. xx Lower GI bleed is bleeding below the level of ligament of Treitz.

His heart cannot be pure whose tongue is not clean.

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SRB's Manual of Surgery Ligament of Treitz is a fibromuscular band, which extends from right crus of diaphragm to duodeno­jejunal flexure with upper part made up of striped muscle fibres, lower part smooth muscle fibres and middle part with elastic fibres.

Clinical Features Acute Bleed xx Features of shock. xx Haematemesis. xx Melaena.

Chronic Bleed xx Hypochromic microcytic anaemia, glossitis, koilony­chia,

congestive cardiac failure. xx Mortality in upper GI bleed is 10%.

Investigations

Fig. 25.90: Anatomy of ligament of Treitz.

UPPER GI BLEED It is considered as: xx Variceal. xx Nonvariceal.

xx Gastroscopy to see the spurting vessel, oozing, clot in the ulcer, collected blood in the lumen of the stomach. xx CT angiography of coeliac trunk and SMA. xx Hb%, packed cell volume, CVP measurement, blood grouping and crossmatching. Ultrasound abdomen. xx LFT; prothrombin time; platelet count; blood urea and serum creatinine; serum electrolytes. xx Modified Forrest classification (refer Chapter 20—Stomach) and Rockall scoring system (better) is used. In Rockall scoring system parameters used are—age (60 [0], 60–79 [1], >79 [2] Years); shock (none [0], pluse >100 [1],) pluse >100 with hypotension [2]); comorbidity (none [0], IHD [2], renal/liver failure/advanced maligancy [3]); condition diagnosed (Mallory Weiss [0], all but mailigancy [1], upper GI maligancy [2]); endoscopic finding (none [0], dark spot, blood/ clot/visible vessel [2]). Score: 8 high.

Treatment

Causes

Treatment of upper GI bleed

xx Peptic ulcer 55%. Ulcer bleeding is precipitated by NSAIDs, steroids, alcohol. Ulcer bleeding is overall common in men. But NSAID induced ulcer bleeding is common in females. Duodenal ulcer (35%) more commonly bleeds than gastric ulcer (20%) xx Gastroduodenal erosions. xx Oesophageal varices. xx Oesophagitis and erosions. xx Carcinoma stomach—5% xx Mallory-Weiss syndrome—5–15%. xx Vascular anomalies—Dieulafoy’s syndrome (A-V malformation in the fundus of the stomach), Osler-Weber-Rendau syndrome, Ehlers-Danlos syndrome. xx Aortoduodenal fistula. xx Bleeding disorders. xx H/o drug intake—anticoagulants, clopidogrel, ecospirin. Factors which aggravate the bleeding Gastric acid which inhibits the platelet aggre­gation Pepsin, by its proteolytic action causes erosion of the ulcer into the vessel. It also digests the clot, so as to aggravate the bleeding ™™ Mucosal blood supply pattern ™™ Gastric motility ™™ Alcohol, drugs Major haemorrhage occurs when erosion of gastroduodenal artery or left gastric artery or splenic artery occurs or when bleeding occurs from varices ™™ ™™

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General Medical—PPI/tranexamic acid/octreotide Endoscopic CT angiography guided embolisation Surgical

xx General: IV fluids, catheterisation, Ryle’s tube aspiration, blood transfusion. xx Injection ranitidine IV 50 mg 8th hourly, or famotidine IV, omeprazole IV, pantoprazole IV. xx Antifibrinolytics like tranexamic acid, EACA. xx Somatostatin or octreotide, PPI infusion. xx Endoscopic therapy (tamponade, laser, haemoclip, banding, sclerotherapy, etc.) is the first line of therapy in all upper GI bleed. CT angiography guided transcatheter embolisation of artery (gastroduodenal) is very useful in bleeding duodenal ulcer if endoscopic therapy fails. Persistent recurrent bleeding needs surgical intervention. xx For varices, vasopressin, propranolol, isosorbide dinitrate, Sengstaken tube tamponade, sclero­therapy, Boerema-crile operation, Hasaab operation (devascula­risation with splenectomy), oesophageal transection, Siguira-Futagawa operation or TIPSS. xx For peptic ulcer, saline wash with 1 : 2,00,000 adrenaline, Nd:YAG laser therapy, cautery coagu­lation, thrombin injection, Finney’s pyloroplasty, partial gastrectomy, ligation of gastroduodenal or left gastriartery, cytoprotectant mesoprostil injection. xx The cause is treated, once acute episode is under control.

Rectum and Anal Canal Lower GI bleed can be: ™™ ™™

Occult bleed: >10 ml/day but not revealed Overt bleed: Bleeding which is revealed –– Overt acute –– Overt acute massive (bleed >1.5 litre/day) –– Overt chronic

Common causes

A

B

Figs 25.91A and B: Bleeding peptic ulcer (duodenal ulcer) is the commonest cause of upper GI bleed. Oesophageal varix causes dangerous severe life-threatening bleed.

Prognosis

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Internal piles Diverticular disease Neoplasia Inflammatory bowel diseases Angiodysplasia

Classification

xx Varices and gastric ulcer bleed has higher mortality. xx Bleeding duodenal ulcer has got better prognosis.

LOWER GI BLEED xx Bleeding in the GIT below the level of the ligament of Treitz. xx Normal faecal blood loss is 1.2 ml/day. A loss more than 10

ml/day is significant.

I.  Bleeding may be: Small bowel bleed: Polyp’, Meckel’s diverticulum, mesenteric ischaemia, intussusception; small bowel tumor. Large bowel bleed: Angiodysplasia, carcinoma, colitis, diverticulitis, carcinoma. Anorectal diseases: Piles, fissure-in-ano, carcinomas. II.  Bleeding may be: Congenital: Polyp’s, Meckel’s diverticulum. Inflammatory: Ulcerative colitis, infective, amoebic, Crohn’s disease. Neoplastic: Adenomas, carcinomas, polyps. Vascular: Angiodysplasia, mesenteric artery ischaemia, colitis. Others: Piles, fissure-in-ano. Angiodysplasia is common in caecum and ascending colon. Bleeding more than 1.5 litres per day is called as acute massive GI bleed. Acute bleed occurs in:

Fig. 25.92: Causes of lower GI bleed.

Causes xx xx xx xx xx xx xx xx xx xx xx xx xx

Angiodysplasia. Diverticular disease—commonest cause in Western countries. Tumours of colon or small bowel. Anorectal diseases—haemorrhoids, fissure-in-ano. Ulcerative colitis, Crohn’s disease. Colorectal polyps; rectal carcinomas. Intussusception. Tumours, either benign or malignant of colon or small bowel. Meckel’s diverticulum. Ischaemic colitis. Stercoral ulcer. Infectious colitis. Mesenteric artery occlusion.

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Mesenteric ischaemia Angiodysplasia Ischaemic colitis Meckel’s diverticulum Intussusception Acute episodes of ulcerative colitis 80% of acute bleed regress spontaneously 20% will become either massive or recurrent

Presentations xx Acute bleeding presents with features of shock. xx Chronic blood loss occurs in piles, fissures, colitis. Presents with hypochromic, microcytic anaemia. xx Tenesmus, subacute obstruction, loss of appetite, decreased weight, bloody diarrhoea is seen in carcinoma distal, large bowel. xx Per-rectal examination is a must which may reveal polyp, growth, ulcerations.

God gives every bird its food, but he does not throw it into the nest.

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SRB's Manual of Surgery xx Haematochezia. xx Mass palpable per abdomen in left or right iliac fossa or mass of intussusception. ™™ ™™ ™™ ™™ ™™

Blood with mucus—colitis, carcinoma Fresh blood as splashes in the pan—piles Maroon coloured stool—Meckel’s diverticulum Red currant jelly in stool—intussusception Bright red blood in stool—polyps

Investigations

Investigations for GI bleed

xx Hb%, packed cell volume, ESR. xx Bleeding time; clotting time; prothrombin time; platelet count; blood urea and serum electrolytes. xx Occult blood in the stool—positive faecal blood test using Guaiac reagent. xx Barium enema. xx Proctoscopy for piles and sigmoidoscopy for rectosigmoid diseases. xx Colonoscopy for colitis, carcinomas, polyps. xx Small bowel enema (enteroclysis).

A

xx Commonly, it is due to either missed common cause or angiodysplasia. xx If it is angiodysplasia, angiography, nuclear scintigraphy, capsule endoscopy; then angiographic embolisation or resection of the part of the bowel is done. xx Enteroscopy, upper and lower GI scopies are needed in other conditions. xx All other conditions are treated accordingly.

B

Figs 25.93A and B: Sigmoid diverticula on colonoscopy. It is the common cause of lower GI bleed in Western countries. xx US abdomen. xx Mesenteric angiogram is very useful investigation in acute bleed, especially in angiodysplasia. xx Technetium scan for Meckel’s diverticulum. xx Capsule endoscopy.

Treatment xx Endoscopic fulguration or therapeutic emboli­sation or right hemicolectomy (for angiodysplasia). xx Endoscopic polypectomy for polyps. xx Treatment for ulcerative colitis with mesacol enema or drugs or total proctocolectomy with ileo-anal anastomosis. xx Surgical resection of colonic carcinoma. xx Massive resection of small bowel in mesenteric ischaemia. xx Sigmoid colectomy in sigmoid diverticula. xx Cause is treated. xx Proper exploration through a lengthy midline incision is essential.

OBSCURE GI BLEED xx It is intermittent GI bleed for which no source has been found endoscopically/radiologically. xx It is 5% common.

Blood ™™ Haematocrit, LFT, blood urea, serum creatinine ™™ Serum ferritin, iron, binding capacity ™™ Coagulation profile—platelet count, BT, CT, PT, APTT Occult stool blood test (1–2 ml/day) ™™ Benzidine test ™™ Guaiac test ™™ Haemoccult—guaiac impregnated electrophoresis paper ™™ Fecal test ™™ Immunological test Endoscopy ™™ Gastroduodenoscopy ™™ Proctosigmoidoscopy ™™ Colonoscopy—often difficult in acute bleed for clarity visualisation, if bleeding point is seen it can be controlled by cautery, laser, haemoclips, injection sclerotherapy, heater probe etc. But still it becomes the test of choice once bleeding has controlled/ stopped temporarily ™™ Small bowel endoscopy—push type (160 cm); Sonde enteroscope (275 cm, 5 mm diameter with balloon tip) are used. Entire small intestine is visualised while withdrawing but therapy or biopsy is not possible Angiography ™™ It identifies when bleeding rate is 0.5 ml / min; useful in active bleed; in therapeutic embolisation, injection vasopressin can be done. Embolisation of small bowel vessel may cause bowel infarction which is dangerous and resection is needed in such situation. Visualisation in angiography can be improved by selective infusion of vasodilators like tolazoline and prostaglandins, using magnification films, using vasoconstrictor drugs ™™ Angiogragraphic criteria in angiodysplasia are—early and prolonged filling of draining veins; cluster of small arteries; visualisation of vascular tuft Nuclear scintigraphy ™™ Identifies 0.1 ml/min of bleed ; Tc sulphur colloid scan is very sensitive and is completed in 1 hour but increased uptake in spleen and liver obscures bleeding point and needs repeated administration due to rapid clearance; Tc labeled RBC recirulates and so effective for 1 day with better localisation ™™ Advantages are—high-sensitivity even with active continued bleed; screening test prior to angiography ™™ Problems are—no specificity; therapy is not possible Other methods ™™ CT angiography; MR angiography ™™ Aortography for aortoenteric fistula ™™ Intraoperative localisation—on table enteroscopy; on table Doppler; on table bowel lavage and colonoscopy

Chapter

26

Urology A. Kidney It is no exaggeration to say that the composition of the blood is determined not by what the mouth ingests but by what the kidneys keep; they are the master chemists of our internal environment, which, so to speak, they synthesize in reverse. —Homer William Smith, 1939

CHAPTER OUTLINE ™™ Anatomy of Kidney and Ureter ™™ Plain X-ray—Kidney, Ureter and Bladder ™™ Intravenous Urogram ™™ Retrograde Pyelography ™™ Renal Angiogram ™™ Micturating Cystourethrography ™™ Ascending Urethrogram ™™ Isotope Renography ™™ Cystoscopy ™™ Catheters –– Foley’s Catheter –– Malecot’s Catheter

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–– Red Rubber Catheter Nephrostomy Suprapubic Cystostomy Haematuria Horseshoe Kidney Cystic Diseases of the Kidney –– Polycystic Kidney Disease –– Solitary Renal Cyst Duplication of Renal Pelvis and Ureter Retrocaval Ureter Uretrocele Injuries to Kindney

ANATOMY OF KIDNEY AND URETER

KIDNEY—ANATOMY xx They are a pair of excretory organs situated retro­peritoneally, on the posterior abdominal wall; one on each side of vertebral column. xx Vertically it extends from the upper border of T12 vertebra to the centre of the body of L3 vertebra. The right kidney is slightly lower than the left, left kidney is slightly nearer to the median plane. xx Each kidney is about 11 cm long, 6 cm broad, 3 cm thick. Lateral border is convex. Medial border is concave with a hilum. Structures seen in the hilum are (from anterior to posterior)—(1) renal vein, (2) renal artery, (3) renal pelvis. xx Upper pole is related to suprarenal gland; lower pole lies 1 inch above the iliac crest.

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Renal Tuberculosis Hydronephrosis Pyonephrosis Carbuncle of Kidney Perinephric Abscess Renal Calculus Ureteric Calculi Staghom Calculus Benign Tumours of Kidney Wilms’ Tumour Renal Cell Carcinoma Approaches to Kidney

xx Capacity of renal pelvis is 10 ml. xx The angle between the 12th rib and the outer border of the sacrospinalis is the kidney angle. Kidney pain is usually referred here and pressure over this point elicits pain in kidney lesions. xx Hepatorenal pouch is a peritoneum lined deep recess, related to the upper pole of kidney. It is the lowest site when the body is in horizontal position, excluding the pelvis. Collection of extravasated fluid is likely to occur in this pouch following surgeries to liver and biliary tract.

Capsules of Kidney 1. Proper capsule—fibrous membrane which can easily be stripped off from the organ.

The remedy for injuries is not to remember them.

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SRB's Manual of Surgery 2. Perirenal fat is in the space of Gerota. 3. Renal fascia of Gerota—has got anterior layer (Fascia of Toldt) and posterior layer (Fascia of Zuckerkandl). 4. Pararenal body of fat.

Structure of Kidney Gross Coronal section shows outer brownish cortex, inner pale medulla, renal sinus. Renal sinus is a space that extends into the kidney from hilus. It contains (1) branches of renal artery, (2) branches of renal vein, (3) renal pelvis. The pelvis divides into 2–3 major calyces which, in turn divides into 7–13 minor calyces.

Histology Each kidney is composed of 1–3 millions of uriniferous tubules; each of which has a collecting part (collecting tubules) and secretory part (nephron).

Blood Supply It is from renal artery, which arises from the aorta at right angles, at the level of intervertebral discs between L1 and L2 vertebrae. About 95% of abdominal aortic aneurysm arises below the level of origin of renal artery.

Lymphatics They are drained into para-aortic nodes. Perinephric fat is removed during nephrectomy (for malignancies), as intrarenal lymphatics freely com­municate with the plexus in the perinephric fat.

URETER—ANATOMY xx Each ureter is 25–30 cm long. It begins within the renal sinus as a funnel-shaped dilatation called renal pelvis. xx It enters the bladder wall obliquely to open at the lateral angle of the trigone. xx It lies in the retroperitoneal space not attached to any fixed structures, so can be displaced or obstructed by retroperitoneal masses like tumours or aneurysms. xx Abdominal portion of ureter lies on the medial portion of psoas major muscle near the tips of transverse processes of lumbar vertebra (which is very well seen in IVP). xx The ureter enters the pelvis crossing the end of common iliac or beginning of external iliac artery. xx In females, uterine artery crosses the ureter from lateral to medial side, about 2 cm lateral to the cervix (this has to be remembered while ligating the uterine arteries in hysterectomy). Normal sites of constrictions: (1) PUJ, (2) At the brim of lesser pelvis, (3) Along its passage through the bladder wall

xx Arterial supply: Upper segment of ureter receives blood supply from branches of renal and adrenal arteries; the middle portion from the branches of arteries of posterior abdominal wall; the pelvic portion from the branches of internal iliac arteries.  Vessels reach the abdominal portion of ureter on the medial side; whereas the pelvic portion receives on the lateral side (This has to be remembered while mobilising the ureter). The vessels form an anas­tomotic plexus in the adventitia of the ureter, which is found to be deficient in 10–15% of individuals leading to necrosis of cut ends of ureter following extensive mobilisation.

PLAIN X-RAY—KIDNEY, URETER AND BLADDER (KUB) Fig. 26.1: Segments of kidney. The kidney is divided into anatomic segments based on blood supply. In the hilum, the main artery divides into anterior and posterior divisions. The anterior division supplies the apical, upper, middle and lower segments; posterior segment is supplied by the posterior division. The knowledge of this is important in the operation of anatrophic nephrolitho­tomy, where a functionally avascular plane (Brodel) between the posterior segment and the upper and middle segments exist on the posterior half of the kidney, about two-thirds of the way from the hilum to the lateral margin of the kidney.

Nerve Supply T10,11,12 through the lesser and lower splanchnic nerves.

xx Preparation of the patient: Enema/bowel wash/laxative is given on the previous day and the patient is asked to fast in order to reduce the bowel gas shadows in X-ray. xx High penetration X-ray is taken in supine position which covers pubic symphysis and lower two ribs. xx Interpreting the film: a. First bony parts are looked for, i.e. the hip, pelvis, lumbar vertebrae for fractures, scoliosis, spina bifida, secondaries in the spine. b. Kidney shadow: Kidney shadows are visua­lised in plain X-ray KUB due to difference in the density between kidney (high vascularity) and perinephric fat (low vascularity). Findings noted are size, location, calcification and stones. In children, perinephric fat is absent and so kidney shadows are not visualised. c. Psoas shadow: It is visualised well in normal KUB.

Kidney Psoas shadow is obliterated in: ™™ ™™ ™™ ™™ ™™ ™™

In enlarged kidney In scoliosis due to inflammatory or infiltrative causes In malignancy Tuberculous spine with cold abscess (psoas abscess) Splenic injury—in left-sided shadow Retroperitoneal tumours

d. Ureteric line: It is looked for any radio-opaque shadow (ureteric stone). It runs along the tips of the transverse processes of the lumbar vertebrae, crosses the sacroiliac joints and reaches up to a point medial to the ischial spine. e. Bladder, prostate and urethral areas are visualised for any lesion.

A

B

Fig. 26.2: Plain X-ray KUB AP-view. Note the psoas shadow.

INTRAVENOUS UROGRAM (IVU) Procedure Renal function must be normal. xx Overnight fasting for 8 hours is advised. Laxa­tives are given to reduce bowel shadow and get a good quality film. xx First, a plain X-ray KUB is taken (IVU should not be read without doing KUB). xx Then 1 ml test dose of sodium diatrizoate (Urograffin) or meglumine iothalamate is injected IV and waited for 5–10 minutes for any reaction. If no adverse reaction occurs, then full dose 1 ml/kg body weight, IV urograffin is given (40–50 ml). xx X-ray is taken in 1–5 minutes, which shows the nephrographic and secretory function of the kidneys. xx Later 15 minutes and then 20–30 minutes films are taken. xx Further films are taken depending on the need. xx Film can be taken as late as 72 hours. Late films show bladder pathology as well as residual urine. xx In case of renal failure with high blood urea, dose of dye is increased to 2 ml/kg body weight to get a better film—Infusion IVU. Often diuretics are used in these patients to have better secretion. xx Lower abdominal compression is done for 10 minutes to have better definition of calyces, but not done in children and patients with abdominal aortic aneurysm. xx Minute IVU: In case of renal artery stenosis, within first minute many films are taken to see nephro­graphic shadow (where a small, concentrated kidney is seen). xx Nonvisualization of kidney: No contrast is seen in the film even after 12 hours.

C Figs 26.3A to C: IVU showing hydronephrosis with clubbing of calyces and dilatation. Delayed post-lasix film often should be taken whenever there is poor secretion in initial films. Film can be taken as late as 72 hours. This delayed film shows dilatation (Courtesy: Dr Navinchandra Shetty, MD, HOD of Radiology, KMC, Mangaluru).

Fig. 26.4: IVU showing hydronephrosis on right side; normal secretion on left side; with bladder filling

Men find it easier to flatter than praise.

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SRB's Manual of Surgery Intravenous Urogram (IVU) Indications

Findings

1. Hydronephrosis

Clubbing of calyces

2. Congenital anomalies a. Horseshoe kidney

Flower vase appearance

b. Duplex kidney and double ureter c. Ureterocele

Adder (cobra) head appearance

d. Polycystic kidney disease

Spider leg appearance

e. Retrocaval ureter

Reverse ‘J’ sign with hydronephrosis

3. Renal cell carcinoma

Irregular filling defect; spider leg appearance

4. To see the function of the kidneys in bilateral diseases

Bilateral stones, obstructive uropathy

5. After surgery for urinary diseases

To see the function of kidneys and outcome of the surgery

6. Renal injury

To see the function of other kidney (a very specific investigation)

Contraindications 1. Iodine sensitivity—may go for anaphylaxis. Hence, all precautions must be taken and essential drugs should be available while doing IVU 2. Multiple myeloma and hypergammaglobulinaemias (Acute renal failure may be precipitated due to dehydration) 3. Toxic thyroid

Procedure xx Under G/A, cystoscope is passed. Ureteric orifice is visualised. xx Ureteric catheter is passed. Dye, sodium diatrizoate is injected. xx Patient is put in 15° head down position to allow the dye to reach upper urinary system. xx X-ray is taken.

Advantages xx Prior to dye injection selective urine sample can be taken from each ureter. xx Brush biopsy from suspected urothelial tumours of upper urinary tract can be taken. xx Better-delineation of anatomy (due to more concen­tration of dye).

Fig. 26.5: Ectopic kidney right sided IVU picture. It is un-ascended kidney. It often presents as mass in the right iliac fossa. CT scan is diagnostic. Differential diagnoses for masses in right iliac fossa are nodal mass; carcinoma caecum; tuberculosis; psoas abscess; retroperitoneal tumour. Sepsis; stones; tumour; can occur in ectopic kidney. Management of whatever problems arise is done through open method. Bilateral ectopic kidney may lead into eventual renal failure. Isotope scan is diagnostic.

RETROGRADE PYELOGRAPHY (RGP) Indications ™™ ™™ ™™

Failure of showing any secretions in an IVU as late as 72 hours film Urinary tuberculosis Urothelial tumours from the renal pelvis

Fig. 26.6: Left RGP—normal study.

Kidney Disadvantage Anaesthesia is required and is laborious.

RENAL ANGIOGRAM Indications ™™ ™™ ™™ ™™ ™™

Renal artery stenosis Renal artery atheroma Renal artery aneurysm Occasionally renal cell carcinoma Arterial anomalies

Procedure Retrograde Seldinger technique: xx Through femoral artery, using Seldinger’s needle selective angiogram is done to visualise tumour vascularity, narrowing, ano­malies. Dye used is Hypaque. Dose: 6–7 ml. xx Therapeutic embolisation, transluminal balloon angioplasty for renal artery stenosis can also be done by this approach. xx Translumbar approach for angiogram (through aorto­gram) is also used. Hypaque used is 30 ml. Complications ™™ ™™ ™™ ™™ ™™

Paraplegia Embolism Dissecting aneurysm Bleeding Renal tubular necrosis

Fig. 26.7: Micturating cystourethrogram showing concomi­tant existence of posterior urethral valve (causing dilatation of proximal urethra) and vesicoureteric reflux (left side).

ASCENDING URETHROGRAM xx xx xx xx xx

It is the investigation of choice for stricture urethra. Red rubber catheter is passed into the external meatus. Water-soluble iodine dye is injected through the catheter. Oblique X-ray films are taken to visualise the urethra. Site, size, extent of stricture and extra­vasation can be found out in urethrogram.

Renal pharmacoangiogram: xx Noradrenaline is injected along with the dye. Normal vessels will constrict in res­ponse to noradrenaline. But since tumour is auto­nomous, vessels in renal cell carcinoma do not respond to noradrenaline and so tumour blush is seen.

MICTURATING CYSTOURETHROGRAPHY (MCU) Indications a. Vesicoureteric reflux. b. Posterior urethral valve.

Procedure

A

Catheter is passed into the bladder. Dilute iodine dye is infused. X-ray is taken during micturition. Free reflux is looked for. Applying pressure over the suprapubic region, X-ray is taken. Pressure reflux is studied. Vesicoureteric reflux is graded depending on the severity of the reflux—as:   I—Ureters seen II—Ureters and pelvis are seen III—Ureters, pelvis, calyces are seen IV—With grossly distended calyces V—Tortuous elongated serpentine ureters It can be unilateral or bilateral. Often it is associated with posterior urethral valve. It is often complicated by infection, pyonephrosis and renal failure Investigations: MCU, IVU, U/S, blood urea and serum creatinine Treatment: Tailoring of ureter with reimplantation

B Figs 26.8A and B: Ascending urethrogram showing stricture urethra.

Excellence is never granted to man but given as the reward of labour.

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SRB's Manual of Surgery ISOTOPE RENOGRAPHY xx A measure of individual kidney function is obtained by this method using a gamma camera. xx Radiolabelled Technetium 99m DMSA (Dimer­capto- succinic acid) or DTPA (Diethylenetriamine-penta acetic acid) is given intravenously. DTPA—renal function. DMSA—renal parenchymal changes.

It shows: xx Early vascular phase. xx Then secretory phase. xx Later excretory phase.  This allows the assessment of renal plasma flow to each kidney and the efficiency and effectiveness of pelvicalyceal excretion also.  Secretion 5 RBC’s/HPF). ™™ ™™ ™™ ™™ ™™

Early (initial) haematuria: Urethral origin, distal to external sphincter Terminal haematuria: Bladder neck or prostate origin Diffuse (total) haematuria: Source is in the bladder or upper urinary tract False haematuria: Discolouration of urine from pigments such as food colouring and myoglobin. Silent haematuria is due to tumours of kidney or bladder unless proved otherwise.

Fig. 26.21: Suprapubic cystostomy (SPC). Malecot’s or Foley’s catheter can be used.

Procedure xx Under local anaesthesia (Xylocaine 2% above the pubis, in the midline) or G/A, a vertical midline incision of 3 cm in length is placed through linea alba. Skin, fascia, anterior rectus sheath are incised. Recti are retracted. In extraperitoneal space, peritoneum with pad of fat is reflected upward. xx Bladder is identified by the pattern of detrusor muscle and vesical venous plexus and is also confirmed by aspirating urine through a syringe.

Causes ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Renal injury Urinary stones Wilm’s tumour Tuberculosis Renal cell carcinoma Cystitis Bladder tumour Urinary bilharziasis BPH, carcinoma prostate Renal infarct Glomerulonephritis Blood dyscrasias

Kidney

A

Fig. 26.23: Causes of haematuria.

Investigations xx Urine culture and sensitivity (urine test for haematuria—

Benzidine test). xx Ultrasound to look for the stone, tumour in the urinary tract. xx Cystourethroscopy to look for bladder or urethral pathology. xx IVU look for function of the kidneys. xx Urinary cytology for diagnosing urothelial malignancy. xx Bleeding time; clotting time; prothrombin time; platelet count. xx CT abdomen. xx Renal function tests—blood urea, serum creatinine.

B Figs 26.24A and B: (A) Horseshoe kidney and (B) Plain X-ray KUB showing horseshoe kidney with renal stones.

Clinical Features xx Presents as a fixed, nonmobile, firm mass in the midline at the level of 4th lumbar vertebra which is resonant on percussion. xx It is more prone for infection, stone formation, hydronephrosis, tuberculosis.

Management

Diagnosis

Cause should be identified and treated. Blood transfusion. Antibiotics. Nephroureterectomy for RCC; removal of stone from kidney, ureter, urinary bladder. xx Treatment of bladder tumour by cystoscopic resection; intravesical chemotherapy using BCG; radiotherapy; systemic chemotherapy. xx Treatment of medical causes like glomerulonephritis. xx Correction of BPH. xx Correction of bleeding diathesis.

xx IVU—medialisation of lower calyces and curving of ureter like a ‘flower vase’. xx Ultrasound abdomen.

xx xx xx xx

HORSESHOE KIDNEY xx It is a developmental anomaly where there is failure of complete ascent of kidneys with the fusion of lower or upper poles. It is due to fusion of subdivisions of mesonephric duct, when the embryo is as early as 30–40 days old. xx This condition is common in males. xx Fusion of lower pole is common (rarely upper poles). xx Most common site is in front of 4th lumbar vertebrae. The part in front of the vertebra is called as isthmus. It has blood supply which freely communicates one kidney to other. Isthmus usually lies in front of aorta.

Fig. 26.25: IVU showing flower vase appearance of horseshoe kidney.

When the patient dies the kidneys may go to the pathologist, but while he lives the urine is ours. It can provide us a serial story of the major events going on within the kidney. —Thomas Addis

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SRB's Manual of Surgery xx Urine analysis, blood urea and serum creatinine are supportive investigations. xx CT abdomen, CT angiogram.

Treatment xx Whatever the complication occurs in horseshoe kidney, it is treated accordingly. xx Per se separation of isthmus is not indicated, unless to approach aorta for aortic diseases.

CYSTIC DISEASES OF THE KIDNEY Types xx Genetic  Adult polycystic kidney disease (Autosomal dominant).  Infantile polycystic kidney disease (Autosomal recessive)— fatal. xx Nongenetic: Simple cyst, multicystic kidney, medullary sponge kidney. xx Acquired renal cystic disease may develop in patient on longterm dialysis.

POLYCYSTIC KIDNEY DISEASE (PCKD) xx Adult PCKD is inherited as autosomal dominant disease. It is common in females. xx It is bilateral and presents in third decade. One side presents little earlier than other side.

xx Associations  Polycystic diseases of liver (18%), pancreas and lungs.  Berry aneurysm in the circle of Willis. xx Cyst formation occurs at the junction of the distal tubule and the collecting duct. xx Grossly it contains multiple cysts with a clear or brownish fluid (due to haemorrhage). Clinical features ™™ ™™ ™™ ™™ ™™ ™™

Bilateral palpable renal mass Loin pain Haematuria Infection Hypertension Uraemia

xx Renal mass, which is lobular, firm, mobile, moves with respiration, ballotable, with dull renal angle and resonant band in front. xx Pain, which is due to stretch of renal capsule or haemorrhage into a cyst. xx Haematuria (25%), due to overdistended cyst rupturing into the renal pelvis. xx Infection is due to stasis. xx Hypertension (75%). xx Uraemia occurs in late stage due to renal failure. Differential diagnosis ™™ ™™ ™™

Renal cell carcinoma Hydronephrosis Solitary renal cyst

Investigations xx Ultrasound confirms the presence of cysts. xx IVU—Spider leg pattern with an elongated com­pressed renal pelvis, narrowed and stretched calyces. xx Blood urea and serum creatinine. xx Urine shows low specific gravity.

Treatment A

xx Wait and watch policy. xx If one of the cysts overdistends causing pain, haemorrhage, infection, then surgical intervention is required. xx Rovsing operation: The kidney is exposed. The cyst is opened. The fluid is evacuated. The cut edge is marsu­pialised. xx Presently US-guided aspiration is done as a simpler approach. xx Laparoscopic/retroperitoneoscopic aspiration/de-roofing of the renal cyst. xx Once renal failure sets in, then initial haemodialysis followed by bilateral nephrectomy, is done and later renal transplantation should be planned for.

SOLITARY RENAL CYST B Figs 26.26A and B: Polycystic kidney disease, picture and CT scan. It is bilateral, multiple.

xx Solitary renal cyst is never congenital. xx It is due to an earlier trauma or infection resulting in blockage of tubule, leading to cyst formation. xx It is usually uni­lateral, presents as a renal mass which is smooth, often tender if infected or haemorrhagic.

Kidney Differential Diagnosis xx xx xx xx

Renal neoplasm. Hydronephrosis. Polycystic disease. Hydatid cyst.

xx Usually unilateral. Common on the left side. xx In 3% of cases, it is associated with duplication of ureter. xx Upper renal pelvis is small, drains the upper calyces. Lower renal pelvis is larger, drains the middle and lower calyces. xx Double ureter when associated, may be partial where two ureters join in lower third or complete where upper ureter opens into the bladder at a lower level and lower ureter opens into the bladder at the upper, normal ureteric orifice. This is called as “Weigert Meyer Law”. xx In partial duplex, there is reno-renal reflux resul­ting in infection, stone formation and hydronephrosis.

Investigations xx xx xx xx

IVU—diagnostic. US to look for complications. Cystoscopy shows double ureteric orifices on the same side. DTPA scan to see the function.

Fig. 26.27: Solitary renal cyst. It is acquired, unilateral.

Investigation xx Ultrasound and IVU confirms the diagnosis. xx CT scan.

Fig. 26.29: Duplex renal system.

Fig. 26.28: Left side renal cyst—CT picture. It could be solitary renal cyst. It can be aspirated or de-roofed by laparoscopy/retroperitoneoscopy.

Treatment xx Kidney is exposed. The cyst is aspirated and a portion of the cyst wall is removed (Kirwin’s operation) and cavity is filled with perinephric fat. xx Occasionally if the cyst is in one of the poles, partial nephrectomy is done. xx Laparoscopic approach.

DUPLICATION OF RENAL PELVIS AND URETER xx It is most common congenital anomaly of the upper urinary tract (4%).

A

B

Figs 26.30A and B: Bilateral complete duplex kidney on table look and X-ray postoperatively. Both duplex ureters are reimplanted into the urinary bladder.

Good health is a serious business: like life itself, it has to be worked at and it takes on added meaning with effort. —Normour Cousins

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SRB's Manual of Surgery Treatment xx Ureteric meatotomy is done if there is narrowing of the orifice. xx The co-existing complications are treated.

B Fig. 26.32B

Figs 26.32A and B: Retrocaval ureter—IVU picture showing reverse J sign. On table finding of retrocaval ureter. It is treated by Anderson’s Hynes operation. It causes hydronephrosis. It is due to anomalous development of IVC. xx IVU shows hydronephrosis with ‘reverse J sign’. xx Treatment:Anderson Hynes’ operation. Fig. 26.31: IVU showing bilateral duplex kidney. xx Often heminephrectomy including removal of corresponding ureter may be essential as treatment. xx In females with complete duplication, lower ure­teric orifice is ectopic, causing urinary incontinence which needs partial nephrectomy or ureteric reimplantation.

URETEROCELE xx It is a cystic enlargement of the intramural portion of ureter due to congenital atresia of the ureteric orifice. Its wall contains mucous membrane only. xx It is common in females, often bilateral (10%). Complications

RETROCAVAL URETER xx It is due to developmental defect of IVC, as a result of which right ureter passes behind the IVC, causing right-sided hydronephrosis with upper third hydroureter.

™™ ™™ ™™

Stone formation Recurrent infection Hydronephrosis

Stephen classification Stenotic, sphincteric, sphinctero­stenotic

A Fig. 26.32A

Fig. 26.33: IVU reveals left-sided ureterocele with duplex kidney. Note the characteristic Cobra (Adder) head pattern of left ureter­ocele.

Kidney Investigations

Types

xx IVU—shows Adder head appearance or cobra head appearance. xx Cystoscopy—shows translucent cyst which is thin walled surrounding the ureteric orifice.

1. Small subcapsular. 2. Large subcapsular. 3. Cortical laceration. 4. Laceration with perinephric haematoma. 5. Medullary laceration with bleeding into the renal pelvis. 6. Corticomedullary complete rupture. 7. Hilar injury (most dangerous). Grading of renal injury 1. Subcapsular nonexpanding haematoma without parenchymal laceration 2. Cortical laceration 1 cm depth; no urine extravasation 4. Parenchymal laceration extending through cortex and medulla with collecting system; with extravasation of urine; expanding subcapsular haematoma 5. Renal pedicle avulsion; shattered kidney

Fig. 26.34: Ultrasound picture of ureterocele—Adder head appearance.

Clinical Features

Treatment

xx Features of shock. xx Haematuria—may be mild to profuse depending on the

xx Cystoscopic ureteric meatotomy with the removal of cyst wall. xx In addition to that co-existing complications should be treated. xx Often ureteric reimplantation is needed.

xx Sudden delayed profuse haemorrhage causing haematuria

INJURIES TO KIDNEY xx Commonly, it is due to a blunt injury. xx Often it is associated with other abdominal injuries—of

liver, spleen, bowel, mesentery, etc. xx Per se renal injury is extraperitoneal.

type of injury. can occur between 3rd day to 3rd week after trauma. xx Clot colic. xx Bruising, swelling and tenderness in the loin. xx Paralytic ileus with abdominal distension occurs due to

retroperitoneal haematoma implicating splanchnic nerves.

Investigations xx CT scan is the investigation of choice. It gives the grading

of the renal injury; identifies the associated injuries; gives idea about the function of the kidney reasonably.

A

B

C

D

E

F

G Fig. 26.35: Renal trauma causing extensive laceration. Patient underwent nephrectomy (Courtesy: Dr Ashfaque Mohammed, DNB; KMC, Mangaluru).

Figs 26.36A to G: (A) Small subcapsular; (B) Large subcapsular; (C) Cortical laceration; (D) Laceration with perinephric haematoma; (E) Medullary laceration with bleeding into the renal pelvis; (F) Corticomedullary complete rupture, (G) Hilar injury (most dangerous).

The value of experience is not in seeing much but in seeing wisely—William Osler

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SRB's Manual of Surgery xx Ultrasound abdomen is also important initial tool to identify

the site and type of injuries, haemoperitoneum and associated injuries. It is very useful tool to check the response for conservative therapy by repeating it at regular intervals. xx IVU is also useful to see the function of the injured kidney as well as opposite kidney; often it is possible that opposite renal artery goes for reflex spasm, temporarily ceasing the function of the opposite kidney. This may lead into uraemia with raised blood urea and serum creatinine and often needs haemodialysis for few times. Presently, IVU is not an essential investigation; but often done for documentation. xx Renal function tests at regular intervals; serum electrolyte estimation, haematocrit assessment, blood grouping—are other needed investigations. xx Chest X-ray, CT scan chest, plain X-ray abdomen often may require to be done.

Treatment

Complications ™™ ™™ ™™ ™™ ™™ ™™ ™™

Clot retention in the bladder and may go for renal failure Pararenal pseudohydronephrosis Infection Perinephric abscess Aneurysm of the renal artery Renal failure Hypertension occurs 3 months later

RENAL TUBERCULOSIS xx Commonly it is secondary. Primary may be in the lung. xx Tuberculous bacilluria occurs with an early lesion in the

renal cortex, and the disease spreads along the ureter causing tuberculous ureteritis and stricture ureter. xx Tuberculous kidney results in any of the following pathological types.

I. Initially always conservative:  Catheterise and watch the urine colour and output.  Blood transfusion.  Strict observation with regular monitoring of the pulse, BP,

temperature, U/S follow-up daily.  Sedation, analgesic and antibiotics.  75% of patients respond to conservative mana­gement.  While treating conservatively, regular moni­toring of blood urea

and serum creatinine is a must.  If the patient goes in for renal failure, haemo­dialysis should be

done for 6–8 weeks. Mean­while, other kidney starts functioning again and patient recovers without any further problem.

II. Indications for surgical intervention:

A

B

C

D

 When there are signs of progressive blood loss with the condi-

tion of the patient deteriorating.  Formation of progressive perinephric haema­toma (pulsatile

haematoma).  When there are associated other injuries.  Hilar injury with PUJ disruption.

Surgery (Only in 10–20% of Patients) Options: xx Gentle suturing of the laceration. Often kidney is friable, this is not possible. xx Then nephrostomy (Cabot’s) is done. xx When the injury is in the poles, partial nephre­ctomy is done. xx In hilar injury and severe laceration, nephrectomy is the only choice. Types

Treatment

I Only bruise/contusion

Conservative

II Breach in calyceal system rupture of one of the small branches of renal artery

Conservative/ nephrectomy

III Rupture of pelvi-calyceal system/ renal substance

Nephrectomy

Figs 26.37A to D: Specimen of kidney showing dilatation and caseous material as content. It is tuberculous pyonephrosis. Ureter is visualised in the specimen. Often there may be ureteric stricture due to tuberculosis.

Pathological Types Through blood, bacteria reach the glomeruli causing caseating granuloma with Langhan’s type of giant cells and epithelioid cells. These granulomas coalesce to form a papillary ulcer and other consecutive different forms.

Kidney xx xx xx xx

Tuberculous papillary ulcer. Cavernous form. Hydronephrosis. Pyonephrosis [due to (secondary) superadded infection by E. coli, Klebsiella]. xx Tuberculous perinephric abscess. xx Calcified tuberculous area (mimics calculi, hence called as pseudocalculi). xx Caseous kidney—often called as putty kidney or cement kidney (it goes for autonephrectomy). xx Miliary tuberculosis. xx Tuberculous bacilluria occurs from an early stage of the disease which causes tuberculous ureteritis and stricture ureter. Most common site is ureterovesical junction; second common site is pelviureteric junction.  Tuberculous cystitis eventually results in golf hole ureter and thimble bladder (cystoscopic findings). This is due to fibrosis causing rigid withdrawn dilated ureteric orifice looking like golf hole. Entire urinary bladder gets fibrosed, stiff and unable to dilate and accommodate urine causing thimble systolic bladder.  Tuberculous prostatitis, seminal vesiculitis (P/R—palpable seminal vesicle), tuberculous epididymitis and funiculitis are other associations. Thickened epididymis with ulcer on the posterior aspect of the scrotum may often be found. Tuberculous funiculitis with beaded, thickened vas deferens.

Clinical Features xx Common in males.

xx xx xx xx

xx xx xx xx xx xx xx xx xx xx

Investigations xx xx xx xx xx

xx xx xx xx

Fig. 26.38: Mode of spread in urinary tuberculosis.

Common on right side. Frequency—both day and night. Polyuria. Sterile pyuria: Urine is pale and opalescent with presence of pus cells without organisms in an acid urine—abacterial aciduria (Other causes: Intersti­tial cystitis, chlamydia). Painful micturition with often haematuria. Haematuria may be overt or microscopic (50%). Renal pain and suprapubic pain. Suprapubic pain is more common due to cystitis. Tuberculous kidney is rarely palpable unless there is hydronephrosis or perinephric abscess. Enlarged prostate and seminal vesicle, thickened beaded vas, thickened epididymis, impotence, infertility are other features. Presentation like acute pyelonephritis. Features of urinary stones; recurrent urinary tract infection; renal failure if both kidneys are diseased; hypertension. Haemospermia; pelvic pain. Dyspareunia; menstrual dysfunction; vaginal discharge; infertility in females. Fever and weight loss. Often cough with expectoration and haemoptysis may be present.

↓Hb%. ↑ESR. Mantoux skin test is usually positive. Chest X-ray. U/S abdomen. Three consecutive early morning samples of urine (EMSU) are collected and sent for microscopy (Ziehl-Neelsen staining), culture (L-J media) or guinea pig inoculation. Plain X-ray KUB—shows calcification. CT scan of abdomen and pelvis to see hydronephrosis, shrunken kidney, stricture, necrosis. IVU—hydrocalyx, narrowing of calyx, stricture ureter which are often multiple with dilatations in between. Often RGP is very useful, as better definition of ureter, pelvis, calyces and selective sampling of urine are possible.

Fig. 26.39: Renal tuberculosis types.

Always make a total effort even when the odds are against you.

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SRB's Manual of Surgery Unilateral

Fig. 26.40: Stricture of left ureter lower part—IVU picture. Common cause is tuberculosis of ureter. xx Cystoscopy reveals multiple tubercles, bladder spasm, oedema of ureteric orifice eventually forming “golf hole ureter”, scarring, ulceration, bleeding, stone formation. xx Polymerase chain reaction (PCR) for tuberculosis. Radioisometric culture. xx Voiding cystourethrography (MCU) to see ureteric stricture and reflux.

Treatment xx Antitubercular therapy is started. INH, rifampicin, ethambutol and pyrazinamide. Duration of treatment is one year. xx After 6–12 weeks of drug therapy, surgical treat­ment is planned. Kidney is exposed. Pyocalyx is drained. Cut edge of the capsule is sutured—Hanley’s renal cavernostomy. xx Hydronephrosis—Anderson Hynes operation or nephrostomy or stenting (“J” stent) of ureter is done. xx Renal tuberculous abscess not resolving for 2 weeks should be drained. xx Ureteral stricture—stenting/reimplantation of the ureter into the bladder/psoas hitch/Boari’s flap/ileal conduit (Koch’s ileal conduit). xx Thimble bladder—hydraulic dilatation/ileocystoplasty/caecocystoplasty/sigmoid colocystoplasty is done. xx In unilateral lesion, with gross impairment of renal function— nephroureterectomy is done.

A. Extramural: 1. Aberrant renal vessels (vein or artery). It is common on left side. 2. Compression by growth (carcinoma cervix, carcinoma rectum). 3. Retroperitoneal fibrosis. 4. Retrocaval ureter. B. Intramural: 1. Congenital PUJ obstruction. 2. Ureterocele. 3. Neoplasm of ureter. 4. Narrow ureteric orifice. 5. Stricture ureter following removal of stone, pelvic surgeries or tuberculosis of ureter. C. Intraluminal: 1. Stone in the renal pelvis or ureter. 2. Sloughed papilla in papillary necrosis.

Bilateral A. Congenital:  Congenital stricture of external urethral meatus, pin-hole meatus.  Congenital posterior urethral valve. B. Acquired:  BPH.  Carcinoma prostate.  Postoperative bladder neck scarring.  Inflammatory/traumatic urethral stricture.  Phimosis.  Carcinoma cervix.  Bladder carcinoma. xx Congenital PUJ is the most common cause of HN. xx Often it is bilateral and presentation on one side is earlier than the other side. xx Aberrant renal artery or vein in the lower pole of kidney can compress the PUJ causing HN. Renal angiogram confirms the diagnosis.

Indications for nephroureterectomy Nonfunctioning kidney Disease extensively involving the kidney ™™ Disease causing hypertension and severe obstruction ™™ Tuberculous pyonephrosis ™™ Coexisting renal cell carcinoma ™™ ™™

HYDRONEPHROSIS (HN) It is an aseptic dilatation of pelvicalyceal system due to partial or intermittent obstruction to the outflow of urine.

Aetiology It can be unilateral or bilateral.

Fig. 26.41: Aberrant renal vessels are one of the known causes of hydronephrosis.

Kidney Pathology xx Initially pressure burden is taken up by the pelvis; later calyces and renal parenchyma. Gradually, parenchyma thins out due to destruction and it dilates. Eventually leading to compromised secretory function. Parenchymal thickness of less than 2 mm is unlikely to function. In bilateral cases such patients will go for renal failure.

A

Fig. 26.43: Hydronephrosis due to congenital PUJ obstruction. It is the common cause of hydronephrosis.

B Figs 26.42A and B: Aberrant renal vessels causing obstruction and hydronephrosis. As this often supplies lower pole of kidney exclusively, it needs to be retained. Treatment of aberrant renal vessels If it is a vein, it can be ligated safely. But if it is an artery, it exclusively supplies the lower pole of the kidney and so cannot be ligated. So kidney is mobi­lised; upper and lower poles are approximated together so that artery is made to slip away from the site of compression—Hamilton Stewart operation. xx In pregnancy dilatation of ureters and both pelvis occur due to atony of ureteric musculature by progesterone. It starts as early as in the first few weeks of pregnancy and lasts until few weeks after delivery. Involution occurs 2–12 weeks after delivery.

A

B Figs 26.44A and B: Specimens showing hydronephrosis.

Classifications Classification I ™™ Unilateral HN ™™ Bilateral HN without renal failure ™™ Bilateral HN with renal failure Classification II ™™ Intermittent HN: Obstruction occurs, swel­ling and pain appear in the loin. After sometime, patient passes large amount of urine following which swelling and pain disappear—Dietl’s crisis ™™ Persistent HN: It is due to persistent partial obstruction Classification III ™™ HN only ™™ HN with hydroureter Classification IV ™™ Extrarenal pelvic HN (80%) ™™ Intrarenal pelvic HN (20%). Destruction of kidney is earlier and severe here, as compared to extrarenal pelvic HN

Fig. 26.45: Stages of HN.

Clinical Features A. In unilateral cases:  Congenital PUJ obstruction and calculus are the most common causes.  M : F : : 2 : 1. –– Right side kidney is affected more commonly. –– Dull aching loin pain with dragging sensation or heaviness.

Variability is the law of life, and so no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions which we know as disease. —William Osler

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SRB's Manual of Surgery –– Mass in the loin which is smooth, mobile, ballotable,

moves with respiration with dullness in renal angle and a band of colonic resonance in front. –– Attacks of acute renal colic. –– Often patient may be having Dietl’s crisis—after an acute attack of renal colic, swelling in the loin is seen which disappears after sometime following passage of large volume of urine. –– Dysuria, haematuria, if infected fever and tenderness in renal angle. –– Occasionally hypertension. B. In bilateral cases:  From lower urinary tract obstruction.

C

B

Figs 26.47B and C

Figs 26.47A to C: CT scan showing hydronephrosis of left kidney with extrarenal pelvis. Patient underwent laparoscopic pyeloplasty (Courtesy: Dr Ashok Padit, MCh, Urologist, Mangala Hospital, Mangaluru). Loin pain Features of bladder outlet obstruction—frequency, hesitancy, poor stream ™™ Kidneys are often not palpable if renal failure develops early ™™ ™™

 From bilateral upper urinary tract obstruction. ™™ ™™

Loin pain, mass in the loin, attacks of renal colic In bilateral cases, when it is severe, features of renal failure like oliguria, oedema, hiccough may be present

A

B Figs 26.46A and B: Types of renal pelvis: (A) Intrarenal; (B) Extrarenal.

A

B

Figs 26.48A and B: (A) IVU showing bilateral hydronephrosis and hydroureter; (B) (IVP showing right hydronephrosis. Note the dilated right renal pelvis and delay in the excretion of the dye from the affected kidney.)

Complications 1. Pyonephrosis. 2. Perinephric abscess. 3. Renal failure in bilateral cases.

Investigations A Fig. 26.47A

xx Blood urea and serum creatinine. xx Urine for microscopy. xx Ultrasound abdomen: Investigation of choice.

Kidney Type of pelvis, thickness of parenchyma, site of obstruction and cause of obstruction, e.g. stones, can be made out.

Fig. 26.49: Ultrasound picture of hydronephrosis showing dilated pelvis. xx IVU: To find out the function of diseased as well as opposite

kidney. Normal calyx is cup shaped. It gets flattened and later club shaped which even­tually becomes broadened in hydronephrosis. xx CT scan is diagnostic.

Fig. 26.52: Isotope scan showing hydronephrosis on the left side. xx Whitaker test: A fine needle is passed into the renal pelvis

through loin. Pelvis is perfused with saline at a rate of 10 ml/minute. Normally, initially the pres­sure increases and later it will remain constant. Persistent increase in pressure suggests HN.

Treatment xx Always conservative surgeries which are aimed at con­­

serving the kidneys are done. Nephrectomy is not done unless indicated. 1. The cause is treated: Stone, congenital anomaly, aberrant renal vessels, stricture urethra (dilatation, urethrotomy, urethroplasty); phimosis (circumcision); BPH (TURP); posterior urethral valve (cystoscopic fulguration of valve). Note: Fig. 26.50: Hydronephrosis as seen in CT scan. xx Isotope renography is also useful to study the function of

the kidney before and after the surgical treatment and also to see the efficacy of surgery as far as function is considered—DTPA scan.

A



Please refer respective topics and highlight the individual treatment.

2. Anderson-Hyne’s operation (Dismembered pyelo­plasty): In congenital PUJ obstruction, the spasmodic segment and redundant pelvis are excised. A new pelvis is created and the cut end of pelvis is anastomosed to the ureter in the dependent position.

B

Figs 26.51A and B: (A) Retroperitoneal tumour causing ureteral obstruction with hydronephrosis; (B) CT scan showing bilateral hydronephrosis. One side large (left side); another side early hydronephrosis.

Fig. 26.53: Anderson-Hyne’s operation.

Difficulties are like mirror on the wall that shows a person what he is in reality.

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SRB's Manual of Surgery 3. Davis T-tube ureterostomy: Placement of T-tube in the ureter by making longitudinal incision. 4. Non-dismembered pyeloplasties: Here PUJ is not transected. Reconstruction is done without PUJ transection by different methods, e.g. Foley’s Y-V plasty. 5. In bilateral HN, without renal failure, kidney which is functioning better should be operated first. Three months later, otherside kidney is dealt with. 6. In bilateral HN with renal failure, bilateral nephrostomy and haemodialysis support is required initially. After 3–6 weeks IVU is done and the functions of both kidneys are looked for. If they function, then treated accordingly by Anderson-Hyne’s operation.  If kidneys are still not functioning (renal function 2 ng/ml/year [rate of change in PSA in one year]); PSA Doubling Time (50 years with PSA >3 ng/ml should undergo prostatic biopsy.

xx BPH arises from submucosal glands of periurethral transitional

zone with stromal proliferation and adenosis. It eventually compresses the peripheral zone and enlarges as lateral lobe. xx BPH arising from subcervical glands of central zone enlarges as middle lobe projecting up into the bladder.

Pathology xx BPH usually involves median and lateral lobes or one of them. xx It involves adenomatous zone of prostate, i.e. submucosal

glands. xx Median lobe enlarges into the bladder. xx Lateral lobes narrow the urethra causing obs­truction. xx Urethra above the verumontanum gets elongated and

narrowed. xx Bladder initially takes the pressure burden causing trabecu-

lations, sacculations and later diverticula formation. xx Enlarged prostate compresses the prostatic venous plexus

causing congestion, called as vesical piles leading to haematuria.

Prostatic calculi It is the calcification of corpora amylaceae which contains calcium phosphate, protein and fat.

BENIGN PROSTATIC HYPERPLASIA (BPH) He was very often, both in the Day and the Night, forced to make Water, seldom in any Quantity, because he could not retain it long enough. —Edward Hyde (first Earl of Clarendon), 1759

It is benign enlargement of prostate which occurs after 50 years, usually between 60 and 70 years. BPH affects both glandular epithelium and connective tissue stroma.

A

B

Figs 26.109A and B: (A) Prostate anatomy; (B) Retention of urine in bladder due to BPH. xx Incrimination of BPH as the source of haematuria before

excluding other causes is termed as “Decoy prostate”.

Aetiology

xx Kidney and ureter: Backpressure causes hydroureter and

Theories xx It is involuntary hyperplasia due to disturbance of the ratio and quantity of circulating androgens and estrogens. xx Hypothalamus → pulsatile release of LHRH → release of luteinising hormone (LH) from anterior pituitary → stimulates Leydig cells of testes → releases testosterone (TS) → reaches prostate → releases 5α reductase type II of prostate → converts TS to DHT (dihydrotestosterone) for its effects. DHT is five times more potent than TS. 90% TS is from testes. Remaining 10% TS is from adrenal cortex. xx With age TS level drops slowly. But fall of oestrogen level is not equal. So prostate enlarges through intermediate peptide growth factor. xx BPH is a benign neoplasm, also called as fibromyoadenoma. The neoplastic theory is old one—not universally accepted now—under debate.

xx Secondary ascending infection can cause acute or chronic

hydronephrosis. pyelonephritis. xx Often severe obstruction can lead to obstructive uropathy

with renal failure. xx BPH causes impotence.

Clinical Features xx Frequency occurs due to introversion of sensitive urethral

mucosa into the bladder or due to cystitis and urethritis. Urgency, hesitancy, nocturia. Overflow and terminal dribbling. Difficulty in micturition with weak stream and dribble. Pain in suprapubic region and in loin due to cystitis and hydronephrosis respectively. xx Acute retention of urine. xx xx xx xx

Prostate xx Chronic retention also can occur in BPH. xx Retention with overflow. High pressure chronic retention

with functional obstruction. xx Impaired bladder emptying with its problems like cystitis,

urethritis, stone formation and residual urine. xx Haematuria. xx Renal failure. xx Prostatism is a combination of symptoms like frequency

both at day and night, poor stream, delay in starting and difficulty in micturition. xx Tenderness in suprapubic region, with palpable enlarged bladder due to chronic retention. Hydronephrotic kidney may be palpable. xx Per rectal examination shows enlarged prostate. It should be done when bladder is empty. xx Features of urinary infection like fever, chills, burning micturition. xx International prostate symptom score is available now. Lower urinary tract symptoms (LUTS) Symptoms of voiding • Hesitancy • Poor flow not improving by straining • Dribbling even after micturition • Intermittent stream—stops and starts • Poor bladder emptying • Episodes of near retention

Symptoms of storage • Frequency • Nocturia • Urgency • Urge incontinence • Nocturnal incontinence

Differential Diagnosis xx Stricture urethra. xx Bladder tumour, carcinoma prostate. xx Neurological causes of retention of urine like diabetes, tabes,

disseminated sclerosis, Parkinson’s disease. xx Idiopathic detrusor activity. xx Bladder neck stenosis; bladder neck hypertrophy.

Investigations

xx xx xx xx

Urine for microscopy and C/S. Blood urea and serum creatinine. Ultrasound abdomen—look for presence of residual urine. Urodynamics.  Urine flow rate >15 ml/sec is normal. 10–15 ml is equivocal; 5% or less of resected tissue ™™ T1c Tumor identified by needle biopsy (due raised PSA) T2 Tumour confined to prostate ™™ T2a—tumour in one half of one lobe or less ™™ T2b—tumour in more than half of one lobe (but NOT both lobes) ™™ T2c—tumour involves both lobes within the capsule T3 Tumour extends through prostatic capsule ™™ T3a—Extracapsular extension (unilateral or bilateral) including microscopic bladder neck involvement ™™ T3b—involving one or both seminal vesicles T4—Fixed tumor invades adjacent rectum/pelvic floor or wall N—Regional Lymph Nodes Nx—Regional nodes cannot be assessed N1—Regional nodes involved

Lymphatic spread:  Into the obturator lymph nodes, then to internal iliac lymph nodes.  Through seminal vesicles, into external iliac and retroperitoneal lymph nodes.  Eventually mediastinal, left supraclavicular lymph nodes get involved. Clinical features ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Commonly asymptomatic Bladder outlet obstruction and so retention of urine Haematuria, frequency Pelvic pain, back pain, arthritic pain in sacroiliac joint—features of secondaries On per rectal examination, prostate feels hard, nodular, irregular often with loss of median groove Incidental carcinoma after TURP or after PSA analysis Features of renal failure Anaemia secondary to extensive bone marrow invasion and also due to renal failure.

M—Distant Metastasis M0—No distant metastases M1—Distant metastases present ™™ M1a—Non-regional lymph node(s) ™™ M1b—Bone(s) ™™ M1c—Other site(s) Gleason grading and scoring Gx—Cannot be assessed G1—Score 2–4 G2—Score 5–6 G3—Score 7 G4—Score >7

Differential Diagnosis xx Are other causes of retention of urine and other causes of

back pain.

Investigations xx Hb%, peripheral smear. In metastatic disease, there may

Stage groups Stage I—T1aN0M0G1;T1aN0M0G2—4; T1bN0M0 AnyG Stage II—T1c/T2N0M0 AnyG Stage III—T3/T4N0M0 AnyG Stage IV—Any TN1M0 AnyG; Any T, any N, AnyG Note: Whitmore Jewett system staging is also used with stages as—A, B, C and D.

Note For T1a progress rate is slow—15–20% in 8 years For T1b and T2 it is 35% For T3/T4 M0 it is 50% in 5 years with bone spread For M1 average survival is 3 years

be leukoerythroblastic reaction with bone marrow invasion causing anaemia, thrombocytopenia, DIC and increased fibrinogen degradation products (FDP). Anaemia may also be due to renal failure. xx Prostate specific antigen (PSA): More than 10 ng/ml is suggestive. xx Prostatic fraction of acid phosphatase is increased. xx Blood urea, serum creatinine, liver function tests. xx Transrectal ultrasound (TRUS) is very useful. xx Transrectal prostatic biopsy. 10 biopsy cores are taken. xx Plain X-ray, KUB, may show dense coarse sclerotic secondaries. Osteolytic or combination of lytic and sclerotic lesions are also often seen.

Spread Local spread: xx Upward into seminal vesicles, bladder neck, trigone, later into

both ureters causing anuria. Downward into distal sphincter. Blood spread: xx Into the bones commonly—pelvic bones, lumbar vertebrae, femoral head, ribs, skull—in that order.  Pathological fractures can occur in long bones and vertebrae.  Paraplegia may occur if spine is involved.  Rarely spread to liver and lung can occur.

A

B

Figs 26.115A and B: (A) A plain X-ray AP view of lumbar spine in a patient with carcinoma prostate. Note the typical osteosclerotic secondaries; (B) Carcinoma prostate showing skeletal secondaries in bone scan.

Look at happiness and misery the same; Look at success and failure the same. —True way of life it is called as.

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SRB's Manual of Surgery xx Technetium radioisotope bone scan to see secondaries. xx Ultrasound abdomen, to see the tumour extension into the

bladder and to see kidneys for hydronephrosis. xx MRI/CT scan is better for staging the disease. MRI is ideal. It can be combined with TRUS to have an accurate staging. Note: Osteoblastic secondaries occasionally can be seen in carcinoma breast.

xx Bilateral subcapsular orchidectomy is done to reduce the

testosterone level. Very useful method. First started by Charles Huggins—Urologist (Nobel Prize winner). (Other condition where orchidec­tomy is done is carcinoma of male breast.) xx TURP + Bilateral orchidectomy + External radio­therapy for bone secondaries + Flutamide or Honvan—commonly advocated method. xx Drugs:  Phosphorylated diethylstilbestrol (Honvan)—initially given intravenously and later orally. It is very effective. Complications are cardiac congestion, DVT, gynaecomastia. Phosphorylated diethylstilbestrol

A

B

Figs 26.116A and B: Osteoblastic secondaries in pelvic bones and lumbar spine.

™™ ™™ ™™ ™™

Initially IV 100 mg/daily later orally 100 mg/daily Can cause cardiac congestion, DVT, gynaecomastia Prior RT to breasts to prevent gynaecomastia often advocated Response starts appearing in 48 hours.

 LHRH agonists (Medical castration)—Leupro­lide, Goserelin.  Androgen receptor blocking agents like fluta­mide, bicaluta-

mide. Remember ™™

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

What we taught and thought as carcinoma prostate is slow growing, easy to manage, will not kill the patient is not right; actual fact is there is increase in incidence, inexorable progression despite proper treatment, with increased mortality. Cure is possible only when disease is organ confined. 45% of men over 50 years have carcinoma prostate on autopsy; but only detected in 17%. Most men die with carcinoma prostate, not of carcinoma prostate. It will take 8–10 years for carcinoma prostate to progress to metastasis. Even indolent carcinoma prostate can rapidly progress after 10 years. Metastatic disease becomes Castrate Resistant Prostate Cancer (CRPC) in 1.5–3 years. In CRPC death occurs in 1.5–3 years. Treatment of metastatic disease does not increase survival. Disease should be identified early – by PSA, digital rectal examination (DRE), transrectal US (TRUS). Staging work-up is done using – MRI, PET scan (choline), MDP bone scan.

 Cyproterone acetate (also has got proges­togenic effect).

xx In elderly people with early carcinoma prostate inactivity with wait and watch policy is practised. xx Sometimes permanent suprapubic cystostomy (SPC) is required in these patients. xx Castrate Resistant Prostate Carcinoma (CRPC) – Abiraterone– Cytochrome P 17 (17 Hydroxylase and 17, 20 Lyase) inhibitor– used with prednisolone–to prevent hypokalaemia and fluid overload due to mineralocorticoid excess. Chemotherapy using docitaxel, cabazitaxel, prednisolone is also tried. xx Tumour vaccines—Sepuleucel–T—Autologous peripheral blood mononuclear cells harvested and activated with prostatic acid phosphatase construct (increase in survival 4 months). Allogenic cell line based vaccines, Peptide and mRNA vaccines (CV9103). xx T-cell checkpoint inhibitors ( Ipilimumab – CTLA 4 inhibitor). xx Bone secondaries are treated using—Radioactive strontium 89 (Metastron)/Samerium 153/Radium 223; Palliative RT to specific bone involved; Bisphosphonates – Zoledronic acid; Denosumab ( RANKL inhibitor – down-regulation of osteoclasts); calcium, vitamin D3.

Treatment In prostatic cancer with marked elevation of acid phosphatase, castration or injection of large amounts of estrogen caused a sharp reduction of this enzyme to or towards the normal range…. In 3 patients with prostatic cancer, androgen injections caused a sharp rise of serum acid phosphatase. —Charles Brenton Huggins, Clarence Vernard Hodges, 1941

Remember ™™ ™™ ™™

xx Radical prostatectomy is done in early growth with removal

of prostate, seminal vesicle, distal sphincter along with reconstruction of the urethra. Open/laparoscopic/robotic assisted/nerve sparing approaches are used nowadays. xx Radical radiotherapy for early carcinoma prostate can be given using both interstitial and external radiation. xx Pelvic lymph node dissection with I125 radiation seeds implantation.

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Wait and watch policy is ideal in elderly patient with early carcinoma (P/R; PSA) above 70 years. TURP if there is obstruction with bilateral subcapsular orchidectomy; LHRH agonists; androgen blockage. Radical prostatectomy/radical RT in young T1a or T1b—early disease. The criteria for radical prostatectomy—life-expectancy should be more than 10 years; PSA 5 cm M0 – Distant spread not present M1 – Distant spread present M1a – Distant spread to nonregional nodes or to lungs M1b – Distant spread to other than nonregional nodes or lungs

Serum tumour markers (S) Sx – Marker study not done S0 – Normal marker study S1 –LDH 10000 ng/ml

In torsion testis, affected testis lies higher than its fellow.—Clyde L Deming

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SRB's Manual of Surgery Stage groups in testicular tumour Stage 0—Tis N0 M0 S0 Stage I—T1–4 N0 M0 Sx Stage IA—T1 N0 M0 S0 Stage IB—T2–4 N0 M0 s0 Stage IS—Any T N0 Mo S1–3 Stage II—Any T N1–3 M0 Sx Stage IIA—Any T N1 M0 S0–1 Stage IIB—Any T N2 M0 S0–1 Stage IIC—Any T N3 M0 S0–1 Stage III—Any T Any N M1 Sx Stage IIIA—Any T Any N M1a S0–1; Any T N1–3 M0 S2 Stage IIIB—Any T Any N M1a S2; Any T N1–3 M0 S3 Stage IIIC—Any T Any N M1a S3; Any T Any N M1b Any S

Investigations No FNAC; No scrotal approach; No incision biopsy. xx Through inguinal approach, cord and testis are exposed.

A soft clamp is applied to the cord at or above the level of the deep ring so has to prevent dissemination through blood. Frozen section biopsy is done from the suspected area. If tumour is positive, high orchidectomy is done (Chevassu manoeuvre). xx Measurement of tumour markers (β-HCG, AFP, LDH).  AFP and β-HCG are elevated in nonseminomatous germ cell tumours (teratomas)—65%.  Raised AFP always indicates teratomatous tumour. AFP level increase is not seen in pure seminomas.  β-HCG may be elevated in advanced cases of seminomas (10%).  LDH level depends on growth rate/cellular proliferation/ tumour burden. LDH is increased in 80% of advanced seminomas and 60% of nonseminomatous germ cell tumour.  β-HCG is never found in normal individual. It is secreted by syncytiotrophoblasts. Half life is 18–36 hours. It is increased in choriocarcinoma (100%); embryonal carcinoma (65%); teratoma testis; recurrent or residual disease in testicular tumour after therapy.

 Placental alkaline phosphatase (PLAP) is increased in

seminoma. xx Chest X-ray to look for lung secondaries. HRCT scan is ideal. xx Ultrasound abdomen to see nodal status like para-aortic

nodes and liver secondaries. CT abdomen is better. xx Ultrasound scrotum to see echogenicity of testis and tumour

within. xx CT scan abdomen and pelvis to look for secondaries, iliac

and para-aortic nodes. xx CT chest is needed to confirm lung secondaries. xx Based on presence of AFP; β-HCG; LDH; Nonpulmonary

visceral secondaries (bone/liver/brain), germ cell tumour risk group classification is done to both seminomatous germ cell tumour (SGCT) and also to nonseminomatous germ cell tumour (NSGCT).  Good risk and intermediate risk group for SGCT.  Good risk; intermediate risk and poor risk for NSGCT.

Treatment xx Seminomas are radiosensitive. So after high orchidectomy,

radiotherapy is given to increase the cure rate and also to reduce relapse. It is the treatment of choice in stage I seminomas. Opposite testis should be shielded during radiotherapy.  Seminomas with high levels of tumour marker are treated as nonseminomatous tumours.  Chemotherapy is also effective. Cisplatin is very useful drug in seminoma. xx In teratoma, Retroperitoneal Radical Lymph Node Dissection (RPLND) is beneficial after high orchidectomy. Even in stage I disease, chances of existing retroperitoneal spread is 30%. So, RPLND (infrahilar) has a major role especially in teratomas which are relatively radioresistant. It involves removal of precaval, retrocaval, paracaval, interaortocaval, retroaortic, para-aortic, common iliac nodes along with removal of gonadal vein and adjacent fibrofatty tissues from internal ring level to its insertion into renal vein on left side and inferior vena cava on right side. Commonly bilateral RPLND is done as contralateral nodes also can be

Fig. 26.200: Staging of testicular tumour.

Testis  Complications: Haemorrhage; injury to main struc-

tures like major vessels/ureter/bowel; chylous ascites; lymphocele; retrograde ejaculation.  Radiotherapy is not beneficial in teratoma.  Chemotherapeutic drugs for teratoma are cisplatin, bleomycin, vinblastine, etoposide, ifosfamide, mesna, paclitaxel. BEP regimen is commonly used.

A

Follow-up xx Measurement of tumour markers at regular intervals for

5 years and yearly after 5 years. xx CT abdomen and chest once a year.

Factors Affecting the Prognosis B Figs 26.201A and B: High orchidectomy showing testis with cord structures which is ligated at or above the internal ring; it is done through inguinal approach.

xx Histological appearance of tumour. xx Staging of the tumour: II—90%; III—70% 5-year survival. xx Age of the patient, younger the age group poorer the progxx xx xx xx

nosis. Seminoma has got better prognosis than teratomas. Spermatocytic seminoma has got good prognosis. Hurricane type has got worst prognosis. Seminoma responds well to RT (melts-like snow). Teratoma is less sensitive RT.

PARATESTICULAR TUMOURS Types xx xx xx xx xx

Adenomatoid. Cystadenoma of epididymis. Mesenchymal neoplasms. Mesotheliomas. Metastases.

Features

Fig. 26.202: High orchidectomy is done for testicular tumour through inguinal approach. Not through scrotal incision. Cord is ligated at the level of the internal ring.

involved. Mortality in RPLND is only 1%. RPLND may cause ejaculatory problems. Nerve sparing RPLND is ideal, if technically possible. Nerve sparing dissection is done on opposite side of the tumour. Laparoscopic RPLND is also advocated safely. Modified RPLND is same side lymph node dissection both above and below the inferior mesenteric artery (IMA); opposite side dissection is limited to above the level of IMA so that sympathetic chain on opposite side is preserved to retain ejaculation.

xx Generally sarcomatous. xx Rhabdomyosarcoma occurs in 40% cases. Occurs during first two years of age. It can be localised or with distant spread (lungs). xx US scrotum; CT scan. xx Treatment—radical orchidectomy and chemotherapy.

ORCHITIS xx It is an inflammation of the testis. It is commonly associated with inflammation of the epididymis. Hence, called as epididymo-orchitis. xx Orchitis is due to infection through blood, lymphatics or epididymis.

Causes xx xx xx xx xx xx

Viral infection—mumps. Filarial disease. Leprosy. Bacterial. Brucellosis. Infectious mononucleosis.

In torsion testis, testis always twists away from midline—John P Sparks

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SRB's Manual of Surgery xx It can be precipitated by retrograde spread due to stricture urethra, after prostate or bladder surgery, after instrumentation. xx Syphilis involves testis—causing formation of gummatous ulcer on front of the scrotum. Syphilitic orchitis Syphilis involves only testis; never vas deferens. It can be: ™™ Bilateral interstitial orchitis seen in congenital syphilis causing pigeon—egg testes in infants; if infant becomes syphilitic boy, then he becomes lame (Clutton’s joints), deaf (neurolabyrinthitis), blind (interstitial keratitis), impotent (atrophy of testes) ™™ Interstitial fibrosis, bilateral causing gradual destruction of the seminiferous tubules with loss of testicular sensation without any enlarged testes. Testis is dense, rounded hard and mobile— billiard testis’ ™™ Gumma of testis is most common type of presentation with unilateral painless slowly enlarged hard testis with loss of testicular sensation. Testis is adherent to anterior part of the scrotal skin leading to softening and gummatous ulcer formation. Shotty groin, epitrochlear and popliteal lymph nodes may be palpable

Fig. 26.204: On table operated hydrocele case—showing thickened epididymis.

Fig. 26.205: Tuberculous epididymitis presenting as multiple ulcers on the posterior aspect.

Causes Fig. 26.203: Ulcer scrotum—it could be nonspecific. Syphilitic ulcer develops in front (gumma); but nowadays it is very rare.

Features xx Pain in the testis often radiates into groin due to associated funiculitis. xx Fever, tenderness in the testis. xx Secondary hydrocele is common. xx Urinary infection often noticed. xx Differential diagnosis:  Torsion testis.  Testicular tumour. xx Treatment:  Antibiotics, analgesics, DEC.  Treating the cause.

EPIDIDYMITIS Inflammation of epididymis is commonly associated with orchitis— epididymo-orchitis.

xx Nonspecific, viral like mumps. xx Bacterial. xx Filarial. xx Tuberculosis: It involves mainly epididymis not testis and so ulcer/ sinus occurs over the posterior aspect of the scrotum not in front. xx Gonococcal. xx Schistosomiasis. It can be acute or chronic.

Features xx xx xx xx xx

Pain and tenderness in the epididymis. Swollen, tender epididymis. Thickened epididymis. Often secondary hydrocele may be present. Beaded vas with craggy epididymis—in tuberculosis.

Treatment xx Analgesics, antibiotics, diethyl carbamazine citrate (DEC) 100 mg for 3 weeks.

Testis Tuberculous epididymitis ™™

™™

™™

Fig. 26.206: Tuberculous epididymitis.

™™

xx Specific cause should be ruled out. xx Long-term epididymitis causes real psychological disturbance to the patient and so reassurance is required.

™™ ™™

It is commonly due to retrograde spread from tuberculous cystitis. It involves globus minor (tail) first and later entire epididymis and testis is involved in late stage. Blood spread from lungs directly involves globus major first. Thickened, craggy, firm nodular epididymis is common. Cold abscess, sinus or undermined ulcer may be present on the posterior aspect of the scrotum. Lesion will be on the anterior aspect in anteverted testis. Scrotal skin loses its normal rugosity with wasting of the tissue under the skin. There is restricted mobility (upward and downward) of testis. Thickened beaded vas (due to tubercles) is typical. Secondary hydrocele develops in 30% cases. 60% will be having renal tuberculosis. Digital examination of rectum (P/R) shows tender thickened palpable seminal vesicles and irregular prostate. Pulmonary tuberculosis is evident in 50% of cases.

The young patient is asked to sit on a chair and hug his knees to the chest. Pressure then directed on the inguinal canal causes a retractile testis to descend into the scrotum. — Louis Orr

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Neurosurgery CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™

Head Injuries Extradural Haematoma Subdural Haematoma Subarachnoid Haemorrhage Fracture Skull Depressed Skull Fracture CSF Rhinorrhoea

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Hydrocephalus Intracranial Abscess Intracranial Aneurysms Intracranial Tumours Pituitary Tumours Craniopharyngiomas Spinal Dysraphism

HEAD INJURIES Now as soon as thou findest that smash which is in his skull like those corrugations which form on molten copper, (and) something therein throbbing and fluttering under thy fingers like the weak place of an infant’s crown before it knits together-when it has happened there is no throbbing and fluttering under thy fingers, until the brain of his (the patient’s) skull is rent open- (and) he discharges blood from both his nostrils and both his ears, (and) he suffers stiffness in his neck. — (Anonymous), circa 2500 BC

Head injuries are one of the common causes of death in road traffic accidents. Young males are commonly affected. It can be open or closed injuries depending on whether there is fracture skull with meningeal injuries causing CSF leak or not. CSF (Cerebrospinal fluid) can leak through scalp wound or through ear or nose depending on site of injury. Open injury has more risk of intracranial infection including meningitis. In closed head injury CSF leak is not present. Otherwise both are equally dangerous depending on the extent of intracranial injury. Intracranial haematomas/haemorrhages can be extradural or subdural or intracerebral or subarachnoid. Scalp injury can be incised/lacerated/multiple/or scalp avulsion or degloving. Blood vessels in the scalp are attached to galea and so once galeal aponeurosis disrupts profuse bleeding from the scalp is common. Fracture skull can occur at various bones which may be indirect evidence about the extent, type and side of intracranial injury. Scalp should be sutured including galea as interrupted sutures. Bleeding can be controlled by catching galea using series of arteries. Loss of scalp skin with periosteum of the skull bone is difficult to

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Meningocele Spina Bifida Intervertebral Disc Prolapse Tuberculosis of Spine Spinal Tumours

manage which may require creation of multiple perforations on the outer table of the skull to facilitate the formation of adequate granulation tissue over which skin grafting can be done at a later ideal period. Injuries can be blunt or sharp (heavy) or missile injuries. Complicated head injury is one which shows life-threatening secondary changes; whereas uncomplicated head injury does not show life-threatening secondary changes but should be observed for. Features of malignant cerebral oedema wherein it shows diffuse cerebral oedema with intracranial hypertension (ICP). It has got high mortality (>90%). It is treated by steroids, mannitol, ventilator support and symptomatic management including prevention of sepsis.

Mechanism xx Distortion of the brain: Brain is a soft structure, therefore has a ‘mobility’ and readily distorts. This distortion and mobility is accentuated by CSF and vascular components. Any impact creates shearing forces in the brain causing damage to neurons, supporting tissues and blood vessels. This leads to loss of consciousness, focal neurological deficits. Such distortive damage may be temporary or permanent. xx Mobility of the brain in relation to the skull and membranes causes cerebral damage and bleeding in dural spaces from torn vessels in the dura, commonly the veins. In old age, the brain shrinks, as a result of which ‘mobility’ of brain increases favouring rupture of veins which cross the subdural space. xx Configuration of interior of skull: Damage is less severe over the smooth area but is more severe over the rough and sharp areas. So the damage is severe over the anterior cranial fossa, over the falx, and over the tentorium.

Neurosurgery xx Coning: It is due to raise in intracranial pressure causing either: i. Herniation of contents of supratentorial compart­ment through the tentorial hiatus or ii. Herniation of the contents of infratentorial compartment through the foramen magnum. In supratentorial herniation, there is com­pression of ipsilateral third cranial nerve and midbrain. Midbrain is displaced away from the mass (haematoma) and midbrain is pressed by the sharp edge of tentorium cerebelli of opposite side leading to dysfunction of corticospinal fibres (which after decussation supplies the opposite side of the body, i.e. same side of the injury).

Fig. 27.1: Exposed skull after trauma with sepsis. It needs multiple burr holes to allow granulation tissue formation from depth. Later skin grafting can be done. Otherwise local rotation flap is needed. xx Deceleration and acceleration injuries: Deceleration injuries occur when moving head strikes an immovable object (like in road traffic accidents). Acceleration injuries occur when stationary skull is struck by a moving object (like in assault). xx Cerebral concussion is slight distortion causing temporary physiological changes leading to transient loss of consciousness with complete recovery. xx Cerebral contusion is more severe degree of damage with bruising and cerebral oedema leading to diffuse or localised changes. xx Cerebral laceration is tearing of brain surface with collection of blood in different spaces and with displacement of dural parts.

Effects of Brain Injuries xx Brain oedema is accumulation of fluid, both intra­cellular and extracellular. It is due to congestion and dilatation of blood vessels. It may be diffuse or localized. xx Brain necrosis is of severe variety with des­truction and is due to haemorrhagic infarction. xx Extradural haematoma occurs usually in temporoparietal region. It is commonly due to tear in middle meningeal veins and often middle menin­geal artery. It causes intracranial hyper­tension, displacement, Kernohan’s effect and often death. xx Subdural haematoma is due to tear of veins between cerebrum and dura due to shearing forces. It is diffuse and commonly associated with cerebral injury. xx Intracerebral haematoma can occur in different parts of cerebrum may be in frontal lobe, temporal lobe. xx Intraventricular haemorrhage is very severe type of haemorrhage. xx Brain ischaemia is due to increased pressure. This in turn leads to alteration in the perfusion of brain which itself aggravates the ischaemia and this forms a vicious cycle, causing progressive diffuse ischaemia of brain. xx Coup injury occurs on the side of the blow to the head. Contre-coup injury occurs on the side opposite to the blow on the head.

Fig. 27.2: Coning with Kernohan’s notch.

This leads to: a. Deterioration in the level of consciousness. b. Dilatation of pupil on the side of compressing mass (haematoma). c. Hemiparesis on the same side of the mass lesion (haematoma) due to compression of the contralateral corticospinal tract. This effect is called as “Kernohan’s notch”. Herniation of infratentorial contents through the foramen magnum causes obstruction of cerebral aqueduct which further damages the brain function. xx Respiratory failure altering PO2 and PCO2 levels.

A Fig. 27.3A

For the resolute and determined, there is time and opportunity.

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SRB's Manual of Surgery Clinical Approach of a Patient with Head Injury 1. Detail history of injury has to be taken and also the process of deterioration—rapid or gradual. 2. History of alcohol intake: Alcohol intake mimics head injury and alcoholism itself may mask the features of head injury. 3. Neurological assessment: By ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

B Fig. 27.3B

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Figs 27.3A and B: Black eye in two different patients. xx Raised intracranial pressure causing bradycardia, hypertension, vomiting. Raised intracranial pressure may precipitate coning and thus aggravates brain ischaemia. xx Fluid and electrolyte imbalance. xx Hyperpyrexia. xx Convulsions due to irritation of grey matter. xx CSF rhinorrhoea or CSF otorrhoea.

Pathology of Head Injury Primary lesions • Diffuse neuronal damage • Shearing lesions • Contusions • Lacerations

Cerebral concussion • Temporary physiological paralysis of nervous system • Loss of consciousness • Post-traumatic amnesia • Full recovery is expected • Residual complications may develop

Secondary lesions Brain swelling • Oedema, venous con-gestion, hypoxia Intracranial haemorrhage • Extradural • Subdural • Intracerebral Infections • Open head injury –– Generalised meningitis –– Subdural empyema • Closed head injury –– Pott’s puffy tumour Cause of death in head injury • Brain hypoxia • Coning • Diffuse severe irreversible neuronal injury • Death may be due to other injuries like abdominal/ thoracic • Metabolic changes • Aspiration in unconscious patient

Level of consciousness Glasgow coma scale Pupillary reaction to light and size Pulse Temperature Blood pressure Respiratory rate Reflexes Limb movements—normal/mild weakness/ severe weakness/ spastic flexion/extension/no response

4. Status and protection of airway. 5. General assessment and other injuries like frac­tures, abdominal organ injuries, thoracic injuries are looked for. 6. Presence of any scalp haematoma, fractures of skull bone which may be depressed has to be looked for. 7. Any blood from nose or ear, CSF rhinorrhoea or CSF otorrhoea has to be looked for.

Indications for Hospitalisation ™™ ™™ ™™ ™™ ™™ ™™ ™™

Any altered level of consciousness Skull fracture Focal neurological features Persistent headache, vomiting, systolic hyper­tension, bradycardia Alcohol intoxication Bleeding from ear or nose Associated injuries

Other features ™™ ™™ ™™ ™™ ™™ ™™

CSF leak or bleeding from nose Blood collection in the orbit Black eye Battle’s sign—ecchymosis over the mastoid Haematoma of scalp Panda sign—bilateral black eye

Fig. 27.4: Degloving injury scalp. Note all layers of the scalp stripped off.

Neurosurgery

Fig. 27.5: Patient with head injury having black eye. Adelaide coma scale It is used in children Scores for eye opening and motor responses are same as Glasgow coma scale   But verbal response score differs—Oriented-5. Words-4. Vocal sounds-3. Cries-2. Nil-1   Orientation cannot be evaluated below 5 years. For first 6 months, the best verbal response is CRY

Fig. 27.6: CT scan head showing scalp haematoma on both sides. There is no internal injury.

Investigations xx X-ray skull: To look for fracture, relative position of the

calcified pineal gland, presence of intra­cranial air. xx Serum electrolyte measurement. xx Blood grouping and cross matching. xx CT scan: Plain (not contrast) to look for cerebral oedema,

haematomas, midline shift, fractures, ventricles, brainstem injury. xx Carotid arteriography. xx Investigations for other injuries like ultrasound of abdomen. xx Monitoring of intracranial pressure.

Fig. 27.7: CT scan head showing intracerebral haematoma.

Glasgow coma scale Eye opening Spontaneous To speech To pain None

Verbal response –4 –3 –2 –1

Oriented Confused Inappropriate words Incomprehensible words None

Motor response –5 –4 –3 –2 –1

Obeys commands Localises pain Flexion to pain Abnormal flexion Extension to pain None

Total score: 15 Mild head injury: score 13–15 Moderate head injury: 9–12 Severe head injury: less than 8 (3–8)

In great attempts, it is glorious even to fail.

–6 –5 –4 –3 –2 –1

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SRB's Manual of Surgery Treatment General xx Protection of airway using mouth gag, endo­tracheal intubation or tracheostomy, whenever required. xx Throat suction, bladder and bowel care and good nursing are very essential. xx Nasal oxygen, or often ventilator support. xx IV fluids initially, later Ryle’s tube feeding has to be done. xx Electrolyte maintenance.

Drugs xx Sedation is avoided. xx Analgesics and anticonvulsants like phenytoin or phenobarbitone is started. xx Diuretics are given to reduce cerebral oedema—either mannitol 20%, 200 ml IV 8th hourly or frusemide 40 mg IV 8th hourly. It should not be given in case of intracranial haematoma. xx Antibiotics like penicillins, ampicillins are given to prevent the onset of meningitis.

xx Corticosteroids, either dexamethasone or beta­metha­sone is used commonly, but its beneficial effect is not confirmed. Indications for surgery  Acute extradural haematoma.  Acute subdural haematoma.  Depressed skull fracture.

Procedure Craniotomy is done and cranial flap is raised. Clot is evacuated followed by applying hitch stitches between dural layer and scalp. Postoperative antibiotics, analgesics, anticonvulsants are given.

Complications of Head Injuries Early xx Brainstem injury—due to coning. xx Compression over cerebellum and medulla. xx CSF rhinorrhoea: Due to communication between intracranial cavity and the nose. There is a tear in the dura following the fracture involving the sinuses—frontal, ethmoid, sphenoid sinuses. Meningitis is the common complication of CSF rhinorrhoea. Treatment: Initial management is only conservative, for 10 days— by antibiotics and observations. Indications for surgical intervention ™™ ™™ ™™ ™™ ™™

A

Fracture of middle third face CSF rhinorrhoea persisting for more than 10 days Fracture of sinuses An aerocoele An attack of meningitis

Surgeries: i. Reduction of fracture of middle third face. ii. Exploration of anterior cranial fossa. xx Meningitis—common. xx Pituitary damage and endocrine failure—requires high dose of hydrocortisone 200 mg, 6th hourly. xx Aerocoele. xx CSF otorrhoea.

B Figs 27.8A and B: CT scan head showing sharp head injury causing through and through cut across skull and brain. Patient survived and went home.

Fig. 27.9: Multiple burr holes done to promote formation of granulation tissue from vascular diploe of the skull. Once granulation tissue covers the entire defect, skin grafting can be done.

Neurosurgery xx Depressed fractures, often causes injury to dural venous sinuses and may lead to torrential haemorrhage, which may be life threatening. So such depressed fractures should never be elevated.

Late xx Chronic subdural haematoma. xx Early post-traumatic epilepsy—they need anti­convulsants for 3 years. xx Late post-traumatic epilepsy is due to scarring and gliosis of cerebrum. xx Post-traumatic amnesia. xx Post-traumatic hydrocephalus. xx Post-traumatic headache.

EXTRADURAL HAEMATOMA xx It is collection of blood in the extradural space between the

dura and skull. xx Most common site is temporoparietal region. It can be

unilateral or bilateral. Vessels commonly involved ™™ ™™ ™™

Middle meningeal veins Anterior branch of middle meningeal artery Posterior branch of middle meningeal artery

Usually, it is associated with fracture of temporoparietal region.

Pathology Direct blow, like from cricket ball or road traffic accidents or fall and impact or coup and contre-coup injuries ↓ Fracture of thin temporal bone ↓ Tear of vessels ↓ Bleeding initially outward towards the scalp and under temporalis muscle ↓ Formation of haematoma ↓ Gradual stripping of dura from skull and collection of blood occurs ↓ In 6–12 hours extradural haematoma occurs which raises the intracranial pressure ↓ Coning of supratentorial content (uncus of temporal lobe) through tentorial hiatus ↓ Shift of midbrain towards opposite side which gets injured by sharp edge of the tentorial cerebelli ↓ Corticospinal tract before decussation on opposite side gets injured

↓ So hemiparesis, and pupillary changes occur on the same side of haematoma ↓ This effect is called as Kernohan’s notch effect. xx Immediately after injury, there is transient loss of conscious-

ness and the patient soon becomes normal. Later after 6-12 hours, he again falls ill and the condition deteriorates. This is the time taken to develop raised intracranial pressure, coning and its effects. This crucial time gap which is unnoticed and often missed is called as “lucid interval”.

Clinical Features xx History of transient loss of consciousness following a history

of blow or fall. xx Patient soon regains consciousness and again after 6–12

hour starts deteriorating (Lucid interval). xx Later the patient presents with confusion, irrita­b ility,

drowsiness, hemiparesis on same side of the injury. Initially pupillary constriction and later pupillary dilatation occurs on the same side, finally becomes totally unconscious— Hutchinsonian pupils. Initial pupillary constriction is due to irritation of the ipsilateral 3rd cranial nerve (oculomotor) by the herniation of the temporal lobe at the tentorial hiatus. But eventually pupillary dilatation occurs by constrictor paralysis due to persistent compression of ipsilateral 3rd cranial nerve. There is ischaemia of the nucleus of 3rd nerve at midbrain due to compression of the posterior cerebral artery. So burr hole decompression is done on the side of Hutchinsonian pupil. xx Death can occur if immediate surgical intervention is not done. xx Features of raised intracranial pressure like high blood pressure, bradycardia, vomiting is also seen. Occasionally, convulsions may be present. xx Wound and haematoma in the temporal region of scalp may be seen. xx Glasgow coma scale gives clear idea about the neuronal injury. xx Autonomic disturbances with bradycardia, systolic hypertension, deep, slow respiration and later Cheyne Stokes ventilation. Cushing’s triad of raised intracranial pressure is obvious—bradycardia; hypertension; respiratory irregularities. xx Features like—restlessness, irritability, headache, vomiting, progressive deterioration—are common.

Investigations xx X-ray skull may show fracture of temporal bone. xx Electrolyte estimation. xx CT scan head is diagnostic. Extradural haematoma shows

biconvex lesion.

Fourth nerve when paralysed causes diplopia when going downstairs (that is on looking downwards). —Sir Benjamin W Ryeroft

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A

B1

B2

Figs 27.10A and B: (A) Extradural haematoma. Note the biconvex configuration of the haematoma; (B1 and B2) CT scan head showing extradural haematoma with biconvex lesion.

Treatment Immediate surgical intervention is a must to save the life of the patient. xx Craniotomy is done and cranial flaps are raised. The dura is not opened and the clot is evacuated. The dura is fixed to galea using interrupted sutures—Hitch stitches. xx Antibiotics and anticonvulsants are given postoperatively. xx Recovery is good after surgery. Treatment of extradural haematoma ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Earliest surgery and evacuation is the need 5 cm vertical incision in parietal region above the zygoma Galea is incised. Skull is opened using perforator and burr Meninges are kept aside Black currant jelly clot is evacuated Bleeding vessels are cauterized—bipolar cautery Dural hitch stitches are placed Opposite side if needed should be evacuated Antibiotics; anticonvulsants Analgesics General measures—catheter; fluid therapy Prevention post-traumatic complications

™™ ™™ ™™

Post-traumatic epilepsy Meningitis Post-traumatic amnesia

Complications

SUBDURAL HAEMATOMA Types ™™ ™™

Acute Chronic

Acute Subdural Haematoma xx It is a collection of blood between the brain and dura. It is

due to injury to the cortical veins and often due to laceration

of cortex of brain which bleeds and blood gets collected in the subdural space forming a haematoma. xx Here haematoma is extensive and diffuse. There is no lucid interval. There is severe primary brain damage. xx Haematoma may be of coup and contre-coup type. xx Loss of consciousness occurs immediately after trauma and is progressive. xx Convulsion is common. xx Features of raised intracranial pressure is obviously seen— high BP, bradycardia, vomiting. xx Focal neurological deficits or hemiparesis can occur. xx CT scan shows concavo-convex lesion.

Treatment xx Antibiotics, anticonvulsants. xx Surgical decompression is done by craniotomy.

Chronic Subdural Haematoma xx It is due to the rupture of veins between dura and brain

(cerebral hemispheres), causing gradual collec­tion of blood in subdural space. xx It is commonly seen in elderly people following any minor trauma like fall, slipping (which might have gone unnoticed). xx In elderly people, brain atrophies and even minor injuries can cause shearing and bleeding from these veins. xx Blood collects gradually over 2–6 weeks. Plasma and cellular components get separated. Eventually cellular part gets absorbed leaving only fluid component. It is called as chronic subdural hygroma. xx Usual haematoma collection is 60–120 ml. Often in 50% of cases, it is bilateral.

Clinical Features xx Common in old age, with history of minor trauma. xx Patient presents with confusion, disorientation, gradually

with altered level of consciousness and drowsiness.

Neurosurgery xx Later convulsions, features of intracranial hyper­tension,

features of coning develops. xx Extensor plantar response and pupillary changes develop eventually.

Investigations xx CT scan (shows concavo-convex lesion). xx Serum electrolytes. xx Blood grouping and cross matching.

Differential Diagnosis xx Electrolyte imbalance. xx Intracranial space occupying lesion.

Treatment xx Craniotomy and evacuation of clot is done when required

on both sides. xx Antibiotics. xx Anticonvulsants for 3 years. Complications ™™ ™™ ™™ ™™

Epilepsy Meningitis Coning Neurological deficits

Chronic Subdural Empyema xx It may be primary infection of subdural space from sinusitis focus causing suppuration and pus formation. xx It can be complication of the chronic subdural haematoma. xx It is due to secondary bacterial infection of collected clot/fluid. xx Infection is from sinusitis scalp (common)/through earlier trauma wound/haematogenous. xx Commonly Gram positive organisms cause empyema like streptococci (viridans/milleri) but other virulent organisms like Gram negative bacteria occasionally can cause. xx There is cortical venous thrombophlebitis and cortical infarction. xx Headache, fever, meningism and convulsions are the features. xx MRI is ideal than CT to diagnose. xx Treatment: Antibiotics, craniotomy and drainage; anticonvulsants, ICU care, proper monitoring, regular follow up. xx Condition has got 10% mortality.

SUBARACHNOID HAEMORRHAGE (SAH) Fig. 27.11: Subdural haematoma. Note the concavo-convex configuration of the lesion.

The Abbot by chance wished to decide with him the fate of the servants, found (him) prostrate upon the ground, insensible to shouts, to shaking and pinching of the body…senseless…. I saw him livid from pallor, deprived of all sensation and animate motion…. The first hour after midday of the same day he ceased to live…. By the indulgence of the Most Reverend Lord Abbot… I opened the head…. Much blood flowed from the space…. The (blood) covered (the brain) all over…. The ventricles laid open I found them all filled up with blood. —Johann Jakob Wepfer, 1658

It is a type of intracranial haemorrhage into the subarachnoid space usually from basal cisterns. It may be spontaneous or following trauma. Causes

Fig. 27.12: CT scan head showing subdural haematoma with concavo-convex lesion.

™™ ™™ ™™ ™™ ™™ ™™

Intracranial aneurysms—commonest cause (50%) Hypertension A-V malformations Blood dyscrasias Anticoagulant drugs Brain tumours (malignant)

Two black eyes following one injury indicate fracture of the base of skull.—Sir Earnest Finch

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Treatment

xx xx xx xx xx xx

xx xx xx xx xx xx

Sudden onset of severe headache with vomiting. Features of raised intracranial pressure. Photophobia. Neck stiffness. Focal neurological deficits: hemiplegia, dysphasia. Eye changes: ptosis, dilated pupil, changes in the eyeball movements. xx Sudden loss of consciousness. xx Features of brain oedema and cerebral ischaemia. In 40% of recovered patients, rebleeding occurs in 6–8 weeks which is commonly fatal. Hunt and Hess grading for subarachnoid haemorrhage Grade 1: Grade 2: Grade 3: Grade 4: Grade 5:

Asymptomatic Severe headache and neck stiffness Drowsy, confused or mild focal deficit Stupor, hemiparesis Decerebrate rigidity, coma

Fischer grading of SAH I—minimal 15 mm size

Differential Diagnosis xx Meningitis. xx Coning due to any cause.

Investigations xx xx xx

Lumbar puncture should be done to differentiate from meningitis. It has to be done carefully as it may precipitate coning. In subarachnoid haemorrhage, blood stained CSF is collected. CT scan. Carotid and vertebral angiogram.

Clipping, or wrapping the aneurysm. Craniotomy and proceed. Ligation of common carotid artery—there is risk of hemiplegia. Therapeutic embolisation. Excision of vascular malformations. Coiling of aneurysm with instruments.

FRACTURE SKULL Fracture skull is important as by itself may cause different problems and often it may be an indicator of the site of intracranial injury. It may be fracture of both tables of the skull or depressed fracture which is common in children but do can occur in adult. Fracture site may be single or multiple. It may be in anterior or middle or posterior cranial fossa. Fracture segments adjacent to dural venous sinuses may tear them causing life-threatening haemorrhage which is difficult to manage. Anterior cranial fossa fracture—Here cribriform plate may be fractured causing CSF rhinorrhoea; subconjunctival haemorrhage can develop when fracture extends to orbit. Anosmia due to olfactory nerve injury, blindness either partial or complete due to optic nerve injury or oculomotor nerve palsy can also occur. Middle cranial fossa fracture—Here maxillary or sphenoid or other sinus cavities can get fractured causing epistaxis, CSF otorrhoea, abducent (6th), facial (common, 7th), and vestibulocochlear (8th) nerve palsies can occur. Posterior cranial fossa fracture—It can cause glossopharyngeal, vagus or spinal accessory nerve palsies with boggy swelling in the nape of the neck.

Clinical Features xx Features of brain injury with altered Glasgow coma scale,

convulsions, localizing signs depends on the location of the fracture and amount of intracranial injury. xx Cranial nerve palsies as mentioned earlier. xx Features of raised intracranial pressure (ICP—normal is 8-–12 mmHg) when present – vomiting, systolic hypertension, headache, bradycardia, altered level of consciousness.

Investigations xx CT head, CT angiogram (carotid/vertebral if indicated

only). xx Serum electrolytes, haematocrit.

Treatment

Fig. 27.13: CT scan showing intracerebral brain haemorrhage.

If there is no intracranial injury fracture segment can be treated conservatively. Fracture site close to the dural venous sinuses are usually treated conservatively as intervention may cause more damage. Often it needs formal craniotomy and elevation of the fracture segment.

Neurosurgery Complications

Anterior or middle cranial fossa injury with fracture cribriform plate or injury to paranasal sinuses can tear dura causing CSF leak and rhinorrhoea.

xx Haemorrhage. xx Meningitis. xx Post-traumatic epilepsy.

Causes

DEPRESSED SKULL FRACTURE xx It is a common neurosurgical problem among the head

injuries. xx It means fracture depression is more than the depth of inner

table of the skull.

xx Investigations: CT scan. Problems in depressed fracture Tear in the dura beneath Haematoma in the deeper plane Injury to the cerebrum Injury to the venous sinuses—may cause life-threa­ten­ing haemorrhage. Fracture should not be elevated in such occasion, as it itself can precipitate bleeding ™™ Convulsions ™™ Meningitis ™™ ™™ ™™ ™™

xx Traumatic. xx Iatrogenic during base of skull surgeries or other neurosurgical procedures. It occurs in 5–7 days after the procedure usually. Nasal surgeries like FESS or septoplasty can cause CSF rhinorrhoea. xx Spontaneous/idiopathic—Due to high pressure hydrocephalous or congenital. xx Tumour related causes which erode the bony plate to create communication.

Features xx Rim of blood in the linen or filter paper with a layer of clear fluid—ring/double ring/halo sign. xx Change in position causes gush of CSF—reservoir sign. xx CSF leak may be immediate (within 48 hours) or delayed. Delayed leak occurs as initial haematoma prevents leak but haematoma dissolves or reduces CSF leak begins. xx CSF rhinorrhoea may be unilateral or bilateral or paradoxical (due to injury to midline structures like crista galli or vomer wherein CSF leaks into opposite nostril). xx Salty or metallic taste is typical. xx Anosmia, features of other cranial nerve palsies, infection or meningitis or pneumocephalous may be present. xx Traumatic leak resolves spontaneously in 70% of cases and will not recur; whereas nontraumatic leak is unlikely to resolve which requires intervention either endoscopically or by open method. Note:

CSF mixed with blood will not clot.

Fig. 27.14: Depressed skull fracture.

Treatment xx Antibiotics, anticonvulsants. xx Elevation of the depressed fracture: Burr holes are made in the adjacent normal skull. Fracture is elevated. Bony fragments and necrotic materials are removed. Dural tear is closed with interrupted sutures.

CSF RHINORRHOEA It is the CSF leak through the nose due to communication between subarachnoid space and nasal cavity. It is due to tear in the dura of various causes. CSF normally is produced by choroid plexus and absorbed by arachnoid villi. Normally CSF production is 20 ml/h or 500 ml per day. 150 ml of CSF is on circulation in CNS.

xx Complications: meningitis, persistent leak for long time due to prevention of dural healing by brain matter interposition. Streptococcus pneumoniae and haemophilus influenzae are most common bacteria causing meningitis. xx Beta 2 trasnferrin assay is best method to identify the CSF leak. It is produced by neuraminidase in CNS. It is present only in CSF, perilymph and aqueous humor. 0.5 ml of leak fluid is assayed by electrophoresis. Beta trace proteins, glucose test of leak fluid are other less sensitive methods. xx CT head confirms the site of injury. MRI head or CT or MR cisternography or injection of intrathecal fluorescein are different methods used to identify the site of leak.

Treatment xx Avoid straining, coughing, sneezing, nasal blowing as much possible as with head end 300 elevation. xx Acetazolamide 250 mg tid reduces the CSF volume and hence the leak. xx Antibiotics coverage to prevent ascending meningitis. xx Surgical treatment—CSF leak which doesn’t stop, needs surgical intervention. Dural flap or muscle patch or mucosal graft or bone graft is used to cover the defect at the site of leak. Approaches may be intracranial, external approach through paranasal sinuses or endoscopic approach.

The blessing of health is realised on the sick bed—Mr Tut-Tut

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SRB's Manual of Surgery xx Lumbar drainage as an adjuvant therapy can be used with drainage of 5–10 ml/h for 48 hours.

HYDROCEPHALUS The heads of children sometimes grow enormously large, the sutures give way, and the membranes of the brain are pushed up with the water within, and make a soft tumour rising above the edges of the sutures…. They daily become more and more stupid, with a pulse not above seventy-two. —William Heberden, 1802

It is dilatation of ventricles due to blockage of cerebrospinal fluid flow (CSF) or due to increased secretion or due to defective absorption of CSF.

Classification I xx Communicating type: Ventricles communicate freely into the subarachnoid space.   Here there is defective absorption of CSF fol­lowing any inflammation, subarachnoid haemor­rhage or trauma. xx Noncommunicating type: Obstruction is in the ventricle or its exit, due to any tumours or any inflammatory process. CSF drains from lateral ventricle to 3rd ventricle through foramen of Monro; from 3rd ventricle to 4th ventricle through aqueduct of Sylvius; from 4th ventricle through foramen of Lushchka and Magendie to reach over the convexity to get absorbed by arachnoid tissue.

Classification II Congenital

Acquired

Associated with spina-bifida and myelomeningocele. It is due to:

May be unilateral or bilateral (midline obstruction), due to:

• Failure of formation of CSF pathways

• Chronic meningitis

• Arnold-Chiari malformation

• Trauma

• Congenital stenosis of aqueduct of Sylvius

• Subarachnoid haemorrhage

• Presents with widening of • Brain tumours—(pineal/ cerebellar/craniopharyngiomas) sutures, tense fontanelles and decreased cortical • Colloid cyst of 3rd ventricle thickness • Arachnoid cysts • Enlargement of head occurs, either prenatal (can cause obstructed labour) or postnatal

Surgery xx Tapping of the lateral ventricles. xx Ventriculocysternostomy using polythene catheters— Torkildsen operation. xx Ventriculo-atrial (VA) or ventriculo – peritoneal (VP) shunts. xx Complications of shunt surgery – obstruction or infection of the shunt; subdural haematoma, convulsions, spontaneous pneumothorax, ascites.

Clinical Features xx Large head often causes obstructed labour. There will be raised head circumference more than 2 cm/month and craniofacial disproportion. xx Bulging of anterior fontanelle which is more prominent on crying, engorged scalp veins, scalp is thin and shiny, suture line separation. xx Decreased upward gaze (sunsetting sign); on percussion cracked pot sound due to dilated ventricle (Macewen’s sign). xx Delayed milestones, mental retardation and difficulty in retaining feeds. xx Features on raised ICP mainly in adult, lethargy, irritability, ataxia, papllioedema, blindness due to ophthalmoplegia, abducens palsy and respiratory failure.

Investigations xx CT scan; MRI brain, CT or air ventriculography. xx Evaluation for the cause.

Treatment Drugs—acetazolamide, frusemide, isosorbide, glycerol.

A Fig. 27.15A

Neurosurgery Clinical Features xx Evidence of focus of infections are seen, i.e. middle ear (CSOM), sinusitis. xx Focal neurological features are seen, depending on the location of abscess. In temporal lobe abscess features of dysphasia, contralateral hemipa­resis are seen; in cerebellar abscess, all cerebellar symptoms are seen. xx Epilepsy. xx Features of raised intracranial pressure: (a) slow pulse, (b) rising BP, (c) headache and vomiting, (d) papillo­edema, (e) deterioration in level of con­sciousness, (f) visual distur-bances.

Differential Diagnosis xx Intracranial tumour. xx Tuberculoma. xx Meningitis.

B Fig. 27.15B

Figs 27.15A and B: Hydrocephalus child. CT scan head picture in hydrocephalus.

INTRACRANIAL ABSCESS Types xx Extradural abscess: Caused by:  Osteomyelitis of skull.  Middle ear infection.  Frontal sinusitis.   Pott’s puffy tumour is subperiosteal swelling with infection and inflammation of the scalp. There is acute localised headache and tenderness in the skull, localised pitting oedema of the scalp usually in the frontal region. xx Subdural abscess: is caused by septic thrombo­phlebitis from the frontal sinusitis or other infections. It is often very severe with extension into the venous sinuses. xx Intracerebral abscess: is caused by  Extension from middle ear or sinuses.  Blood-born infection.  After intracranial injuries.

Investigations xx xx xx xx xx xx xx xx

CT scan. MRI. Carotid angiogram. Ventriculography. EEG. Isotope brain scan. Total count, ESR. Investigation specific for focus of infection. Lumbar puncture should be avoided in acute abscess as coning can occur.

Common sites: Temporal lobe, cerebellum, frontal lobe. It can be: a. Acute—There is acute septic encephalitis without pus formation. It may cause ventriculitis or localized abscess formation b. Subacute—Occurs in 3 weeks, by the formation of a glial wall, i.e. thickness is more near the cortex and less towards ventricle c. Chronic—Occurs in 6 weeks with thick wall which may persist or may get enlarged behaving like a space occupying lesion d. Metastatic—Abscess in brain occurs either in cere­brum (parietal or temporal lobes) or in ventricles (Ventriculitis is more dangerous and often fatal)

Fig. 27.16: Intracranial abscess. It needs drainage. It could be tuberculosis. It is a space occupying intracranial lesion, mimics malignancy often.

Disease is no absolute physical entity but a complete intellectual construction, an amalgam of biological state and social definitions. —Charles E Rosenberg

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SRB's Manual of Surgery Treatment xx Antibiotics—high dose penicillins, benzyl penicil­lins are given. xx Burr hole exploration is done and Dandy’s brain cannula is placed. Pus is aspirated and sent for culture and cytology. xx In case of chronic abscess, exploration of cranial cavity and excision of brain abscess is done. Complications ™™ ™™ ™™

Intracranial hypertension Coning Neurological deficits

Secondaries are the commonest malignant tumour in the brain. Metastasis occurs usually from lung (commonest), nasopharynx or from any other organ in the body. Secondaries in brain ™™ ™™ ™™ ™™ ™™ ™™

INTRACRANIAL ANEURYSMS Types

™™ ™™

Commonest malignant brain tumour Primary are—lungs (40%), breast (30%), melanoma (15%), others (15%) Usually multiple Headache, focal lesions, convulsions, hypertension, altered level of consciousness are the features CT scan, CT chest or evaluation of primary—needed Radiotherapy and chemotherapy of particular primary is treatment Solitary metastasis can be removed surgically Steroids reduce the cerebral oedema and so symptoms

xx Subclinoid type occurs in the internal carotid artery within the cavernous sinus. It causes ptosis, defective external ocular movements, 5th nerve palsy. It can cause carotid-cavernous fistula. xx Supraclinoid type is commonest type.  Berry aneurysms: A congenital type occurs in circle of Willis in relation to internal carotid artery [40% (most commonly at the origin of posterior communicating artery)], anterior communicating artery, middle cerebral artery, vertebrobasilar artery. It occurs due to weakness in the media of major arteries.  Acquired aneurysms due to atheromas, hyper­tension.  Mycotic aneurysms occurs due to infection in the wall of cerebral vessels, as a result of any bacte­raemia. Common sites are peripheral branches of middle cerebral artery. Presentations ™™ ™™ ™™ ™™

Subarachnoid haemorrhage Pressure effects Convulsions Eye and pupillary signs

Fig. 27.17: Orbital secondaries from adrenal neuroblastoma.

Investigations xx CT scan. xx Carotid and vertebral angiogram.

Treatment xx Clipping or wrapping of aneurysms. xx Therapeutic embolisation. xx Open neurosurgical approaches.

INTRACRANIAL TUMOURS There was discovered on (the corpus callosum) of the brain a remarkable round fleshy tumour like an acorn. It was hard and full of holes and was as large as a medium-sized apple. It was covered with its own membrane and was entwined with veins…. We perceived that this ball by compressing the brain and its ducts with its mass and by flooding them, had been the occasion of the lethargy and listlessness and finally of death. —Felix Platter, 1614 

Fig. 27.18: CT scan head showing brain secondaries.

Neurosurgery Primary Brain Tumours 1. Gliomas (43%). a. Astrocytomas are the commonest type. They are usually malignant. They can occur anywhere in the cerebral hemispheres, medulla, brainstem. Peak incidence is in 4th decade.   They can be diffuse, solid or cystic. They contain starshaped cells resembling adult neuroglial cells. Astrocytic gliomas are graded as Grades I, II, III, IV based on the quantity of adult and primitive cells. Grade I—Cystic Grade II—Diffuse Grade III—Anaplastic Grade IV—Glioblastoma multiforme—It is high grade aggressive type of astrocytoma. It is treated by surgical removal/debulking; high dose radiotherapy, chemotherapy with carmustine inserted into the surgical cavity and oral temozolomide. Median survival is 12 months; 2-year survival rate is 25% or less.

2. Meningiomas (18%): They are usually globular, arising from the arachnoids. Tumour gets attached to the dura. It gets blood supply from dural arteries and veins, from emissary veins and veins of diploe and scalp. Along these veins tumour cells invade the bone, causing bone destruction and reactive hyperostosis.   Meningiomas are classified as fibroblastic, endothelial and angioblastic. Sites ™™ ™™ ™™ ™™

Microscopic: It contains whorls of spindle cells, with central hyaline material, with psammoma bodies. Meningioma ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Fig. 27.19: CT scan showing astrocytoma – aggressive variety— grade IV—gliobalstoma multiforme.

b. Oligodendrogliomas: They are slow growing tumour commonly arising from frontal lobes, lasts for years; shows calcification. c. Spongioblastoma polare: They arise from primitive spongioblasts, affects optic chiasma, 3rd ventricle, hypothalamus. They are both operable and radiosensitive. d. Medulloblastoma: It is highly malignant embryonal tumour grouped under PNETs (primitive neuroectodermal tumours) arising from primitive cell nests; common in children (medulloblastoma is the most common brain tumour in children) and young individuals. It often spreads within the brain itself causing sugarcoat metastases which may extend across the spinal canal. e. Ependymomas: Here cells resemble ependymal cells; can occur throughout the hemispheres. They arise from cells lining the ventricles of the brain and central canal of the spinal cord. They are common in 4th ventricle; common in younger individual; blocks CSF circulation causing hydrocephalous.

Parasagittal Frontobasal Posterior fossa Choroid plexus

18% common Arising from arachnoids 80% are supratentorial; but occasionally can occur in the sphenoid wing, olfactory groove or lateral ventricle Common in females of middle aged Multiple meningiomas may be present in patients with neurofibromatosis type 2 Gets blood supply from dural vessels Invades the skull bone through emissary and diploe veins Destruction and reactive hyperostosis of bone is common Psammoma bodies are often seen histologically CT/MRI diagnostic Surgery is the choice therapy It has got good prognosis

3. Schwannoma (8%): Common in auditory nerve, also called as acoustic neuroma.   Occurs in the internal auditory meatus which projects into the cerebellopontine angle (C- P angle), compressing 5, 6, 7, 8th nerves. It presents with compressive features like unilateral deafness, trigeminal neuralgia, squint, cerebellar compres­sion syndrome. 4. Pituitary tumours (12%). 5. Craniopharyngiomas (5%). 6. Blood vessel tumours (2%).

Clinical Features xx Initial period of silent growth. xx Focal syndromes with epilepsy. xx Raised intracranial pressure with headache, vomiting,

deterioration of level of consciousness, altered vision, slow pulse, high BP, papilloedema. xx Brain displacement and stage of coning. Note:

First sign in acoustic neuroma is loss of corneal reflex.

A very bold surgeon is the one who realise that, his patient takes all the risks.

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SRB's Manual of Surgery Specific Features xx Frontal lobe tumours: Personality and emotional changes,

epilepsy of generalised type, contralateral facial weakness. xx Parietal lobe tumours: Jacksonian epilepsy, progres­sive

hemiparesis, astereognosis, acalculia. xx Occipital lobe tumours: Aura of flashing of light in contralateral field, homonymous hemianopia. xx Temporal lobe tumours: Progressive aphasia, visual, auditory, smell and taste hallucinations, hemipa­resis, superior quandrantic hemianopia. xx Midline tumours: Produces bilateral hydrocepha­lus. xx Tumours of the third ventricle (colloid cyst is common): Causes bilateral hydrocephalus, progressive cerebral atrophy, dementia, sexual precocity, endocrine disturbances. xx Pineal tumours: Causes precocious puberty. xx Cerebellar vermis tumours: Usually medulloblas­tomas, occur in young children, presents with progressive hydrocephalus and features of hernia­tion of cerebellar tonsils through foramen magnum. xx Cerebellar hemisphere tumours: Commonly are astrocytomas, produce cerebellar syndromes, nystagmus.

A

B Figs 27.21A and B: MRI brain showing glioma brain.

Incidence of malignant brain tumour is 8% In adult brain tumours are commonly (60%) are supratentorial; in children infratentorial – posterior cranial fossa ™™ 50% present with headache which is often (10%) worsening at early morning. Headache is due to raised ICP; focal or generalised convulsions (25%); progressive neurological deficit (65%) motor (mainly and sensory; visual disturbances; cranial nerve palsies; mental changes; drowsiness and irritability – are presentations ™™ Features may suddenly worsen or progress when there haemorrhage in the tumour ™™ ™™

Fig. 27.22: MRI brain showing glioblastoma multiforme. It is very aggressive malignant tumour.

Investigations xx X-ray skull:     

Calcifications like in meningiomas, cranio­pharyn­giomas. Separation of sutures. A beaten silver appearance. Lateral displacement of pineal body. Hyperostosis, expansion, destruction in skull bones.

Fig. 27.23: Skull X-ray showing mass calcified lesion. It could be meningioma, dermoid extending intracranially.

Fig. 27.20: CT scan head showing large meningioma frontal region.

xx xx xx xx xx xx xx

Isotope scan. CT scan. MRI. Positron Emission Tomography (PET). Carotid angiogram (Introduced by Egas Moniz). Ventriculography. EEG.

Neurosurgery Treatment

  It secretes excess growth hormone causing acromegaly in adults and gigantism in children.

xx Relief of raised intracranial pressure:

a. Ventricular tap and drainage through a posterior parietal burr hole. b. Tapping of cystic tumours and abscesses. c. Administration of mannitol. d. Emergency decompression by partial removal of tumour. e. Steroid therapy—dexamethasone. xx Establishment of pathological diagnosis: a. Burr-hole and biopsy. b. Craniotomy and biopsy using brain cannula. c. Frozen section biopsy. d. CT guided stereotactic biopsy. xx Removal of benign tumours—by different cranio­tomy approaches. xx Decompressive surgeries for malignant tumours. xx Shunt surgeries to drain CSF—ventriculoperi­toneal shunt or ventriculoatrial shunt. xx Radiotherapy—external radiotherapy is used as pri­mary treatment or as an adjuvant therapy after surgery. xx Chemotherapy is occasionally used—Temozolamide.

A

A

B Figs 27.24A and B: Craniopharyngioma from sellar region.

Prognosis

B

Tumour which is benign and surgically accessible has better prognosis.

PITUITARY TUMOURS A young student…suddenly (sleepy and lethargic) died in convulsions within two weeks. In his brain the ventricles were found swollen with blood… which had gone down to the base of the skull…. The olfactory bulbs were not swollen at all. The pituitary gland…was completely blocked by a…viscous and gelatinous mass about the size of a small bean… Hence a dropsy of the brain ensued. —Richard Lower, 1672

Classifications I 1. Eosinophil (Acidophil) adenomas: Tumour is usually small. Rarely it causes compressive features.

Figs 27.25A and B: Acromegaly due to pituitary tumours. Note the operated scar in the frontal region. 2. Chromophobe adenomas are common in females and in the age group—20–50 years.   Initially, it is intrasellar and after sometime becomes suprasellar. Later, it extends intracranially often massively, causing features of intracranial space occupying lesion. It presents with myxoedema, amenorrhoea, infertility, headache, visual disturban­ces, bitemporal hemianopia, blindness, intracranial hypertension, epilepsy. Differential diagnosis: Meningiomas, aneurysms. CT scan, angiogram, X-ray skull are diagnostic. Treatment is surgical decompression by cranio­tomy through subfrontal approach or trans-s­phenoidal approach. Deep external radiotherapy and steroids are also used. 3. Basophil adenomas are usually small. They secrete ACTH and presents as Cushing’s disease with all its features. 4. Prolactin-secreting adenomas causes infertility, amenorrhoea and galactorrhoea.

Truth always exists; only lies are invented.

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Hypersecreting Hyposecreting by compression and atrophy

™™ ™™

Micronodular: Tumour size less than 10 mm Macronodular: Tumour size more than 10 mm

xx Ventriculocisternostomy—Torkildsen’s operation is done in cases of large masses blocking the 3rd ventricle obstructing the CSF outflow. xx Radiotherapy.

Classification III

Stages ™™ ™™ ™™

Stage of intrasellar development Stage of suprasellar extension Stage of massive intracranial extension

Investigations

SPINAL DYSRAPHISM It is posterior midline congenital deformity of spine due to incomplete fusion of ectodermal, mesodermal or neuroectodermal elements either singly or in combination. It is due to arrest of closure of neural tube.

Types Myelocele

xx X-ray skull—shows calcifications, destruction of sella turcica, mass lesion, enlarged pituitary fossa. xx CT scan. xx MRI. xx Hormone assay—like serum prolactin, growth hormone, ACTH, steroids, sex hormones, etc.

There is failure of closure of neural as well as vertebral arch. There is raw oval defect uncovered over central canal which is incompatible with life and newborn infant dies soon. Loss of lower limb power, incontinence of urine, talipes, CSF discharge, and meningitis is common. Very occasional infant who survives develop a skin coverage from periphery but neurological problems are irreversible. It is common but least survival chance.

Treatment

Syringomyelocele

xx Surgery: By subfrontal craniotomy approach or transphenoidal approach.   Care should be taken not to injure optic chiasma, arteries, cavernous sinus. xx External radiotherapy.

It is rarest type. Central canal of spinal cord is dilated with bulging out of the canal under the skin of the dilated centrtal canal as thin cystic sac containing cord with meninges and nerve roots. Gross paralysis is common. It is identified on table as it is difficult to differentiate from myelomeningocele clinically.

CRANIOPHARYNGIOMAS They are large masses with cystic cavities, lined by ciliated epithelium containing cholesterol crystals. Areas of calcifications may be present and coral-like masses may be formed. They are adherent to the basal arteries and adjacent nerves. They are irremovable. They are tumours of sellar region.

Clinical Features xx Intrasellar craniopharyngiomas inhibits sexual maturation causing obese, impotent dwarf with bitemporal hemianopia (due to compression of optic chiasma)—Frolich’s syndrome. xx Suprasellar craniopharyngiomas produces Frolich’s syndrome; pressure on hypothalamus which controls sleep and water metabolism (causes somnolence and diabetes insipidus). xx Massive intracranial extension causes intracranial hypertension and also hydrocephalus by obstructing CSF flow.

Investigations xx Skull X-ray shows calcification. xx CT scan is diagnostic.

Treatment xx Through craniotomy or through trans-sphenoidal approach cystic tumours are evacuated. xx Ventriculoatrial shunt has to be done to drain CSF in case of hydrocephalus.

Myelomeningocele It occurs 2 in 1000 live births. Here part of the cord or cauda equina or both present as median cystic swelling at back. It is not transilluminant. It is common in lumbosacral region. Adhesion of spinal cord or cauda equina to sac causes neurological deficit. Kinking, compromised blood supply causes neurological deficit (30%). Monoplegia, paraparesis, paraplegia, talipes and incontinence are the features. It is almost always associated with Arnold Chiari syndrome or Dandy Walker syndrome (atresia of foramina Lushka and Magendie).

Meningocele Protrusion of spinal meninges through a congenital defect in the spinal laminar defect.

Spina Bifida Neural arches failure to unite over a limited area and externally there is no protrusion but there is obvious defect.

MENINGOCELE It is the herniation of meninges through a weak point of spine where bony fusion has not taken place effectively. Swelling is covered with pia mater and arachnoid mater without dural covering and contains CSF.

Clinical Features xx Present since birth.

Neurosurgery xx Soft, cystic, fluctuant with transillumination. xx Signs of compressibility. xx Expansile impulse when asked to cough or when child cries.

Location xx Lumbosacral—commonest. xx Occipitocervical—2nd most common.

 Initially there is no neurological deficit but later due to teth-

ering, traction on dura, infection, can lead neurological deficits. 2. Spina bifida aperta  Here neurological deficit is present. It may be myelomeningocele wherein spinal cord and nerve roots are in the sac. It may be meningocele wherein sac consists of meninges and fluid only.  Meningocoele is brilliantly transilluminant. Myelomeningocoele is not transilluminant.

Investigations

Clinical features

xx CT scan head to look for hydrocephalus. xx MRI spine.

Treatment Excision as early as possible. Transverse elliptical incision. Closure of defect by plication. Approximation of muscles. Early closure prevents infection.

Motor paralysis Sensory paralysis Visceral paralysis with incontinence of urine and faeces Swelling in the spine at the site of the lesion, may be lipoma or dermoid, with impulse on coughing ™™ Bony defect at the site ™™ Hydrocephalus ™™ ™™ ™™ ™™

Complications xx Ulceration. xx Haemorrhage. xx Closure may cause hydrocephalus which needs shunting of CSF. Meningocele

Meningomyelocele

• • • • • •

• • • •

Membranes content Soft, cystic Brilliantly transilluminant Longitudinal furrow absent No neurological defect Good prognosis after repair

Membranes with nerve roots Soft to firm Nontransilluminant Longitudinal furrow is seen due to adherence of nerve roots • Trophic ulcer, bowel/ urine incontinence, motor problems • Neurological deficit present • Not good results

Fig. 27.26: Spina bifida occulta. Note the dimple and tuft of hair.

SPINA BIFIDA xx It is also classified under spinal dysraphism. xx It is failure of enfolding of nerve elements within the spinal canal during developmental period. xx It is usually seen in lumbosacral region. There is failure of fusion of one or more posterior vertebral arches. xx It is often associated with other anomalies.

Sites ™™ ™™

Lumbosacral Thoracolumbar

Types 1. Spina bifida occulta—commonest type  There is dimpling of skin with dermoids, lipomas in the site. Impulse on coughing can be seen.

A

B Figs 27.27A and B: Spina bifida with protruding dermoid through the defect.

Investigations xx Plain X-ray of the spine. xx CT scan/MRI of spine and head.

The first sign of Pott’s disease is deepened midline spinal sulcus at about T10 level due to increased muscular tonicity of sacrospinalis muscle. It is a NATURE’S PLASTER CAST. —Francis E Jardine

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SRB's Manual of Surgery Treatment xx xx xx xx

Correction of deformity. Maintaining the visceral function. Development of limb function. Ventriculoperitoneal shunt or ventriculoatrial shunt surgery for hydrocephalus.

xx Central-posterior is not common. It is due to trauma. It is severe type, even though rare. Secondary changes: Osteoarthritis of joints.

Clinical Features xx Pain in the distribution of the root which gets aggravated by straining, coughing, twisting, stooping. xx Pain radiates along the distribution of the nerve with tingling and numbness. xx Lumbar scoliosis is significant. xx Restricted forward flexion but free lateral flexion. xx Positive straight leg raising on the affected side with positive Lasegue’s manoeuvre. xx Wasting in the muscles with blunting of sensation, with absence knee and ankle jerks. xx Loss of bladder sensibility and retention of urine.

Fig. 27.28: Infant with encephalocoele. It is non-transilluminant whereas meningocoele is brilliantly transilluminant.

INTERVERTEBRAL DISC PROLAPSE (IVDP) xx Herniation of part of the gelatinous nucleus pulposus through a rent in the annulus fibrosus, commonly at postero-lateral part which is a weak point. xx In cervical spine discs between C5 and C6 ; C6 and C7 are commonly affected impinging 6th and 7th nerves res­pectively. xx In lumbosacral region, discs between L5 and S1; L4 and L5 are commonly affected impinging first sacral nerve and 5th lumbar nerve respectively. xx Initially protrusion bulges through the pain sensitive posterior longitudinal ligament causing back pain. xx Later it herniates through the posterior ligament compressing the nerve causing typical root pain.

Fig. 27.30: Intervertebral disc prolapse.

Differential Diagnosis xx xx xx xx xx xx xx

Spinal cord tumours. Tuberculosis of the spine. Osteoarthritis. Ankylosing spondylitis. Spondylolisthesis. Vascular problems. Retroperitoneal and pelvic tumours.

Investigations

Fig. 27.29: Intervertebral disc prolapse.

Types xx Posterolateral is common.

xx xx xx xx

X-ray spine both AP and lateral. It is not useful in acute prolapse. Myelography or radiculography. CT scan. MRI is very useful method.

Treatment xx Rest in bed. xx Spinal jacket.

Neurosurgery xx Continuous or intermittent traction. xx Analgesics and relaxants. xx Intradiscal injection of the chymopapain enzyme which dissolves the fibrocartilaginous tissue and nucleus pulposus. xx Surgical treatment: Indications:  Persistent pain for 12 weeks which is not relieved by drugs.  Severe neurological disturbances like involve­ment of bladder, bowel or sexual functions. Surgery: Discectomy.

TUBERCULOSIS OF SPINE (CARIES SPINE) xx It is commonly of secondary type. xx Primary focus is in the lungs or lymph nodes. xx Commonly involved vertebra is dorsilumbar vertebra T10.

Differential diagnosis ™™ ™™ ™™ ™™

Cervical spondylosis Congenital torticollis Secondaries Spinal cord tumours

Investigations xx X-ray cervical spine, chest X-ray. xx MRI is ideal.

Treatment xx Antitubercular drugs. xx Anterolateral decompression of vertebra. xx Drainage of cold abscess.

Mode of infection: Mainly haematogenous.

A.  Tuberculosis of Cervical Vertebra Common in C6 and C7 vertebra.

Clinical Features xx Pain in the neck, often referred to occipital region through suboccipital or posterior auricular nerves. xx Pain, when referred through anterior cervical primary rami causes brachial neuralgia. xx Rigidity in the neck. xx Patient supports the chin on the palm of his hand (Rust sign). xx Tenderness and paraspinal spasm with rigidity of the skull muscles. xx All passive and active movements of spine are painful and restricted. xx Cold abscess may be present in the neck, posterior to sternomastoid muscle or in the retropharyngeal region or in the axilla. xx Chronic tuberculous retropharyngeal abscess in midline, situated behind the prevertebral fascia. It is painless, soft, often causing dysphagia and dyspnoea.

Fig. 27.32: Compression fracture spine—traumatic, pathological.

B. Tuberculosis of Thoracolumbar Vertebra (Pott’s disease, caries dorsilumbar spine) Commonest site is dorsilumbar region—T10. Reasons ™™ ™™ ™™ ™™ ™™ ™™ ™™

It is the junction of fixed (thoracic) and mobile (lumbar) segments of spine It bears the maximum stress It has got large amount of cancellous bone Bulky nucleus pulposus Relative avascularity of the body of dorsilumbar vertebra Close proximity to the thoracic duct through which infection can occur Adjacent prevertebral veins

Types Fig. 27.31: Tuberculosis of spine.

xx Tuberculosis of the body of vertebra  Tuberculous metaphysitis—Here contiguous surfaces of the vertebra are involved. It is the most common type in children.

Great minds must be ready not only to take opportunities, but also to make them.

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SRB's Manual of Surgery  Tuberculous osteomyelitis (central type—through central artery

of the vertebra)—It occurs in the centre of the body of vertebra.  Tuberculous periostitis (peripheral or periosteal) — It is seen in adults. It is situated deep to the anterior longitudinal ligament. xx Tuberculosis of the appendages  Spinous process.  Pedicle.  Transverse process.  Lamina.

Features xx Contiguous surfaces of paired vertebra are involved. xx Lower half of one vertebra and upper half of adjacent vertebra below, with intervertebral joints are involved as they share a common blood supply.



It passes through psoas sheath. It causes psoas spasm causing flexion of hip with inability to extend. If abscess extends below the inguinal ligament, then it is cross-fluctuant. 3. Spinal cord involvement—causes paraplegia (10%). This is common in thoracic spine, as the spine is narrow. a. Early paraplegia (‘Paraplegia in flexion’ , ‘paraplegia with active disease’). It is due to: –– Pressure by caseating material, granulation tissue and sequestrum. –– Tuberculous meningitis. –– Spinal cord oedema. –– Endarteritis of segmental spinal artery. –– Pressure from distended disc. b. Late paraplegia (‘Paraplegia with a healed disease’, ‘paraplegia with extension’). It is due to: –– ‘Gibbus’ causing stretching of the spinal cord. –– Longitudinal shrinkage of the spinal cord due to gliosis.

Clinical Features xx Pain in the back, often with tingling sensation along the distribution of nerve roots. xx In upper thoracic tuberculosis, typical ‘military attitude’ with raised shoulder which is drawn back­wards is seen. xx Kyphosis (gibbus) is the commonest deformity. It can be angular but also can be rounded. xx Tenderness in the spine with paraspinal spasm. xx All active and passive movements of spine are restricted. xx ‘Coin test’—inability to pick up a coin is positive. xx Weakness and decreased power in the limb muscles, with altered sensation.

Investigations

Fig. 27.33: Tuberculosis of spine. Note the area of involvement. xx Destruction of the vertebra and intervertebral disc; collection of caseous material behind the anterior longitudinal ligament.

Pathology ™™ ™™ ™™ ™™ ™™

xx X-ray spine shows:  Narrowing of the disc space.  Wedging of the vertebra.  Rarefaction of the adjacent vertebra.  Soft tissue shadow of cold abscess. xx Chest X-ray PA view. xx ESR. xx Radioisotope bone scan. xx CT scan or MRI of spine.

Tuberculous endarteritis Decreased blood supply Formation of tubercles with caseation Destruction of bone Failure of subperiosteal new bone formation

Effects 1. Deformity—Kyphosis (Gibbus) is excessive posterior curvature of the spine. It is due to complete anterior collapse of the vertebra. 2. Cold abscess formation: a. Close to the midline, when caseating material passes through the medial dorsal cutaneous nerves. b. Away from the midline, when caseating material passes through the lateral cutaneous nerve. c. Cold abscess may form in relation to psoas muscle (in dorsilumbar or lumbar).

A

B

Figs 27.34A and B: Typical tuberculosis of spine involving L4 and L5 spine X-ray features.

Neurosurgery Differential Diagnosis xx xx xx xx xx

2. Intramedullary (25% of intradural) –– Commonest is diffuse gliomas (50%).Others are ependymomas, vascular malformations. –– Common in cervical cord.

Secondaries in the spine. Spinal tumours. Scheuermann’s disease (osteochondritis). Old compression fracture of the vertebra. Ankylosing spondylitis. Complications of Pott’s spine

™™ ™™ ™™ ™™ ™™

Kyphosis Cold abscess Paraplegia Sinus formation Dissemination

Treatment xx Anti-tuberculous drugs for one year. xx Rest with plaster jacket (SPICA).

Patient gains weight, X-ray shows re-calcification and healing. ESR becomes normal. Pain and spasm disappears. Indication for surgery ™™ ™™ ™™

When the disease is progressive When there is neurological manifestation Cold abscess formation

Surgeries Note:

No posterior approach, no laminectomy for TB spine.

• • •

Anterolateral approach and costotransversec­tomy with removal of all caseating material with bone grafting. Drainage of cold abscess. Posterior spinal fusion using bone graft. Bone graft is taken from the iliac crest.

SPINAL TUMOURS Classification A. Extradural tumours  Commonest is secondaries. –– They lie between the dura, bone and liga­mentum flavum. –– Primary sites are bronchus, breast, prostate, kidney. Rare extradural tumours are sarcomas, osteoclastoma, chondroma, lipoma. B. Intradural tumours 1. Extramedullary (75% of intradural) –– Neurofibromas are the commonest, more common in males. -- Arises from the posterior nerve root. It can be ‘dumbbell’ tumours. –– Spinal meningiomas are seen exclusively in females.

Fig. 27.35: MRI spinal cord showing spinal cord tumour—ependymoma.

Clinical Features xx xx xx xx xx

Weakness of limbs, often with paraplegia. Tingling and numbness. Disturbance in micturition. Changes in tendon reflexes. Pain in the back. Spinal cord or cauda equina compression is a surgical emergency.

Investigations xx xx xx xx

X-ray shows widening of space and destruction. Myelography. Lumbar puncture per se has no role, as it is dangerous. CSF below the block may be yellow and protei­na­ceous and is called as ‘Frolin’s syndrome’. xx Protein levels in lumbar CSF is usually raised in the presence of lumbar tumours, commonly ‘Schwannomas’. xx CT scan. xx MRI.

Surgery xx Surgery is the main treatment—Decompression of spinal cord and removal of tumour by doing laminectomy. xx Adjuvant therapy: Radiotherapy and chemo­therapy. xx Intrathecal methotrexate is also beneficial.

No head injury is so slight that it should be neglected, or so severe that life should be despaired of. —Hippocrates, Father of Medicine

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Thorax CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Chest Injuries Fracture Ribs Flail Chest and Stove in Chest Pneumothorax Tension Pneumothorax Haemothorax Pleural Tap Bronchoscopy Empyema Thoracis Empyema Necessitans Lung Abscess Intercostal Tube Drainage

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Shock Lung Pulmonary Embolism Surgical Emphysema Lung Cysts Mediastinal Tumours Thymomas Lung Cancers Pancoast Tumours Chest Wall Tumours Pericarditis – Acute Pericarditis – Chronic Constrictive Pericarditis ™™ Pericardial Tap

CHEST INJURIES Types xx xx xx xx

xx xx xx xx xx xx

Crush injuries involving lung, pleura, ribs. Single rib fracture. Two or more rib fractures. Steering wheel injury—causes multiple rib frac­tures, bilaterally often with flail chest, with fracture dislo­cation of upper end of sternum. Stove in chest or flail chest. Traumatic pneumothorax. Haemothorax, haemopneumothorax, with fracture ribs. Tension pneumothorax. Pericardial, cardiac injuries and rupture of bron­chus. Associated injuries in liver, spleen, diaphragm, major vessels.

Causes xx xx xx xx xx

Road traffic accidents. Industrial accidents. Blast injuries. Crush injuries. Stab injuries.

™™ Cardiac Tamponade ™™ Diaphragmatic Hernia ™™ Pulmonary Complications during Postoperative Period ™™ Surgical Management of Pulmonary Tuberculosis ™™ Video-assisted Thoracoscopic Surgery

 In children, ribs are malleable and so fracture ribs are rare.  In elderly because of rigid ribs fracture is common.  First and second ribs are protected by clavicle and so their

fracture is uncommon.  11th and 12th ribs are floating ribs and so their fracture is rare.

Classification of Chest Injuries As per the American College of Surgeons Committee on Trauma chest injuries are classified as (deadly dozen): 1. Immediately life-threatening injuries. 2. Potentially life-threatening injuries. Immediately life-threatening injuries

Potentially life-threatening injuries

• Airway obstruction

• T racheobronchial disruption

• Tension pneumothorax

• Aortic disruption

• Open pneumothorax

• Diaphragmatic disruption

• Massive pneumothorax

• Esophageal disruption

• Cardiac tamponade

• Cardiac contusion

• Flial chest

• Pulmonary contusion

Thorax Pathological Effects of Chest Injuries Immediate

Late

Hypoxia

Empyema, fibrothorax

Hypercarbia

Lung abscess

Acidosis

Mediastinitis

Hypovolemic shock

Cardiac arrhythmias

xx Ventilator support with IPPV (Intermittent positive pressure ventilation), with regular monitoring of blood gas. xx Tracheostomy/endotracheal intubation is done whenever required. xx Antibiotics, bronchodilators, often steroids are other supportive measures required. Indications for thoracotomy ™™

Bronchospasm

Clinical Features of Thoracic Injuries xx History of trauma, painful breathing, cough, haemoptysis, pain in the chest wall, sometimes external wound may be present (in communicating wounds). xx Features of shock when major vessels are involved, i.e. tachycardia, hypotension, cold periphery. xx Respiratory distress—tachypnoea, cyanosis, res­pira­tory difficulties. xx Tenderness over the fracture site. xx Dullness on percussion with decreased breath sounds signifies haemothorax. Resonant with decreased breath sound confirms pneumothorax. xx Surgical emphysema with palpable crepitus may be present.

Investigations Chest X-ray shows haemothorax, pneumothorax, fracture ribs. Hb%, PCV to assess blood loss. Blood grouping and cross matching. Blood gas analysis, i.e. PO2 and PCO2. Ultrasound abdomen to look for associated abdominal injuries. FAST (Focused abdominal sonar trauma). xx CT chest and CT abdomen. xx xx xx xx xx

Treatment Initial First Aid xx Airway: Prevention of aspiration, plastic airway, intubation, tracheostomy. xx Breathing: ICT placement, supportive measures. xx Circulation: Fluid therapy, CVP line, blood transfusion. xx Look for disability. xx Expose the patient properly for proper breathing and assisting. xx Assess the patient properly. xx Examine the patient thoroughly. xx Evaluate the patient for associated injuries like of head, abdomen, fracture limbs, spine.

Further Treatment xx Fracture rib without complication is treated with analgesics and rest. xx Haemothorax, pneumothorax should be treated with intercostal tube drainage (ICT) with underwater seal. xx Flail segment should be treated accordingly. xx Blood transfusion is done whenever required. xx Antibiotics like penicillin, cefotaxime, etc. to prevent infection. xx Nasal oxygen, throat suction.

™™ ™™ ™™ ™™ ™™ ™™

Haemothorax more than 1500 ml found when ICT is placed or hourly collection in ICT is 200–300 ml ICT placed shows persistent drainage of blood Diaphragmatic injury When associated with liver and spleen injuries Bronchus and major vessel injuries Haemopericardium Oesophageal and thoracic duct injuries

Principles of Management of Chest Injuries xx Pulmonary physiotherapy. xx Aspiration of secretions—trachea, nasotracheal, oral, pharyngeal. xx Pain relief—oral narcotics, intercostal nerve block, epidural anaesthesia. xx Respiratory supports—encourage coughing, chest percussion, deep inspiration efforts, humidification, mobilisation. xx ICT placement for haemo/pneumothorax. xx Management of shock. xx Focused abdominal sonography on trauma (FAST). xx Surgery when indicated—thoracotomy and proceed. xx Management of complications—DVT and embolism, tracheostomy problems, ICT problems, sepsis, ARDS, empyema treatment, bronchopleural fistula, bronchial stenosis, chylothorax, clotted haemothorax, atelec­tasis.

Complications xx xx xx xx xx xx

Infections—empyema, lung abscess, pneumonia, septicaemia. Respiratory failure. Traumatic asphyxia. Traumatic shock lung. Disseminated intravascular coagulation (DIC). ARDS (Adult respiratory distress syndrome).

Note • Incidence of thoracic injury is 25% of all injuries. • 75% to 80% of them are managed nonoperatively—transfusion, ICT placement, critical care. • Mortality due to thoracic injury is 20% to 25%. • Chest X-ray is the immediate (first choice) investigation required; chest X-ray may be require to be repeated in 12-24 hours even if earlier X-ray is apparently normal. Pneumothorax, haemothorax, diaphragmatic hernia with bowel in the thoracic cavity are indentified in chest X-ray. • Imaging thorax (USG chest) during ultrasound abdomen (FAST) is also useful in initial assessment. • CT scan is the most reliable investigation in major thoracic injury. It reveals injuries to lungs, major vessels, pericardium, oesophagus, bronchi, etc. • ICT placement is the most common intervention done and lifesaving procedure in majority of thoracic injuries. In emergency situation one should not wait for chest X-ray or ultrasound chest

Old age is always fifteen years older than I am—Bernard M Baruch

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SRB's Manual of Surgery • • • • •

•

if it causes delay instead should place ICT at the earliest. ICT is diagnostic and therapeutic. Sucking chest wound should not be closed without any ICT placement to avoid formation of unstable tension pneumothorax. Often bleeding may be due to injury to intercostal vessels or internal mammary vessels mainly in blunt injury chest; it is managed by ICT placement and ligation of the specific vessels. Blood transfusion may be required in massive haemothorax. Associated injuries like fractures, spine injury, head and abdominal injuries should be looked for. Diaphragmatic injury is often silent. Serial chest X-rays, CT chest, video-assisted thoracoscopy (VATS) with laparoscopy gives the diagnosis. Immediate surgery is required. Nasogastric tube should be passed. Through thoracotomy or laparotomy approach contents are reduced; diaphragm is sutured using interrupted nonabsorbable sutures—number one polypropylene mattress sutures are usually placed. ICT is placed: Deadly dozen chest injuries should be remembered. They are: − Immediately life-threatening injuries are—Airway obstruction; tension pneumothorax; open pneumothorax; massive haemothorax; flail chest; pericardial tamponade.

−

Potentially life-threatening injuries are—Aortic and tracheobronchial injuries; myocardial contusion; rupture of diaphragm; oesophageal injuries; pulmonary contusion.

xx Emergency thoracotomy is required to have internal cardiac

massage, to control major bleed from lungs, heart or major vessels, oesophageal injury, massive air leak.

FRACTURE RIBS xx Rib fractures are rare in children as ribs are malleable. xx Fracture ribs are common in elderly as ribs are rigid and nonmalleable. xx 1st and 2nd ribs are covered by clavicle and so rarely fractures. xx Floating 11th and 12th ribs rarely get fractured.

Causes for Fracture Ribs xx Road accidents, chest injuries. xx Direct trauma. xx Blast injuries.

A

B

C

D

Figs 28.1A to D: Traumatic diaphragmatic hernia—chest X-ray showing stomach in the left hemithorax; on table finding of injury to the diaphragm; repaired diaphragm.

Thorax Features of Rib Fracture xx xx xx xx xx xx

Difficulty and pain during breathing. Tenderness over fracture site. Spring test is positive. Propped up position is more comfortable than lying down. Features of haemothorax, lung injuries. Features of abdominal injuries like of liver and spleen injuries.

Problems in Fracture Ribs xx xx xx xx xx xx xx

Surgical emphysema. Haemothorax, pneumothorax. Cardiac and or major vessel injury. Diaphragmatic injury. Flail chest. Asphyxia, cyanosis, respiratory failure. Pneumonia.

Investigations xx Chest X-ray is diagnostic. xx CT chest or abdomen to check deep or solid organ injury. xx Arterial blood gas analysis.

Non-traumatic rib fracture ™™ ™™ ™™ ™™ ™™ ™™

Stress fracture Metastatic fracture Metabolic cause like hyperparathyroidism Osteogenesis imperfecta Child abuse Old age—osteoporosis

FLAIL CHEST AND STOVE IN CHEST xx It is fracture of two or more consecutive ribs, with each rib

having two or more fracture sites. Such segment is called as flail segment. xx Stove in chest is depression of a portion of chest wall due to severe chest injury, otherwise features and management are like flail chest.

Pathophysiology Flail segment moves independent of the adjacent thoracic cage. During inspiration flail segment moves inwards (unlike normal thoracic cage which moves outward), and during expiration the segment moves outwards (unlike normal cage which moves inward) causing pathophysio­logical derangements. xx This paradoxical respiration causes reduction in venti­latory lung surface and so respiratory dys­function. xx Mediastinal flutter: Movement of mediastinum during different phases of respiration occurs, often causing kinking of great vessels and sudden cardiac arrest. xx Pendular movement of air from one lung to other occurs, and thus preventing atmospheric air to get into both injured and otherside normal lung leading to respiratory failure. xx All these derangements gets aggravated by haemo­thorax, pneumothorax and other associated injuries. xx There is hypoventilation: Carbon dioxide retention and respiratory failure.

Flail chest Derangements Fig. 28.2: CT reconstruction image of thoracic cage showing fracture lower ribs—left sided; haemothorax, splenic injury, diaphragmatic injury should be suspected.

Treatment xx xx xx xx

Control of pain. Prevention of infection. Respiratory physiotherapy. Treatment for definitive conditions like flail chest, ICT placing for haemo/pneumothorax.

• Paradoxical respiration • Mediastinal flutter • Pendular movement of air • Pulmonary contusion

Types • Anterior—near costochondral junction • Lateral—in rib shafts • Posterior—safer, due to support of scapula

Problems • Cardiac arrest • Respiratory failure • Haemothorax • Infection • ARDS

Note Flail chest is a clinical diagnosis.

There are no disease of aged but diseases among the aged.—Leonard Larson

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SRB's Manual of Surgery First Aid The paradoxical movement of flail segment is prevented by applying pressure over it using hand or clothes (It is often life saving.) It makes other lung function adequately.

Additional drain is often justified. Respiratory care, early mobilization and physiotherapy is useful.

Causes xx Traumatic. xx Spontaneous.

Investigations xx Chest X-ray—to identify the fracture segment. xx Blood grouping. xx Arterial PO2 and PCO2 and serum electrolytes.

Treatment xx Intercostal tube drainage. xx Applying clips to fracture ribs and fixing above and below

1. Tuberculous. 2. Non-tuberculous: a. Rupture of emphysematous bullae. b. Rupture of solitary lung cyst. c. Honeycomb or cystic lung. d. Idiopathic. Spontaneous pneumothorax can be acute, chronic, recurrent.

to normal ribs. Antibiotics like penicillins, cefotaxime. Blood transfusion, IV fluids. Bronchodilators, steroids. Ventilator support with IPPV—IPPV is treatment of choice. Assisted ventilation is required for several days until the chest wall stabilises. If ventilator support is required for more than 10 days, then tracheo­stomy is done to prevent laryngeal stenosis which can occur due to prolonged endotracheal intubation. xx Thoracotomy—when required only. xx xx xx xx

PNEUMOTHORAX The means we possess of reducing (a diseased lung) to a state of collapse, or of divesting it for a time of its peculiar functions, are equally simple and safe. In those cases in which the disease is placed in one of the lungs only, the remedy (i.e. induced pneumothorax) would appear to be simple, safe, and complete —James Carson, 1820

It is the presence of air between the layers of pleura. Classification I a. Pneumothorax. b. Hydropneumothorax. c. Pyopneumothorax. d. Haemopneumothorax. e. Artificial pneumothorax. f. Tension pneumothorax.

Classification II a. Open pneumothorax b. Closed pneumothorax  Simple  Tension

Open pneumothorax is a sucking chest wound, with wound usually more than 3 cm in size. Here lung collapses and causes severe hypoventilation. A large sized chest tube should be placed; sucking wound is closed with creation of three side flutter valve. Often thoracic tube may be connected to suction apparatus with a low pressure to facilitate lung expansion.

Fig. 28.3: Plain X-ray chest PA-view showing air-fluid level and collapsed lung margin (Hydropneumothorax)

Clinical Features Hyperresonant, absence of breath sounds, tracheal deviation. Chest X-ray reveals ™™ ™™ ™™

Radiolucency on the affected side Absence of lung markings Collapsed lung margin

Treatment xx In tension pneumothorax, emergency needle aspiration is done followed by ICT placement. xx ICT placement. xx The cause is treated. xx Often thoracotomy is required, if there is persistent broncho-pleural fistula or ruptured cyst or bullae.

TENSION PNEUMOTHORAX xx During inspiration, air is pumped into the pleural cavity

through a valvular opening in the visceral pleura and underlying injured lung. xx Lung collapses first, and as air continuously collects in the pleural cavity, mediastinum shifts towards the opposite side, further decreasing the volume of the functioning lung.

Thorax xx Further increase in the pleural pressure, reduces the venous

return, atrial filling, and ventricular filling and so cardiac output and cardiac function.

xx Tumours of lung, mediastinum, pleura. xx Leaking aneurysms. xx Spontaneous.

There may be rib fractures in traumatic haemo­thorax. Clinical features Pain in the chest, tenderness Difficulty in breathing, dullness on percusion diminished breath sounds ™™ Features of shock ™™ ™™

Investigations xx Chest X-ray. xx Aspiration (pleural tap). xx Chest CT scan.

Treatment Fig. 28.4: Emergency decompression through 2nd intercostal space.

It causes sudden death and hence emergency treatment is required. Clinical features Tachypnoea and tachycardia Decreased/absent breath sounds ™™ Resonant on percussion with severe mediastinal/tracheal shift ™™ Cyanosis and hypotension ™™ Chest pain, distended neck veins ™™ ™™

1. ICT placement in the mid-axillary line in the 6th intercostal space. 2. Antibiotics, bronchodilators. 3. Thoracotomy: Indications of thoracotomy Initial chest tube output of 1500 ml of blood or persistent drainage of 200–300 ml/hr. ™™ Clotted haemothorax is difficult to manage. It requires thoracotomy, evacuation and decor­tication of lung. Initially liquefaction of the clot is tried by infusing of streptokinase and trypsin into the pleural cavity ™™

Complications xx Infection and empyema. xx ARDS: respiratory failure.

Management xx Once clinically diagnosed, a wide bore needle is immedi-

ately placed in the second intercostal space in midclavicular line, and a sterile glove is kept on the hub (blunt) end of the needle to create a valve so as to prevent inward sucking of air from outside—thoracocentesis. xx Nasal oxygen is used. xx Once patient is better, chest X-ray is done. xx Later an intercostal tube is passed (ICT placement). xx Antibiotic, analgesics are given. xx In severe cases ventilator support with IPPV is required.

PLEURAL TAP Indications xx Pleural effusion—both for diagnostic as well as thera­peutic purpose. The fluid is sent for culture, cytology, microscopy, specific gravity, biochemical analysis of proteins for diagnosis of tuberculosis, malignancy. xx In empyema thoracis, for diagnostic purpose before placing an ICT.

HAEMOTHORAX It is blood in pleural cavity. It causes pain, shock, as it is very irritant to pleural cavity. It is a good culture media for bacteria and so infection is quite common.

Causes xx Trauma. xx Postoperative: Pulmonary, cardiac, oesophageal surgeries,

cervical sympathectomy, leak from CVP monitor line.

Fig. 28.5: Sites of pleural tap.

Experience teaches slowly at the cost of mistake.

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SRB's Manual of Surgery Position In sitting position, leaning forward over a wooden support.

Site Tip of scapula at 7th intercostal space (posteriorly). Under local anaesthesia wide bore needle (Abraham needle) is passed to tap the fluid. Complications ™™ ™™ ™™ ™™

Infection Dry tap or bloody tap Sudden vagal shock Pain and respiratory distress

Fig. 28.8: Bronchoscope.

Types xx Rigid bronchoscopy—it is used for removal of foreign body and bronchial wash. It reaches up to third generation bronchioles. It is used to take biopsy from carcinoma of proximal divisions but not from carcinoma of peripheral lung. Rigid scope has got multiple holes to allow ventilation during the procedure (Oesophagoscope does not have side holes). It is done under general anaesthesia. xx Flexible bronchoscopy—it reaches up to 5th generation bronchioles. It can be done under local anaesthesia. It is mainly used for diagnosis and biopsy. Complications ™™ ™™ ™™ ™™

Fig. 28.6: Position for pleural tap is sitting and leaning forward over a support. Site is below the scapula, posteriorly through the seventh intercostal space.

BRONCHOSCOPY Indications Diagnostic: To take biopsy in conditions like carcinoma lung, lung abscess, pulmonary tuberculosis. Therapeutic: To remove foreign body, to suck out the bronchial secretions.

Bleeding Infection Perforation Bronchospasm

EMPYEMA THORACIS The pleurisie is an inflammation of the membrane, investing the ribs, caused by subtile and cholerick blood…. If it tend to suppuration, it commonly infers a pricking pain, a fever and difficulty of breathing…. If nature being too weak…the disease is turned into an empyema, wherefore the Chirurgeon must then be called, who…may make a vent between the third and fourth true and legitimate ribs…. The pus or matter must be evacuated by little and little at several times; and the capacity of the chest cleansed from the purulent matter. —Ambroise Paré, 1575

It is collection of pus in pleural cavity.

Fig. 28.7: Foreign body in trachea. This can be removed using a bronchoscope. Patient may develop collapse of lung, pneumonia, respiratory failure and ARDS.

Fig. 28.9: Causes of empyema.

Thorax Causes

Clinical Features

An empyema is never primary. Secondary causes are: xx From chest wall: Wounds, osteomyelitis of ribs. xx From lung: Pneumonia, abscess, bronchiectasis, tuberculosis, growth. xx Postoperative: After thoracotomy. xx From oesophagus: Perforations, carcinoma. xx From below diaphragm: Subphrenic abscess. Tuberculosis and pneumonia are common causes in developing countries.

xx xx xx xx xx

Pathology xx Initially serous fluid collects, which eventually becomes

purulent. Intrapleural clotting of pus occurs with thickening of pleura and later fibrinous adhesion forms resulting in matured empyema. xx Chest is withdrawn inwards and is immobile, mediastinum is drawn inwards, diaphragm gets elevated. xx It leads to rigid contracted immobile chest with functionless lung underneath—frozen chest. Often pus perforates through intercostal space and forms empyema necessitans.

Pain in the chest, tenderness, fever. Difficulty in breathing. Features of toxicity in acute type of empyema. Dullness on percussion, absence of breath sounds. Decreased chest wall movement. Complications

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Frozen chest (functionless lung) Empyema necessitans Osteomyelitis/chondritis of ribs or vertebra Pericarditis Mediastinitis Bronchopleural fistula Dissemination of infection

Investigations xx xx xx xx xx xx

Chest X-ray, ESR. Peripheral smear. Diagnostic aspiration. Pus C/S, AFB. Bronchoscopy. CT scan and MRI for carcinoma bronchus.

Treatment Stages of empyema ™™ ™™ ™™

Acute empyema Subacute empyema Chronic empyema

Organisms: Initially staphylococci, streptococci, pneu­mococci, and later Entamoeba coli, Pseudomonas, drug-resistant staphylococci. Clinical types ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Acute empyema Acute fulminant toxic empyema Subacute empyema Chronic empyema Latent empyema Persistent empyema Empyema necessitans Chronic empyema with sinus Interlobar empyema

™™ ™™ ™™

Exudative Fibrinopurulent Organising

Stage 1 xx Antibiotics. xx Repeated aspirations. xx Intercostal tube drainage. xx Antituberculous drugs. Stage 2 xx ICT drainage. xx Rib resection (Eloiser’s method). xx Antibiotics, antituberculous drugs. xx Respiratory physiotherapy. Stage 3 xx Decortication is very useful and favourable method. Here, thickened pleural sac is stripped off from the lung through thoracotomy approach. xx Often lobectomy may be required, rarely pneumo­nectomy is done. xx Physiotherapy, antibiotics, ATD’S are also essen­tial.

EMPYEMA NECESSITANS

Pathological types

Anatomical types (Depending on the anatomical location) ™™ ™™ ™™ ™™ ™™

Apical Mediastinal Interlobar Diaphragmatic Lateral

Fig. 28.10: Empyema necessitans.

For all the happiness mankind can gain, is not in pleasure but in rest from pain.—Dryden

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SRB's Manual of Surgery It is a complication of empyema thoracis, wherein empyema which is not drained perforates through the chest wall presenting as subcutaneous collection of pus communicating directly or often with a tortuous route with the pleural cavity.

Causes xx Neglected empyema either of tuberculous or non­tuberculous aetiology. xx Following incomplete aspiration of pus of empyema through a thin needle—needle track itself allows pus to form a track and leads to empyema necessitans.

Clinical Features A diffuse, tender, smooth, soft, fluctuant, swelling in the intercostal space having impulse on coughing.

Clinical features ™™ ™™ ™™ ™™ ™™

Acute onset of fever, but often it is recurrent in nature Cough with expectoration Haemoptysis with foul smelling sputum Chronic illness with debilitation Pleuritic pain

Complications xx Spread into other areas of the lung. xx Metastatic cerebral abscess—Lung abscess is the commonest focus for metastatic cerebral abscess. Occurs as a result of pyaemic emboli through paravertebral veins. xx Haemorrage, may be torrential due to erosion of the vessel in the abscess wall. xx Empyema thoracis.

Features of empyema necessitans ™™ ™™ ™™ ™™ ™™

Bulge in the intercostal space Restricted movement of chest wall Tenderness Dullness on percussion without breath sounds Impulse on coughing

Investigations xx Chest X-ray. xx Total count is increased. xx ESR.

Treatment xx Antibiotics. xx Empyema is drained by placing an ICT. Pus is sent for C/S and AFB. xx If it is tuberculous, antitubercular drugs are started. xx Empyema necessitans subsides on its own when empyema is treated. xx But often may require separate incision and drainage when track is tortuous.

Differential Diagnosis xx xx xx xx xx

Pulmonary tuberculosis. Carcinoma lung. Fungal infections like aspergillosis. Pneumoconiosis. Lung cysts.

Investigations xx Chest X-ray shows localised opacity with smooth margin and fluid level. xx Bronchoscopy and biopsy is done to rule out carcinoma. xx Sputum for culture, AFB and cytology. xx CT scan.

LUNG ABSCESS xx It is localised suppuration in the lung with tissue necrosis. xx It is end-stage of suppurative pneumonitis with thrombosis

of associated artery.

Aetiology xx Pneumonias due to Streptococcus, Pneumococcus, Haemophilus, Staphylococcus, anaerobic and other bacteria. xx Bronchial obstruction due to tumours or foreign body. xx Chronic upper respiratory infection due to sinusitis, tonsillitis and dental infection (anaerobic infection). xx Septicaemia. xx Aspiration. As pus accumulates, tension increases inside the abscess cavity causing spread into other areas of the lung or may rupture into the bronchus. Note:

Lung abscess secondary to aspiration is commonly seen in apical lower lobe.

Fig. 28.11: CT scan of lung showing right-sided lung abscess with fluid level.

Treatment Medical xx Appropriate high dose antibiotics are started depending on

sputum culture like penicillins, third generation cephalosporins like cefoperazone, ceftriaxone for 3–6 weeks. xx Postural drainage for 2–3 hours, 3 times daily.

Thorax INTERCOSTAL TUBE DRAINAGE

xx Periodic culture of sputum is done to study the response

of treatment. xx 80–90% of acute abscesses resolve by medical therapy.

Surgical xx External surgical drainage with rib resection is done in

severe acute lung abscess only. Not commonly used procedure. xx Lobectomy is done when medical treatment fails.

It is the method of draining fluid/blood/air collected in the pleural cavity safely, so as to allow the underlying lung to expand. Indications ™™ ™™ ™™ ™™ ™™ ™™

Haemothorax, hydrothorax, chylothorax Pneumothorax Haemopneumothorax Empyema thoracis Traumatic lung contusion After thoracotomy, to drain pleural cavity

A

A

B

Figs 28.13A and B: (A) Intercostal tube drainage underwater seal; (B) Intercostal tube drainage showing haemothorax.

Procedure xx Technique is also called as tube thoracostomy; tube is called

B1

B2 Figs 28.12A and B: Lung abscess X-ray picture and CT of the same patient.



as chest or intercostal tube or drain (Bulau drain). Concept was first introduced by Hippocrates but popularized by Dr C Pope in 1922. xx Chest tube is made up of clear plastics or PVC; it has got multiple fenestrations on the side which resides inside the thoracic cavity. Ranges from 6 French to 40 French sizes are available. Tube has got a radio-opaque strip. Silastic channel styled chest drains (Blake drains) are available which drain through capillary action and suction; it is less painful. xx Drainage canister is used to collect the blood, air, fluid and so on through a water seal apparatus. Triple chamber canisters are often used for better function; here first chamber collects the fluid content. Second chamber acts as water seal which allows the air escape acting as one way valve; it also indicates the air leak from pleura or lung. Third chamber is the suction control chamber; height of water column in

Clubbing is frequently present in those with a chronic discharging empyema sinus. —Hippocrates, Father of Medicine

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SRB's Manual of Surgery this regulates the negative pressure so controls the suction system. Only water seal and water column regulator system is ‘wet’ type; water seal with mechanical regulator is ‘wetdry’ type; system without water seal but uses mechanical check valve and mechanical regulator is called as ‘dry’ system. xx Site: Triangle of safety—British Thoracic Society describes the safe zone as—bounded by the lateral border of pectoralis major, a horizontal line inferior to the axilla, the anterior border of latissimus dorsi and a horizontal line superior to the nipple; commonly the tube is inserted into the 5th intercostal space slightly anterior to the midaxillary line; but it may be 6th space below in haemothorax or empyema or it may be upwards in 4th space in pneumothorax. In this point muscle bulk is less and so easy to pass the intercostal tube. xx Position: Patient is kept in supine (with head end up if possible 45°) position. Arm should be abducted and externally rotated with palm of the hand is kept over the patient’s head. Cleaning and draping is done. Local anaesthesia xylocaine 1% or 2% is injected at the site of insertion of the tube in the space under the skin, muscle and to parietal pleura; site is just above the rib, i.e. in the lower part of the intercostal space so as to avoid injury to neurovascular bundle which are located in the groove in the lower part of the rib close to the upper part of the intercostal space. xx Horizontal skin incision is made using no 11 blade, 4 cm in length; fascia and intercostal muscles are opened and separated; adequacy of the separation should be confirmed using finger tip; fenestrated end of the selected (No. 28 in adult; No. 18 in children; No. 12 in infants; No. 10 in neonates) chest tube is held firmly using long curved haemostat (Kelly’s clamp); outer end is clamped which will be released later; tube is gently forced across the parietal pleurae which gives ‘a given way’ feel. Tube is easily pushed into the thoracic cavity. Air or blood or fluid will pass through the tube; tube is connected to under water seal apparatus which should be filled with sterile normal saline up to the mark in the canister (Tube is often clamped prior to insertion and released after that). ICT is sutured to the skin using nonabsorbable polyethylene suture; often additional suture bites are taken around and kept untied which will be tied immediately firmly after removal of the ICT (central vertical mattress suture—sealing suture). Air tight plaster dressing is placed around to keep the ICT in position. xx Movement of the air column during respiration (and during the act of coughing) should be checked; quantity of fluid or blood collecting also should be observed. Check chest X-ray should be taken immediately to assess the position of the ICT. O2 supplementation is often needed; patient should be monitored throughout. xx Canister or underwater seal bottle or bag should be kept 100 cm below the patient level. xx Trocar ICT or guide wire directed ICT placement is also used in few centres but they are not popular.

Fig. 28.14: ICT bottle with blood—haemothorax.

Fig. 28.15: Immediate check chest X-ray should be done to confirm the position of the ICT.

Postoperative Care xx ICT care is crucial. Movement of the column, quantity of fluid collected should be observed. Mechanical manipulation (tapping, milking) gently may be done to correct kinking, clot inside or to facilitate free flow of fluid but they are painful. xx Closed chest tube clearing device using sterile magnetically wired loops can prevent clogging and blocking of the tube so as to prevent formation of retained blood syndrome (haemothorax, pleural effusion, tamponade, atrial fibrillation). xx Lung expansion should be checked at regular intervals. xx Usually ICT is placed for 3–5 days for pneumothorax until lung expands adequately which should be confirmed by chest X-ray; for haemothorax for 4–7 days. For bronchopleural fistula ICT should be kept for longer period. xx Respiratory physiotherapy using spirometer or football balloon and breathing exercise should be done.

Fig. 28.16: Spirometer. Respiratory physiotherapy should be done using spirometer.

Thorax ICT Removal xx It is done once chest X-ray confirms that lung gas has expanded properly, pleural fluid drain becomes serous and less than 25 ml/ day for 3 consecutive days, water column movement becomes less than 1 cm. xx It is removed under all aseptic precaution; suture is removed; patient is asked to take deep inspiration; often outer end of the tube may be connected to low volume suction. At the summit of deep inspiration, tube is pulled out; wound is cleaned quickly and if sealing suture is present it should be tied firmly; sealed plaster dressing is placed to avoid re-entry of air into the plural cavity. Contraindications for ICT placement ™™ ™™ ™™ ™™

Traumatic diaphragmatic hernia Refractory coagulopathy Pleural adhesions Emphysematous bullae

xx xx xx xx xx

Antibiotics. High dose of steroids. Monitoring the patient with PCWP and cardiac monitor. Bronchodilators. The cause is treated.

PULMONARY EMBOLISM (PE) From my Stanford days… I had known that excessive bed rest gave rise to thromboembolic complications…. The death rate from thrombo­ embolism was always much less at the County Hospital than it was at Stanford Hospital…. When (the County Hospital patients) got up to go to the bathroom, (they) dislodged only tiny clots from their veins and these did not harm them when they got to the lungs and were dissolved, while the wealthier patients (at Stanford) who remained in bed and formed large clots in their legs and pelvises suffered the major conse­quences of large pulmonary emboli. —William Dock, 1984

Complications ™™

™™ ™™ ™™

™™ ™™

Clogging of the ICT (40%) is the main complication which commonly goes unnoticed as the part inside the thoracic cavity is gets often clogged. It can cause retained blood syndrome, tension pneumothorax, effusion, haemothorax. Injury to intercostal nerve and vessels, diaphragm, liver, spleen, aorta and heart can occur. Improper placement of the tube. Re-expansion pulmonary oedema can occur if large quantity of fluid or pus drained in effusion or empyema; it may cause sudden onset cough, breathlessness and respiratory arrest (potentially fatal). In such situation gradual decompression is better. Subcutaneous haematoma, seroma, subcutaneous emphysema can occur. Displacement, pain, intercostal neuralgia, dyspnoea, cough, infection can occur.

SHOCK LUNG (Stiff lung) Causes xx xx xx xx

Major chest trauma. Septicaemia. Massive blood transfusions. DIC.

Pathogenesis Development of microthromboembolism in small lung vessels following extensive intravascular coagu­lation, leading to pulmonary consolidation, which reduces the lung compliance markedly, causing severe depression of gas exchange in the lung—a stiff lung. It has got high mortality as lung cannot expand at all. Outcome is fatal if emergency treatment is not given.

Treatment xx Endotracheal intubation. xx Ventilator support with IPPV.

xx It is due to deep venous thrombosis (DVT) which gets detached to cause pulmonary embolism. xx It may be from femoropopliteal or ileo-femoral region. The thrombi most commonly develop in the leg veins due to stasis and hypercoagulable state. They subsequently enlarge and propagate proximally, dislodge to form emboli.

Types xx Small emboli: Causes pulmonary hypertension of features of bronchopneumonia. xx Medium emboli lodges in branches of pulmonary artery causing chest pain, haemoptysis, dyspnoea. xx Large (massive) emboli causes block at bifurcation of pulmonary artery trunk or right/left pulmonary artery leading to sudden chest pain, severe dyspnoea, shock, raised venous pressure and sudden death. Effects of pulmonary embolism ™™ ™™ ™™ ™™

Decreased cardiac output Pulmonary vasospasm and pulmonary hyper­tention Bronchospasm Defective oxygenation of blood

Risk Factors xx xx xx xx xx xx xx

Postoperative and trauma patients who are bed ridden. Pregnant women. Old age. Obesity and heart disease. Varicose veins. All aetiologies which cause DVT. Carcinoma. Clinical features

™™ ™™ ™™

Dyspnoea, chest pain and haemoptysis Tachycardia, tachypnoea and cyanosis Pleural rub and cardiac gallop

The patient dyspnoeic due to pulmonary embolism prefers to lie flat.—Ronald Gibson

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Features

xx Chest X-ray PA view—hyperlucency in an area of oligaemia— Westermark sign. xx CT scan and MRI—can detect PE. xx Pulmonary angiography: It is diagnostic (100%). xx Arterial blood gas analysis. xx Isotope radionuclide ventilation—perfusion (V/Q) lung scanning:While normal scan rules out PE, evidence of V/Q mismatch is highly suggestive of pulmonary embolism. xx Doppler study and venogaphy—To rule out DVT.

xx Pain, diffuse swelling of the subcutaneous region. xx Palpable crepitus is diagnostic. xx X-ray chest and neck is confirmatory.

B

A

Figs 28.18A and B: Chest X-ray PA and lateral views showing surgical emphysema.

Fig. 28.17: Chest X-ray showing wedge shaped pulmonary infarct.

Management xx Thrombolytics: Streptokinase, 6 lakhs units to begin with and later one lakh units hourly. xx Pulmonary embolectomy with or without bypass by immediate thoracotomy. xx Venous thrombectomy using Fogarty catheter. xx Ventilator support. xx To prevent further embolisation of embolus into the lungs, IVC filters can be placed. xx Treatment of DVT.

Fig. 28.19: Surgical emphysema. Note the demonstration of crepitus.

Treatment xx Conservative treatment—treat the cause. xx In severe cases—ICT one side or both sides placement.

LUNG CYSTS

Note:

Heparin should not be combined with thrombolytics.

SURGICAL EMPHYSEMA It is collection of gas/air in the subcutaneous or and fascial planes.

Causes xx xx xx xx

Lung injury. Tracheal injury. Chest wall injury. After laparoscopic procedure.

Types xx Localised—observed at the site of trauma. xx Generalised—extensive in the neck, face, eyelids, chest wall, etc.—in the injury of bronchus, oesophagus and mediastitum.

Types ™™ ™™ ™™ ™™

Epithelial cyst Emphysematous cyst Parasitic cyst (Hydatid cyst) Pseudocyst of the lung

Epithelial Cyst xx xx xx xx xx

It is of developmental origin. It can be large single cyst or small, multiple cysts. It is lined by respiratory epithelium. It is often associated with cervical rib or cardiac anomalies. It is common in infants and children.  Usual clinical features are dyspnoea and chest pain. When infected, presents with fever, cough and haemo­ptysis.  Treatment is excision of the cyst. Antibiotics are given when infected.  Here spontaneous pneumothorax is uncommon. Infection and haemorrhage are common.

Thorax Emphysematous Cyst xx It is a progressive disease of lung with rupture of alveolar wall and distension with air. xx It is an acquired condition. xx Cyst does not have epithelial lining. xx Compression of adjacent lung tissue with poor gaseous exchange is common. Usual clinical features are dyspnoea and severe, persistent cough. Pseudocyst of the lung: It occurs in a cavity due to tuber­culosis, lung abscess or Staphylococcus pneumonia.

Complications xx Spontaneous pneumothorax. xx Severe chronic bronchitis.

xx Complement fixation test. xx Indirect haemagglutination test. xx CT scan—diagnostic. Complications ™™ ™™ ™™ ™™ ™™ ™™ ™™

Rupture of the cyst Anaphylaxis Secondary infection Collapse of lung Pleural effusion Secondary pleural hydatid formation Hepatobronchial fistula formation (produces bilious sputum)

™™ ™™ ™™

Lung abscess Epithelial lung cysts Aspergillosis

Differential diagnosis

Treatment xx Thoracotomy and enucleation of the cyst: It is achieved by taking a good anaesthetist’s help by creating positive pressure ventilation. Cyst extrudes intact. It should not be held with forceps to avoid rupture. xx Lobectomy is done in cases with difficulty and compli­cations. xx Drugs like praziquantel or albendazole is given for a long period.

A

Figs 28.20A and B: (A) Hydatid cyst in lung; (B) Ruptured hydatid cyst with water-lily sign.

Treatment xx Localised cyst is excised. xx Generalised cysts are treated conservatively. xx Pleurodesis is often required. Here spontaneous pneumothorax is very common. Infection and haemorrhage are uncommon.

Hydatid Cyst of the Lung xx xx xx xx

MEDIASTINAL TUMOURS

B

It is caused by the parasite, Echinococcus granu­losus. It is often associated with hydatid cysts of the liver. Incidence is 15%. It is usually single. But multiple hydatids can occur.

xx It occurs at any age group, in both sexes. xx It is often identified on a routine chest X-ray, as about 50% are symptomless.

Presentations Chest pain and back pain. Respiratory distress. Venous congestion (SVC syndrome). Hoarseness of voice (due to compression over recurrent laryngeal nerve). xx Dysphagia, due to oesophageal compression. xx xx xx xx

Presentations xx Dyspnoea, chest pain and haemoptysis. xx Rupture into bronchial tree causes anaphylaxis. xx Rupture also causes expectoration of fluid and grape skins (vesicles). xx Fever, cough and expectoration due to secondary infection. xx Asymptomatic hydatid, identified during chest X-ray.

Investigations xx Chest X-ray: 1. Dense homogenous opacity. 2. Collapsed laminated membrane produces an irregular projections in a fluid level due to rupture of the cyst—Water-lily appearance. 3. Crescentic cap of air, when it communicates into bronchial tree. xx Positive Casoni’s test. xx Blood shows eosinophilia.

Fig. 28.21: Superior mediastinal tumour— could be thymoma, nodal mass.

Endurance is not just the ability to bear hard things but to turn it into glory.

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Horner’s syndrome, due to compression over sympathetic chain. Scabbard trachea. Later diaphragmatic paralysis may occur. Pleural effusion. Haemorrhage, due to erosion of major vessels by malignant tumour.

Investigations xx xx xx xx

Chest X-ray, both PA view and lateral view. CT scan. MRI. Mediastinoscopy and biopsy.

Treatment xx Thoracotomy and removal of tumour. xx If malignant, adjuvant therapy like radiotherapy and chemotherapy are given. xx Sternotomy for superior and anterior mediastinal tumours. xx Thoracoscopic and mediastinoscopic approaches.

Fig. 28.22: Sites of mediastinal tumours.

Classification Superior mediastinal tumour: Retrosternal goitre. Anterior mediastinal tumours ™™ Retrosternal goitre, aortic arch aneurysm lymph node enlargement. ™™ Thymic tumours—thymomas are commonly asso­ciated with myasthenia gravis. ™™ Teratomas and dermoids. ™™ Pleuro-pericardial cyst (spring water cyst). Midmediastinal tumours ™™ Lymphadenopathies of all causes—secondaries, lymphomas, tuberculosis—common. ™™ Foregut duplication cysts. ™™ Lipomas.

A

B Figs 28.24A and B: CT scan showing mediastinal tumour.

A

B Figs 28.23A and B: Chest X-ray showing mediastinal tumour.

Posterior mediastinal tumours xx xx xx xx

Neurofibromas—commonest, 75%. Ganglioneuromas. Aneurysm of descending aorta. Lymph node mass.

A

B Figs 28.25A and B: Plain X-ray chest showing posterior mediastinal mass.

Thorax Features of myasthenia gravis ™™ ™™ ™™ ™™ ™™ ™™ ™™

An autoimmune disease Presence of antibodies to acetylcholine recep­t ors in NMJ resulting in reduced muscular contraction Weakness of muscle on exertion Ptosis, diplopia, dysarthria, dysphagia Drooping of jaw Paralysis of respiratory muscle Periodic remission

LUNG CANCERS xx Lung cancers are either secondary or primary. xx Secondaries are commonly from breast, thyroid, sarcomas,

Fig. 28.26: Malignant effusion—right-sided.

kidneys and bones. They usually show typical cannonball secondaries. Primary should be evaluated by CT scan, endoscopies, tumour markers. PET scan is useful investigation. It is treated with chemotherapy, RT.

THYMOMAS xx Thymomas are the most common tumours of the antero­superior mediastinum in the adult. xx They are most common in the fifth and sixth decades of life. Both sexes are equally affected. Histological types ™™ ™™ ™™ ™™



Epithelial cell—has poor prognosis Lymphocytic Mixed Spindle—has better prognosis 50% of thymomas are malignant

Staging I — Confined to the capsule II — Tumour spread to periglandular fat III — Tumour spread to adjacent tissue

Clinical Features xx xx xx xx xx

Asymptomatic—50%. 30-40% of thymomas have associated myasthenia gravis. Chest pain. Dysphagia and dyspnoea. Superior vena caval obstruction.

Fig. 28.27: Multiple cannonball secondaries in lung. Primary sites are—breast, kidney, sarcomas, testis, prostate, thyroid. xx Bronchogenic carcinoma is the commonest primary; common

in smokers and males. Cough, chest pain, haemoptysis, loss of weight and appetite, features of metastases and paraneoplastic syndromes are—common presentation. It is evaluated with chest X-ray, CT chest and metastatic work up, tumour

Investigations xx Tensilan diagnostic test: By injecting 10 mg IV to symptomatic myasthenia will be relieved in one minute temporarily. xx Chest X-ray, lateral view shows opacity in the mediastinum. xx CT scan.

Treatment xx For myasthenia—tablet neostigmine bromide 15 mg tds, daily. xx Thymectomy is very useful.  When the disease is less than 5 years.  Myasthenia gravis without thymoma.  In young, females.

Fig. 28.28: Bronchogenic carcinoma—X-ray picture.

Comedy is the Tragedy that happens to other people.

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SRB's Manual of Surgery markers, sputum cytology and bronchoscopy. Commonly it is advanced when present with. When operable, pneumonectomy is done provided opposite lung is normal. Inoperable cases as commonly are managed with chemotherapy, radiotherapy and symptomatic measures. Condition carries poor prognosis.

PANCOAST TUMOURS (Superior sulcus tumour) When the tumour extends its feet from all sides of its body into the veins, the sickness produces the picture of a crab. —Galen, (130-200)

xx It is a type of peripheral lung carcinoma arising from the apex of the lung (5% of lung cancers).

Investigations xx xx xx xx xx

Chest X-ray. CT scan. Bronchoscopy and biopsy. CT-guided biopsy. MRI is better than CT in Pancoast tumour as brachial plexus and sympathetic chain is involved which better visualised in MRI.

Treatment xx Lobectomy/pneumonectomy. xx Radiotherapy—external tele cobalt. xx Chemotherapy—methotrexate. Prognosis: Poor.

CHEST WALL TUMOURS

Features xx It invades brachial plexus, sympathetic chain, upper ribs

xx Tumours arising from the chest wall components like muscles or ribs. They can be benign or malignant.

and vertebrae.

xx Intractable pain in upper chest, arm and also weak­ness in

the arm.

Fig. 28.30: Chest wall tumour. Benign tumours are usually chondromas. xx Commonest benign tumour is chondroma arising from ribs. xx Malignant tumours are secondaries (commonest), chondrosarcoma arising from ribs (common among primary malignant tumours), rhabdomyosarcoma from muscles, fibrosarcoma from ribs/muscles/ other soft tissues, Ewing’s sarcoma and invasion from other tumours like from pleura or lungs or breast. Fig. 28.29: X-ray showing right sided Pancoast’s tumour.

Presentations Pancoast’s syndrome ™™ ™™ ™™ ™™

Lower brachial plexus palsy Horner’s syndrome Rib erosion Apical shadow

Horner’s syndrome ™™ ™™ ™™ ™™ ™™

Miosis Enophthalmos Anhydrosis Ptosis Loss of spino-ciliary reflex

Fig. 28.31: Fungating tumour invading chest wall.

Thorax Benign Tumours

CHRONIC CONSTRICTIVE PERICARDITIS (Pick’s Disease)

xx They are slow growing, nonmobile, painless and usually from the rib cartilage, near costochondral junction. xx X-ray is diagnostic, shows rib expansion with intact cortex. xx One or more ribs can be involved. Treatment is rib resection.

xx Here pericardium is thickened, fibrosed and calcified. Heart is encased in a rigid cavity which decreases the cardiac function as well as the venous return.

Primary Malignant Tumour

Causes

xx It has got all features of sarcoma—progressive rapid enlargement, attaining large size, warm, vascular, nonmobile, often extends into the thoracic cavity or with skin ulceration. xx Secondaries in lung/brain/liver can occur. xx Chest X-ray, CT chest, US abdomen should be done to see secondaries. xx CT scan can also give idea about the tumour extension and operability. xx Open incision/trucut biopsy is essential for histological confirmation. xx Treatment is wide excision with chest wall reconstruction using different osteomyocutaneous flaps, rib grafts, mesh or acrylic plates. xx Postoperative adjuvant chemotherapy is always needed to prevent relapse. In advanced cases radio­therapy to chest wall is advised.

xx xx xx xx

PERICARDITIS

Tuberculous pericarditis is the commonest cause. Trauma. Viral pericarditis. After cardiac surgery.

Clinical Features xx Decreased cardiac output and tachycardia. xx Dyspnoea on exertion, easy fatigability. xx Raised jugular veins, hepatomegaly, ascites and oedema feet.

Investigations xx xx xx xx

ECG. Echocardiography. Chest X-ray. CT scan.

Treatment

Water contained in the sac of the heart, likewise if the sac contain within either a fluid putrid and smelling badly, or stones, it causes throbbing…. Adhesions of the pericardium to the body of the heart itself…was observed in two dropsical patients.

xx Pericardiotomy with biopsy. xx Pericardiectomy. xx Antitubercular drugs is started when tuberculosis is the cause.

PERICARDIAL TAP

—Guillaume de Baillou (Ballonius), 1735

Indications

Types 1. Acute pericarditis. 2. Chronic pericarditis. 3. Chronic constrictive pericarditis.

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Pericardial effusion due to any cause—viral, tubercular Haemopericardium Purulent pericardium

ACUTE PERICARDITIS

Procedure

Usually by bacteria like Staph. aureus, H. influenzae, Streptococci, Neisseria. It is uncommon at present, because of availability of good antibiotics.

A 16 or 18-gauge needle is passed into the pericardium just below the Xiphoid process, directing upwards and backwards, towards left side with an angle of 45° to the surface.

Other causes ™™ ™™ ™™ ™™ ™™

Viral infection Uraemia Trauma Malignancy Connective tissue disorders

xx Here pus collects in the pericardial space causing decreased cardiac function and toxicity.

Treatment xx Antibiotics. xx Pericardial aspiration. xx Drainage of purulent fluid by open pericardio­tomy.

Fig. 28.32: Pericardial tap for pericardial effusion/tamponade.

Don’t let the skin stand between you and the diagnosis.

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This site is used because: Most dependent aspiration ™™ Unlikely to traumatise heart ™™ Pleura is not punctured ™™ Coronary vessels are not interfered ™™

It is herniation of abdominal content through dia­phragm into the chest.



Congenital

Acquired

Presently US guided aspiration is commonly done. Traumatic

Complications xx Injury to heart. xx Infection.

Oesophageal hiatus (Commonest type of diaphragmatic hernia)

May be associated with malrotation with Ladd’s band

CARDIAC (PERICARDIAL) TAMPONADE Rapid accumulation of fluid or blood in the pericardial space causing increase in the intrapericardial pressure is called as cardiac tamponade. This results in compression of cardiac chambers. ↓ ↓ venous return ↓ ↓ cardiac output Causes Trauma Progressive pericardial effusion due to tuber­culosis, viral, bacterial infections ™™ Often, uraemia can cause significant pericardial effusion ™™

Eventration

Hernia through foramen Bochdalek

Hernia through foramen Morgagni

Congenital oesophageal hernia (rare)

Etiology of congenital diaphragmatic hernia Genetic Decreased lung fluid pressure Failure of the closure of pleuroperitoneal canal (foramen of Bochdalek) ™™ Early return of bowel into peritoneal cavity from physiological hernia ™™ ™™ ™™

™™

Features xx xx xx xx xx

Hypotension. Widened cardiac dullness. Muffled or decreased heart sounds. Increased venous pressure with raised jugular veins. Pulsus paradoxus (pulse becomes weaker on inspiration than expiration). xx In severe cases, heart is unable to expand causing shock and often sudden death. Beck’s triad ™™

Hypotension

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Muffled heart sounds

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Raised jugular venous pressure

xx Investigation: Chest X-ray and US confirms the diagnosis. xx Differential diagnosis: Tension pneumothorax.

Treatment xx Pericardial tap is done for immediate temporary relief under

US guidance—needle pericardiocentesis.

xx But eventual open pericardiotomy (occasionally pericar-

diectomy) and drainage is required in most of the patients.

Eventration xx It is weakening of diaphragm due to atrophy and loss of muscle of a part or all of one leaf of the diaphragm, with thin fibrous tissue formation, covered with pleura and peritoneum on either side. xx Diaphragm is attenuated and inactive. xx Classification of eventration: 1. Congenital—marked decrease in the muscle fibres in the diaphragm, clinically it may mimic CDH with sac. 2. Acquired or secondary—(a) Phrenic nerve palsy due to trauma (with Erb’s palsy); viral—usually in adults (Polio, Herpes zoster, Influenza, Diphtheria). (b) Neoplasia. (c) Autoimmune neuropathy involving diaphragm or phrenic nerve. (d) Iatrogenic. xx Most of them present in the infancy and childhood. A few of them escape to adulthood. x x This thin diaphragm is raised higher and immobile. It is actually not a true herniation. But features mimic hernia. xx Presentation: Asymptomatic, wheezing, recurrent LRTI, exercise intolerance, extreme respiratory distress. xx Symptomatic patients have functional deficit in ventilation perfusion (V/P) ratio because lung growth is affected. xx Larger the defect more the hypoplasia. More the hypoplasia lesser the perfusion and severe the symptoms. xx Paradoxical movement compromises the gas exchange. xx Sniff test—fluoroscopic evaluation for paradoxical movement. xx Chest X-ray (CT scan/MRI) shows the abnormality xx Differential diagnosis are diaphragmatic hernia through foramen Bochdalek. xx Condition causes respiratory embarrassment.

Thorax

Fig. 28.35: Anatomy of diaphragm showing different sites where hernia can occur.

Types

A

Fig. 28.36: Diaphragmatic hernia.

B Figs 28.33A and B: Eventration of diaphragm on table look (Courtesy: Dr Sadashiva Rao, MCh, Paediatric Surgeon, KMC, Mangaluru).

Treatment is plication of diaphragm through laparotomy. Indications for surgery ™™ ™™ ™™ ™™ ™™

Symptomatic patients Decreased ventilation perfusion ratio Prolonged (>3 to 6 months) exertional dyspnoea Impairing daily activity in idiopathic/viral Phrenic nerve palsy

Hernia Through Foramen Bochdalek (Through Pleuroperitoneal Canal) (95% Left Sided, Only 5% Right Sided)

Fig. 28.34: Chest X-ray showing left sided diaphragmatic hernia. Note the bowel shadows in the left side thorax.

xx It is commonest congenital diaphragmatic hernia. xx This is a developmental defective condition, due to failure of fusion of pleuroperitoneal canal leaving a direct communication between pleura and peri­toneum on left side. This allows herniation of contents of abdomen into the left side thorax. xx Common content is colon. Occasionally small bowel, stomach are the contents. xx 80% cases do not have hernial sac. Only 20% cases has got sac.

Words that enlighten are more precious than jewels.

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Fig. 28.37: Postmortem look of a newborn baby with classical diaphragmatic hernia (Courtesy: Dr Subramanya Bhat K, Sonologist Kanhangad). Note the entire bowel occupying the left side thorax.

Pathogenesis

Pulmonary hypoplasia → Acidosis → Pulmonary vascular bed spasm                Persistent pulmonary hypertension

Antenatal

Postnatal

• Fetal interventions • Discontinue the pregnancy (poor prognosis) • Continue pregnancy and observation • Shift the mother to higher centre • Mode of delivery—LSCS/ normal

• Stabilise the neonate • Do not resuscitate with Ambu bag • Tracheal intubation and ventilation • Pass nasogastric tube Surgical correction of CDH after stabilisation

Triad of congenital diaphragmatic hernia (CDH) ™™ ™™ ™™

Respiratory distress Scaphoid abdomen Mediastinal shift (Pseudodextrocardia)

Association of CDH    Persistent fetal circulation Hypoplasia not only on left side, it may be bilateral. Generations of bronchial branches decreased. Extension of tunica media beyond respiratory bronchioles. Decreased total lung mass Incidence: 1 in 3000 live births, M:F—2:1. 90% present in newborn period. 90% of CDH are Bochdalek hernias Left—80%, right—15%, bilateral—5%. Defects are large in babies and small in adults. Associated anomalies—10 to 50%, commonest—nonfixation/ midgut malrotation. Other anomalies—CNS, cardiac are known to occur and commoner with large/bilateral CDH. xx Very small percentage of patients escape and pass on to adulthood. Incidence—0.17 to 6% xx Incidental detection while evaluating for some other problem. So usually they are asymptomatic. xx xx xx xx xx xx xx xx xx xx

Poor prognostic criterias in Bochdalek hernia ™™ ™™ ™™ ™™ ™™

Early antenatal detection (before 5th month) Small left ventricle Large diaphragmatic defect / hemiagenesis Stomach in chest Polyhydramnios

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Respiratory embarrassment Scaphoid abdomen Bowel sounds in left side of chest Mediastinal shift towards right side Occasionally features of intestinal obstruction

Clinical features

Pulmonary hypoplasia with persistent fetal circulation—is the actual cause for hernia ™™ Respiratory acidosis ™™

Hernia through Foramen of Morgagni xx The defect lies between the sternal and costal attachments of diaphragm and is situated in front, towards right. Colon is commonest content. Usually, it is symptom free.

Oesophageal Hiatus Hernia xx Oesophageal hiatus hernia can be congenital or acquired (common).

Traumatic Diaphragmatic Hernia xx Either on right or left side, resulting from road traffic accidents, crush injuries, penetrating injuries, or blunt injuries. xx Patient is under shock. xx On right side along with the liver, the intestines may also get herniated. xx Patient is pale, presents with respiratory distress, guarding and rigidity over the abdomen.

Investigations xx X-ray chest and abdomen. xx US abdomen. xx Often CT scan of abdomen and chest is done.

Investigations: Chest X-ray, barium enema (common) or barium meal, arterial blood gas analysis (ABG). Treatment xx Laparotomy and dissection of the sac (when present) and closure of the defect in the diaphragm (using nonabsorbable suture material). Note:

Persistent fetal circulation is the major problem in these newborns. It aggravates the postsurgical mortality.

A

B

Figs 28.38A and B: (A) Plain X-ray chest; (B) Barium enema, showing bowel loops within thoracic cavity on the right side (diaphragmatic hernia).

Thorax SURGICAL MANAGEMENT OF PULMONARY TUBERCULOSIS

Treatment xx Immediate laparotomy and exploration is done. Tear in the diaphragm is sutured. xx Associated injuries in liver or spleen or bowel are treated accordingly. xx Adequate blood transfusion and antibiotics is required. xx Ventilator support is often necessary.

PULMONARY COMPLICATIONS DURING POSTOPERATIVE PERIOD

xx xx xx xx xx xx xx xx

Age: Common in infants and elderly. Sex: Common in males. Common in smokers. Common in people with chronic bronchitis, asthma, tuberculosis or COPD. Postoperative pain. Deep venous thrombosis and pulmonary embolism. Type of surgery: Common in thoracic or upper abdomen surgeries. Septicaemia. Paralytic ileus. Anaesthetic complications. Aspiration and its problems. Obesity.

Bronchopneumonia. Lung collapse. Bronchitis. Lung abscess. Adult respiratory distress syndrome (ARDS). Respiratory failure. Alkalosis. Pleural effusion or empyema.

xx Pleural tap. xx Intercostal tube drainage for empyema. xx Rib resection and Eloisier’s drainage. xx Lung resection is undertaken when medical treatment fails or when there is tuberculoma. It is commonly used method. xx Lobectomy or pneumonectomy. xx Decortication. xx Thoracoplasty collapse therapy—it causes elastic relaxation of lung around the lesion leading to closure of cavity. xx Creation of artificial pneumothorax (nitrogen is used). xx Temporary phrenic nerve palsy. xx Extrapleural pneumothorax. xx Plombage: It is extrapleural pneumolysis using lucite spheres.

It is visualisation and doing surgical procedures through video thoracoscopy. It can be: xx Diagnostic—lung cyst, pleural pathology, malignancy, tuberculosis, lung abscess, emphysematous bullae. xx Therapeutic—cervical sympathectomy, oesophageal mobilisation for carcinoma of oesophagus, lung resection, excision of lung cysts, etc.

Requirements xx Expert skilled personal. xx Double lumen endotracheal tube for one lung anaesthesia. xx Instruments.

Investigations xx Chest X-ray. xx Arterial blood gas analysis.

Advantages

Management xx xx xx xx xx xx

Failure of medical therapy. Tuberculoma. Tuberculous bronchiectasis. Destruction of lobe. Persistent foci, persistent cavity. Empyema thoracis. Presence of neoplasm with tuberculosis.

VIDEO-ASSISTED THORACOSCOPIC SURGERY (VATS)

Complications xx xx xx xx xx xx xx xx

xx xx xx xx xx xx xx

Surgeries Done

Precipitating Factors xx xx xx xx

Indications for Surgery

Suction—aspiration of tracheobronchial tree. Respiratory physiotherapy. Analgesics to control pain. Ventilator support with endotracheal intubation. Tracheostomy. Control of sepsis by proper antibiotics.

xx Open thoracotomy and its complications are avoided. xx Less painful, fast recovery. xx Magnification and precise dissection.

Disadvantages xx Injury to major structures. xx Longer duration of surgery. xx Learning curve.

An error gracefully acknowledged is a victory.

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B. Cardiac Surgery CHAPTER OUTLINE ™™ Anatomy ™™ P reoperative Assessment and Preparation of the Cardiac Patient ™™ Cardiopulmonary Bypass ™™ Congenital Heart Diseases ™™ Patent Ductus Arteriosus ™™ Coarctation of Aorta

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Atrial Septal Defect Ventricular Septal Defect Pulmonary Stenosis Transposition of Great Vessels Tetralogy of Fallot Acquired Heart Disease Mitral Regurgitation

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Aortic Stenosis Aortic Regurgitation Valve Replacement Surgery Ischaemic Heart Disease Cardiac Pacemakers Postoperative Care

ANATOMY Heart consists of right and left atrium, right and left ventricle with mitral (bicuspid) valve between left atrium and left ventricle and tricuspid valve between right atrium and right ventricle. Aorta begins from the left ventricle to have systemic circulation. Superior vena cava (SVC) and inferior vena cava (IVC) enters the right atrium to return venous blood. From right ventricle, pulmonary artery begins which transport the unoxygenated venous blood into the lungs. From lungs, four pulmonary veins collect the oxygenated blood to reach right atrium and to complete the cycle. Pressure in the right ventricle is low. Pressure in the left ventricle is high. Chordae tendinae act as guy ropes which connect valves (mitral and tricuspid) to heart through papillary muscles. Aortic and pulmonary valves are semilunar valves. First heart sound is produced by closure of atrioventricular valves. Second heart sound is produced by closure of semilunar valves. Valvular heart disease may be congenital or acquired. Rheumatic heart disease is the commonest acquired cause for valvular disease. Mitral stenosis is the commonest type. Right and left ventricles are separated by interventri­cular septum. Right ventricle is thinner than left ventricle. SVC and IVC opens into right atrium. Heart derives its blood supply from two coronary arteries—right and left. Left coronary artery once origins at ostium runs for 2 cm, divides into anterior descending and circumflex artery. Anterior descending artery runs in the anterior interventricular groove to reach apex and ascends short distance in posterior interventricular groove. The circumflex artery runs around the base of left ventricle. Right coronary artery through atrioventricular groove reaches the posterior interventricular groove and runs along it. Right coronary artery supplies right atrium, entire right ventricle except anterior part, posterior part of the interventricular septum, conducting system except left branch. Left coronary artery supplies left atrium, entire left ventricle except posterior part, anterior part of the interventricular septum. There are collaterals within the heart and extra­cardiac but is not sufficient enough to maintain the adequate perfusion in case of coronary block to the dynamic heart leading into myocardial infarction.

Fig. 28.39: Normal heart anatomy. Venous drainage of heart is through superficial and deep veins. Superficial veins (great cardiac, middle cardiac, small cardiac, oblique and posterior veins) form coronary sinus ending at right atrium. Deep veins directly enter the heart called as Thebesian veins. First blood passes to the elastic vessels then resistant vessels and capillaries later to veins and then back to heart. In capillary because of great cross-sectional area, rapid transfer of substances across tissues occur. Flow of blood from left side heart through aorta and its branches to capillaries and return to right heart is called as systemic circulation. Blood from right heart through pulmonary artery to lungs and from lungs through pulmonary veins to left heart is called as pulmonary circulation. Conduction system of heart consists of SA node (Sinu atrial node) which is pacemaker of the heart, AV node (Atrio- ventricular node) located in lower part of the atrial septum, AV bundle (Atrio ventricular bundle) with right and left branches and terminal Purkinje fibres in subendocardial region.

Cardiac Surgery

xx xx

xx

xx

Fig. 28.40: Conduction system of heart. Surface marking of the heart: Upper border is between 2nd and 3rd costal cartilage at the level of sternum. Lower border is from 2 cm to the right of sternal margin at 6th costal cartilage to the apex of heart at 5th intercostal space 9 cm from the midline.

xx

xx

PREOPERATIVE ASSESSMENT AND PREPARATION OF THE CARDIAC PATIENT xx xx xx

ejection fraction are found through this. Usually cardiologists do this test and give opinion about it. Treadmill stress test to find out the response of heart to work. Coronary angiogram is done to find out the amount of coronary function or its block. Special coronary artery catheter is passed through the brachial or femoral artery like in seldinger angiogram. This catheter is negotiated into the coronary arteries both right and left. Radio-opaque water soluble dye is injected into the catheter and coronaries. X-ray film will confirm the status of the coronaries. Procedure is done under guidance using C-arm. Amount of block is assessed and categorised. Cardiography is the procedure wherein dye is injected into the heart chambers using specialised catheters and size, shape, presence of clot in the chambers, valvular incompetence are studied. Cardiac catheterisation is done to get cardiac oximetry and pressures in different chambers of the heart. Cardiac catheter is flexible 100 cm long tube passed to the heart under guidance. Right and left sides are assessed separately. Catheter is infused with heparinised solution to prevent intravascular clotting during procedure. Catheter to the right side of the heart is passed through the cubital vein, subclavian vein, SVC. Pressures at systole and diastole are studied in right atrium, right ventricle, pulmonary artery. Blood samples are collected from these three levels to study oxygen saturation (oximetry). Left side of the heart is approached by two approaches—one is through the right atrium penetrating the atrial septum, catheter reaches the left atrium, and so to left ventricle and aorta. Pressure is recorded in each chambers. Blood samples are collected for oxygen saturation. Pressure will alter in valvular diseases like stenosis or regurgitation. Oxygen saturation is altered in shunts between right and left sided. Shunt occurs between systemic and pulmonary circulation. Cardiac isotope scanning.

™™ ™™ ™™ ™™ ™™

Fig. 28.41: Surface marking of the heart. xx Since cardiac surgery is a major surgery, proper evaluation is essential. Consent, explanation, dis­cussion in initial phases is absolute need. xx Patient will be anxious. He needs proper consolation, moral support. xx Proper history related to smoking, alcohol intake, diabetes, previous cardiac surgery, drug intake is essential. xx ECG, chest X-ray, haemoglobin, haematocrit, blood urea, serum creatinine, blood sugar, lipid profile, blood grouping are essential basic investigations. xx Echocardiography is ultrasound examination of heart. Heart chambers, pericardium, pumping capacity, valves and their structure,

Pressure in atrium is low 0–10 mmHg. Right atrium is little lower than left Pressure in the right ventricle is 15–30 mmHg systolic and 0–8 diastolic Pressure in pulmonary artery is 15–30 mmHg systolic and 3–12 diastolic Pressure in left ventricle is 100–140 systolic and 3–12 mmHg diastolic Pressure in aorta is 100–140 systolic and 10–80 mmHg diastolic

xx Pulmonary function study is done by chest X-ray, spirometry, blood gas analysis. xx Focus of infection should be looked for like dental infection, throat infection, skin infection.

CARDIOPULMONARY BYPASS Here functions of the heart and lungs are temporarily replaced by heart-lung machine which acts as a pump and oxygenator to the body. Heart is exposed through a midline sternotomy incision. Venous blood from the SVC and IVC is diverted to the heart lung machine by placing tubes to them. From the heart-lung machine, oxygenated blood is pumped through a tube which is passed to the ascending aorta so as to bypass the heart and lungs with retaining the function so tissues will have adequate required perfusion. Blood should be heparinised to prevent clotting. Often venous tube is placed in the right atrium.

Hatred never gets ceased by hatred; it gets ceased only by love. Hate is the subtlest form of violence.

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SRB's Manual of Surgery Temperature is lowered over the heart by pouring cold saline. Ventilation is discontinued. Once procedure in the heart is over, air in the chambers of the heart is cleared. Coronary artery perfu­sion is restored and heart is made to beat spontaneously or using DC shock. Acidosis and hypocalaemia is corrected. Patient is warmed. Heart is allowed to fill gradually and slowly heart lung machine blood flow is reduced. Cannulas are removed from the veins (SVC and IVC) and also from the aorta. Protamine sulphate is given to reverse the effect of heparin.

In PDA, part of the blood from aorta flows back to pulmonary artery because of high pressure in aorta (left-to-right shunt). This causes pulmonary hypertension. Occasionally, pressure is so severe that flow may reverse and deoxygenated blood from pulmonary artery may flow towards aorta causing reversal of left-to-right shunt converting acyanotic shunt to a cyanotic one. It is called as Eisenmenger‘s syndrome. It can occur in other left-to-right shunt also (ASD, VSD). Child presents with dyspnoea, chest pain, machinery murmur. Aortogram and echocardiography are diagnostic.

Fig. 28.42: Figure showing cardiopulmonary bypass.

Fig. 28.43: Patent ductus arteriosus.

Myocardial protection is achieved by:

Treatment—closure of the PDA either through interven­tional cardiology or more conveniently through open surgery.

Infusion of solution with 20 mmol/litre of potassium into the coronaries ™™ Cooling cardioplegic infusate to 6°C ™™ Surface of the heart is sprayed with 4°C Hartmann‘s solution ™™ Body temperature is reduced to 20–27°C Heart can be kept arrested for 2 hours. ™™

CONGENITAL HEART DISEASES

Complications of PDA—congestive cardiac failure, bacterial endocarditis.

COARCTATION OF AORTA—5% Narrowing of the aorta just distal to the origin of left subclavian artery. It is often associated with PDA, VSD.

Left-to-right shunt—It leads into overloading of the pulmonary circulation. Usually it is acyanotic. PDA—patent ductus arteriosus. ASD—atrial septal defect. VSD—ventricular septal defect. Right-to-left shunt—Blood from the systemic veins enter the systemic arteries bypassing the lungs allowing severe hypoxic blood to enter the systemic circulation. It will cause cyanosis. Examples are tetralogy of Fallot and transposition of great vessels. Conditions without shunts—Coarctation of aorta, aortic stenosis, pulmonary stenosis. Also classified as cyanotic and acyanotic heart diseases.

PATENT DUCTUS ARTERIOSUS (PDA)—10% Ductus arteriosus is essential in foetal life wherein blood from pulmonary artery reaches the aorta through this ductus arteriosus by passing the lung. Once child is born, this ductus closes because of the beginning of the lung function. Prostaglandin prevents closure. Indomethacin promotes closure. If it persists in child it is called as PDA.

Fig. 28.44: Coarctation of aorta.

Cardiac Surgery There is increased perfusion of upper limb, cranium, face. But less blood supply occurs to lower limb, kidneys.

Types xx It can be preductal or postductal depending on relation to the ligamentum/ductus arteriosus.

Features xx It causes left ventricular hypertrophy, differential blood pressure (pressure upper limb is higher but pressure in lower limb is lower). Often there is differential cyanosis. xx Visible dilated intercostal vessels through collateral perfusion is more obvious when patient leans forwards. xx X-ray will show dilated proximal aorta, notching of ribs due to erosion of the intercostals vessels. xx Aortogram is diagnostic.

Features xx There is shunting of blood from left atrium to right atrium. It causes left ventricular hypertrophy, pulmonary hypertension, eventually occasionally reversal of shunt as right to left leading into cyanosis. xx Dyspnoea, fixed split of second heart sound, systolic murmur due to increased blood flow through the pulmonary valve are the clinical features. xx It is diagnosed by echocardiography, cardiac catheterisation and angiocardiogram.

Treatment xx Closure of the defect by direct suturing or using patch either pericardium or Dacron.

Treatment is widening of the narrowed segment of aorta with Dacron patch graft, or removal of stenosed segment and arterial graft.

Fig. 28.46: Atrial septal defect.

VENTRICULAR SEPTAL DEFECT (VSD)—15% Fig. 28.45: Collaterals development in intercostal vessels in coarctation of aorta.

Types

Complications xx Congestive cardiac failure, bacterial endocarditis, aortic rupture.

ATRIAL SEPTAL DEFECT (ASD)—7% xx An ASD is the hole in the atrial septum, thus causing communication between left and right atrium. Types Secundum type is the commonest one. It is elliptical, in the middle of the atrial septum and is due to defect in the site of foramen ovale ™™ Primum type is lower part. It is rare ™™ Sinus venosus type is near SVC opening ™™

xx VSD is defect in the ventricular septum causing left-to- right shunt. There is pulmonary hypertension, ventricular hypertrophy.

xx Four types of VSD are present depending on location of the defect. Defect can be small or large. xx It may be associated with tetralogy of Fallot. xx Severe cases of shunt become reversal causing Eisenmenger‘s syndrome.

Clinical Features xx Pansystolic murmur, palpable thrill, split second sound with pulmonary accentuation, recurrent respiratory infections. xx 40–50% of defects especially when they are small, will close spontaneously. Spontaneous closure will not occur after the age of 6.

Investigations Echocardiography, cardiac catheterisation.

When man is hungry he dreams food. Hunger is the greatest anarchist in man, next to egoism.

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SRB's Manual of Surgery Treatment Closure of the defect using pericardial patch or Dacron. While suturing care should be taken not to inure atrioventricular conduction system.

Complications of VSD Recurrent respiratory infection, pulmonary hypertension, cardiac failure.

Fig. 28.48: Transposition of great vessels.

TETRALOGY OF FALLOT It is a cyanotic congenital heart disease. Components Fig. 28.47: Ventricular septal defect.

PULMONARY STENOSIS It is narrowing of the pulmonary valves due to fusion of cusps. Narrowing may be as less as 2–4 mm. Patient develops right ventricular hypertrophy and later right ventricular failure. Pressure in the right ventricle is higher, in pulmonary artery is lower. Treatment is pulmonary valvotomy.

Ventricular septal defect Infundibular and pulmonary stenosis causing right ventricular outflow obstruction ™™ Right ventricular hypertrophy ™™ Dextroposition of aorta ™™ ™™

Because of right ventricular outflow obstruction venous blood gets diverted through the existing VSD into the left ventricle and so to the aorta. So systemic circulation is provided with unoxygenated venous blood causing cyanosis.

TRANSPOSITION OF GREAT VESSELS Here aorta begins from right ventricle and pulmonary artery begins from left ventricle. So venous blood enters the aorta and causes hypoxia and cyanosis. It is usually not compatible with life but often through bronchial collaterals communication may develops and become compatible. When it is often associated with ASD or VSD or PDA mixing occurs and is compatible. It is cyanotic heart disease. It is diagnosed by an emergency echocardiography and aortocardiogram.

Treatment xx Immediate palliative method is Rashkind balloon septostomy. A balloon is passed into the right atrium and through the septum into the left atrium. Balloon is inflated and rapidly pulled out through the atrial septum causing widening of the defect in the septum. It allows flow of oxygenated blood from pulmonary veins through the septum and so to the right ventricle and aorta. xx Albert-Mustard atrial redirection of flow of blood: Atrial septum is excised and using either pericardial or Dacron patch left atrial blood is directed to the right ventricle and right atrial blood is directed to the left ventricle. xx Later definitive correction is done either at atrial level or at great arterial level.

Fig. 28.49: Tetralogy of Fallot.

Features xx Cyanosis with dyspnoea. Ejection systolic murmur which diminishes during cyanotic attack. xx Echocardiography, cardiac catheterisation are the essential investigations.

Cardiac Surgery Treatment xx Blalock-Taussig operation—it is done as initial treatment in newborn baby with Fallot‘s tetralogy. Left subclavian artery and pulmonary artery is connected using a graft which allows the pulmonary arterial perfusion. xx Second stage definitive correction by relieving the right ventricular outflow obstruction completely and closure of VSD using Dacron patch.

allow the finger to pass inside. Left ventricular tip is incised with a purse string suture and Tubb‘s valve dilator is passed. Under finger guidance through left atrial purse string wound, valve and cusps are separated using Tubb’s dilator.

ACQUIRED HEART DISEASE Mitral Stenosis Commonest acquired heart disease. Valve here cannot open completely during left atrial contraction. It is scarring and thickening of the mitral valves due to inflammation of valves with valve area less than 2.5 cm 2 (normal is 4–6 cm2). It will later lead into fusion of chordae tendinae, calcification of the valve cusps. It is commonly due to rheumatic fever with streptococcal pharyngitis. Fig. 28.50: Mitral valvotomy using Tubb’s dilator.

Features Mitral stenosis ↓ Hypertrophy of the left atrium ↓ Sluggish blood flow, left atrial hypertrophy ↓ Atrial fibrillation → atrial thrombus → emboli ↓ Pressure in pulmonary vein increases ↓ Lung congestion, oedema ↓ Pulmonary artery hypertension ↓ Right ventricular failure and tricuspid regurgitation (CCF). Mitral stenosis—clinical features and investigations ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Dyspnoea, orthopnoea Cough, haemoptysis Mid-diastolic murmur, with loud heart sound Features of atrial fibrillation Chest X-ray shows straightening of the left border of the heart ECG and echocardiography will demonstrate mitral stenosis, clot Cardiac catheterisation shows increased right atrial pressure Pulmonary capillary wedge pressure (PCWP) shows increased left atrial pressure

Indications for surgery ™™ ™™ ™™ ™™

Severe stenosis Calcification of cusps Clot in the left atrium Right ventricular hypertrophy

Surgeries for mitral stenosis xx Closed mitral valvotomy—through left thoracotomy incision, heart is exposed. Left atrium is opened with purse string suture so as to

xx Open mitral commissurotomy—it is done with cardiopulmonary bypass, left atrium is opened, valve and commissures are separated, valve is dilated using finger, clot in the left atrium is removed. xx Open valvuloplasty by doing repair of the valve. xx Percutaneous balloon valvotomy. xx Valve replacement surgery.

MITRAL REGURGITATION Mitral valve here cannot close completely during left ventricular contraction. It can be associated with mitral stenosis also.

Causes xx Rheumatic heart disease causing fibrosis, rigidity and shortening of chordae tendinae leading to inability to close the mitral valve. xx Myxomatous degeneration of the valve. xx Marfan’s syndrome. xx Connective tissue disease. xx Sarcoidosis.

Mitral regurgitation ↓ Left ventricular hypertrophy but reduced cardiac output ↓ Left atrial enlargement with increased pressure ↓ Pulmonary venous pressure increases ↓ Lung congestion, oedema (CCF)

Features ™™ ™™ ™™ ™™ ™™ ™™

Cough, haemoptysis, chest pain, dyspnoea Pansystolic murmur Features of failure Often associated features of mitral stenosis Features of associated diseases Echocardiography, cardiac catheterisation and PCWP are the investigations

Every light has darkness just beneath it. Darkness is ignorance and no knowledge.

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AORTIC STENOSIS Narrowing of the aperture of aorta is due to rheumatic heart disease, bicuspid stenosis, calcification. Valve is thickened, fibrosed, calcified and narrowed.

Features xx There is left ventricular hypertrophy with reduced left ventricular capacity. xx Because of the narrowing of the valve, cardiac output decreases. xx Systolic murmur is better heard over aortic area. xx Later may lead into failure. xx Echocardiography is diagnostic.

2. Mechanical valves  Starr-Edwards ball—valve prosthesis.  Bjork-Shiley tilting disc—valve prosthesis. Mechanical valves are long lasting but they are thrombogenic. Embolic phenomenon can occur. Patient requires oral anticoagulant to keep prothrombin time twice normal. If anticoagulants cannot be used, then aspirin, dipyridamole can be used. Problems with mechanical valves Thrombogenic Require warfarin anticoagulant therapy Prone for severe epistaxis, intracranial haemorrhage while on warfarin therapy ™™ Prone for infections by bacteria, fungi, yeasts ™™ Mechanical haemolysis and anaemia ™™ Valve malfunction may occur ™™ ™™ ™™

3. Free homograft valve.

Treatment Valve replacement surgery.

AORTIC REGURGITATION There is incompetence of aortic valve.

Causes xx xx xx xx xx xx

Fig. 28.51: Different types of valve prosthesis.

Rheumatic disease. Connective tissue disorder. Marfan‘s syndrome. Tertiary syphilis. Endocarditis. Aortic dissection.

Features ™™ ™™ ™™ ™™ ™™ ™™

There is left ventricular hypertrophy, and cardiac failure later Early diastolic murmur is characteristic Collapsing pulse Dyspnoea, chest pain Echocardiography is diagnostic It may be associated with ischaemic heart disease

Treatment Valve replacement surgery.

VALVE REPLACEMENT SURGERY Indications ™™ ™™ ™™

Severe valvular disease with fixity, stenosis Valve disease with thrombosis like in mitral stenosis Multivalvular disease

Types 1. Biological valves—Capentier’s glutaraldehyde preserved porcine valve with a sewing ring and frame is used. It is not thrombogenic. So, it is used in child bearing age and in whom warfarin is contraindicated. But its life span is less. So it is useful in elderly.

ISCHAEMIC HEART DISEASE (IHD) Main major arteries of the heart are right coronary, left coronary and circumflex artery. Blockage can occur in one or two or all three vessels. Involvement of all three vessels is called as triple vessel disease. IHD presents as asymptomatic with sudden massive cardiac ischaemia with sudden death. Or symptomatic angina, is progressive if not treated and eventually may lead in to severe MI. Atherosclerosis is the commonest cause. Risk factors are: ™™ ™™ ™™ ™™ ™™

Hypercholesterolaemia Cigarette Diabetes mellitus Hypertension Family history and age

Atheroma plaques deposits in the coronary artery and narrows it. Block above 70% is called as critical block. Angina is initially treated with calcium antagonists, beta blockers, nitrates.

Investigations xx xx xx xx

ECG. Coronary angiography is diagnostic. Echocardiography. Lipid profile (done on empty stomach).

Treatment 1. Coronary balloon angioplasty is done in case of angina, only one or two vessels are involved. It is done by interventional radiologists

Cardiac Surgery Contd... Permanent Pacing It is done in congenital and acquired atrioventricular block, sick sinus syndrome (SA node dysfunction), atrial fibrillation, certain tachycardia.

Routes of Pacing Transvenous route is commonly used. A needle is passed into the subclavian vein and guide wire is passed through the needle into SVC. Dilators are passed through the guide wire. Then sheath is passed. Electrode is passed into the atrium or ventricle. It is endocardial pacing.

Fig. 28.52: Coronary artery: Anatomy and sites of CABG. in presence of cardio­logists. Balloon tip catheter is passed through femoral or radial artery to reach proximal aorta and entered into the coronary artery opening. Coronary angiogram is done after injecting the dye. Balloon tip of the catheter is passed across the site of the block. Balloon is inflated to crush the atheroma. Problems with angioplasty ™™ ™™

Restenosis May precipitate block

Indications Triple vessel stenosis Left main stem stenosis Chronic stable angina Angina with persistent chest pain Block more than 70%

™™ ™™ ™™ ™™ ™™

Arrhythmias Infection Phlebitis, haematoma, thrombosis, bleeding Failure of battery, electrode Electrode displacement

™™ ™™ ™™

Fixed rate—ventricular pace—no sensing Demand release—ventricular pace—sensing-triggered mode Inhibited rate—ventricular pace—sensing-inhibited mode

Types of electrode activity

Grafts Used xx Patient’s own long saphenous vein—commonly used graft. xx Patient’s own internal mammary artery—choice graft as it is reliable, less occlusion, long-term patency. Usually 3–4 grafts are used. Technique—It is done under cardiopulmonary bypass. Aortic cross clamps are used to help proper graft anastomosis. Complications of CABG ™™ ™™ ™™ ™™

POST-OPERATIVE CARE xx Proper monitoring and ICU care is essential. xx ECG, temperature, BP, CVP, cardiac monitor, urine output has to be assessed regular intervals. xx Serum electrolytes, blood gas analysis, assessment of isoenzymes, haematocrit, blood urea, creatinine. xx Acidosis and hypercalcaemia to be corrected early. Complications of pacing

2. Coronary artery stenting after balloon angioplasty. 3. Coronary artery bypass graft (CABG).

™™ ™™ ™™ ™™ ™™

Transthoracic pacing—it is not commonly used. It requires open thoracotomy. One lead is placed to the atrium and two other to ventricle. Pacemaker may be external usually used as tempo­rary. Internal pacemaker is placed in the upper chest wall below the middle of the clavicle in subfacial plane under local anaesthesia (pacemaker pocket).

Graft thrombosis Narrowing Atherosclerosis in the graft Respiratory infection

CARDIAC PACEMAKERS Cardiac rate is made regular using specialised device which stimulates the heart and acts as pacemaker. Temporary Pacing It is done in myocardial infarction, arrhythmias, and cardiac surgery.

Contd...

xx Pacemakers are sensitive to electromagnetic interference. xx Drains from pericardium, mediastinum should be assessed carefully. xx Hypovolaemia, cardiac tamponade, myocardial infarction, hypoxia, acid-base imbalance has to be corrected. xx Dopamine, dobutamine, isoproterenol are the drugs used when there is low cardiac output. xx Digoxin, pacing, cadioversion may be required if there is cardiac arrhythmias. xx Management of respiratory system—when the patient is alert and having adequate cough reflux, endo­tracheal tube is removed. Breathing exercises, physiotherapy, observation for respiratory distress, prevention of pneumonia to set in are important care required. xx Care of the endotracheal tube, suctioning, checking the parameters in intermittent positive pressure ventilation (IPPV). xx Neurological system should be observed—alertness, speech, level of consciousness, any deficits are looked for. xx Strict asepsis is undertaken in cardiac postoperative period by avoiding unnecessary visitors, separate dress in postoperative ward, wearing gloves, cap, masks while attending the patient.

Perfection is the best excuse.

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Adjuvant Therapy CHAPTER OUTLINE ™™ Radiotherapy ™™ Chemotherapy ™™ Cell Cycle

™™ Antimalignancy Drugs ™™ Hormone Therapy in Cancer ™™ Immunosuppression

RADIOTHERAPY The effect of radiations on living cells is the more intense: (1) the greater their reproductive activity, (2) the longer their mitotic phase lasts, and (3) the less their morphology and function are differentiated. —Jean Alban Bergonié, Louis Mathieu Frédéric Adrien Tribondeau, 1906

™™ Immunotherapy ™™ Hybridoma ™™ Gene Therapy

3. Redistribution of the cells. Cells in the ‘S’ phase of the cell cycle (where DNA is being synthesised) are radioresistant. These, cells after radiotherapy will go to ‘G2’ or ‘M’ phase. 4. Reoxygenation of the cells which were hypoxic at the time of radiotherapy. Hypoxic tumour cells are radioresistant. About 10% of tumour cells are in hypoxic state. Thus, fractionation of the radiotherapy allow retained cells to go for active and sensitised phase making radiotherapy more effective.

xx Radiotherapy is the use of ionizing radiation as therapy, mainly in malignant conditions. xx Megavoltage X-rays or gamma rays which genera­tes energy greater than 1 × 106 V are used.

Oxygen is a good radiosensitiser. So hyperbaric oxygen is used many times as radiosensitiser.

Principles and Factors in Radiotherapy

It is called as grey unit. It is defined as the absorption of 1 J of radiation energy by 1 kg of tissue.

xx Penetration of the beam into the deep seated tumour. xx Building of the radiation dose under the skin over the tumour tissue so as to minimize the skin reactions. xx Precise targeting of radiation towards the tumour. xx Radiosensitivity, tumour volume and tumour size are the factors which determine the radiation efficacy.

Physicochemical Effects of the Radiation xx Direct action on the target tissues. xx Indirect action, by releasing free radicals which cause cell destruction. xx It acts on the different phases of cell cycle to destroy the cell.

Changes in the Tumour Cells after Irradiation 1. Repair of the damaged but retained cells. 2. Repopulation is by proliferation and reproduction of the retained cells.

Radiation Unit

Types of Radiotherapy (Therapeutic) 1. Curative (radical) radiotherapy: It is given in early malignancies as a curative or primary method to tumours which are radiosensitive. 2. Palliative radiotherapy: It is used to alleviate the symptoms when the tumour is beyond cure. Symptoms are: xx Pain in secondaries in the bone  Myeloma.  Carcinoma breast.  Advanced lymph node metastasis. xx Bleeding  Carcinoma oral cavity, cervix.  Carcinoma bladder, rectum.  Advanced secondaries in the lymph nodes.

Adjuvant Therapy Common tumours Seminoma testis Hodgkin‘s lymphoma Squamous cell carcinoma Ewing‘s sarcoma Carcinoma lung Gliomas Bladder tumours Carcinoma cervix, vagina, nasopharynx, head and neck, oesophagus ™™ Basal cell carcinoma ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Dose is 60 Gy in 30 fractions over 6 weeks. xx Fungation  Breast carcinoma.  Rectal carcinoma. xx Obstruction  Bronchogenic carcinoma obstructing inferior vena cava.  Carcinoma cervix causing obstruction to the ureter. xx Pathological fracture due to secondaries. xx Spinal cord compression due to secondaries.

Kilovoltage machines. Linear accelerator. Betatron/Microton. Radioactive materials like Cesium 137 (pellets), Iridium 192 (wire), Gold 198 (seeds), Iodine 125 (seeds).

Measurement of Ionising Radiation Roentgen unit is a measure of ionisations produced per unit volume of air by X-rays and gamma rays but it is not used for photon energies above 3MeV. SI unit for exposure is Coulomb per kg.

Radiation Absorbed Dose (RAD) Absorbed dose is De/dm. It is mean energy imparted by the ionizing radiation to material of mass dm. Old unit is rad which is equivalent to 100 ergs of energy per gram.

Newer International Unit is Presently Used One Grey (Gy) is one joule of energy deposited per kilogram of material. One Gy = 100 rads = 100 cGy. 1 cGy = 1 rad.

Dose is 10–25 Gy in 1 to 5 fractions.

Principle Radiation is used to kill actively proliferating malignant cells at their mitotic level. Common malignancies which are radiosensitive ™™ ™™ ™™ ™™ ™™ ™™

xx xx xx xx

Squamous cell carcinoma Basal cell carcinoma Bladder tumours Carcinoma cervix Seminoma testis Hodgkin‘s lymphoma

Radiotherapy Plan Type and doses of radiotherapy is decided by following factors: xx Site of tumour. xx Lymphatic field. xx Tumour size and extent. xx Histological type and grading. Types of radiotherapy (Technical)

Other areas where radiotherapy is used commonly: xx In carcinoma breast during postoperative period: For secondaries in bone, sometimes as preoperative radiotherapy, as part of QUART Regime. xx In follicular carcinoma of thyroid: For secondaries radioactive I131 5 m curies is given orally. External radiotherapy is also given for bone secondaries along with internal fixation if there is pathological fracture. xx Malignant brain tumours like astrocytomas. xx Many sarcomas. xx Carcinoma prostate. xx Carcinoma oesophagus. xx Carcinoma lung. xx Fixed secondaries in neck as palliation to palliate pain, fungation and erosion into major vessels. xx Multiple myelomas.

Radioresistant Tumours Include xx All GI malignancies. xx Melanoma. xx Medullary carcinoma of the thyroid.

™™ ™™ ™™ ™™ ™™

Superficial X-ray therapy (100 KV) Orthovoltage X-ray therapy (200/300 KV) Caesium (137Cs) or cobalt (60Co) teletherapy Intracavitary or intralesional radiotherapy (Brachy­therapy) Radioactive I131 therapy for follicular carcinoma thyroid

Brachytherapy xx xx xx xx xx xx xx xx

It is radiation given with source close to the tumour. It is given using iridium192 caesium137. It is curative radiotherapy. It is used in carcinoma oral cavity, penis, breast, cervix and bladder. Radiation material placed in the cavity is called intracavitory RT. Radiation material is inserted into the tissues—interstitial RT. Implants can be kept permanently or temporarily. Radioactive material is placed into the cavity/tissue through applicators under general anaesthesia. xx Intraoperative radiotherapy is also becoming popular. xx It has only localised effect with adjacent tissue being spared.

External beam radiation: Given using cobalt 60 teletherapy or X-ray source. Advantages—Deep penetration, skin sparing, better dose distribution.

Internal radiation:

Source of Radiotherapy xx Cobalt-60 machine—most commonly used.

Used for diagnostic and thera­peutic purpose, e.g. in carcinoma thyroid for treatment of secondaries.

“Cancer” word itself is lethal many times than cancer.

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Classification

Efficacy depends on:

• X-rays, electrons-from high energy X-ray machine, i.e. Linear accelerator • Gamma and beta rays from radioactive isotopes like Cobalt-60, Caesium 137, Iridium 197 • Protons, neutrons and heavy ion nuclei from cyclotrons

• Low LET (Low Energy Transfer) radiation— X-rays, gamma rays, electron • High ET radiation—Neutrons, protons, alpha particles and negative ions. It has heavier mass with dense localisation and hence biologically more effective

• Cell cycle phase • Oxygen content of cells

Preoperative radiotherapy Advantages

Postoperative radiotherapy

Radiotherapy and chemotherapy combined

• Down-stage the tumour and reduces the tumour bulk • No change in oxygenation of tissues • Blockage of lymphatics by RT prevents tumour spread during surgical dissection • Reduces the chances of microscopic spread Disadvantages • Delayed healing due to reduced vascularity • Flap necrosis, fistula formation • Carotid blow-out

• More effective and extent of RT is welldefined • Flap necrosis, fistula complications are less Indications • When resected margin is positive for tumour • When bone/cartilage are involved • Extracapsular nodal spread • Multiple neck nodes/node more than 3 cm in case of neck disease • Poorly differentiated tumour

• Commonly used before or during RT • Chemotherapy after RT is not commonly followed • Chemotherapy before RT is called as induction chemotherapy which reduces the bulk of tumour without altering the vascularity • Chemotherapy with RT is called as concomitant RT which improves the effect of RT. Methotrexate and bleomycin are radio sensitisers

Complications of Radiotherapy

Methods of delivery • External beam radiation (Teletherapy) • Brachytherapy • Systemic irradiation using radioisotopes like I131

CHEMOTHERAPY

xx Oral mucosal oedema, ulceration, dysphagia, dyspnoea, loss of taste, oral thrush. xx Bone marrow suppression. xx Oophoritis in women and oligospermia in men. xx Affecting lens, eyelashes and lacrymal glands causing dryness, cataract. xx Mucosa in GIT is very sensitive causing nausea, vomiting and diarrhoea. xx Radiation dermatitis, pigmentation in skin. xx Radiation myelitis of the spinal cord—causing hemiplegia, paraplegia. xx Radiation pneumonitis and pulmonary fibrosis. xx Radiation nephritis and renal failure. xx Radiation osteomyelitis. xx Radiation-induced malignancies. xx Radiation-induced thimble bladder. xx Radiation-induced frozen pelvis. xx Infection—bacterial, viral, candidial (oral thrush).

xx Chemotherapy, today is an important modality of treatment

in managing a case of cancer. xx It is the main modality of treatment in most of the advanced

malignancies. xx It is used preoperatively to downstage the tumour so as to

increase the possibilities of surgical resection. xx When used postoperatively it reduces the rate of recurrence. xx It is the primary treatment for NHL, leukaemia. xx These drugs mainly act by blocking the mitotic activity in

the nucleus in different phases of the cell cycle. xx It is given either oral, intravenous (systemic), intra-arterial,

intrathecal and intravesical (regional) or as isolated limb perfusion. xx Intra-arterial chemotherapy is used in head and neck cancers and hepatic cancers. xx Isolated limb perfusion is used in melanoma.

Brachytherapy Type

Advantages

Disadvantages

• Intracavitary like in uterus, urinary bladder, maxillary antrum, bronchial or oesophageal tree • Interstitial wherein radioactive needles/ wires/ribbons/seeds are inserted into the tumour area like in bladder or oral cavity • Surface brachytherapy using moulds like in tumours of skin/eye/breast • Radionuclides used are Caesium 137 (Cs137), Iridium 192 (Ir192), Gold 198 (Au198) and Iodine 125 (I125) • Brachytherapy is often combined with external beam radiotherapy

• High, localised, single continuous dose of RT • Deeper and adjacent tissues are spared • High dose rate with short time • Less side effects • Curative and effective in early cancers • After loading devices are available which reduces personal exposure • Surgery is avoided and part is retained

• Technically difficult • Availability of the facility • Local complications like displacement/ erosion

Adjuvant Therapy CELL CYCLE The cell cycle is composed of: 1. ‘G0’—resting phase or nonproliferative phase. 2. Presynthetic phase (G1)—resting cells that are not preparing for cell division are said to be in this subphase G. 3. ‘S’ phase—DNA synthesis takes place during this phase. 4. ‘M’ phase—formation of mitotic spindle, i.e. period of mitosis. 5. Postsynthetic phase (G2)—premitotic interval, which follows the termination of DNA synthesis. Most potent cytotoxic agents act by damaging DNA. Their toxicity is high during the DNA synthetic phase, ‘S’ phase of the cell. Some agents block the formation of mitotic spindle in M phase (vinka alkaloids and taxanes). So the agents have activity only against cells that are in the process of division. Hence, tumour with high fraction of actively dividing cells are more susceptible to chemotherapeutic agents.

II.  Classification of antimalignancy drugs based on the action on cell cycle S-phase specific agents: Cytosine arabinoside, hydroxyurea, 6-mercaptopurine. M-phase specific agents: Vincristine, vinblastine, palcitaxel. Phase nonspecific agents: Alkylating agents, nitrosoureas, antitumour drugs, procarbazine, cisplatin, dacarbazine.

Mode of Action These drugs damage the active cells by affecting the process of cell division. Hence, they also affect haemo­poiesis, cellular activity, epithelial tissues and gonads. They also suppress the immune system.

Adverse Effects in General Bone marrow suppression, alopecia, hepatotoxicity, nephrotoxicity, damage to gonads, damage to GI mucosa and ulceration.

HORMONE THERAPY IN CANCER

Ablative Procedures xx Oophorectomy and adrenalectomy in carcinoma breast. xx Orchidectomy in carcinoma prostate.

Added Hormone xx Prednisolone, progestogens, estrogens and androgens.

Hormone Antagonists

Fig. 29.1: Cell cycle. When chemotherapy is given with interferons and interleukins, it is called as biochemotherapy.

ANTIMALIGNANCY DRUGS I.  Classification 1. Alkylating agents: a. Nitrogen mustards: Mechlorethamine (mustine hydrochloride), cyclophosphamide, chloram­bucil, melphalan. b. Ethylenimines. c. Alkylsulfonates—busulfan. 2. Antimetabolites: a. Folic acid antagonists—methotrexate. b. Purine antagonists—azathioprine, 6-mercap­topurine. c. Pyrimidine antagonists—5-fluorouracil, 3. Antibiotics: Actinomycin-D, mitomycin, doxoru­bicin, bleomycin. 4. Vinca alkaloids: Vincristine, vinblastin. 5. Miscellaneous: Cisplatin, procarbazine.

xx Tamoxifen is estrogen receptor antagonist. Estrogen receptor level is assayed. If it is more than 10 units/g of tissue, it is called as ER positive and if less than 10 units, it is called as ER negative. xx Cyproterone acetate, competes with testosterone for binding receptors. xx LHRH analogue—Goserelin (Zoladex) acts as an antagonist to carcinoma breast. xx Phosphorylated diethylstilbestrol (Honavan) is used in carcinoma prostate.

Drugs that Interfere with Hormone Synthesis or Release xx Aminoglutethimide is an adrenal inhibitor. It is also an aromatase inhibitor inhibiting the peripheral conversion of androstenedione to estrogen. xx Papillary carcinoma of thyroid is (TSH) hormone dependent. TSH can be very well-suppressed by giving L-thyroxine, suppressive dose, daily 0.3 mg for life long. Steroids (corticosteroids) are used as component of chemotherapy regime. They also improve the anorexia and also control hypercalcaemia seen in patients with malignancies on treatment. They reduce cerebral oedema in intracranial malignant neoplasms.

The miserable have no other medicine but only hope.—William Shakespeare

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Used in

Adverse effects

1.

Mustine hydrochloride

Hodgkin‘s lymphoma

Alopecia, bone marrow suppression

2.

Cyclophosphamide: Dose: 3 mg/kg IV daily for 5 days in dextrose, as monthly cycle for 6 months Orally as 50 mg tablets

Ovarian carcinoma, lymphomas, colonic and bronchogenic carcinoma

Alopecia, bone marrow suppression, haemorrhagic cystitis

3.

Melphalan: Dose:10 mg daily × 3 weeks Available as 2 mg tablets

Multiple myeloma and melanoma

4.

Busulfan: 10 mg for 3 weeks

Chronic myeloid leukaemia

5.

Chlorambucil: 10 mg for 3 weeks

Chronic lymphatic leukaemia

6.

Methotrexate: 2.5–5 mg/d orally;10 mg intrathecally 1–2 times a week

Choriocarcinoma, ALL, soft tissue sarcoma, breast cancer

Oral and GIT ulceration, bone marrow suppression, hepatic damage

7.

6-Mercaptopurine: Dose: 2.5 mg/kg/d orally

Leukaemias and choriocarcinoma

Hyperuricaemia

8.

5-Fluorouracil Dose:15 mg/kg/d IV

Adenocarcinomas of GIT, breast cancers and cancer cervix

Neurotoxicity, stomatitis, bone marrow suppression

9.

Vinca Alkaloids. Vincristine: Dose:1.5 mg/sq.m Vinblastine: Dose: 0.1 mg/kg body weight

Leukaemia Hodgkin’s lymphoma

Neurotoxic Bone marrow toxicity

10.

Rubidomycin: Dose: 40 mg/m/day IV

Acute myeloblastic leukaemia

Myocardial depressant

11.

Adriamycin: 60 mg/m2 IV

NHL, hepatoma, medullary carcinoma thyroid, osteosarcoma and soft-tissue sarcomas

Cardiotoxic

12.

0‘-p DDD(Mitotane): Dose: 10 gm orally for 8 weeks

Carcinoma adrenal cortex

13.

Bleomycin: 20 units IV or IM

Squamous cell carcinoma of skin and other Pulmonary fibrosis regions and lymphomas

14.

Cytosine arabinoside: Dose: 4 mg/kg IV

Leukaemias and lymphomas

15.

Lomustine (CCNU) and Carmustine (BCNU)

Brain tumours and lymphomas

16.

Procarbazine

Hodgkin‘s lymphoma and oat cell carcinoma lung

Bone marrow and CNS depression

17.

Cisplatin: Dose: 20 mg/m2/d

Testicular and ovarian tumours

Nephrotoxicity

18.

Etoposide: Dose: 100 mg/sq.m

Testicular tumour, bladder tumour, lymphomas

19.

Hydroxyureas

Myeloma, leukaemias

IMMUNOSUPPRESSION xx It is mainly used in transplantation to prevent graft rejection, e.g. in transplantation of kidney, liver, heart, small bowel, pancreas. Drugs used are: xx Azathioprine (Imuran, Purine analogue): Inhibits purine synthesis. xx Cyclosporine: It is a very good immunosuppressant, derived from fungus. It causes inhibition of lymphocytic activity, delayed hypersensitivity, inter­leukins, memory cells, etc. It binds to cyclo­p hilin, decreases IL-2 and other cytokine release from T cells. It is initially given intra­v enously and later given orally. It is given usually for long duration, for 12–24 months. It is nephrotoxic as well as bone marrow suppressant. So, constant monitoring by blood urea, serum creatinine,

xx xx xx xx xx xx

Pulmonary fibrosis

Leukopenia and thrombocytopenia

blood count, Hb% at regular intervals is required. Dose should be adjusted depending on these parameters. Cyclosporine is very effective immunosuppressant in transplantation. Antilymphocytic globulin: Antibodies against T-cell receptors (CD2, CD3, CD4, CD8), B-cells and macrophages. Steroids (methylprednisolone): Alters trans­crip­tion and translation, affects T-cells and macro­phages. Cytosine arabinoside: Anti-inflammatory and immunosuppressive effect. Tacrolimus (FK506): Bind to FK binding proteins, effects are similar to cyclosporine. OKT3: Acts against CD3 and T-cells. Mycophenolate mofetil: Inhibits inosine mono­sphosphate, affects lymphocytes.

Adjuvant Therapy HYBRIDOMA

Types of Immunosuppression 1. Induction regimens: Mainly aims to avoid rejection and to establish a good graft function during the immediate post-transplant weeks (2 weeks). Antilymphocytic sera, along with either cyclosporine or azathioprine or steroids are used here. 2. Antirejection regimens: It aims at reversing the acute rejections. High dose steroids and anti­lymphocytic sera are used here. 3. Maintenance therapy: Using cyclosporine or FK506 along with steroids and azathioprine. Complications ™™ ™™ ™™ ™™ ™™ ™™

Infection—commonest Malignancy—squamous cell carcinoma, lymp­homa, Kaposi’s sarcoma Nephrotoxicity Bone marrow toxicity GIT toxicity Neurotoxicity

IMMUNOTHERAPY It is enhancing the host response of patient whenever required, commonly against malignant cells. Often it is used in other conditions also, where there is severe immunosuppression due to any reason like bone marrow suppression or in specific conditions like severe hepatitis. Immunotherapy can be: ™™ ™™ ™™ ™™

Active Passive Restorative Adaptive

Immunotherapy agents xx xx xx xx xx xx xx xx xx xx

Monoclonal antibodies. Bone marrow transplantation. Cell transfer. Lymphokines. Thymic hormones. Levamisole and BCG (as immunomodulators). Prostaglandins. Interferons, interleukins. Immunoglobulins. Antibody derived specific to certain tumour like melanoma. Tumours where immunotherapy is used

™™ ™™ ™™ ™™ ™™

Melanoma Bladder tumour Carcinoma colon Renal cell carcinoma In many tumours it is under trial

Disadvantages xx Very costly. xx Nonavailability. xx Effect is not 100%.

xx It is a biotechnological process wherein multi­plication property of Myeloma cells is combined with synthetic property of some other required cells, to achieve rapid and large quantity manufacturing of required chemical. xx Myeloma cells with only retained multiplication activity is fused with human cells or lymphocytes or other cells (of nature to produce the required product) by hybridisation. The resulting cell has got the capacity to multiply rapidly and to produce required product in large quantity. It is called as hybridoma. xx It is used to generate monoclonal antibodies, insulin and many other antibodies, immunoglo­bulins, etc. Monoclonal antibodies are used for ™™ ™™ ™™ ™™ ™™ ™™

Immunodiagnosis—for radioimmunoassay, radionuclide scan Antibody for detection of tumour antigen For cancer therapy For serotherapy As conjugates (with drugs, toxins, isotopes) For production of other chemicals and as a research tool

GENE THERAPY The ability to alter specific genes of interest is, nowadays an exciting and powerful tool in the potential manage­ment of a wide range of diseases. Instead of giving a patient a drug to treat or control the symptoms of the genetic disorder, physicians may be capable of treating the basic problem by altering the genetic makeup of the patient’s cell. Typically, two methods have been considered: Germ line and somatic cell gene therapy. xx Germ cell therapy involves insertion of a gene into fertilised egg for the correction of a genetic disease. Because these genes are dispersed throughout the tissues of the egg, they end up in the germ cells of the foetus, and hence are passed on to the future generations. xx Somatic cell therapy involves the insertion of genes or otherwise manipulating the gene machinery of a cell to treat a disease. In this case the cells are restricted to the population that has been treated and any genetic change remains restricted to these cells and is not passed onto the germ cell line. The goals of human somatic therapy are usually one of the following: xx To repair or compensate for a defective gene. xx To enhance the immune response directed at a tumour or pathogen. xx To protect vulnerable cell populations against treatments such as chemotherapy. xx To kill tumour cells directly. Several single gene disorders are candidates for gene therapy and in addition, current thinking has expanded to include treatment of AIDS and athero­sclersis using gene therapy techniques. Vectors used for gene therapy fall into two main classes—Viral and nonviral. xx Viral: Initially retroviruses were used as vectors. Other potential vectors include Adenovirus, Herpes virus and Vaccinia virus. xx Nonviral systems  Liposome mediated DNA transfer.  DNA protein conjugates. However exciting and appealing the prospects of gene therapy may appear, this technique is still in the experimental stages.

Life so short, the craft so long to learn.—Hippocrates

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Anaesthesia

It has long been an important problem in medical science to devise some method of mitigating the pain of surgical operations. An efficient agent for this purpose has at length been discovered. A patient has been rendered completely insensible during an amputation of the thigh, regaining consciousness after a short interval. —Henry Jacob Bigelow, 1846

CHAPTER OUTLINE ™™ Preoperative Assessment ™™ General Anaesthesia –– Anaesthetic Agents –– Oxygen –– Muscle Relaxants –– Reversal Agents –– Instruments in Anaesthesia –– Complications of General Anaesthesia

–– Postoperative Care –– Monitoring the Postoperative Patient ™™ Regional Anaesthesia –– Topical Anaesthesia –– Infiltration Block –– Field Block –– Nerve Block

PREOPERATIVE ASSESSMENT History xx Chronic cough, smoking, alcohol, drug intake, drug allergy. xx Any previous diseases like hypertension, diabetes mellitus,

epilepsy, bronchial asthma, tuberculosis, hepatitis, cardiac diseases. xx Drug therapy: Steroids, antihypertensives, sedatives, antibiotics, antiepileptics.

Examination General: Posture, teeth, mouth opening, dilated veins, neck movements, tremor, airway, anaemia, oedema, jaundice, cyanosis. Respiratory system: To look for asthma, tuberculosis, emphysema, COPD. Airway: Mouth opening, Mallampati scoring, thyro­men­tal distance, temporomandibular joint assessment. Thyromental distance: It is the distance between mentum and thyroid

–– Intravenous Regional Anaesthesia ™™ Spinal Anaesthesia –– Saddle Block ™™ Epidural Anaesthesia –– Caudal Anaesthesia

cartilage, measured externally. If it is more than 6.5 cm (i.e. more than 4 fingers breadth) intubation is easier, if it is less than 6.5 cm intubation is difficult. Cardiovascular system: Hypertension, ischaemic heart disease, arrhythmias, cardiac failure, valvular diseases. Spine: Curvature, intervertebral space, skin over the area for any infection. Other systems: Abdomen, skeletal system. Scoring to assess intubation Mallampati scoring: Class I — Faucial pillar, soft palate, uvula are seen Class II — Faucial pillar, soft palate are seen Class III — Only soft palate is seen Samsons Young modification: Class IV — Only hard palate seen Class I, II: Easy intubation Class III, IV: Difficult intubation

Anaesthesia Preoperative Investigations Haematocrit, blood sugar, blood urea, serum creatinine, electrolytes, chest-X ray, ECG, blood grouping, blood-gas analysis, cardiac assessment.

Preoperative Treatment xx xx xx xx xx xx

Control of respiratory and cardiac diseases. Improvement of Hb% status, if anaemia is present. Preoperative antibiotics are given. Blood should be kept ready for major cases. Starvation for 4 hours for liquids and 6 hours for solids. Bladder and bowel should be emptied to prevent soiling on the operation table. Urinary catheter may be passed and enema may be given. xx Dentures, contact lenses, jewellery must be removed. xx Surgical area should be cleaned and properly prepared.

GENERAL ANAESTHESIA It means abolition of all sensations, i.e. touch, pain, posture and temperature with a state of reversible loss of consciousness. It has got three components: (1) Analgesia; (2) Hypnosis; (3) Muscle relaxation.

AnaestheTIC Agents xx Volatile anaesthetics: They vaporise in room air.  Agents used are: Ether, trichloroethylene, halothane, enflurane, isoflurane, sevoflurane.  Ether which is irritant, unpleasant, flammable, is commonly used agent in developing countries.  Enflurane and isoflurane are non-inflammable, non-explosive, non-irritant and stable. Here anaesthesia is rapid with faster recovery. xx Gaseous anaesthetics:  Nitrous oxide: It is non-inflammable, non-irritant, good analgesic but weak anaesthetic agent. It is given along with 30–50% oxygen for balanced anaesthesia (blue coloured cylinder in India).  Cyclopropane is highly flammable. xx Intravenous anaesthetics:  Thiopentone: It is ultrashort acting barbiturate which causes hypnosis during induction of anaesthesia. It does not have analgesic effect. It causes hypotension, respiratory depression, laryngeal and bronchospasm. Recovery is rapid. Extravasation of drug can cause skin ulceration. Intra-arterial injection causes vasospasm and gangrene. Dose: 4–7 mg/kg. Methohexitone sodium. Propanidid: 4–7 mg/kg. It can cause anaphylaxis.  Ketamine: Dose: 2 mg/kg IV. It is a good analgesic. It causes dissociative anaesthesia. It can lead to hypertension, apnoea, laryngospasm. In children it can be given IM-5 mg/kg. It does not require intubation for small procedures.  Propofol: It is widely used induction agent which has got predictable onset and recovery. It has got least side effects on CVS and respiratory system. It is also used for total IV anaesthesia. Dose: 1–2.5 mg/kg.



 Fentanyl is neuroleptanalgesic. It causes sedation, catatonia,

dissociation, hypotension and preferred in asthmatics.

OXYGEN xx Oxygen is given through Boyles apparatus (33.3%). xx Oxygen in high concentration is respiratory depressant and also affects eyes. xx A 5% CO2 mixture in oxygen is called as carbogen. xx Oxygen is available in black and white coloured cylinder.

MUSCLE RELAXANTS Depolarising Muscle Relaxants They act at the level of acetylcholine receptors which widens the refractory period after depolarisation causing paralysis. It is shortacting muscle relaxant. a. Suxamethonium chloride (scoline):  It lasts for 2–4 minutes.  It causes muscle twitching—fasciculations—paralysis.  It is metabolised by plasma pseudocholinesterase. Atypical or deficiency of this enzyme prolongs the action of the scoline.  Side effects are hyperkalaemia, myotonia, apnoea and cardiac arrest. b. Suxthonium bromide.

Non-depolarising Muscle Relaxants They block the channels of entry of acetylcholine. They are long acting relaxants. 1. Tubocurarine: It lasts for 45 minutes. 30 mg is the dose. 2. Gallamine. (Flaxedil): Dose is 1–2 mg/kg. It is cheaper. It is contraindicated in renal diseases. 3. Pancuronium bromide (Pavulon): It is synthetic steroid muscle relaxant. Its action lasts for 45 minutes. Dose is 0.08–0.1 mg/kg. 4. Vecuronium bromide: It is a steroid muscle relaxant, given at a dose of 0.05–0.1 mg/kg. 5. Rocuronium is short-acting steroid muscle relaxant. It starts its action in one minute. 6. Atracurium: It lasts for 20–30 minutes. Dose is 0.6 mg/kg. 7. Mivacurium: Dose is 0.15–0.25 mg/kg.

REVERSAL AGENTS They are anticholinesterase drugs which increase the acetylcholine, and thus act as antagonising agents for non-depolarising muscle relaxants. They cause brady­cardia. Neostigmine (2.5 mg) is used commonly along with atropine (1.2 mg). Edrophonium (short acting) and pyridostigmine (long acting) are other drugs.

INSTRUMENTS IN ANAESTHESIA 1. Boyle’s apparatus: It consists of: a. Cylinders for N2O and O2. b. Pressure gauge—to know the amount of gas remaining. c. Pressure regulator—to regulate the pressure of gas used. d. Rotameter—to know the flow of gas. e Vapouriser.

When giving mouth-to-mouth resuscitation, the important thing to remember is to remove your denture first. —WU McClenahan

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Fig. 30.1: Different sized airways have different colours. Fig. 30.4: Direct laryngoscope with endotracheal tube and tongue depressor. Note: • Pin index code: It is safety mechanism to fix gas cylinder onto the Boyle’s machine. Different gases have different pin index codes, so that interchanging of cylinders does not take place. • Pin index code for N2O is 3, 5. • Pin index code for O2 is 2, 5. • Pin index code for air is 1, 5.

Fig. 30.2: Different sized masks used during anaesthesia.

2. Endotracheal tube: These are tubes inserted into the trachea and is used to conduct gases and vapours to and from the lungs. Depending on the diameter, it is available in various sizes. It has a cuff at one end which, when inflated stabilises the tube in position and also prevents regurgitation. Non-cuffed tubes are also available. The other end near the mouth is connected to the breathing circuit through which anaesthetic gases are delivered. The tube is inserted using a direct laryngoscope. The proper placement in the airway is confirmed by auscultating for the breath sounds over the chest when the gases are delivered. Complications ™™ ™™ ™™

Postoperative sore throat Hoarseness after intubation Upper airway oedema

3. Magill’s forceps. 4. Mouth gag.

Fig. 30.5: Magill’s forceps. Fig. 30.3: Boyle’s apparatus used for anaesthesia.

5. Laryngoscope. 6. Connectors.

Anaesthesia 7. Laryngeal mask airway (LMA):  Laryngeal mask consists of a wide bore tube whose proximal end connects to breathing circuit and distal end is attached to an elliptical cuff which can be inflated.  These come in various sizes for various age groups. It is made up of silicone rubber.  The deflated cuff is lubricated and inserted into the hypopharynx, so that once inflated, the cuff forms a low pressure seal around the entrance into the larynx. Advantages ™™ ™™ ™™ ™™

Does not require laryngoscope for insertion Does not cause irritation of airway Less incidence of laryngospasm In case of inability to intubate can save the life of the patient

Contraindications ™™ ™™ ™™

Pharyngeal pathology Full stomach as it can cause aspiration Bronchospasm

Components of general anaesthesia ™™ ™™ ™™ ™™

Premedication Induction Maintenance Recovery

POSTOPERATIVE CARE Immediate postoperative period is important and critical, because patient may not be fully conscious. Patient should be kept in recovery room until he/she recovers from anaesthesia. 1. Care of respiratory system: Adequate breathing is important, otherwise hypoxia sets in, which gradually leads to cardiac arrest. Respiratory problems may be: ™™ ™™ ™™ ™™ ™™ ™™

Laryngeal spasm Falling of tongue backwards blocking the airway Aspiration Bronchospasm ARDS Respiratory failure

  Oxygen supplement through mask, observa­tion, proper positioning are the treatment. 2. Hypercarbia. 3. Circulatory problems:

Premedication It is given one hour before surgery: xx For sedation and relief of anxiety. Pethidine 50 mg/ mor­phine 10 mg/diazepam 10 mg, midazolam 1–2.5 mg. xx To suppress vagal activity. Atropine 0.6 mg IM. xx To reduce vomiting. Promethazine (phenargan) 12.5 mg. Induction: Patient is preoxygenated with 100% oxygen for 3 minutes then induced with IV thiopentone, given 4–5 mg/kg. Patient loses consciousness. Induction is maintained by 67% nitrous oxide and 33% oxygen. Scoline is given IV to relax muscles so as to facilitate endotracheal intubation. Once intubated, ventilation can be either controlled using muscle relaxants or spontaneous using a volatile anaesthetic agent. Reversal is done using neostigmine and atropine or glycopyrrolate.

COMPLICATIONS OF GENERAL ANAESTHESIA xx xx xx xx xx xx xx xx

xx Pneumothorax. xx Anaphylaxis. xx Malignant hyperthermia: It is an inherited myopathic disorder occurs under anaesthesia due to drugs like halothane, scoline. There is marked increase in metabolic rate, with rise of temperature. There is high levels of CPK enzyme. Condition will cause metabolic acidosis and hyperkalaemia. It has got high mortality. Treatment is IV dantrolene, cooling, oxygen and cold IV fluids. xx Hypothermia.

Intra-arterial injection of the drug. Myocardial depression and cardiac arrest. Hypertension. Laryngeal and bronchial spasm. Cardiac arrhythmias. Respiratory failure. ARDS. Mendelson’s syndrome: It is due to regurgitation of the acid from the stomach causing aspiration of acid leading into bronchospasm, pulmonary oedema and circulatory failure. This is treated with oxygen, suction, hydrocortisone, aminophylline, antibiotics, Ryle’s tube aspiration and ventilator support. xx Hypoxia.

™™ ™™ ™™ ™™

Hypotension Arrhythmias Hypertension Cardiac arrest

4. GIT: ™™ ™™ ™™

Vomiting Regurgitation Mendelson’s syndrome

5. Renal problems: Oliguria, i.e urine output is less than 30 ml/hour. It may be due hypovolaemia, hypo­tension, acidosis, sepsis, transfusion reaction, toxins.   The ratio of urine/plasma osmolality of 2:1 signifies pre-renal failure. Ratio of 1.7:1 indicates renal failure.   Blood urea and serum creatinine is done at regular intervals.   Fluid and electrolyte imbalance, if any is corrected.   100 ml 20 % mannitol or frusemide 40–80 mg are often required. 6. Other problems: Restlessness, shivering, pain.

MONITORING THE POSTOPERATIVE PATIENT xx xx xx xx xx xx xx

Pulse, temperature, BP chart. Breathing type. Level of consciousness. Urine output. Oxygen saturation and heart rate using pulse oximeter. Checking and encouraging limb movements. Skin colour, tongue colour for adequacy of oxyge­nation.

The future belongs to those who believe in the beauty of their dreams.

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Tongue for hydration. Cardiac monitor. Blood gas analysis in case of patient on ventilator. Serum electrolytes assessment.

REGIONAL ANAESTHESIA Carl Koller, an ophthalmologist introduced cocaine as local anaesthetic in ophthalmic practice. Mode of action: It causes temporary conduction block of the nerve, thus preventing the propagation of nerve impulse. Advantages of local anaesthetic agent: xx Technically simpler. xx General anaesthesia is avoided. xx Consciousness is retained. xx Patient can have food earlier after surgery. Drugs used: xx Cocaine, procaine, cinchocaine—amino esters. xx Lignocaine, prilocaine, bupivacaine, ropivacaine—amino amides. Lignocaine/Lidocaine/Xylocaine: It is the com­monest local anaesthetic agent used. It is available as 0.25–5% concentrations. It is metabolised in the liver and excreted in the kidney as xylidines. It is also an antiarrhythmic drug and so commonly used in cardiology and cardiac surgery. Side effects: Giddiness, headache, postural hypo­tension, tinnitus, circumoral anaesthesia. Dose: 4 mg/kg effect lasts for 90 minutes. Uses xx Topical: 4%. xx Infiltration block: 0.25%. xx Field block: 0.5%. xx Nerve block: 1.0 %. xx Epidural: 1.5, 2.0%. xx Spinal: 5%. It can be used with or without adrenaline. Xylocaine with adrenaline has got longer duration of action. It creates relatively bloodless field. But it should not be used in places where end arteries are present like glans penis, ear lobule, tip of the nose, lip, fingers and toes. Bupivacaine (Marcaine): It has got prolonged action. It is a vasodilator also. xx Dose: 3 mg/kg. xx Epidural block: 0.5% xx Spinal: 0.5% 3 ml.

TOPICAL ANAESTHESIA xx It is used for minor surgeries of eye, laryngoscopy, bronchoscopy, cystoscopy, gastroscopy. xx It is available as instillation, spray, viscous, ointment, gel, EMLA (Eutectic mixture of local anaesthetic).

INFILTRATION BLOCK Direct injection of local anaesthetic under the skin for small procedures.

FIELD BLOCK It is achieved by blocking the entire field of excision where lesion is located.

NERVE BLOCK xx Block of inferior dental nerve and lingual nerves in the region of the mental foramen for extraction of teeth. xx Finger block of digital nerves. Here plain xylocaine is used (without adrenaline). xx Intercostal block. xx Ankle block. xx Median and ulnar nerve block. xx Brachial plexus block (Winnie’s block). It can be given through:  Interscalene.  Axillary.  Supraclavicular approaches. Supraclavicular approach is commonly used. 1 cm above the midpoint of the clavicle, needle is passed downwards, backwards and medially towards first rib. Once needle hits the first rib, 15–20 ml of 1.5% xylocaine is injected (with walking or stepping over the first rib). Complications are pneumothorax and injury to the great vessels. Other blocks: xx Cervical plexus block. xx Sciatic nerve block. xx Femoral nerve block.

INTRAVENOUS REGIONAL ANAESTHESIA (BIER’S BLOCK) Limb is exsanguinated and occluded with tourniquet. Pressure in the tourniquet must be 30 mmHg more than the systolic pressure of the patient. Needle is placed in the selected vein. 40 ml of 0.5% xylocaine for upper limb and 80 ml of 0.25% of xylocaine for lower limb is injected into the vein. Xylocaine with adrenaline should not be used. It gives very good analgesia for 2 hours. Side effects: Sudden release of drug into the circulation can cause hypotension, convulsions and often death. Bupivacaine should not be used.

Indications For upper and lower limb surgeries, it can be used without G/A or S/A.

SPINAL ANAESTHESIA It is the injection of local anaesthetic into the subara­chnoid space causing loss of sympathetic tone, sensation and motor function. The sympathetic block is 3 segments higher than sensory block, motor block is 3 segments lower than sensory block. Position: Lateral decubitus position with head, hips and knees being fully flexed so as to open the inter-laminar spaces. Highest point of iliac crest corresponds to 4th lumbar vertebra. Drugs used: xx Lignocaine 5% in 6% dextrose, 2 ml. xx Bupivacaine 0.5% in 5% dextrose, 3 ml. xx Cinchocaine 0.5% in 6% dextrose, 2 ml. Technique: 24–26 gauge needle with stillette is used. Needle is passed through the interspinous space and ligamentum flavum to reach the subarachnoid space to get clear fluid (0.5 ml/sec). Needle is rotated 360 degrees and drug is injected slowly. Patient is repositioned to supine. Drug takes 15 minutes to act.

Anaesthesia Types 1. 2. 3. 4. 5.

xx It is spinal anaesthesia using xylocaine or bupi­vacaine given in sitting position.

Caudal (up to L5) Low spinal (up to L1) Mid-spinal (up to T10) High spinal (up to T6) Unilateral spinal

EPIDURAL ANAESTHESIA

Advantages ™™ ™™ ™™ ™™

Economical Hypotension reduces the bleeding Adequate relaxation is achieved Respiratory complications are less

xx It is a potential space between dura anteriorly and ligamentum flavum posteriorly which has got negative pressure inside. It extends from foramen magnum to sacral hiatus. xx Touhy needle is used for epidural anaesthesia. Once the needle is in the space there will be sudden indrawing of air or saline drop. xx An epidural catheter is placed in the space and fixed. 2% xylocaine with adrenaline or 0.5% bupivacaine is injected into the space to achieve anaesthesia up to the desired level.

Advantages xx It can be used for continuous repeated prolonged anaesthesia. xx It can be used for postoperative analgesia. xx It can be kept for several days.

Fig. 30.6: Spinal anaesthesia being given. Note the position of the patient.

Disadvantages and Complications xx xx xx xx xx

CSF leak and aseptic inflammation of meninges causing headache. Meningism. Infection. Paraplegia. It is very rare. Occasionally, it can become total spinal which requires intubation and ventilator support. Contraindications

™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Cardiac patient Allergy Increased intracranial pressure. It may precipitate coning Sepsis Spinal tumours Back pain and spinal diseases Neurological conditions like syringomyelia Kyphosis, scoliosis

Fig. 30.7: Epidural anaesthesia with epidural catheter placed.

CAUDAL ANAESTHESIA Caudal space is the sacral component of epidural space and access is through the sacral hiatus.

Indications ™™ ™™ ™™

Haemorrhoidal surgery Circumcision Small procedures in the perineum like cystoscopy

Procedure It is given in lateral position. Needle is inserted through the sacral hiatus to enter the caudal epidural space. Drug is then injected into the space.

Complications Trauma to anal canal Intravascular injection ™™ Failure of caudal block ™™

SADDLE BLOCK

™™

xx It is used for surgeries in perineal and anorectal region.

Greater the obstacle more the glory in overcoming it.

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Advanced Imaging Methods

What would it be like in a radiologist’s shoes? To spend most of my day dealing with images of people: plain black-and-white X-ray images, or speckled images caused by sound waves bouncing off organs, or images caused by dyes outlining arteries and veins, or contrast medium filling loops of bowel, or images reconstructed by computers into cross sections of the body—all without speaking to a patient. —Abraham Verghese, 1994

CHAPTER OUTLINE ™™ Ultrasound ™™ Doppler

™™ CT Scan ™™ Magnetic Resonance Imaging

ULTRASOUND Ultrasound contains waves with a frequency of more than 20,000 cycles/second which the human ears cannot hear. In medical sonography, frequencies used are commonly 2–10 MHz. The transducer or the probe works as both transmitter of sound waves and receiver of echoes. The piezoelectric crystal is the producer of ultrasound waves. Received signals from the patient are fed into the computer which forms the image. There are three types of ultrasound image display. 1. A-mode: Only one dimensional static display as spikes are obtained. It is used only in eye scan. 2. B-mode: Two dimensional real-time images in the form of grains. It is most widely used type. Using this mode Transverse, Longitudinal or Oblique sections can be taken. 3. M-mode: Here images are recorded as dots. It is mainly used in moving parts like echocar­diography. M-mode is also called as TM mode, i.e. Time Motion Mode.

Uses xx Used in all abdominal and pelvic conditions, often in thoracic conditions. xx Ultrasound of thyroid is very useful method to differentiate between solid and cystic lesions. xx Ultrasound is used in testicular tumours, epidi­dymo­­orchitis, trauma to testis, erectile dysfunction, etc.

™™ Radionuclide Imaging ™™ Positron-emission Tomography Scan

xx Ultrasound breast is used to differentiate solid from cystic tumours. xx Soft tissue and musculoskeletal ultrasound. xx Ocular ultrasound is ideal method to image eye and intraocular structures. Advantages ™™ ™™ ™™ ™™ ™™ ™™ ™™

No radiation Noninvasive Effective with efficiency Painless Low cost Available even as portable machines Stones are well-visualised with acoustic shadow

Disadvantages Interpretation can be inadequate ™™ Bowel shadow may prevent proper visualisation ™™ In obese patient image will be inadequate ™™ Interpretation is based on echogenicity either hyperechogenic or hypoechogenic ™™

Advanced ultrasound techniques Endosonography (EUS) is used in visualisation of walls of oesophagus or stomach through gastro­scopy ™™ Transvaginal ultrasound ™™ Transrectal ultrasound to see prostate ™™ Doppler ultrasound to study arterial and venous diseases ™™

Advanced Imaging Methods

A

Fig. 31.1: US showing abdominal aortic aneurysm.

Fig. 31.2: US showing appendix—appendicitis.

Fig. 31.3: US showing liver mass.

Fig. 31.4: Cranial sonography is done to see intracranial problems through suture lines—usually done in infants and children.

B Figs 31.5A and B: US thyroid showing thyroid both lobes in one; solid and cystic components in another.

It’s your imagination that can take you anywhere.

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SRB's Manual of Surgery CT Scan Computerised tomography scan was invented by Godfrey Hounsfield in 1963. He was a physicist. He received Nobel prize (1972) for the same. The first CAT scan is in the London museum. Narrow X-ray beams are passed from rotating X-ray generator through the gantry where patient is placed. When X-rays pass through the tissues, some of the X-rays get absorbed and some pass through, depending on the tissue density. The different grades of absorption in different tissues are detected through sensitive detectors which are translated to a Grey scale image by a computer. Density of tissues is numbered as Hounsfield Number (HN) Water—Zero HN Air—Minus 1,000 Bone—Plus 1,000 The density of other tissues come in between air and bone with different HNs ™™ ™™ ™™ ™™

Fig. 31.6: US picture of a pelvic mass. Ultrasound as therapeutic use ™™ ™™

To guide aspiration of amoebic liver abscess, pericardial tap On table ultrasound can be done to assess the ope­ra­bility of tumour. (During laparotomy to assess the extent of tumour, lymph node status, etc.)

DOPPLER Doppler effect is a change in the perceived frequency of sound emitted by a moving source. So it measures blood flow. Spectral Doppler wave form and ultrasound image are combined in Duplex scanning.

Presently spiral CT scan has become popular. They are faster and in a single breath holding time, whole CT scan can be taken. Both plain and contrast CTs are done whenever required.

Contrast Agents xx Ionic: Water soluble iodide dyes like Sodium diatrizoate, Meglumine iothalamate (Conray, Urograffin, Angiograffin). They are cheaper but often toxic and cause anaphylaxis. xx Non-ionic are safer but expensive, like Iohexol (Omnipaque), Iopamiro. In abdominal CT, contrast agents can be given orally to delineate bowel properly.

Types 1. Continuous waves. 2. Pulsed waves. Doppler will provide both audio and video signals. Colour Doppler imaging displays flowing blood as red when direction of flow is towards the transducer. Image will be blue if flow is away from transducer.

Uses xx To study cardiovascular system. xx To study vascularity of tumours. xx To study blood flow and velocity in arterial diseases so as to assess stenosis (its extent, cause, etc.) like in atherosclerosis, TAO, cervical rib, aneurysm, A-V fistulas. xx To find out deep venous thrombosis (DVT), varicose veins, perforator incompetence. xx To study grade of varicocele in males.

Advantages xx It has replaced venogram and angiogram in many places as a diagnostic tool. xx It is reliable and non-invasive.

Fig. 31.7: CT scan picture showing liver secondaries.

Indications xx Trauma like head injury, chest injury, abdomen trauma. In trauma only plain CT scan is taken. xx Neoplasms: To see the exact location, size, vascularity, extent and operability. For example, brain, abdominal, retroperitoneal, thoracic and spinal tumours.

Advanced Imaging Methods xx Inflammatory conditions, in various sites. For example, psoas abscess, pseudocyst of pancreas.

Fig. 31.11: CT scan showing brain secondaries. Secondaries are the commonest malignant tumours of brain. Breast is the common site of primary. Advantages of CT scan

Fig. 31.8: CT scan showing ascites (gross). ™™ ™™ ™™ ™™ ™™

One to two mm sized sections are possible Amount of exposure to radiation is less More accurate, sensitive, and specific Small lesions are also detected CT-guided biopsies are done at present, safely

Fig. 31.9: CT scan abdomen showing right renal mass (RCC).

Fig. 31.12: CT picture showing astrocytoma. Disadvantages Interpretation by an experienced radiologist is important Artefacts can be present ™™ Cost factor and availability ™™ ™™

Findings Fig. 31.10: CT scan showing retroperitoneal tumour.

xx Extradural haematoma—Biconvex lesion. xx Subdural haematoma—Concavoconvex lesion.

Ultrasound and CT scan are conveyors of morphological information.

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SRB's Manual of Surgery xx Smooth margin in benign condition. xx Irregular margin in malignant condition. Advantages of spiral CT scan Reduced scan time. Useful in children and critically-ill patients Imaging in both arterial and venous phases is possible ™™ Improved lesion detection. Missing a lesion is uncommon ™™ Multiplanar and 3-dimensional analysis like CT angiography, complex joint imaging, facial bone imaging is possible ™™ ™™

High resolution CT (HRCT) is a CT technique used in chest scan where thin sections are taken to have better quality images.

Magnetic Resonance Imaging (MRI) Earlier, named as Nuclear magnetic imaging, the term is not used now. It can be Plain MRI or Contrast MRI. Contrast agent is Gadolinium, given intravenously.

Principle

Fig. 31.14: MRI showing AV malformation.

When patient is placed in an external high magnetic field, protons of hydrogen atoms rotate in phase with each other and gradually return to their original position releasing small amounts of energy which is detected by sensitive coils. Proton density and relaxation time are assessed by radiofrequency pulse and the computer generates a grey scale image from this data. T1 relaxation time is the time taken to return to original axis. T1 images are used to find out normal anatomical details. It has got high soft tissue discrimination. Here fluid (CSF) looks black. T2 relaxation time is the time taken by the proton to diphase. It is used to assess pathological processes. In T2 images fluid looks white. In proton density images fluid looks in between black and white.

Fig. 31.15: MRI picture, which shows extradural schwannoma.

Uses of MRI

Fig. 31.13: MRI showing spine tuberculosis. Note the lesion and vertebral collapse.

xx It is very useful in intracranial, spinal and muscu­loskeletal lesions including joint pathologies. xx It gives direct anatomical sections of the area, with lesions at a high resolution. xx MR angiogram is done without injecting IV contrast agents. xx Cardiac MRI is very useful. xx Breast MRI is used in multifocal recurrent cancers. xx Magnetic resonance cholangiopancreatography (MRCP) is a very useful noncontrast diagnostic tool which may replace diagnostic ERCP. xx MR spectroscopy is chemical analysis of elements in a tissue to differentiate between tumour, inflam­mation, and degeneration.

Advanced Imaging Methods Advantages xx Artefacts are not common. xx More sensitive and specific than CT scan. Contraindications Patients with prosthesis in the body, metallic foreign bodies, pacemakers, cochlear implants, cranial aneurysm clips should never undergo MRI

Precaution Before entering the MRI room, the patient and other personnel should remove all magnetically attractive materials

Tc99m  labelled DMSA (Dimercapto succinic acid) which is taken up by the renal cortical cells, is used in renal function tests Tc99m labelled DTPA (Diphenyl triamine penta acetic acid) measures GFR Tc99m labelled HMPAO (Hydroxy methyl pro­pylamine oxime) is used in Alzheimer’s disease and schizo­phrenia as it crosses the blood brain barrier

Other radionuclides used: xx Thallium 201 chloride for cardiac imaging. xx Gallium 67 nitrate to detect tumours and inflam­mation. xx I123 Advantages Safer Easier No side effects

Disadvantages xx xx xx xx xx xx

Availability and cost factor. It is time consuming. Patient compliance is poor. It is not feasible in patients suffering from Claustrophobia. It is not ideal in emergencies and critically-ill patients. It is not useful in lung pathology and subarachnoid haemorrhage.

RADIONUCLIDE IMAGING xx It represents function of an organ than morphology. Rays: xx α-particles are emitted by the natural radionuclides like radium, which are no longer used in medicine. xx β-particles are useful for therapy but not for diagnosis. xx γ-rays pass out of the body and so used for the diagnostic purpose. xx Mapping is done using sophisticated gamma camera.

xx It is commonest radionuclide used (99- is mass number; m- metastable.). xx It is administered IV. xx Pure γ-rays emitter. xx Short half-life. xx Widely used gamma ray detectors are specified to Tc99m.

Uses Tc

POSITRON-EMISSION TOMOGRAPHY (PET Scan) xx It is a non-invasive diagnostic method to assess the biochem-

ical and physiological status of a tissue. xx It is used in complimentary with CT scan and MRI. xx Two protons are used, they are positive electrons (positrons). xx Most clinically used positron emitting radionuc­lides is

fluoro-deoxyglucose (FDG), others are 82Rb,15O,13N. xx Detectors used are bismuth germanate (BGO) crystals or sodium iodide crystals. xx Principle of electronic collimation is used to produce images from the radiation emitted from positron emitting tracers.

Uses

Technetium 99m

99m

Disadvantages Availability Cost factor Not specific Fast half-life

labelled serum albumin is used to detect pulmonary emboli Tc99m labelled phosphate is used to image bone Tc99m labelled sulphur colloid is used to detect the functions of liver, spleen, bone marrow Tc99m labelled HIDA (Hippuric immuno diacetic acid) or PIPIDA is used to study the functions of hepatocytes and biliary tract

xx xx xx xx xx xx xx xx

To assess myocardial perfusion (82Rb) and viability (FDG) study. Epilepsy—To localise temporal lobe epilepsy (FDG). Cancer imaging—Lung cancer (detection and staging). Colorectal cancer. Melanoma. Head and neck cancer and breast cancer. Musculoskeletal tumours. Thyroid cancer (I131).

Advantage Very specific.

Disadvantage Very expensive and limited availability. Note:

•

Most of the U/S pictures, CT and MRI pictures in this book are from Balmatta Scan Centre, Mangalore, I am thankful to consultants Dr Raghavendra Bhat and Dr Ravichandra there.

Radioisotope studies are indicators of physiological processes

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Operative Surgery A. Asepsis and Sterilisation Bearing in mind that it is from the vitality of the atmospheric particles that all the mischief arises, it appears that all that is requisite is to dress the wound with some material capable of killing these septic germs, provided that any substance can be found reliable for this purpose, yet not too potent as a caustic. —Joseph Lister, 1867

CHAPTER OUTLINE ™™ Sterilisation ™™ Disinfection

™™ Antisepsis ™™ Asepsis

Sterilisation xx It is freeing an article by removing or killing all bacteria,

spores, fungi and viruses.

DISINFECTION xx It is killing of all bacteria, fungi and viruses but not spores.

ANTISEPSIS xx It is inhibition of growth of microorganisms.

ASEPSIS xx Asepsis means—organisms are prevented to access the

patient or individual.

DIFFERENT METHODS OF DISINFECTION/ STERILISATION Physical Agents xx Burning or incineration is used to disinfect contaminated articles like dressings.

™™ D  ifferent Methods of Disinfection/ Sterilisation

xx Hot-air oven: Here temperature used is 160 to 180 degree for one hour. xx Boiling: It kills bacteria but not spores and viruses. Temperature is between 90 to 99 degree. It is used to disinfect syringes, utensils. It is not useful for gloves, rubber materials. xx Autoclave: It is steam under pressure. Temperature attained is between 120–135 degree. It is sterilised for 20 minutes with 15 pounds/sq. inch pressure. It kills all organisms including spores. Completeness of sterilisation is confirmed by using specific gelatin protein which precipitates only in steam underpressure for 20 minutes. Green coloured strip turns to black if autoclave is complete (signaloc). Surgical gloves, linen, cotton, dressings, surgical instruments are sterilised by this method. Sharp and plastic instruments cannot be sterilised by this method. Bacillus thermophilus spores are used to assess the completeness of the sterilisation in mass scale. Double autoclaving is done for instruments of orthopaedic or ophthalmic surgeries. xx The Bowie-Dick method is also used to check the completeness of sterilisation. xx Radiation: Ionising type of radiation: Atomic gamma radiation is used as commercial method to sterilise suture materials, disposable materials in packets. It is viable, safe and cheaper. xx Non-ionizing radiation either infrared radiation or ultraviolet radiation is used to reduce the bacteria in air, water. Bacteria and

Asepsis and Sterilisation Materials

Method of sterilisation

• All theatre appliances

Autoclave

• Sharp instruments (scissors, needles, blades) plastic materials

Glutaraldehyde 2%, lysol

• Endoscopes

Glutaraldehyde

• Rubber equipments

Glutaraldehyde

• Syringes

Autoclave, hot air oven, gamma radiation

• Heart-lung machine

Ethylene oxide

• Disposable articles

Gamma radiation

• Operation theatre and rooms

Ideally by U-V radiation or by formaldehyde

• Sera and biological materials

Filtration

• Lab glassware

Hot-air oven

• Ward, sick room, furniture

Formaldehyde, iodophor spray, glutaraldehyde

• Clothes, bed sheets especially for burns patients

Autoclaving

• Soiled dressings, materials, animal carcasses

Incineration, lysol, iodophors

• Excreta

Lysol, iodophors

• Cleaning of skin before surgery

Iodophors 2%, savlon, spirit

• For cleaning infected wounds

Iodophors, acriflavine, savlon, H2O2

• To remove slough from the wounds

EUSOL, H2O2

• Before injection

Spirit is used to clean the skin

• Cleaning the ward

Phenol, cresol, lysol

• Hand wash

Chloroxylenol, savlon, spirit, iodophors

• Bladder wash

0.1% potassium permanganate solution (Condy‘slotion), solution of acetic acid and silver nitrate

• Water

Chlorination, potassium permanganate

• Fruits, vegetables

Potassium permanganate

virus are vulnerable to ultraviolet rays below 3000Å. Exposure to eyes and skin can cause burn injury.

Fig. 32.2: Signaloc used for confirmation of completion of proper sterilization.

Chemical Agents

Fig. 32.1: Autoclave machine for sterilisation.

xx Phenol: It is used as standard to compare the efficacy of other agents. xx Cresol is more powerful and nontoxic. 5% solution is used. xx Lysol is emulsified cresol with soap. 2% solution is effective. xx Chlorhexidine (hibitane) is useful antiseptic.

Treat the patient as a whole, “Half a sheep is mutton”.

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SRB's Manual of Surgery xx Hexachlorophane: It is not used in infants and children because it can get absorbed through intact skin in this age group causing severe neurotoxicity. xx Dettol (chloroxylenol) 5% solution is used. xx Cetrimide is cationic surfactant (cetavlon) 2% solution is used. xx Savlon is combination of cetrimide and hibitane. It is very commonly used antiseptic in operation theatres, wards.

Halogens xx Bleaching powder. xx Sodium hypochlorite. xx EUSOL: Edinburg University Solution contains sodium hypochlorite, boric acid and calcium hydroxide. Eusol bath is dipping the ulcer bearing part in dilute eusol solution for 30 minutes 2–3 times a day. xx Iodine xx Iodophors: These are antiseptics and also sporicidals. They are non-irritant and do not stain skin. Povidone-iodine is a good example which is commonly used. xx Alcohols: Ethyl or isopropyl alcohols are used. xx Formaldehyde: It is useful to disinfect the rooms like operation theatre. It is effective at a high temperature and humidity of 80–90%. It is commonly used to fumigate the room. 500 ml of formalin with one litre of water is boiled to get formaldehyde vapour. Formaldehyde vapour can be created by adding potassium permanganate to the same solution. Room is kept closed for 12 hours. xx Glutaraldehyde (cidex 2%): It is used to sterilise sharp instruments. Instrument should be dipped for 10 hours to achieve complete steri-

A

B

Figs 32.3A and B: Operation theatre mop rack to keep ‘used mops’ during surgery after use.

lisation. It is potent bactericide, sporicide, fungicide and viricide. xx Hydrogen peroxide (H2O2): It is used as topical oxygen therapy. Because of its effervescence and release of nascent oxygen it removes the tissue debris. It is used to clean wounds, cavities, ulcers, as mouth wash and as ear drops to clear earwax. xx Acriflavine and proflavine are orange-red coloured dyes used as antiseptics. It is effective against Gram-positive and few Gram-negative organisms. It retains its activity in pus and body fluids.

C. Suture Materials CHAPTER OUTLINE ™™ Classification I ™™ Classification II

™™ Classification III ™™ Classification IV

™™ Classification V

Features of ideal suture material ™™ ™™ ™™ ™™ ™™ ™™

Adequate tensile strength Good knot holding property Should be least reactive Easy handling property Should have less memory Should be easily available and cost effective

Uses of absorbable suture materials ™™ ™™ ™™ ™™

CLASSIFICATION I Absorbable Suture Materials xx Plain catgut is derived from submucosa of jejunum of sheep.  It is yellowish white in colour.  It is absorbed by inflammatory reaction and phagocytosis— absorption time is 7 days.  It is used for subcutaneous tissue, muscle, circumcision in children. xx Chromic catgut is catgut with chromic acid salt.  It is brown in colour.  Its absorption time is 21 days.  It is used for suturing muscle, fascia, external oblique aponeurosis, ligating pedicles, etc. xx Vicryl (Polyglactic acid):  It is synthetic absorbable suture material.  It gets absorbed in 90 days.  Absorption is by hydrolysis.  It is violet in colour (braided).  It is multifilament and braided.  It is very good suture material for bowel anasto­mosis, suturing muscles, closure of peri­toneum. xx Dexon (Polyglycolic acid) is synthetic absorbable suture material like vicryl. It is creamy yellow in colour (braided). xx Maxon (Polyglyconate) monofilament. xx PDS (Poly Dioxanone Suture material) is absorbable suture material. It is creamy in colour with properties like vicryl. It is costly but better suture material than vicryl. xx Monocryl (Polyglecaprone) monofilament. xx Biosyn (Glycomer) monofilament.

™™

In bowel anastomosis like gastrojejunostomy, resection and anastomosis. Vicryl is used In cholecystojejunostomy (CCJ), choledochojejuno­stomy (CDJ), pancreaticojejunostomy. Vicryl is used In suturing muscle, fascia, peritoneum, sub­cutaneous tissue, mucosa In ligating pedicles. 1-zero chromic catgut or vicryl are used, e.g. ligation of pedicles during hysterec­tomy In circumcision, usually 3-zero plain or chromic catgut are used

Absorbable suture materials should not be used for suturing tendon, nerves, vessels (vascular anastomosis).

Non-absorbable Suture Materials xx Silk is natural, multifilament, braided, non-absorbable suture material derived from cocoon of silkworm larva. It is black in colour. It is coated suture material to reduce capillary action. xx Polypropylene (Prolene) is synthetic, monofila­ment suture material. It is blue in colour. It has got high memory. (Memory of suture material is recoiling tendency after removal from the packet. Ideally suture material should have low memory.) (Prolene mesh used for hernioplasty is white in colour). xx Polyethylene (Ethylene) is synthetic monofilament nonabsorbable suture material. It is black in colour. xx Cotton is twisted multifilament natural nonabsor­bable suture material. It is white in colour. xx Linen is derived from bark of cotton tree. xx Steel, polyester, polyamide, nylon are other non­absorbable suture materials. Uses of non-absorbable suture materials In herniorrhaphy for repair For closure of abdomen after laparotomy For vascular anastomosis (6-zero), nerve suturing, tendon suturing ™™ For tension suturing in the abdomen ™™ For suturing the skin ™™ ™™ ™™

Suture Materials CLASSIFICATION II

Types of suturing

Natural xx xx xx xx

™™ ™™ ™™ ™™ ™™ ™™

Catgut. Silk. Cotton. Linen.

Continuous suturing Interrupted simple suturing Interrupted mattress suturing Subcuticular suturing Horizontal tension suturing Vertical tension suturing

Synthetic xx Vicryl, dexon, polydioxanone suture (PDS), maxon. xx Polypropylene, polyethylene, polyester, poly­amide.

CLASSIFICATION III xx Braided: Polyester, polyamide, vicryl, dexon, silk. xx Twisted: Cotton, linen.

CLASSIFICATION IV xx Monofilament: Polypropylene, polyethylene, PDS, catgut, steel. xx Multifilament: Polyester, polyamide, vicryl, dexon, silk, cotton.

CLASSIFICATION V xx Coated. xx Uncoated.

Numbering of Suture Material 2-Thick. For pedicle ligation. 10-zero. 1-zero. 2-zero. For bowel suturing. 3-zero. 4-zero. 5-zero. For vascular anastomosis. 6-zero. 7-zero. 8-zero. 9-zero. For ophthalmic surgery. Requires operating microscope.

Fig. 32.46: Types of suturing. Types of knots ™™ ™™ ™™

Reef knot Granny knot Surgeon’s knot

Fig. 32.45: Photo showing different types of suture materials (with pack). Fig. 32.47: Types of knots.

Sadness is a form of fatigue.

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D. Diathermy (Electrocautery) It is the method to control bleeding or to cut the tissues during surgery.

Types Based on type of current used: xx Unipolar cautery. xx Bipolar cautery. It is safer because its effect is seen only in between electrode points. Adjacent tissues will never get damaged. Based on type of action: xx Coagulation cautery which causes haemostasis by tissue coagulation. Here temperature is 100 degree (blue switch). xx Cutting cautery: Here temperature is 1,000 degree which disintegrate the tissues. It is not haemostatic (yellow switch). xx Blended current is combination of both coagulation and cutting.

Disadvantages xx xx xx xx

Infection. Cauterisation of normal tissues. Problem of explosion. Diathermy burn to the patient at the site where diathermy plate is kept. xx Burn injury or electrical shock to surgeon and assisting personnel.

Precautions xx Proper earthing. xx Avoid loose contact of electrodes. xx It should be kept off when not in use during procedure.

Differences between unipolar and bipolar cautery Unipolar cautery

Bipolar cautery

• C  an be used for both coagulation and cutting

• Only for coagulation

• C  onducting plate should be kept

• No need

• C  annot be used in patient with artificial valves

• Can be used

• S hould be careful about adjacent tissues

• A  djacent tissues will never get damaged

Uses xx For coagulation of bleeders during surgery to achieve haemostasis. xx To cut muscles, fascia, etc. xx It is essential for laparoscopic surgical procedures. Bipolar is commonly used. xx It is used to remove small cutaneous lesions, to control bleeding duodenal ulcer.

Fig. 32.48: Diathermy machine with plate, foot switch for use.

E. Operative Procedure CHAPTER OUTLINE ™™ ™™ ™™ ™™ ™™

Abdominal Incisions Vasectomy Circumcision Hydrocele Inguinal Hernia

™™ ™™ ™™ ™™ ™™

Appendicectomy Thyroidectomy Tracheostomy Cryosurgery Lasers in Surgery

™™ staplers in Surgery ™™ Nasojejunal Tube Feeding ™™ Gossypiboma

ABDOMINAL INCISIONS Principles xx xx xx xx

Incision should be long enough for a good exposure. Splitting the muscle is better than cutting, except rectus muscle. Avoid cutting nerves and vessels in the abdominal wall. Retract muscle, abdominal organs towards the neuro-vascular supply. xx Insert a drainage tube through a separate incision. xx Transverse incisions are better than vertical incisions. xx Close the wound layer by layer. Requirements ™™ ™™ ™™

Accessibility Extensibility Security

Factors affecting the strength of the scar ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Type of surgery (acute abdomen, surgery for malig­nancy, major surgery) Obesity Pregnancy Straining Cough Ascites Nutrition Diabetes Immunosuppression Type of incision

Complications of Abdominal Incision xx xx xx xx xx xx

Wound infection. Burst abdomen. Fistula formation. Wound pain. Incisional hernia. Adhesion and its complication.

Fig. 32.49: Different incisions in the abdomen.

Different abdominal incisions are: xx xx xx xx xx xx xx xx xx xx xx xx xx

Upper midline. Upper right paramedian. Upper left paramedian. Kocher’s incision (right subcostal). Left subcostal. Bucket handle. Upper horizontal. Thoracoabdominal. Subumbilical. Incision for lumbar sympathectomy. Lower midline. Lower right or left paramedian. Incisions for appendicectomy—McBurney’s, Rutherfold Morrison’s, Lanz, laparoscopic.

Surgery is an irreversible repair but often it can be irreversible damage also !!!

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SRB's Manual of Surgery xx Pfannenstiel incision. xx Lower horizontal.  Upper incisions are always better.  Horizontal incisions are better.  Paramedian is better than midline.

xx When there is hernia or hydrocele, vasectomy is done along with specific procedures for hernia or hydrocele. xx No scalpel vasectomy, using specialised instru­ments is becoming popular. Procedure does not require any suturing.

CIRCUMCISION

VASECTOMY

Indications

Indications xx Family planning (parents should have two healthy children,

consent should be obtained). xx After prostatectomy, vasectomy is done to prevent retro-

grade infection of testes.

Procedure

xx xx xx xx xx

Religious. Phimosis. Paraphimosis after doing initial dorsal slit. Balanitis and balanoposthitis (common in dia­betics). Early carcinoma of prepuce or glans penis—both diagnostic as well as therapeutic purpose. xx Certain sexually transmitted diseases, e.g. herpes infection.

Types

Procedure

xx Classical method – Scalpel technique. xx No scalpel technique (Shunqiang Li- China).

In children, it is done under General Anaesthesia (G/A). In adults, it is done under local anaesthesia. After cleaning and draping, LA (1% lignocaine (plain) is injected circumferentially near the root of the penis) is given (ring block). Dorsal skin is cut up to the corona and later circumferentially and ventrally. The

Classical method After cleaning and draping the scrotum, 2–5 ml of xylocaine plain 1 % is injected into root of the scrotum on lateral aspect. Skin, dartos are incised (1–2 cm vertical incision). Once spermatic fascia is incised cord structures are identified. Vas deferens is seen and felt as thickened whitish cord like structure. It is dissected using mosquito artery forceps. It is held using Babcock’s forceps as loop outside the wound. Vas is clamped in two different places with a gap in between using two artery forceps. A piece of the vas (5–10 mm) is excised. Cut ends are ligated using non-absorbable sutures like silk. Skin is closed with sutures. Procedure is repeated on the other side. Dressing is placed. Sutures removed after 7 days.

No Scalpel Technique Two special instruments are used here. An extracutaneous ring clamp and Chongquing’s sharpened curved mosquito clamp. After cleaning and draping, xylocaine 2% of 2–3 ml is injected under the skin of midline raphe proximal aspect. Vas deferens of one side is felt and pushed under the raphe. It is carefully held with extracutaneous ring clamp. Skin is incised using sharp tip of the curved mosquito clamp. Whitish cord like vas which is held with ring clamp is dissected → clamped → a small piece of 5 mm is cut. Cut ends are ligated using silk. Opposite vas is also similarly brought into the same wound by manipulation and clamped and ligated after cutting. Skin is not closed. It gets apposed automatically and heals on its own. Post-operatively antibiotics and analgesics are given. It is a single incision procedure also.

A

Advice To avoid sexual contact or to use contraception for 3 months. Complications ™™ ™™ ™™ ™™ ™™ ™™

Haematoma Haematocele Infection Pyocele Sperm granuloma Recanalisation occurs rarely but dangerous

B Figs 32.50A and B: No scalpel vasectomy instruments and technique.

Operative Procedure skin is cut with inner layer. Care is taken to see that optimum (less) skin is cut ventrally to prevent the occurrence of chordee. Frenular artery as well as dorsal vein is transfixed and ligated ventrally using chromic catgut (2-0 or 3-0). Small bleeders are also ligated. Skin is apposed to the cut edge of corona using interrupted chromic catgut sutures. Postoperatively, antibiotics and analgesics are given. Note:

Monopolar cautery should not be used during circumcision as penis may go for necrosis. Bipolar cautery can be used judiciously.

Complications xx Reactionary haemorrhage due to slipping of ligature from frenular artery and dorsal vein. xx Infection. xx Stricture urethra near the external meatus in children. xx Chordee due to removal of excess skin on the ventral aspect. xx Rarely priapism can occur.

xx After evacuation, the sac with the testis is placed in a newly created pocket between the fascial layers of the scrotum (Sharma and Jhawer’s technique). xx Aspiration must be avoided as much as possible as it is only a temporary measure (recurrence occurs very early) and chances of haematocele, infection are higher. xx A drain is placed near the root of the scrotum on the lateral aspect because, it becomes the most dependent portion once scrotal support is given. Scrotal support is given to reduce the scrotal oedema. xx Wound is closed in layers. xx Drain is removed in 48 hours. Surgeries for hydrocele ™™ ™™ ™™ ™™ ™™

Subtotal excision of the sac Jabouley’s operation Evacuation and eversion Lord’s plication Sharma and Jhawer’s technique

™™ ™™ ™™ ™™ ™™

Reactionary haemorrhage Infection Pyocele Sinus formation Recurrent hydrocele

HYDROCELE Types of Surgery xx xx xx xx xx

Subtotal excision. Partial excision and eversion (Jabouley’s operation). Evacuation and eversion. Lord’s plication. Sharma and Jhawers technique.

Procedure xx Under G/A or spinal or L/A, after cleaning and draping, vertical incision of about 6–8 cm in length is made over the scrotum, anteriorly 1 cm lateral to the median raphe. xx Skin, dartos, external spermatic fascia, internal spermatic fascia are incised.   Bluish hydrocele sac is identified, i.e. parietal layer of the tunica vaginalis of testis.   Fluid is evacuated using trocar and cannula. Sac is opened. xx If the sac is small, thin and contains clear fluid, either Lord’s plication, i.e. tunica is bunched into a “ruff” by placing series of multiple interrupted chromic catgut sutures so as to make the sac form a fibrous tissue which is relatively avasular and so haema­toma will not occur, or evacuation and eversion of the sac behind the testis (after eversion, everted sac is sutured with chromic catgut by continuous sutures) is done. xx If the sac is thick, in large hydrocele and chylocele, subtotal excision of the sac is done (as tunica vaginalis is reflected on to the cord structures and epi­didymis posteriorly, total excision of the sac leads to orchidectomy with division of cord). xx Often the sac is excised partially and eversion is done, which is called as Jabouley’s operation.

Fig. 32.51: Trocar and cannula used for tapping hydrocele. It prevents spillage of fluid.

Complications of surgery

Conditions where orchidectomy is done in hydrocele ™™ ™™

Pyocele with testicular destruction Clotted haematocele with testicular des­truction

INGUINAL HERNIA Surgery is the treatment of choice for inguinal hernia. In infants, whether it is hernia or hydrocele, only herniotomy is done through inguinal approach (Michaelis plank operation). In adults: It includes herniotomy, i.e. excision of hernial sac and herniorrhaphy (strengthening of the posterior wall of inguinal canal either by repair or mesh).

1. Herniotomy Anaesthesia: Spinal or General Procedure: After cleaning and draping, skin is incised 1.25 cm above and parallel to the medial two-third of inguinal ligament. Two layers of superficial fascia (outer Camper’s fascia and inner Scarpa’s fascia) are incised. External oblique aponeurosis is incised. Upper leaf is reflected above and lower leaf is reflected downwards to visualise and expose the inguinal ligament. Ilioinguinal nerve is safeguarded. Cremasteric muscle is opened. Cord structures are dissected. Sac which is anterior and lateral to cord is identified and is pearly white in colour. Dissection is usually started from the fundus and extended towards the neck which is identified by extraperitoneal fat. The neck is narrow and is lateral to inferior epigastric artery. Sac is opened at the fundus. Finger is passed to release any adhesions. Sac is twisted so as to prevent the contents from coming back. It is transfixed using absorbable suture material (chromic catgut 2-0) and is excised distally.

A surgeon should have a heart of lion, eyes of a hawk and hands of a woman.—John Halle

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SRB's Manual of Surgery 2. Modified Bassini’s Herniorrhaphy Conjoined tendon and inguinal ligament are approxi­mated using interrupted nonabsorbable monofilament sutures [polypropylene (prolene, blue in colour)]; medial most stitch is taken from the periosteum of pubic tubercle (called as key or Bassini’s stitch); external oblique is closed and other layers are closed. Complications of herniorrhaphy Haemorrhage Haematoma Infection Haematocele Postherniorrhaphy hydrocele Hyperaesthesia over the medial side of inguinal canal due to injury to ilioinguinal nerve ™™ Recurrence ™™ Osteitis pubis ™™ ™™ ™™ ™™ ™™ ™™

Hernioplasty Prolene mesh is used for hernio­plasty (white in colour). Other materials which can be used are Dacron, tensor fascia lata, skin. Relation of sac to the cord ™™ ™™

Indirect inguinal hernia—anterolateral Direct inguinal hernia—posteromedial

APPENDICECTOMY Approaches: xx G r i d - i r o n i n c i s i o n ( M c B u r n e y ’s i n c i s i o n ) : I n c i s i o n is placed perpendicular to the right spino-umbilical line at the McBurney’s point, i.e. at the junction of lateral one-third and medial two-third of spino-umbilical line. xx Rutherford Morison muscle cutting incision (Cut upwards and laterally). xx Lanz crease incision centering at McBurney’s point-cosmetically better. xx Right lower paramedian incision—when in doubt or when there is diffuse peritonitis. xx Laparoscopic approach: Becoming popular. xx Fowler-Weir approach: Medial muscle cutting incision.

Procedure Under general anaesthesia, skin is incised. Two layers of superficial fascia are cut. External oblique aponeu­rosis is opened in the line of incision. Internal oblique and transverse muscles are split in the line of fibres. Peritoneum is opened in the line of incision. Caecum is identified by taeniae, and ileo-caecal junction. Omentum when adherent is separated. Appendix is held with Babcock’s forceps. Mesoappen­dix with appendicular artery is ligated. Using thread or silk, a purse-string suture is placed around the base of the appendix. Base of the appendix is crushed with artery forceps and transfixed using vicryl (absor­bable). Appendix is cut distal to the suture ligature and removed. Stump is cleaned with anti­septics. Purse-string suture is tightened so as to bury the stump. In difficult cases Retrograde appendicectomy can be done. In presence of pus or burst appendix, the peritoneal cavity is drained.

Postoperatively, IV fluids, antibiotics are given. Once bowel sounds are heard, oral diet is started.

Complications after Appendicectomy xx Paralytic ileus. xx Reactionary haemorrhage due to slipping of ligature of the appendicular artery. xx Residual abscess (pelvic, paracolic, local, sub­diaphragmatic). xx Pylephlebitis (Portal pyaemia). xx Adhesions, kinking and intestinal obstruction. xx Right inguinal hernia (direct) due to injury to ilioinguinal nerve. xx Wound sepsis. xx Faecal fistula.

THYROIDECTOMY Types xx Hemithyroidectomy: Along with removal of one lobe, entire isthmus is removed. It is done in benign diseases of only one lobe. xx Subtotal thyroidectomy: Commonly done in toxic thyroid either primary or secondary and also often for nontoxic multinodular goitre. Here about 8 grams or a tissue, size of pulp of the finger is retained at the lower pole, one or both sides and rest of the thyroid gland is removed. xx Partial thyroidectomy is removal of the gland in front of trachea after mobilisation. It is commonly done in nontoxic multinodular goitre. xx Near total thyroidectomy: Here both lobes, except the lower pole which is very close to recurrent laryngeal nerve and parathyroid is removed. It is done in case of papillary carcinoma of thyroid. xx Total thyroidectomy: Entire gland is removed. It is done in case of follicular carcinoma of thyroid, medullary carcinoma of thyroid.

Procedure Position: Under general anaesthesia patient is put in supine position, with neck hyperextended by placing a sand bag under shoulder—with table tilt of 15 degree head up to reduce venous congestion. Incision: Horizontal crease incision is done, two finger breadth above the sternal notch, extending from sterno­mastoid of one side to the other. Skin and platysma are incised—upper flap raised up to thyroid cartilage, lower flap up to sternocla­vicular joint. Deep fascia is opened vertically in the midline. Strap muscles are retracted or cut in between two Kocher’s forceps. Pretracheal fascia is opened to mobilise the thyroid. First, short stout middle thyroid vein is ligated, then superior thyroid pedicle is ligated close to the gland so as to avoid injury to external laryngeal nerve. Inferior thyroid artery is ligated away from the gland so as to avoid injury to recurrent laryngeal nerve. Mobilised gland is removed. Bed is sutured with catgut so as to prevent bleeding. Drain is placed. The wound is close in layers. Thyroid steal: Patient with thyrotoxicosis is taken to operation theatre daily for few days before doing surgery so as to reduce the anxiety of the patient.

Complications of Thyroidectomy xx Haemorrhage: May be due to slipping of ligatures, either of superior thyroid artery or other pedicles. It causes tachycardia,

Operative Procedure

xx

xx

xx

xx



xx xx xx xx

hypotension, breath­lessness and compression over the trachea which inturn may cause severe stridor, respiratory obstruction. As a first aid, immediate release of sutures including that of deep fascia has to be done and pressure over the trachea is released. Then patient is shifted to operation theatre and under general anaesthesia exploration is done and bleeders are ligated. Blood transfusion may be required. Respiratory obstruction: It may be due to haematoma (if it is so, the haematoma has to be evacuated), or due to laryngeal oedema. For laryngeal oedema, immediate emergency endotracheal intubation is done along with steroid injections. Often emergency tracheostomy may be required as a life-saving procedure. Recurrent laryngeal nerve palsy: It can be transient or permanent. Transient is 3% common. They usually recover in 3 weeks to 3 months. Often they require steroid supplement and speech therapy. Permanent paralysis is rare. Hypoparathyroidism is rare (0.5%). Mostly it is temporary due to vascular spasm of para­thyroid glands, occurs in 2nd–5th postoperative day. Presents with weakness, +ve Chvostek’s sign, carpopedal spasm, convulsions. Serum calcium estimation is done and then 10 ml of 10% calcium gluconate—is given IV 8th hourly. Later supple­mented by oral calcium 500 mg 8th hourly. After 3–6 weeks, patient is admitted, drug is stopped and serum calcium level is repeated. Thyrotoxic crisis (Thyroid storm): Occurs in a thyrotoxic patient inadequately prepared for thyroidectomy and rarely a thyrotoxic patient presents in a crisis following an unrelated operation or stress. They present in 12–24 hours with severe dehydration, circulatory collapse, hypotension, hyperpyrexia and often cardiac failure. Treatment is injection hydrocortisone, oral antithyroid drugs, tepid sponging of whole body, beta blocker injection, oral iodides, large amount of IV fluids for rehydration, digitoxin. Cardiac monitor, often ventilator support with close observation is necessary. It has got high rate of mortality with critical period of 72 hours. Correction of fluid and electrolyte imbalance and cardiac monitoring are the important aspects of management. Injury to external laryngeal nerve causes weakness of cricothyroid muscle leading to alteration in pitch of voice. Hypothyroidism: Revealed clinically after 6 months. Wound infection, stitch granuloma formation. Keloid formation.

xx Red rubber tracheostomy tube. xx Polyvinylchloride tracheostomy tube. Modern tracheostomy tubes are made of plastic. They are soft, least irritant and disposable. They have inflatable cuff which makes it easier to give assisted ventilation. Cuff should be deflated at regular intervals to prevent tracheal pressure necrosis. (For assisted ventilation endotracheal tube can be kept for 7 days. Beyond that period patient needs tracheostomy for further ventilation.) Indications for tracheostomy In head, neck and facial injuries Tetanus Tracheomalacia after thyroidectomy Laryngeal oedema/spasm/surgeries Major head and neck surgeries like commando’s operation, block dissection, etc. ™™ ICU ventilation after 7 days ™™ ™™ ™™ ™™ ™™

Fig. 32.52: Tracheostomy tube with inflation part and syringe (Inflated with air)

TRACHEOSTOMY Types xx Emergency tracheostomy. xx Elective tracheostomy.

Tracheostomy Tube xx Fuller’s bivalved tracheostomy tube: It has got outer tube and inner tube. Outer tube is biflanged and so insertion is easier. Inner tube is longer with an opening on its posterior aspect. Inner tube can be removed and re-inserted easily whenever required. xx Jackson’s tracheostomy tube: It has got outer tube, inner tube and an obturator.

Fig. 32.53: Figure showing the position of tracheostomy tube.

Surgery is not just cutting, but it is an art; it is not only an art but also a merciful art.

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SRB's Manual of Surgery Complications of tracheostomy ™™ ™™ ™™ ™™ ™™ ™™ ™™

Tracheal stenosis Bleeding Aspiration Pneumothorax Surgical emphysema in the neck Mediastinal emphysema Tracheostomy dependency

CRYOSURGERY Fig. 32.54: Vertical midline or transverse incisions are used for tracheostomy. Vertical midline extends from cricoid cartilage to sternal notch. It is used both in emergency and elective tracheostomy and commonly used incision. It gives rapid access with less dissection but leads into poor scar. Transverse incision can be used in elective tracheostomy. It is placed two finger breadths above the sternal notch with a length of about 5 cm transversely. It has got a better cosmetic scar.

Technique of Tracheostomy Neck of the patient is hyperextended by placing sand bags under the shoulder. Vertical (midline) or horizontal incision is made. Deep fascia is opened. Strap muscles are retracted laterally. Isthmus is divided or retracted below. 2nd and 3rd tracheal rings are opened and circular opening is made. Tracheo­stomy tube is placed. It is tied around the neck. Note:

Endotracheal tube can be kept in situ only for 7 days.

xx It is the destruction of tissues by controlled cooling. xx System contains an automatic defrosting device with a cryoprobe. Gases used are: xx xx xx xx

Nitrous oxide—minus 98°C temperature. CO2—minus 60°C. Liquid N2—minus 180°C. Freon—minus 190°C. Commonly nitrous oxide is used as it is easily available, cheaper and achieves optimum tempe­rature required for different procedures.

Mode of Action xx It produces intracellular crystallisation, dehy­dration and denaturation of proteins and cell death. xx It causes the obliteration of microcirculation and so cell death.

Indications xx To remove warts and lesions in the skin. xx Cryotherapy for piles. xx For chronic cervicitis.

Advantages xx Relatively bloodless and painless. xx Adequate control of extent and depth in freezing. xx Equally effective.

Disadvantages xx Infection. xx Discharge from the site.

LASERS IN SURGERY Fig. 32.55: Advanced secondaries in neck with tracheostomy tube to control respiratory stridor.

Tracheostomy Care xx Regular suctioning of the tube. xx Cleaning of tracheostomy tube. xx Humidification of the inspired air.

It is Light Amplification Stimulated Emission of Radiation. Electrons in high energy status leave towards excited level from ground state and eventually return to ground state releasing its energy as photon particle of light. This laser light has got one specific wavelength and is monochromatic. Laser light is unidirectional with one specific colour and is coherent with a tight, strong and concentrated beam. Power density and laser energy are two important parameters. Power density is the measure in unit beam area; it is Watts/cm2. Laser energy is power delivered/second.

Operative Procedure Molecules are placed in a compact area and power is passed through this so as to activate the molecules. Molecules get activated at different periods and move in different directions, which they hit each other releasing energy; this energy is allowed to act through optical system to area wherever required. Depending on the molecules used laser is being named like Nd YAG (Neo dymium Ytrium Aluminum Garnet Laser), CO2, Neon, Holmium, Erbium, etc.

Types Based on Generation of Power 1. Continuous wave laser: Generates continuous power for longer duration; it is commonly used in medical field. 2. Pulsed laser: Generates high power for short intervals in pulses. Nd YAG pulsed laser is used in ophthalmology; diode pulsed laser is used in varicose veins.

Types, Based on Material Used xx Solid state laser: Nd YAG laser (infrared light of 1064 wavelength). Nd YAG laser is invisible which is absorbed easily by tissues; requires a visible guiding beam like red helium or neon beam; it penetrates tissues deeply for 5 mm; easily and effectively vaporizes tissues; it is used in endoscopic procedures, LITT (light induced thermal therapy). xx Gas lasers: helium, neon, CO2 lasers are gas lasers. CO2 laser has got wavelength of 10.6 mm; it penetrates tissues very poorly; it is absorbed rapidly by water in the tissues; it is invisible and needs helium or neon beam; it is used I surface lesions of skin and for haemorrhoids. xx Dye lasers: Rhodamine organic dye laser. xx Semiconductor lasers: They are diode lasers use low power. xx Excited dimer (Excimer) lasers: Argon, Krypton, Xenon which are mixed with chlorine or fluorine creating dimer. Argon laser has got two wavelengths 514 (green) and 488 (blue); it is absorbed by haemoglobin red pigment; tissue vaporization is poor; has got limited penetration and so useful for surface lasers in skin, eye; it is useful in photodynamic therapy also.

xx In gynaecology—in endometrial ablation, in removing precancerous lesion of cervix, adhesiolysis, fimbrioplasty.

Advantages It is bloodless, small incision, fast recovery.

Complications Damage to normal tissues, adjacent bowel, vessels. Problem to operating beam—injury to skin, eyes causing corneal or retinal damage, cataract formation.

Precautions xx All operating team staff should wear safety goggles. xx Drapes should be wet; dry materials should be used. xx Instruments ideally should be non-reflective (coated to avoid reflection). xx Audible signals should be used. xx Emergency shutter devices should be present.

STAPLERS IN SURGERY Staplers are used for apposition of tissues. Used in skin, bowel, lungs, etc.

Types xx Cutaneous staplers give clean apposition. It is faster and technically easier. Problem is removal requires specific instrument and costlier than sutures. xx Linear staplers are used to close the bowel either completely or partially. xx Circular staplers also called as EEA stapler—End to End Anastomosis. It is commonly used for colorectal anastomosis in anterior resection for carcinoma rectum, oesophagogastric anastomosis after oesophagogastric resection in case of carcinoma at O-G junction.

Applications xx Focused heat beam of laser light is used to coagulate, excise, vaporize the tissues. xx It is used to cut tissues, cauterize blood vessels, photocoagulation. xx Photodynamic or photoradiation therapy using dye or diode laser after injecting photosensitizer photofrin intravenously.

Uses in Surgery xx In gastroenterology—piles; debulking luminal malignancies like oesophagus, rectum; arrest gastrointestinal bleeding; to remove small tumour or angiodysplasias. xx In urology—to remove superficial low grade bladder tumours. xx In eye—in retinopathy, laser photocoagulation, retinal detachment, in glaucoma. Lasik surgery is done for myopia using microkeratome to reshape the cornea. It is laser- induced keratoplasty. xx In ENT – removal of small mucosal lesions xx In skin – argon or CO2 lasers are used. Used in removal of tattoos (Ruby laser, pulsed); excision of small lesions, haemangiomas. xx Vascular – Laser angioplasty can be done.

Fig. 32.56: Circular stapler for colorectal anastomosis.

Parts: Stapler gun, and cartridge with two rows of stapler pins for apposition. Loaded cartridge is detachable. Cut ends of bowel are placed over gun and cartridge. Once gun is shot, cartridge moves to the gun and creates anastomosis.

Remember, the most important person in an operation theatre is the patient. —Berkehy George Andrew Moynihan

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SRB's Manual of Surgery xx GIA stapler (Gastrointestinal anastomosis stapler) for side to side anastomosis, like small bowel or ileocolic anastomosis. xx Stapler for lung apposition. xx Endostaplers: These are used during laparoscopic surgeries. It is commonly used for bowel anasto­mosis. Endovascular staplers are used to ligate vascular pedicles like renal pedicles during laparoscopic nephrectomy. xx Stapled haemorrhoidopexy—costly. Disposable staplers are available but are costly. Advantages: Technically easier and faster. Disadvantages: Cost factor, availability. Problems with staplers: xx It is not completely haemostatic and so bleeding can occur. xx Leak from anastomosis, improper apposition. xx Intestinal obstruction.

Nasojejunal Tube Feeding xx It is one of the methods of enteral nutrition. It is commonly used in acute pancreatitis. It is also useful in other enteral nutrition needs.

Fig. 32.57: X-ray showing nasojejunal tube for enteral nutrition purpose. It is useful and effective method of enteral nutrition. Its passage needs expertise, C-ARM guidance. It can be kept for long time for 3 months. Its position often to be confirmed by X-ray.

xx It is passed under C-ARM guidance per nasally. It is passed up to the first loop of the jejunum across the duodenal C loop. It should be fixed properly to the nostril. Its position should be confirmed by X-ray. One should take care not to displace the tube. xx Advantages are—it is safer, easier and can be kept for 3 months. Complications of long-term TPN are not there. xx Disadvantages—irritation by tube, displacement, aspiration.

Gossypiboma (Gossypiboma—cotton based in latin) xx By definition, it is the presence of cotton based foreign body that is in place of concealment following surgery. xx Forgotten foreign bodies (mop, gauze, etc.) intraoperatively especially in abdominal cavity (can occur in any cavities (thorax, pelvis) cause adhesions, provoke sepsis, often get encapsulated. xx It may cause an inflammatory mass, bowel erosion/perforation/ peritonitis, intra-abdominal abscess, septicaemia, fistula formation. xx Presentations may be as—asymptomatic, pseudotumour, abscess, septicaemia, fistula. xx Often foreign body erodes and enters the bowel lumen and with peristalsis reaches ileocaecal valve causing intestinal obstruction. There are incidences patient has passed the foreign body like mop per anally few months after surgery (in 6% gossypiboma). xx Ultrasound, CT scan and MRI identifies the foreign body (gossypiboma). Plain x-ray is of less value. xx Incidende of gossypiboma is 1 in 3,000 surgeries. Migration commonly occurs into intestine either small or large but can occur into urinary bladder or stomach. xx 70% of retained foreign bodies are sponges/mops; 30% are instruments. xx Commonest site is abdominal cavity 55%, vagina (20%), thorax (10%) and rest on other cavities. xx Commonly gossypiboma present 3–12 weeks; rarely it can present as later as 5–7 years. xx It is more commonly observed in emergency surgery, trauma, and surgery for malignancies. xx Treatment: Surgical exploration and extirpation of the foreign body, antibiotics. xx Legal problem: Gossypiboma amounts for criminal negligence. Surgeon or team or hospital can be sewed for negligence either in consumer court or criminal court.

F. Laparoscopic Surgery CHAPTER OUTLINE ™™ A  dvantages of Laparoscopic Surgery ™™ Laparoscopic Cholecystectomy

™™ Laparoscopic Appendicectomy ™™ Advanced Laparoscopic Surgeries ™™ Diagnostic Laparoscopy

™™ Retroperitoneoscopy ™™ Natural Orifice Transluminal Endoscopic Surgery

History First laparoscopic cholecystectomy was done by Muhe of Germany in 1985 and by Mouret in Lyon in 1987. McKeran and Saye performed the first laparoscopic cholecystectomy in USA in 1988. First laparoscopic appendicectomy was done by Semm as prophylaxis. First laparoscopic appendicectomy for acute appendicitis was done by Schreiber in 1987. Semm changed 75% open gynaecological surgeries into laparoscopic surgeries. Professor TE Udwadia, Mumbai did first laparoscopic cholecystectomy in India.

Advantages of Laparoscopic Surgery xx Relatively less painful compared to open surgery. Trauma of access is very less. xx Shorter hospital stay and early return to work. xx Faster postoperative recovery. xx Better visualisation of the anatomy, i.e. better approach for dissection and visualisation of other parts of abdomen for any other pathology. xx Instrumental access to different abdominal loca­tions is many times better compared to open method. xx Minimal scar on the abdomen.

Instruments Used xx Zero degree laparoscope is commonly used. Side viewing scopes are also used to have better visualisation 30°. xx Cold light source either halogen lamp or xenon lamp is used. Halogen lamp is used commonly and is cheaper. Xenon lamp gives high visualisation. xx Camera: 3 chip camera is commonly used with high resolution. xx Video-monitor to display images. xx CO2 insufflator. xx Long fine dissectors like in open surgical techniques. xx Hooks and spatulas are used along with cautery for dissection. xx Clip applicators. xx Needle holders. xx Endostaplers. xx Veress needle. xx Suction-irrigation apparatus. xx Trocars of different sizes—10 mm, 5 mm. xx Reducers to negotiate smaller instruments through larger ports.

A

B

Figs 32.58A and B: Laparoscopic set showing trolley, telescope and monitor instruments.

Preparation Always general anaesthesia. Other preparations are same as for open method.

Technique Pressure bandages are applied to both legs to improve the venous return and to decrease the stasis. Head end of the table is lowered to have easier insertion of veress needle and scope. Ryle’s tube and Foley’s catheter are essential before insertion of the trocars. Pneumoperitoneum is created using veress needle through umbilical incision. Access can be achieved by open method through an umbilical incision. CO2 is commonly used to create pneumoperi­toneum as: ™™ ™™ ™™ ™™ ™™ ™™

It is readily available It is cheaper It suppresses the combustion It is easily absorbed by tissues It has a high diffusion coefficient It is quickly released via respiration

Other gases used are: Air, nitrous oxide, helium, argon. Pneumoperitoneum is created upto a pressure of 15 mmHg which distends the abdominal cavity adequately to have proper visualisation of the abdominal contents.

A quiet, vacant mind is distressed, depressed mind.

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SRB's Manual of Surgery Laparoscope is inserted through the umbilical port (10 mm). Abdomen is evaluated for any pathology. Liver, gallbladder, pelvic organs are visualised. Additional ports (3–4) through trocars are placed depending on the procedure to be done. It may be either 5 mm port or 10 mm port. These ports are placed in such a way to have a proper triangulation of instruments for dissection. To use clip applicator 10 mm port is required.

Physiologic Changes due to Pneumoperitoneum xx CO2 causes hypercarbia, acidosis and hypoxia. xx Pneumoperitoneum exerts pressure on the IVC, decreases the venous return and so the cardiac output. xx It increases the arterial pressure also. xx It compromises the respiratory function by compres­sing over the diaphragm impairing the pulmonary compliance.

Fig. 32.59: Portals for laparoscopic cholecystectomy.

Complications

Relative Contraindications

xx xx xx xx xx xx

xx End stage cirrhosis, ascites or portal hypertension. xx Cholangitis: Cholecystectomy should be done after the control of cholangitis. xx CBD stones: Here, initially ERCP and stone extraction is done from CBD, then laparoscopic cholecystectomy is done.

xx xx xx xx xx xx xx xx xx

CO2 narcosis and hypoxia. Sepsis—subphrenic abscess, pelvic abscess, septicaemia. IVC compression. Bleeding. Leak from the site, e.g. bile leak. Organ injury during insertion of ports, e.g. major vessels, bowel, mesentery, liver. Subcutaneous emphysema and pneumomedia­stinum. Gas emboli, though is rare but fatal. Postoperative shoulder pain due to irritation of diaphragm. Cardiac dysfunction due to decreased venous return. Injury to the abdominal wall vessels and nerves. Cautery burn to abdominal structures. Abdominal wall hernias. Wound infection. Mortality—0.5%.

Relative Contraindications xx xx xx xx xx xx xx

Patients with compromised cardiac status. Peritonitis. Previous abdominal surgeries. Bleeding disorders. Morbid obesity. Third trimester pregnancy. Portal hypertension.

Technique After pneumoperitoneum, patient is placed in head up and slight left tilt position so as to make bowels to fall below and towards the left side. One 10 mm trocar is placed at umbilicus and through this umbilical port, laparoscope is passed. One 10 mm port in the epigastric region and two 5 mm ports in the right subcostal line are placed for grasping the gallbladder and for dis­section. Initially, through the working channel gallbladder is held and Calot’s triangle is dissected. Cystic duct and cystic artery are clipped. An intraoperative cholangiogram is done with C-arm. Through the epigastric port, clips or ligatures are applied to the cystic duct and cystic artery, close to the gallbladder. Care should be taken to avoid bleeding and not to injure or clip the CBD or hepatic ducts. Gallbladder is separated from its bed using cautery and spatula and removed through the epigastric port. Abdomen may be drained. Patient is discharged after 48–72 hours.

Basic Laparoscopic Surgeries xx Laparoscopic cholecystectomy. xx Laparoscopic appendicectomy.

LAPAROSCOPIC CHOLECYSTECTOMY It is becoming popular method of treatment. Indications ™™ ™™ ™™

Gallstones—symptomatic Cholecystitis Biliary colic

Fig. 32.60: Laparoscopic cholecystectomy. Applying clip to cystic duct is shown.

Laparoscopic Surgery Complications ™™ ™™ ™™ ™™ ™™ ™™

Common bile duct (CBD) injury Bile leak Haemorrhage Postoperative jaundice Subphrenic and other intra-abdominal abscess Septicaemia

When problem arises, one should be ready to convert into open cholecystectomy. Conversion rate to open cholecystectomy is 2–10%. It is indicated when there is uncontrolled bleeding, dense adhesions, suspected CBD injury, when anatomy is indistinct. When required one should not be hesitant to do conversion.

LAPAROSCOPIC APPENDICECTOMY Indications Acute appendicitis. Here main advantage is confir­mation of the diagnosis. Other parts of the abdomen are also visualised.

Relative Contraindications Appendicular mass and abscess. Technique: Laparoscope is passed through the umbilical port. Two additional ports are placed, one in lower midline (5 mm), another at right lumbar region. Mesoappendix is clipped or cauterized, using bipolar cautery. Appendix base is clipped or ligated using Roeder knot and ligature.

Procedures xx xx xx xx xx xx xx xx xx

Laparoscopic hernia repair. Laparoscopic splenectomy. Laparoscopic fundoplication. Laparoscopic vagotomy and gastrojejunostomy. Laparoscopic Nissen’s fundoplication. Laparoscopic colectomy. Laparoscopic hysterectomy. It is becoming very popular. Laparoscopic urologic surgeries. Laparoscopic paediatric surgeries.

Laparoscopic Inguinal Hernia Repair It is becoming popular method, lately. It is a skilled laparoscopic surgery. 1. Transabdominal preperitoneal repair (TAPP repair): Through abdomen, using laparoscope Hesselbach’s triangle is exposed and mesh is placed in the preperitoneal space. Peritoneum is sutured back or stapled. 2. Totally extraperitoneal repair (TEP repair): Through sub-umbilical incision, preperitoneal space is created with the help of a balloon. Laparoscope is passed to this space. Inguinal canal is dissected and mesh is placed. Triangle of ‘Doom’: It is bounded by ductus deference medially, testicular vessels laterally, with apex at internal ring. This is dangerous area in laparoscopic hernia repair as dissection may injure iliac vessels and cause torrential haemorrhage.

Complications xx xx xx xx

Subcutaneous emphysema. Abdominal wall haematoma. Injury to major vessels. Recurrence.

DIAGNOSTIC LAPAROSCOPY Indications

Fig. 32.61: Ports used for laparoscopic appendicectomy. 10 mm umbilical camera port (1); 5 mm working left lower abdominal port (2); another 5 mm port (3) either in suprapubic midline or right lower abdomen.

xx xx xx xx xx xx xx

Acute pelvic conditions. Tubal pregnancy. Ovarian diseases. Infertility. Staging of the malignancy. Biopsy from the tumours. In chronic pain abdomen where ultrasound, endo­scopies, barium studies are negative, then diagnostic laparoscopy is useful.

Complications xx xx xx xx

Appendicular stump leak. Pelvic abscess. Bleeding. Injury to caecum, ileum.

ADVANCED LAPAROSCOPIC SURGERIES xx Presently most of the abdominal surgeries can be done through laparoscopy. xx It requires advanced technology and skill. Surgeon should be expert in doing intracorporeal and extra­corporeal knotting.

A Fig. 32.62A

When light pressure is exerted over area of surgical emphysema, a sensation similar to that of likewise pulpating a horse hair mattress is experienced. —Denis Dooley

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SRB's Manual of Surgery Complications xx Injury to vessels. xx Paralytic ileus. xx Bowel (colon) injury.

Advantage xx Complications of pneumoperitoneum is not present and so respiratory reserve is well-maintained.

NATURAL ORIFICE TRANSLUMINAL ENDOSCOPIC SURGERY (NOTES) B Fig. 32.62B Figs 32.62A and B: Diagnostic laparoscopy showing ectopic pregnancy in right fallopian tube. It is removed by salpingectomy through laparoscopy. Needle laparoscopy of 2 mm sized becoming popular (especially for diagnostic purpose).

Advantages xx Laparotomy is avoided. xx Once diagnosis is made, therapeutic procedure also can be carried out in the same sitting.

RETROPERITONEOSCOPY xx It is becoming popular in urology to assess kidney, ureter, adrenals for various urologic procedures. xx Through a small loin approach, retroperitoneum is expanded by inflating balloon in the space. Once space is created, different ports are placed to do dissections. Procedures done through retroperitoneoscopy are: ™™ ™™ ™™ ™™ ™™ ™™

Nephrectomy Pyeloplasty Adrenalectomy Pyelolithotomy Uretero-lithotomy Retroperitoneal lymph node dissection (RPLND)

Fig. 32.63: Port positions for retroperitoneoscopy.

It is an experimental surgical technique whereby “scar less” abdominal operations can be performed with an endoscope passed through a natural orifice (mouth, urethra, anus, etc.) then through an internal incision in the stomach, vagina, bladder or colorectum, thus avoiding any external incisions or scars. xx This technique has been used for diagnostic and therapeutic procedures in animal models, including transgastric (through the stomach) organ removal. The transvesical and the transcolonic approaches are also used. Transgastric and transvesical combined approach is also used to increase the feasibility of moderately complex procedures such as cholecystectomy. xx NOTES was originally described in animals by researchers at Johns Hopkins University (Dr Anthony Kalloo, et al.), and was recently used for transgastric appendectomy in humans in India (by Dr GV Rao and Dr N Reddy). xx On June 25, 2007, Swanstrom and colleagues reported the first human transgastric cholecystectomy. In late 2008, surgeons from Johns Hopkins School of Medicine removed a healthy kidney from a woman donor using NOTES. The surgery was called transvaginal donor kidney extraction. xx The transvaginal access to NOTES seems to be the safest and feasible. In 2007, the NOTES Research Group in Rio de Janeiro, Brazil, lead by Dr Ricardo Zorron, performed the first series of transvaginal NOTES cholecystectomy in four patients. With fewer potential complications, the procedure has a disadvantage of being possible only in women. xx Proponents and researchers in this field recognize the potential of this technique to revolutionize the field of minimally invasive surgery by eliminating abdominal incisions. NOTES could be the next major paradigm shift in surgery, just as laparoscopy was the major paradigm shift during the 1980s and 1990s. xx Advantages are—lower anaesthesia requirements; faster recovery and shorter hospital stays; avoidance of the potential complications of transabdominal wound infections (e.g. hernias); less immuno­ suppression; better postoperative pulmonary and diaphragmatic function; and the potential for “scar less” abdominal surgery. xx Disadvantages are—it is single port surgery and difficulty in visualisation of the area in need from all directions which is essential for proper surgical dissection. Poor manoeuverability is the problem. Sepsis through this potentially infected area into sterile peritoneal cavity is a real risk. After procedure non closure of the port site opening in these approach sites or if closing their inadequacy are the real risk in NOTES. xx The general impression is that NOTES will be accepted as the newest frontier in minimally invasive surgery. As of today nonBariatric minimally invasive surgery fellowships offer the best opportunity to train in this new approach.

G. Dressings and Bandages CHAPTER OUTLINE ™™ Dressings

™™ Bandages

DRESSINGS

Indications

They are the materials used to cover wounds, ulcers to provide support and to encourage healing.

Advantages xx It covers the wound and so prevents further contamination. xx It gives comfort to the patient.

Disadvantages xx It may get soaked. xx It may delay the epithelial layer formation.

Types xx Dry dressings: It is used in clean, sutured operated wound. It is not changed at regular intervals. xx Wet dressings: It is used in ulcers and wounds. Dressings are made wet by using jelly or sofra tulle sheets.

Components of Dressing xx Inner contact layer. It is non-absorbent and only allows secretion to pass into the absorbent layer. It does not allow penetration of granulation tissue. It is usually kept wet. Either mesh gauze or sofra tulle is used. xx Intermediate absorbent layer made up of cotton which absorbs the secretions. xx Outer layer as supportive is made up of gauze. Dressings are fixed to the place by: ™™ ™™ ™™ ™™

Bandages Plasters Dynoplast Crepe bandages

Depending on the condition and amount of discharge from the wound/ulcer it is changed as required—twice a day/once a day/once in two days. Small dressings are done without anaesthesia. Large areas like burn wounds or dressing in children require general anaesthesia.

™™ ™™ ™™ ™™

To reduce the swelling like in lymphoedema To keep dressings in position To support splints To stop bleeding/oozing

Types of Bandages a. Roller bandages  It is a continuous roll of material, which is rolled over the part to cover the area.  It is used in limbs.  It is available in different lengths and widths—1 inch, 2 inches, 4 inches or 6 inches.  It is used in different ways. –– Circular turns: Continuous rolls placed over the same place. –– Spiral turns: After the initial turn of the bandage, it ascends proximally overlapping the distal 2/3 of the previous turn. –– Reverse spiral turn: Here each spiral turn is reversed in opposite direction so as to attain uniform pressure. It is used in limbs and areas which end as cones. –– Figure eight turn: It is used in knee, elbow, wrist, ankle and for clavicle. –– Recurrent turn: It is used in head, amputation stump. Here initially circular rolls are made and over that half turns are made to cover other parts of the area required. –– Spica bandage: It has got ascending and descending turns, with each turn overlap and cross each other. It is used in hip, groin, shoulder, breast or thumb. Spica means eye of a bean. b. ‘T’ bandages: It is used in perineum and groin. c. Tailed bandages: It may be four tailed bandages or many tailed bandages. It is used to support dressings on a wide area like in burns dressing, over abdomen or chest wall. d. Tubular bandages: These are stockings which are unrolled over the limb to give pressure effects. It is used in lymphoedema, varicose veins and in the postoperative period following surgeries of the limb (Tubifix, Tubipress). e. Triangular bandage: These are used for supporting the elbow or forearm. Here a wide gauze is used to cover the arm, forearm and elbow, which again winds around the neck. f. Cravat bandages: It is a folded type of triangular bandage, which is used as sling around the neck, when elbow requires to be rested.

Principles of Bandaging

BANDAGES Technique of bandaging is called as Dysmergia.

xx Bandage is applied to the part from distal to proximal end. xx Proper positioning of the limb is a must before bandaging.

Genius is one percent inspiration 99% perspiration.

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SRB's Manual of Surgery xx After initial few circular turns, the required type of bandaging is then done. xx Bandage is unrolled outwards. xx During bandaging, latter turn should overlap 2/3rd of earlier turn. xx Firm, adequate pressure should be used during bandaging. xx After completing the procedure, the knot should not lie over the area or over the bony points or over the back. xx It should not cause venous or arterial compression. xx Digits should be left open and circulation in the digits should be observed for:

Anatomical place • Finger/toe • Arm • Leg • Thigh • Trunk

Types of bandage • 1 inch • 2 and 1/2 inches • 4 inches • 6 inches • 6 inches

• Head

• 4 inches

H. Day Care Surgery CHAPTER OUTLINE ™™ Day Care Surgery

™™ Surgical Audit

DAY CARE SURGERY xx Day care surgery is discharge within 23 hours (USA); surgery done without night stay (UK). xx Day care surgery means patient is fit to return home in 23 hours usually with overnight stay. Ambulatory surgery means patient recovers after surgery and returns home on the same evening. Office surgery means patient recovers from surgery and returns home in few hours. Outpatient surgery is different from day care surgery in that, patient is not previously fully assessed in outpatient surgery. Only minor procedures are done in this. Patient is not admitted in outpatient surgery. In day care and ambulatory surgery patient is admitted in the hospital. xx Day care surgery has been defined by the Royal College of Surgeons as when the surgical day case patient is admitted for investigation or operation on a planned non-resident basis and who nonetheless requires facilities for recovery. This definition excludes upper and lower GI endoscopies, outpatient procedures such as flexible cystoscopy, and minor superficial surgery under local anaesthetic, none of which require full day case facilities for recovery. xx Day care surgery is an upcoming field in surgical practice. It is an unique method wherein general practitioner, nurse at day care ward and theatre, surgeon, anaesthetist work in hand so that hospital stay and so the cost is reduced. xx Patient comes to hospital at morning for surgery and leaves the hospital on same day evening. Advantages ™™ ™™ ™™

™™ Surgeon and Law

xx Patient selection, patient information, patient acceptance are important parts in day care surgery.

Selection Criteria are American Society for Anesthesiologist (ASA) category I and II patients can be taken up for day care surgery. ASA III/or beyond are contraindicated for day care surgery. ASA (American Association of Anesthesiologists) grading of the patient for surgery Normal individual mild-moderate systemic disease—diabetes and hypertension under control ™™ Severe systemic disease—uncontrolled diabetes and hypertension ™™ Incapacitating systemic disease ™™ Moribund status Class E—emergency surgery ™™ ™™

Exclusion criteria for day care surgery are: ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™ ™™

Minimal hospital stay Becomes cheaper Patient acceptance

xx Contraindications for day care surgery are—age >70 years; high-risk cardiac and respiratory patients; patients with bleeding disorders.

Basic requirements are: xx In house anaesthesiologist; recovery room; theatre and recovery room/ward nurse; all essential surgical set up including monitor, ventilator. xx Alertness; ambulation; analgesia and alimentation—basis for day care of surgery.

Assessment done prior to surgery are by: xx Pre-anaesthetic clinics with system evaluations; health questionnaire by surgeon and physician; telephonic interviews.

™™

ASA grade beyond III or more Obesity (BMT >35). Hypertension—not controlled Surgery requiring more than one hour Surgery with anticipation of major fluid/blood loss or needs post-operative critical care Preterm babies and infants less than 3 month’s age Patient living in far and not easily reachable or able transport easily Unstable psychiatric illness If proper caregiver is not available Uncontrolled diabetes, alcohol abuse, Chronic obstructive pulmonary disease (COPD), severe asthma, epilepsy Pregnancy

Levels of day Care Surgery Three levels are used but minor procedures in outpatient clinic, accident cases are not included. xx Minor ambulatory surgery. xx Major ambulatory surgery. xx Inpatient surgery—patient stays overnight and get discharged within a day. Day care surgery unit (DSU) is present in many centres. It may be hospital integrated or hospital based or free standing or officer based. It should have a separate dedicated unit with reception, surgery team, theatre, recovery unit, anaesthetist. Patient selection is done prior to surgery including all evaluations.

So long as enthusiasm lasts, so long is life still with us.

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SRB's Manual of Surgery Many surgeries are done as day care surgery—hernia, haemorrhoidal procedures, laparoscopic surgeries, excisions, biopsies, laparoscopic cholecystectomy, appendicectomy, ovarian cystectomy, varicose vein surgery, all endoscopies, circumcision, orchidectomy, hydrocele surgery, vasectomy, renal stone procedures like ESWL, skin grafting, liposuction, fracture manipulation, arthroscopy, surgical decompression of carpal tunnel syndrome, most of the eye surgeries, tympanoplasties, myringoplasty, adenoidectomy, laryngoscopy, orthodontic surgeries, laparoscopic sterilization etc. Any surgery which has got low-risk with less bleeding and early ambulation can be done as day care surgery with fulfilling the selection criteria. Advantages are—less infection, home food, less chance of DVT, early ambulation, reduced cost, reduced waiting list, early return to work, psychological benefit. Guidelines for safe discharge—stable vitals; proper orientation and recovery of the patient; tolerant for oral food adequately; ability to pass urine; able to move with or without support; no features of vomiting, nausea, severe pain, swelling or bleeding. Responsible relative to take care of the patient at home should be present. Problems Postoperative nausea and vomiting (50%); postoperative pain and postoperative drowsiness/dizziness (50%) are the common complications in day care anaesthesia.

Precautions xx Patient should be assessed properly before sending to day care surgery. xx The nurse should give proper instruction to the patient as patient stays in the hospital for a short period. xx Patient should be warned about possible problems like bleeding, vomiting, pain, discomfort, and sedation. xx Before discharging, patient should be seen by the doctor for the fitness. xx All records should be carefully documented. xx Patient should be advised to rush to hospital if any problems arise or to communicate immediately. xx Now hernia; small gynaecology procedures; ENT, cataract surgeries are done as day care procedures. Nurses hold an important role in day care surgery.

SURGICAL AUDIT ‘Clinical audit’ is a process used by clinicians who intend to improve the patient care. The process involves comparing various aspects of

patient care that includes structure, process and outcome against explicit criteria.

Aspects of Patient Care xx Structure—includes what is there in that place—the people in place, their training and knowledge, the equipments and facilities provided, the organization, management and their payment, etc. xx Process—includes what procedure is followed in that place in managing referred patients, what antibiotics used, what diagnostic tests done, use of ICU facilities, use of postoperative rehabilitation care, what procedure used for discharge of patients, etc. xx Outcome—includes the overall results that include the morbidity, mortality, readmission, improvement /deterioration of the patient’s condition.

Explicit Criteria Proposal for changes can be made in the care of the patient if it falls short of the criteria chosen which can be undertaken at one or more levels: xx Individual level—more training can be given to the doctors. xx Infrastructure—upgrading of the newer diagnostic tools. xx Team level—nurses getting more trained in handling the procedures along with the doctors. xx Institution—change in the treatment strategy, or antibiotic policy. xx Regional level—providing a good referral centre with all facilities and trained personnel. xx National level—introduction of screening programmes and health campaigns. Surgical audit is a systematic, critical analysis of the quality of surgical care that is reviewed by peers against explicit criteria or recognised standards, and then used to further inform and improve surgical practice with the ultimate goal of improving the quality of care for patients. In surgical practice, there will be definitely variations in the results of the surgery done by a trainee or an experienced surgeon, variations in outcome of the operation done in peripheral setup and in referral institutions, usage of modern equipments and technique used.

Step 1 Determine scope It should be clearly defined, otherwise results in ineffective/inappropriate data collection. It should also be relevant, easily measurable. Common areas in scope of an audit include—duration of hospital stay/unplanned admissions/readmissions/operative specific complications/30 days mortality /morbidity/investigations done/management strategy/patient satisfaction.

Fig. 32.64: Surgical audit cycle

Day Care Surgery Step 2 Select standards Standards for the selected topic/practice area is decided based on relevant information obtained from: xx Evidence-based research and guidelines. xx Local guidelines for local relevance. xx New guidelines developed based on references from a library. The standard which was already existing or developed must be clearly described, measurable, specific, and realistic.

xx xx xx xx

Step 3 Collect data It is important aspect of the audit which has to be informative for the audit to be successful. The best quality data collected depends on by whom it is being collected; when—retrospective/prospective collected; how—on form/PDA/computer; at/fter the time of surgery; follow-up data when collected; patient identification in a prospective/ retrospective study. Collected data must be relevant to the objectives of the surgical audit. Sometimes, the standards may need to be expanded or reduced/ or the data collection methods may need to be modified.

Step 4 Present and interpret result with peer review

Audit aims in continuous improvement by experience and by making changes which is ultimately rewarding. The outcome of the audit should be presented and discussed in a clinical meeting. It should undergo peer review. It involves viewing and analyzing one’s outcome by one’s own peers who are none other than other experienced trained surgeons. It should be conducted in an atmosphere of confidentiality, trust and teamwork, should not be an opportunity to blame or brag but exchange of frank, non-confrontational discussions between the colleagues. Mortality/morbidity meetings, grand rounds are one form of peer review.

Step 5 Introduce changes and monitor progress Based on the conclusion of the audit and meetings certain changes to be made in respect to the patient care are decided and all the personnel involved in the process are informed or educated. The outcome due to changes made are monitored by follow-ups either by reauditing the whole process/ or only the part that has been changed.

SURGEON AND LAW xx It is important to a surgeon to know legal aspects in relation to his profession. Consumer protection act and criminal negligence

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xx xx

xx xx xx xx xx

are the two things surgeons are regularly worried about and face often problems. It is better to have a fair idea about consumer protection act in relation to patient treatment. Surgeon should keep all documents regarding the patient with him or in the hospital. Case sheet should be written in detail. Daily follow-up should be written with date and time of visit with progress about the patient. It is better to take detailed consent after proper explanation about the disease and treatment protocol to patient and his close attender/ relative. It is better to get signature about discussion given from them with date and time. In many centres, it is practiced to record the explanation part to keep it as document. Surgical method, its problems, risks due to anaesthesia, high-risk if any, risk of bleeding, complications, duration of hospital stay should be discussed. One should make sure that anaesthetist will do preanaesthetic check up prior to surgery; he should also write his preoperative/operative/ postoperative anaesthetic notes. Daily information sheet should be used wherein patient or party should be informed about the condition of the patient. Timing of this and signature of surgeon and party should be taken. After surgery detailed surgical procedure technique should be written in case sheet and should be informed to patient. Specimens should be shown to patient party and should be sent for histology. Approximate cost of the procedure and entire bill in the hospital should be informed. One should also inform that it may change depends on complications, number of days in ICU, critical care, need for higher antibiotics, etc. Negligence about retaining mops/instruments are legally not acceptable; it is better to take care of enough precautions about that. Surgeon has got vicarious liability about the mistakes done by ward boys, nurses, theatre nurses, etc. So it is better to train them for proper care in OT, postoperative wards and ICU. It is ideal to show all reports to patient party and discuss/brief with them about the condition especially when patient is in ICU. If patient or party become arrogant or aggressive it is better to make a note of it in case sheet and inform police people about the same. It is better to make a professional indemnity insurance policy always to cover these problems in case if needed. It is again ideal to have an advocate to discuss these matters whenever needed. It is care which surgeon gives not cure always.

Duty makes us do things well, but love makes us do them beautifully.

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Miscellaneous A. Fascinating Signs in Surgery “If it is a question of doubt in diagnosis, you may often observe that one man solves the doubt when the others could not, and the way in which one man happened to solve it is this: he applied to the diagnosis of the case some method of examination which others had not applied.” —Charles Barrett Lockwood, 1856–1914

SIGN: Sign is an indication of existence of an objective evidence of a disease, i.e. such evidence as is perceptible to the examining physician, as opposed to the subjective sensation (symptoms) of the patient. PATHOGNOMONIC SIGN (patho = disease, gnoma = signature, pathognomonic = signature of the disease): Specially distinctive or characteristic sign of a disease or pathological condition on which a diagnosis can be made. ACCESSORY SIGN (Assident sign): Any nonpathognomonic sign of disease, which adds on to the surety of the diagnosis when present. ANTECEDENT SIGN: Any precursory indication of an attack of disease. These signs are to be identified at the earliest. 1. Aaron’s sign: A sensation of pain and/or distress in the epigastric or precordial region on pressure over McBurney’s point in appendicitis. 2. Abadie’s sign: Charles Abadie—Spasm of levator palpebrae superioris muscle—A sign of Graves’ disease. Jean Abadie—Insensibility of Achilles tendon to pressure, seen in tabes dorsalis. 3. Air cushion sign (Syn: Klemm’s sign): In the radiograph of chronic appendicitis, there is often an indication of tympanitis in the right lower quadrant. 4. Alder’s sign of shifting tenderness: This sign is useful to diagnose acute appendicitis in pregnancy. Locate the most tender spot and mark it on the skin. Now request the patient to turn on the left side and wait for a full minute. If the tenderness is of uterine origin it will shift with the uterus while the position remain constant in case of appendicular origin. 5. Angell’s sign: Helpful in diagnosing “Torsion testis” due to developmental anomaly—The presence of mesentery between the testis and the epididymis is invariably bilateral. The sign is usually obscured on the affected side and can be made out by examining the patient in the standing position wherein the opposite testis will be found to lie horizontally instead of in the normal vertical position. 6. Anghelescus’ sign: Seen in Pott’s disease of spine (TB spine) wherein the victim is unable to bend the spine while lying on the back so as to rest on the head and heel alone. 7. Argyll Robertson pupil sign: Typically described for neurosyphilis wherein light reflex is lost while accommodation reflex is retained. Such an eye responds poorly to mydriatics. This is due to destruction of fibres between pretectal nucleus and Edinger-Westphal nucleus. Other conditions where this sign may be seen—encephalitis, vascular and traumatic lesions, cerebral tumours, diabetes mellitus and chronic alcoholism. 8. Auenbrugger’s sign: Bulging of the epigastrium due to massive pericardial effusion. This sign highlights the importance of examining thorax in patients with abdominal symptoms. 9. Babinski’s sign (Not syn with Babinski’s reflex): a. Loss or weakening of the Achilles tendon reflex in sciatica. This sign helps distinguish true sciatica from hysterical sciatica. b. In hemiplegia the contraction of platysma muscle in the healthy side is more pronounced than on the affected side. It can be elicited by asking the patient to open the mouth, whistling, blowing, etc.

Fascinating Signs in Surgery

c. When a hemiplegic patient is lying with arms crossed upon the chest and makes an effort to sit up, the thigh on the paralyzed side is flexed upon the pelvis and the heel lifted from the floor while limb on the healthier side does not move. d. When the paralyzed forearm is placed in supination it turns over to pronation. It is seen in organic paralysis and is also called ‘Pronation sign’. 10. Baid sign: Described for pseudocyst of pancreas and is well appreciated in thin individuals. When Ryle’s tube is passed into the stomach, it may be palpated over the swelling because the stomach is displaced anteriorly by the pseudocyst pancreas. 11. Ballances’ sign: Seen in about 25% of ruptured spleen. There is a dull note in both the flanks due to haemoperitoneum. The dullness on the right side can be made to shift, but that on the left side remains constant/fixed because the blood in the vicinity of the ruptured spleen gets coagulated soon. 12. Ballet’s sign: This sign is helpful in Graves’ disease and hysteria wherein there will be persistence of involuntary pupillary and reflex eye movements with loss of all voluntary eye movements (external ophthalmoplegia). 13. Bamberger’s sign: A sign described in pericardial effusion—Presence of signs of consolidation at the angle of scapula which disappears when the patient leans forwards. 14. Banana sign: An ultrasonographic sign described for Arnold-Chiari deformity—a cause for congenital hydrocephalus. Sonography of the fetal skull reveals flattened and curved (banana like) shape of the cerebellar hemisphere. 15. Bastede’s sign: A sign described in a case of appendicitis—Mentioned to be condemned—when colon is inflated with air through a rectal tube, pain and tenderness can be elicited in the right iliac fossa in a suspected case of appendicitis. Such manoeuvre carries risk of perforation and hence should not be entertained. 16. Battle’s sign: It is relevant in middle cranial fossa fracture—bruising/ecchymosis over the mastoid process in the line of posterior auricular artery is a tell-tale sign of underlying middle cranial fossa fracture (temporal bone fracture). 17. Bergman’s sign: A urologic radiographic sign: a. The ureter is dilated immediately below an obstructing neoplasm rather than collapsed as seen in cases of obstructing stones. b. The ureteral catheter passed in such cases tends to coil in this dilated portion of the ureter. 18. Berry’s sign: Indicated by the absence of carotid artery pulsation in a patient presenting with goitrous swelling, is an ominous sign of thyroid malignancy (due to carotid sheath infiltration by the malignant tissue). 19. Bezold’s sign: Described in a case of mastoiditis—An inflammatory swelling seen below the apex of the mastoid process. 20. Biederman’s sign: A dark colour instead of normal pink colour of the anterior pillar of the throat is seen in some patients with syphilis. 21. Bird’s sign: Described for hydatid disease of lung wherein a definite zone of dullness with absence of the respiratory sounds may be appreciated. 22. Biernacki’s sign: Analgesia of ulnar nerve in general paresis and tabes dorsalis. 23. Blatin’s sign (Syn: Hydatid thrill): A sign elicited in cases of hydatid cystic disease. It is due to displacement of daughter cysts in the fluid of the mother cyst. 24. Boas sign: An area of hyperaesthesia, posteriorly extending 2.5 cm lateral to the spinous process of vertebrae to the posterior axillary line and vertically from the level of the 11th dorsal to the 1st lumbar spine—A definitive sign of the presence of cholecystitis. 25. Blumberg sign (Syn: Rebound tenderness; Release sign): It is a sign of peritonitis due to presence of an inflamed organ underneath it. 26. Bonnet’s sign: Pain on thigh adduction in sciatica. 27. Boston’s sign (Syn: von Graefe’s sign): It constitutes the lid lag elicited in cases of thyrotoxicosis. 28. Bowler’s hat sign (Syn: Double ring sign): A radiological sign which describes the appearance of a gastric polyp seen on end-on position in a double contrast barium meal study. There will be a central lucency with two rims of barium around. May also be seen in cases of sessile intestinal polyp or a diverticulum. 29. Boyce’s sign: A gurgling sound heard on pressure by the hand on the side of neck, in cases of oesophageal diverticulum. 30. Bozzolo’s sign: A visible pulsation of the arteries in the nostrils. A sign believed to indicate the presence of aneurysm of the thoracic aorta. 31. Branham sign (Syn: Nicoladoni sign): This sign is elicited when arteriovenous fistula is suspected. A pressure on the artery proximal to the fistula will cause: a. Reduction in size of the swelling. b. Disappearance of bruit. c. Fall in pulse rate. d. Pulse pressure returns to normal. 32. Brodie’s sign: A black spot on the glans penis—a sign of gangrene due to urinary extravasation into the corpus spongiosum. 33. Bald fundus sign: A radiological sign described for atrophic gastritis.  The fundus of the stomach looks like a small dome with absence of mucosal pattern indicated by a very thin smooth appearing gastric wall. 34. Bent inner tube sign: A radiological sign described for sigmoid volvulus—an important diagnostic sign. A plain X-ray abdomen taken in the supine position reveals a massively distended ahaustral sigmoid colon arising from the pelvic loop. 35. Bird of prey sign: A radiological (Barium enema) sign which helps in confirming the diagnosis in doubtful cases of sigmoid volvulus. Barium enema reveals a smooth tapered narrowing at the point of torsion of the colon. Mucosal folds show a screw pattern around the point of twist. 36. Border sign: Describes the appearance of ventral hernia in barium study follow through done in suspected cases, in the postoperative period. Lateral and inferior border of the hernia are sharply outlined while the medial and upper border blends with the abdominal shadows.

Everything is funny as long as it is happening to somebody else.

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SRB's Manual of Surgery 37. Cardarelli’s sign: Transverse pulsations in the laryngotracheal tube in suspected cases of aneurysms and dilatation of the aortic arch. 38. Chvostek’s sign (Syn: Chvostek Weiss sign; Schultze’s sign): A clinical sign typically described for hypocalcaemic tetany. The sign is elicited by tapping over the muscles and/or superficial nerves to induce the muscle spasm. It may be: a.  Facial sign: A light tap over the facial nerve branches in front of the ear lobe causes muscular twitching over the whole of that side of the face. b.  Peroneal sign: Tapping the peroneal nerve near the fibular neck will cause dorsiflexion and abduction of the foot. 39. Cobra head sign (Adder head appearance): A radiological sign seen in cases of ureterocele—congenital dilation of lower end of ureter. Urography done in suspected cases produces a characteristic appearance which resembles a cobra head and hence the name. 40. Crescent sign: A radiological sign described in relation to two different conditions affecting the lungs and the kidneys: a. In plain chest X-ray taken in a patient suspected of hydatid disease or aspergilloma (fungus ball) of the lung reveals a crescent of air in the shadow of partially ruptured hydatid cyst or in the cavity containing fungus ball. b. On IVP, the nephrogram reveals a crescent sign in cases of congenital hydronephrosis. 41. Cullen’s sign (Syn: Cullen Hofstatter sign): A clinical sign which was typically and initially described for ruptured ectopic pregnancy wherein there is discolouration (ecchymosis) of the umbilicus and the surrounding skin (aptly referred to as umbilical black eye). It is due to haemoperitoneum and may be seen in conditions like ruptured ectopic pregnancy (a bluish tinge), acute haemorrhagic pancreatitis (a yellowish tinge). 42. Carman’s sign (Syn : Carman-Kirklin meniscus sign): A radiographic sign helpful in the analysis of gastric ulcers in barium meal study. It is a reliable indicator of malignancy. Nonprojecting ulcers lying intraluminal in all projections surrounded by an elevated rim of tumour produces a curval interface resembling a meniscus and is called Carman’s meniscus sign. Whether the meniscus is convex or concave towards the lumen is mainly dependent upon the site of ulcer in relation to incisura angularis. Meniscus is concave towards the lumen in cases of ulcer being proximal to the incisura while it is convex when the ulcer is distal to the incisura. 43. Carnett’s sign: A clinical sign which helps differentiate the plane of abdominal swelling. The abdominal wall muscle is made tense by asking the patient to raise both the legs with knee extended. If the lump is intraperitoneal it disappears or becomes less prominent, while it becomes prominent or persists when the lump arises from the abdominal wall. 44. Chilaiditi’s sign (Syn: Chilaiditi’s syndrome; Hepatoptosis): A radiological sign seen in plain X-ray abdomen which is helpful in the diagnosis of this syndrome wherein there is interposition of colon between liver and diaphragm. It needs to be differentiated from the conditions causing gas under the diaphragm. The presence of haustrations in the gas shadow in a plain X-ray abdomen tilts the favour in the diagnosis of Chilaiditi’s syndrome. 45. Coiled spring sign: A radiological sign (Barium enema) classically described for intussusception. The passage of barium beyond the apex of the intussusception into the intussuscipien gives a coiled spring appearance. The sign may also be seen in cases of: a. Post-traumatic haematoma of duodenum. b. Acute appendicitis. c. Mucocele of appendix. d. Endometriosis of appendix. e. Intestinal carcinomas. 46. Coles’ sign: A radiological sign. Barium meal follow through study reveals deformity of the duodenal contour in the presence of duodenal ulcer. 47. Colon cut off sign: A radiographic sign of appendicular perforation or colonic spasm. Absence of gas and feces in the right lower quadrant, reflex dilatation of transverse colon and sharp cut-off of gas at the hepatic flexure. This sign is also seen in acute pancreatitis 48. Coopernail’s sign: Ecchymosis on the perineum and scrotum/labia. A sign of fracture pelvis. 49. Cope’s sign (Syn: Psoas sign): Clinical signs which are relevant in cases of acute appendicitis. This has two tests: a.  Cope’s psoas test: In acute appendicitis there is psoas muscle spasm secondary to the inflamed organ and hence the patient keeps the thigh in a flexed position. This pain can be aggravated by passively hyper-extending the hip joint which stretches the psoas muscle. b.  Cope’s obturator test: Principles are same as above except the muscle involved is obturator internus which is passively stretched by internally rotating the right leg which is flexed at the hip and knee. 50. Cupola sign: A radiological sign helpful in the diagnosis of pneumoperitoneum. A plain X-ray abdomen (erect position) reveals gas under the diaphragm when there is relatively large amount of air in the peritoneal cavity—Cupola sign. 51. Crow foot sign (Syn: Mercedes Benz sign; Seagull’s sign): A radiological sign described in relation to cholelithiasis (Gallstones). Nearly 80–90% of the gallstones are radiolucent with only 10–20% being radio-opaque. However, rarely a non-opaque gallstone can be diagnosed in plain radiography by the presence of gas containing crevices within the stone. These radiolucent crevices give the appearance of the crow foot; Hence the name crow foot sign, Mercedes Benz sign or the Seagull’s sign. 52. Courvoisier’s sign (Syn; Courvoiser’s law): In a patient with obstructive jaundice, if the gallbladder is palpable it is not due to gallstones. 53. Cowen’s sign: A clinical sign elicited in cases of Graves’ disease. In response to a light shone on one eye there is jerky constriction of the contralateral pupil. 54. Crowe’s sign: Refers to axillary freckling seen in neurofibromatosis. 55. Cruveilhier’s sign of the saphena varix: A clinical sign elicited in cases of varicose veins (Saphena varix). A thrill is felt over the saphena varix when the patient is asked to perform a Valsalva manoeuvre/cough in an erect position and is due to a jet of blood entering and filling the pouch. 56. Coleman’s sign: Helps in the clinical evaluation of fracture mandible. There is obvious swelling and bruising over the bony injury and a haematoma in the floor of the mouth if the body of the mandible is fractured.

Fascinating Signs in Surgery 57. (Meniscus) Claw sign: A radiological sign (Barium study) diagnostic of ileo-colic intussusception. The barium in the intussuscipien is seen as a claw around the negative shadow of the intussusceptum. 58. Coffee bud sign: It is a radiological sign seen in volvulus of sigmoid colon. 59. Dalrymple’s sign: It is one of the manifestations of Graves’ ophthalmopathy. It consists of retraction of the upper eyelid so that the palpebral opening is abnormally wide and upper sclera is visible. 60. Delbet’s sign: A prognostic indicator in cases of aneurysm of the main artery of the limb. If the nutrition of the part distal to the aneurysm is maintained then the collateral circulation is said to be sufficient even though the distal pulse is not felt. 61. de Musset’s sign: Rhythmical jerking movement of the head with each heart beat and is seen in cases of aortic insufficiency and aortic aneurysm. 62. Dance sign (Syn: Signe de Dance): A feeling of emptiness in the right iliac fossa—A sign of intussusception. 63. Demarouay’s sign: Fixation or lowering of larynx during phonation and deglutition. A sign of syphilis of trachea. 64. Dew’s sign: A clinical sign described in relation to the diaphragmatic hydatid abscess beneath the right cupola of the diaphragm. The area of resonance moves caudally with the patient in knee-elbow position. 65. Dixon Mann’s sign (Syn: Mann’s sign): In case of Graves’ orbitopathy the two eyes appear not to be on the same level. 66. Dorendorf’s sign: The sign identifies the fullness in the supraclavicular groove on one side in aneurysm of aortic arch. 67. Double bubble sign: A radiological sign described in cases of duodenal obstruction. A plain X-ray abdomen reveals two foci of gas, one in the stomach and the other in the duodenum—a sign of duodenal atresia. A similar feature is observed in the foetus in ultrasonography done in the antenatal period. 68. Drummond’s sign: A whiff sound heard over the open mouth during respiration in cases of aortic aneurysm. 69. DTP sign (Syn: Distal tingling on percussion; Tinel’s sign; Formication sign): A prognostic indicator which is helpful in the evaluation of nerve recovery following nerve injury. If percussion over the site of nerve injury causes tingling sensation in the distal end of the limb it suggests that the nerve injury was a partial one or it heralds the recovery from the nerve injury—a good prognostic sign. 70. Dubois sign: Shortness of the little finger in congenital syphilis. 71. Duchenne’s sign: This clinical sign identifies the sinking of the epigastrium during inspiration (a paradox). It is classically seen in cases of paralysis of the diaphragm and in certain cases of hydropericardium (Pericardial effusion). 72. Dupuytren’s sign: It is described in two conditions: a. A crackling sensation on pressure over a sarcomatous bone. b. In congenital hip dislocation, it refers to free up and down movement of the head of the femur. 73. Dott’s sign: It is helpful in differentiating pain due to acute appendicitis and basal pneumonia with pleuritis. Compression of lower thorax from side to side elicits obvious distress when the lesion is above the diaphragm whereas in appendicitis it has no effect. 74. Dock sign: A radiological sign described in relation to coarctation of aorta. A chest X-ray PA view reveals rib notching on the inferior margins of 3rd-9th ribs while sparing the first two ribs and is indicative of collateral circulation developed in coarctation of aorta. 75. De Weese sign: A clinical sign helpful in cases presenting with history suggestive of intermittent claudications with palpable peripheral pulses. The patient is asked to exercise by walking or running sufficiently to bring on the pain. If prompt re-examination reveals absence of peripheral pulses it suggests that the pain was truly due to intermittent claudication. 76. Echo sign: A percussion sound resembling an echo which is heard over a hydatid cyst. 77. Elliot’s sign: Refers to presence of indurated edge of a syphilitic skin lesion. 78. Enroth’s sign: Identifies the abnormal fullness of the eyelids—a manifestation of Graves’ orbitopathy. 79. Escherich’s sign (Syn: Escherich’s reflex): Described in relation to tetany, where percussion of the inner surface of the lips or tongue produces contraction of lips, tongue and masseter muscles. 80. Ewart’s sign: It is said to be positive in cases of pericardial effusion if there is bronchial breathing and dullness on percussion at the lower angle of the left scapula and is due to pressure and collapse of the lingular lobe due to enlarged pericardial sac. 81. E-sign (Syn: Reverse 3 sign): A radiological sign seen on barium swallow radiograph in patient suspected of coarctation of aorta and is due to indentation produced on the barium filled oesophagus by the aorta. 82. Figure of three sign: A radiological sign seen in the plain chest X-ray PA view in patient with coarctation of aorta. A pair of bulges is seen in the wall of the aortic arch one above and one below the aortic knuckle and is due to pre- and post-stenotic dilatation of the aorta. 83. Frostberg’s sign: A radiological sign seen in barium study in carcinoma of the head of pancreas involving the duodenum. In carcinoma of the head of the pancreas, there is widening of the ‘C’ loop of the duodenum and with the involvement of the ampulla of Vater, the expanded loop assumes a reversed 3 configuration—Frostberg’s sign. Once the carcinoma of the head affects the duodenum the surgical cure is remote. 84. Fox sign: Discolouration near the inguinal ligament—seen in few cases of haemorrhagic pancreatitis. 85. Fuchsig’s sign (Syn: Crossed leg test): This sign is more relevant when popliteal artery is not clinically palpable along with absent distal pulses. The patient is made to sit with his legs crossed. Normally, oscillatory movements of the foot occur synchronously with the pulse if the popliteal artery is patent while a negative result is more suggestive of popliteal artery block in a patient with absent distal pulses. 86. Federici’s sign: An interesting sign described in relation to pneumoperitoneum (due to intestinal perforation) wherein on auscultation of the abdomen, the cardiac sounds can be heard. 87. Flush tank sign: A clinical sign described in relation to hydronephrosis. The patients classically present with features suggestive of Dietle’s crisis, i.e. passage of a large amount of urine with consequent disappearance of a lumbar swelling—Flush tank sign.

Many look but only few see.—Maxwell M Wintrobe

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SRB's Manual of Surgery 88. Flare sign: The precursor of varicose ulcer is a splay of fine venules that courses from the medial (sometime the lateral) malleolus, and spreads out to be lost beneath the thick skin of the heel and is known as the “Flare sign”. 89. Gifford’s sign: A clinical sign which helps in differentiating unilateral exophthalmos and proptosis due to intraorbital tumours. If the upper eyelids cannot be easily everted on the affected side, the exophthalmos is more likely to be due to thyrotoxicosis, whereas if the lid is easily everted it is more likely due to an intraorbital mass. 90. Grey Turner sign: Skin discolouration (bruising) in the left flank (left costovertebal angle) in cases of acute haemorrhagic pancreatitis. 91. Gilbert’s sign: Opsiuria indicative of hepatic cirrhosis (opsiuria means excretion of urine more rapidly during fasting than after a meal). 92. Glasgow’s sign: A clinical sign—presence of systolic murmur over the brachial artery is found in latent aortic aneurysm. 93. Griffith sign: It is one of the clinical signs of Graves’ orbitopathy wherein there is lower lid lag on upward gaze. 94. Guyon’s sign: Ballottement and palpation of a floating kidney. 95. Gaur sign: A clinical sign seen in femoral hernia. Distension of superficial epigastric and/or circumflex iliac veins on the affected side due to pressure on these vessels by the hernial sac. 96. Guerin’s sign: Haematoma at greater palatine foramen seen in maxillary fracture. 97. Homan’s sign: Pain on sudden dorsiflexion of the foot—a sign of deep vein thrombosis of calf veins. 98. Hamilton Bailey sign: A clinical sign described for intussusception. A sausage shaped mass with concavity towards the umbilicus which is felt to harden as a wave of peristalsis commences. 99. Hall’s sign: This sign identifies a tracheal diastolic shock felt in the aneurysm of aorta. 100. Hatchcock’s sign: Refers to the tenderness towards the angle of the jaw in mumps. 101. Haudek’s sign (Haudek’s niche): A radiological sign identified in barium meal X-ray done in patient suffering from gastric ulcer. It describes a projecting shadow (niche) in radiographs due to settlement of barium in pathological niches of stomach wall. 102. Hitzelberger’s sign: A clinical sign described in case of acoustic neuroma wherein there is anaesthesia of medial, posterior or superior areas of the external auditory canal because of the tumour tissue compressing on the facial nerve. 103. Hook sign: This clinical sign identifies flexion of fingers in a case of acute suppurative tenosynovitis. 104. Horn’s sign: This sign identifies the pain produced by traction on the right spermatic cord in acute appendicitis. 105. Howship Romberg sign: A sign described in the patients suffering from obturator hernia. The patient complains of pain passing down the inner side of the knee due to pressure on the obturator nerve by the hernial sac. 106. Harvey’s sign: Two index fingers are placed by the side on a vein. The fingers are now pressed firmly and the finger near the heart is moved proximally keeping the steady pressure on the vein so as to empty the short length of vein between the two fingers. The distal finger is now released. This will allow venous refilling to be observed which will be poor in ischemic limb and increased in arteriovenous fistula. 107. Hamman’s sign (Syn: Hamman’s mediastinal crunch or murmur): A clinical sign—precordial crunching, clicking or knocking sound synchronous with each heart-beat heard on auscultation in conditions such as:  Acute mediastinitis  Pneumomediastinitis  Pneumothorax. 108. Inflammatory signs (Syn: Cardinal signs in inflammation):  Rubor—Redness  Calor—Temperature  Dolor—Pain  Tumour—Oedema/swelling  Functio lesa—Loss of function 109. Jendrassik’s sign: Paralysis of extraocular muscles—A manifestation of Graves’ orbitopathy. 110. Jugular sign (Syn: Quekenstedt’s sign; Tobey Ayer test): On spinal canal block (e.g. spinal tumour) when pressure is applied over jugular veins, in the manometer connected to LP needle, either pressure will not raise or if raises falls slowly. 111. Joffroy’s sign: Absence of wrinkling of the forehead when the head is bent down and the patient is asked to look upwards—A sign of Graves’ ophthalmopathy. 112. Kernig’s sign: A sign which is positive in meningitis. With the hip flexed, the knee is extended, normally it can be done upto 175°. In meningitis it is restricted due to spasm of the hamstrings. 113. Kaposi Stemmer sign: Failure to pick up or to pinch a fold of skin at the base of the second toe. It is characteristic of lymph oedema. 114. Kocher sign (Syn: Mean’s sign): A sign of Graves’ orbitopathy. The examiner places one hand on a level with the patient’s eye and then lifts it higher. The upper eyelid springs up more quickly than the eyeball. 115. Kanavel sign: This sign is useful in the diagnosis of ulnar bursitis. In case of ulnar bursitis the site of maximum tenderness is over that part of the ulnar bursa lying between the transverse palmar creases. 116. Kantor’s sign (String sign of Kantor): A radiological sign described in barium enema follow through in patients suffering from Crohn’s disease. A string like configuration of contrast material through a filling defect is seen in the radiography. 117. Kehr sign: This sign identifies the pain elicited in the left shoulder in patients with suspected splenic rupture. The pain (referred pain) experienced by the patient is due to blood in the peritoneal cavity irritating the diaphragm. 118. Klemm’s sign: It is the radiological sign found in chronic appendicitis where there is often an indication of tympanitis in the right lower quadrant. 119. Knie’s sign: Unequal dilatation of the pupils—a sign of Graves’ orbitopathy. 120. Krisowski’s sign: Cicatricial lines radiating from the mouth in congenital syphilis.

Fascinating Signs in Surgery 121. Kenawy’s sign: A clinical sign usually associated with bilharzial fibrosis of liver (Egyptian splenomegaly) but may be present in any type of portal hypertension. Auscultation over the xiphoid process reveals a venous hum (splenic vein engorgement) which becomes prominent on inspiration. 122. Klein’s sign (of shifting tenderness): A clinical sign useful in acute nonspecific mesenteric lymphadenitis. When patient is shifted to left lateral position, point of maximum tenderness also gets shifted to the left side in contrast to acute appendicitis. It may also be positive in Meckel’s diverticulitis. 123. Lemon sign: A radiological sign of Arnold-Chiari deformity. There is scalloping of the frontal bones giving the skull a lemon shaped configuration in sonography of the fetal skull during second trimester of pregnancy. 124. Lennhoff’s sign: A furrow appearing on deep inspiration below the lower rib and above an echinococcal cyst of liver. 125. Sign of Leser Trelat: Sudden appearance and rapid increase in size and number of seborrhoeic keratoses, a sign of internal malignancy of the GIT. 126. Lloyd’s sign: A clinical sign elicited in a patient with renal calculus. Pain elicited in the loin on deep percussion over the kidney even when there is no pain on applying deep pressure. 127. London’s sign: It is useful in ruptured intestine suspected in an accident case. The presence of pattern of bruising of the skin (i.e. an imprint of the clothing is noted on the skin) indicates that a crushing force has been applied sufficient to rupture the bowel against the vertebral column. This sign is a strong indication to carry a laparotomy. 128. Mallet Guy’s sign: A clinical sign identified in chronic relapsing pancreatitis. It is elicited by placing the patient in the right lateral position with the patient’s hip and knee flexed and deeply palpating the abdomen in the epigastric and the left subcostal region. This will evoke tenderness in chronic relapsing pancreatitis. 129. McBurney’s sign: Finger tip pressure is made over the McBurney point elicits severe tenderness in patients with appendicitis. 130. Murphy’s sign (Moynihan’s method): This clinical sign is classically described in patients suffering from cholecystitis. It is elicited by asking the patient to breath deeply while exerting moderate pressure with the left hand such that thumb lies over the fundus of the gallbladder. The patient catches his breath as the inflamed gallbladder which is pushed down by the diaphragm gets imposed against the thumb. 131. McEwen’s sign: A clinical sign elicited in children with hydrocephalus. On percussion of skull behind the junction of frontal, parietal and temporal bones and auscultation over opposite mastoid bone there is a more resonant note than normal, seen in internal hydrocephalus and cerebral abscess in children (syn: cracked pot sign, cranial cracked pot sound). 132. Meniscus sign: Refer No. 57. 133. Moebius sign: Inability to keep the eyeballs converged due to insufficiency of medial rectus muscle— A clinical sign of Graves’ ophthalmopathy. 134. Milian’s ear sign: A clinical sign which is useful to differentiate facial erysipelas from cellulitis. Erysipelas being a cuticular lymphangitis spreads from the face to the pinna while the cellulitis which is spreading inflammation of the subcutaneous tissue stops short of pinna because of close adherence of the skin to cartilage. 135. Mahler’s sign: A steady increase of pulse rate without corresponding increase of temperature seen in thrombosis. 136. Mann’s sign (Syn: Dixon Mann’s sign): In Graves’ disease the two eyes appear not to be on the same level. 137. Marie’s sign: Tremors of body extremities in Graves’ disease and other types of hyperthyroidism. 138. Mean’s sign (Syn: Kocher’s sign): Refer No. 114. 139. Medusa Lock sign: A radiological sign described in patients with intestinal obstruction due to roundworm infestation. A plain X-ray erect film of the abdomen reveals trapped intestinal gas within the worm mass giving a characteristic appearance of coiled locks of hair—Medusa Lock sign. 140. Meitzer’s sign: Loss of normal second heart sound on auscultation of the heart after swallowing. Seen in occlusion or contraction of lower part of oesophagus. 141. Mercedes Benz sign (Syn: Crow foot sign): Refer No. 51. 142. Mexican hat sign: A radiological sign described in barium enema (filling defect) done in patients with pedunculated polyp of the inferior wall of the colon. 143. Maulage sign: Waxy cast appearance of bowel segments—A radiographic sign of coeliac disease. 144. Mose’s sign: A clinical sign suggestive of deep vein thrombosis. It is elicited by squeezing the relaxed calf muscles from side to side which is painful in case of deep vein thrombosis. 145. Niche sign (Syn: Haudek’s sign): Refer No. 101. 146. Nicoladoni’s sign (Syn: Branham’s sign): Refer No 31. 147. Oliver’s sign (Syn: Porter’s sign; Tracheal tug): Tracheal tug is seen in:  Aneurysm of the aorta.  Neoplasm which fixes bronchus to aorta. 148. Omega sign: A radiological sign observed in patient suspected of sigmoid volvulus on the X-ray. A plain X-ray abdomen taken in the supine position shows a massively distended sigmoid colon with haustrations arising from the pelvis resembling Greek letter ‘omega‘ (w). 149. Payr’s sign: Pressure over the sole of the foot elicits severe pain in cases of thrombophlebitis. 150. Peroneal sign: Tapping the peroneal nerve near the fibular neck causes dorsiflexion and abduction of foot in hypocalcaemic tetany. 151. Perez’s sign: A friction sound heard over the sternum when the patient raises and drops his arms. A sign of mediastinal tumour or aneurysm of arch of aorta.

Learn to see, learn to hear, learn to feel, learn to smell—that is clinical method.

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SRB's Manual of Surgery 152. Parrot’s sign (Syn: Parrot’s nodes, hot cross bun skull, Natiform skull): Bony nodes on the outer table of the skull of infants with congenital syphilis, so that it has a hot cross bun or buttock shape. 153. Pfuhl sign: A clinical sign which helps in differentiating between subphrenic abscess and pyopneumothorax. Inspiration increases the force of flow in paracentesis in subphrenic abscess, but lessens in case of pyopneumothorax. This distinction is however lost in cases where diaphragm is paralyzed. 154. Pitre’s sign: Hypoaesthesia of scrotum and testes in tabes dorsalis. 155. Plummer’s sign (Syn: Quadriceps sign): Inability to step up onto the chair or to walk up steps seen in Graves’ disease and other forms of hyperthyroidism. 156. Pool Schlesinger’s sign: In tetany if patients leg is held at the knee joint and flexed strongly at the hip joint, within a short time there will be an extensor spasm at the knee joint with extreme supination of foot. 157. Porter’s sign: Tracheal tugging in aneurysm of aortic arch and neoplasms which fix the left bronchus to aorta. 158. Potain’s sign: Extension of percussion dullness over the arch of the aorta from the manubrium to the third costal cartilage on the right side—seen in cases of dilatation of the aorta. 159. Prehn’s sign: Elevation and support of the scrotum will relieve the pain in epididymo-orchitis but not in torsion testis. 160. Psoas sign (Syn: Cope’s test): Refer No. 49. 161. Puddle sign: Describes a clinical method to detect small amount of ascites (150–500 ml). Patient lies prone for 5 minutes and then goes for knee-elbow position. In this position dullness is elicited in the umbilicus in case of minimal ascites. 162. Pemberton’s sign: This sign refers to symptoms of faintness with evidence of facial congestion and external jugular vein distension when the arms are raised above the head touching the ears. This manoeuvre reduces the thoracic inlet thereby hampering venous drainage of the face in the presence of retrosternal thyroid. 163. Pointing sign: Ask the patient to point to the site of maximum pain. If this proves to be the site of localized tenderness it is also certainly the site of diseased organ, e.g. appendicitis. 164. Patel’s sign: It is important in paralytic ileus. Apply the stethoscope firmly to the skin just below and right of the umbilicus for full 3 minutes. In paralytic ileus there will be omnious silence, broken by patient’s own heart sounds believed to be transmitted via the over distended coils of the intestine with added succussion splashes if the patient moves and very occasionally by faint tinkles. 165. Pad sign: A radiological sign identified in patients with carcinoma of the head of pancreas wherein the ‘C’ loop of barium filled duodenum may be widened. 166. Panda sign (Raccoon sign, Spectacle haematoma, Black eye): Haemorrhages in soft tissues around the eye and in the eyelids is known as Panda sign as it resembles panda eyes. It is caused by: 1. Direct trauma, such as punch to the eye. 2. Blunt impact to the forehead, the blood gravitating downwards over the supraorbital ridge. 3. Fracture of the floor of the anterior fossa of the skull. 167. Queckenstedt’s sign (Jugular sign; Tobey Ayer test): Refer No. 110. 168. Quenu Muret sign: A prognostic indicator. In aneurysm, when the main artery of the limb is compressed and a puncture is made at the periphery, if the blood flows, then the collateral circulation is probably established. 169. Rat-tail sign: A radiological sign described in relation to oesophageal carcinoma. 170. Ridge sign: A clinical sign of dehydration. In considerable dehydration if the skin is picked up in between the thumb and fingers and then released, instead of it springing back with normal elasticity, a ridge is formed that subsides slowly. 171. Rovsing sign: In acute appendicitis, when left iliac fossa is pressed; pain is felt in right iliac fossa. 172. Release sign (Syn: Rebound tenderness; Blumberg’s sign): Refer No. 25. 173. Reversed 3-sign: Refer No. 81. 174. Reisman sign (Syn: Snellen’s sign): The bruit heard over the closed eye in Graves’ disease. 175. Rocher’s sign: A clinical sign which helps in the differentiation of epididymitis from torsion of the testes. In torsion testes, the epididymis cannot be distinguished from the body the testes, whereas in epididymitis the body of the testes can be felt in the enlarged crescent of epididymis. 176. Rommelaere’s sign: An abnormally small proportion of normal phosphates and of sodium chloride in urine in cancerous cachexia. 177. Rotch sign: A clinical sign identified in case of pericardial effusion. Dullness is felt on percussion on the right 5th intercostal space. 178. Rovighi’s sign: A fremitus felt on percussion and palpation of the superficial hepatic hydatid cyst. 179. Racoon sign (Syn: Panda sign, Spectacle Haematoma, Black Eye): Refer No. 166. 180. Sign of splashing (Syn: Succussion splash): Seen in gastric outlet obstruction. 181. Saegesser’s sign: A clinical sign identified in patients with splenic rupture. An excruciating tenderness is elicited in the Saegesser’s point or splenic point (seen in the lower part of the posterior triangle of the neck between the left sternomastoid and scalenus medius muscle above the clavicle). 182. Sternomastoid sign (Syn: Trail’s sign): The sternal head of the sternomastoid muscle will become more prominent on the side to which trachea is deviated. 183. Saenger’s sign: Refers to the light reflex of the pupil that has ceased, returns after a short stay in the dark. Observed in cerebral syphilis but not in tabes dorsalis. 184. Sansom’s sign: Described in two separate context:  Marked increase in the area of dullness in the second and third intercostal space – Due to pericardial effusion.  A rhythmical murmur heard with a stethoscope applied to the lips in aneurysms of the thoracic aorta. 185. Schlesinger’s sign (Syn: Pool’s phenomenon): Refer No. 156. 186. Schultze sign (Syn: Schultze Chvostek sign): Refer No. 38.

Fascinating Signs in Surgery 187. Silex’s sign: Furrows radiating from the mouth in congenital syphilis. 188. Sisto’s sign: Constant crying in infancy—a sign of congenital syphilis. 189. Setting sun sign: A clinical sign described in patients suffering from raised intracranial tension. There is downwards deviation of the eyes so that each iris appears to set beneath the lower eyelid with white sclera exposed between it and the upper lid. This sign is observed in cases:  Hydrocephalus  Intracranial haemorrhage  Brain tumours 190. Snellen’s sign (Syn: Reisman sign): Refer No. 174. 191. Sumner’s sign: This sign is said to be positive when there is increase in the tone of the abdominal muscle on gentle palpation of the right iliac fossa. It may indicate:  Appendicitis  Right ureteric or renal stones  Torsion ovarian cyst. 192. Simon’s sign: Identifies absence of usual correlation between the movements of diaphragm and thorax, seen in early cases of meningitis. 193. Stierlin’s sign: A radiological sign observed in barium enema study of the colon where there is absence of normal shadow due to an indurating or ulcerative process such as tuberculosis of caecum or colon. 194. String sign (Syn: Kantor’s sign): Refer No. 116. 195. Suker’s sign: Deficient complementary fixation in lateral eye rotation—a manifestation of Graves’ orbitopathy. 196. String of beads sign: A series of round shadows resembling a string of beads or pearls, seen on a radiograph of small intestine, indicating of trapped gas surrounded by the fluid of obstructed and distended bowel. 197. Stellwag’s sign: Identifies the widening of palpebral fissures (staring look) due to retraction of upper eyelids, an early sign of Graves disease. 198. Stemmer sign (Kaposi Stemmer sign): Refer No. 113. 199. Slip sign: A clinical sign which helps in differentiating a solid swelling, e.g. lipoma, from a cystic swelling. Here, when the edge of the swelling is palpated, the margin of the solid swelling does not yield but slips away from it unlike a cystic swelling which yields to the pressure of the palpating finger and does not slip away. 200. Solius sign: A radiological finding observed in a chest X-ray lateral view in patient’s with enlarged thymus. An enlarged thymus being a firm swelling does not get flattened against sternum by the pressure of heart and great vessels. 201. Shrinkage sign: A radiological sign of thymus enlargement. In a chest X-ray there is a paradoxical alteration of the shape of the chest with respiration (Decrease in transverse diameter with deep inspiratory film than the expiratory film). 202. Seagull sign: Refer No. 51. 203. Suzmann’s sign: A clinical sign described in patient with coarctation of aorta. The collaterals which develop display visible and palpable pulsations together with thrills and murmurs which are most obvious in the inter-scapular and infra-scapular regions of the back. The Dock sign is the radiological counterpart of this sign. 204. Trail’s sign (Syn: Sternomastoid sign): Refer No. 182. 205. Tap sign (Syn: The percussion sign; Chevrier’s sign): If the valves are incompetent an impulse will be felt by the fingers overlying the long saphenous vein when the varicosities are percussed below. 206. Thornton’s sign: Refers to the severe pain complained by the patient in the region of the flanks in nephrolithiasis. 207. Tinel’s sign (Syn: DTP sign; Formication sign): Refer No. 69. 208. Tresilian sign: This sign identifies reddish appearance (congestion) in opening of Stensen’s duct in cases of mumps. 209. Trimadeau’s sign: A radiological sign identified in barium swallow X-ray done in patient’s with dysphagia. If the dilatation above an oesophageal stricture is conical, the stricture is fibrous; while it is cup shaped (shouldering) it is likely to be malignant. 210. Tanyol’s sign: In ascites umbilicus shifts downwards and in mass arising from pelvis it shifts upwards. 211. Troisier’s sign: Identifies enlargement of left supraclavicular lymph node (Virchow’s node). Seen in:  Ca stomach  Ca testes  Ca bronchus  Malignancy of any other abdominal organ. 212. Trousseau’s sign: This sign is described under two different context:  The blood pressure cuff is applied to the arm and inflated to pressure above systolic pressure for 3–5 minutes. This will elicit typical carpopedal spasm (obstetrician’s hand) in cases of hypoparathyroidism and other conditions associated with hypocalcaemia.  Migrating superficial thrombophlebitis—a sign of visceral carcinomas especially of pancreas or the stomach. 213. Tracheal fluctuation sign: A unique sign elicited in patients suffering from achalasia cardia. 214. von Graefe’s sign (Syn: Graefe’s sign): Persistent lagging of upper lid behind the corneoscleral limbus when patient is asked to follow the finger moved up and down several times. Seen in Graves’ disease. 215. Vermooten’s sign: A clinical sign helpful in the intrapelvic rupture of urethra. On per rectal examination, the prostate cannot be felt but in its position a doughy swelling (blood and urine) is felt. If prostate is felt, it is displaced upwards. 216. Vas sign: This sign is helpful in differentiating testicular neoplasm and an inflammatory lesion of the testes. Inflammatory lesions causes vas deferens to become considerably thickened which remains normal in cases of neoplasm.

Absolute diagnosis are unsafe and are made at the expense of the conscience.—William Osler

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SRB's Manual of Surgery 217. Vein sign: A bluish cord along the mid-axillary line formed by the swollen junction of the thoracic and superficial epigastric vein. Seen in:  Tuberculosis involving the bronchial glands  Superior vena cava obstruction. 218. Wegner’s sign: A postmortem finding—A broadened discoloured appearance of the epiphyseal line in infants who have died from congenital syphilis. 219. Wilder’s sign: An early clinical sign of Graves’ disease consisting of slight twitch of the eyeball when it changes its movement from adduction to abduction or vice versa. 220. Wimberger’s sign: Symmetrical erosions of the proximal tibia seen radiographically in infants with congenital syphilis. 221. Water lily sign (Syn: Lily pad sign): A radiological sign identified in cases of hydatid cyst of the lung. When the hydatid cyst ruptures, the daughter cyst floating within the cavity appear like a water lily hence the name water lily sign. 222. Smith’s sign: Murmur heard in cases of enlarged bronchial lymph nodes on auscultation over the manubrium with the patients head thrown backwards. 223. ‘H’ Bomb sign: A radiological sign seen in cases of atrophic gastritis. The gastric folds within fundus and the body of stomach are very thin and the thin walled fundus becomes distended with air (in erect posture) or with barium contrast.

B. Triads in Surgery 1. Saint’s triad: Diverticulosis of colon Gallstones Hiatus hernia. 2. Whipples’ triad: Seen in insulinoma. Features of hypoglycaemia Blood sugar less than 45 mg% Symptoms are relieved by glucose. 3. Charcot’s triad: Seen in ascending cholangitis. Intermittent fever Intermittent pain Intermittent jaundice. 4. Virchow’s triad: Change in the vessel wall Diminished rate of blood flow Increased blood coagulability. 5. Murphy’s triad: Seen in acute appendicitis. Pain in right iliac fossa Vomiting Temperature. 6. Hutchinson’s triad: Seen in late congenital syphilis Interstitial keratitis 8th nerve deafness Hutchinson’s teeth. 7. Trotter’s triad: Seen in nasopharyngeal carcinoma. Conductive deafness Elevation and immobility of same side soft palate Pain in the side of the head. 8. Tillaux’s triad: Seen in mesenteric cyst. Soft fluctuant swelling in the umbilical region Freely mobile in the direction perpendicular to mesentery Zone of resonance all around. 9. Triad of portal hypertension: Varices Splenomegaly Ascites. 10. Cushing’s triad: In intracranial hypertension. Increased blood pressure Decreased pulse rate Decreased respiratory rate. 11. Triad of renal cell carcinoma: Anaemia Haematuria Mass in the loin. 12. Borchardt’s triad: Seen in gastric volvulus Acute epigastric pain Violent vomiting Inability to pass nasogastric tube. 13. Beck’s triad: Seen in cardiac tamponade. Muffled heart sounds Distended neck veins Hypotension.

14. Pancoast’s triad: Seen in Pancoast tumour. Excruciating pain in the arm Horner’s syndrome Erosion of ribs. 15. Prune-Belly triad: Seen in Prune-Belly syndrome. Cryptorchidism Abdominal wall defects Genitourinary defects. 16. Mackler’s triad: Seen in Boerhaave’s syndrome. Vomiting Chest pain Subcutaneous emphysema. 17. Triad of Sandblom: Seen in haemobilia Jaundice Pain Melaena. 18. Galezia triad: Dupuytren’s contracture Retroperitoneal fibrosis Peyronie’s disease of penis. 19. Dieulafoy’s triad: Seen in appendicitis Hypersensitiveness of skin Reflex muscular contraction Mac Burney’s tenderness. 20. Triad of congenital diaphragmatic hernia Respiratory distress Apparent dextrocardia Scaphoid abdomen. 21. Carney’s triad Functioning adrenal para ganglioma—nonfamilial Gastric leiomyosarcoma—GIST Pulmonary chondroma. 22. Triad of Ohashi in IPMN in ERCP A bulging ampulla of Vater Mucin secretion Dilated main pancreatic duct. 23. Haimovici triad of revascularisation of an acutely ischaemic limb Muscle infarction Myoglobinuria Acute renal failure. 24. Triad of small bowel obstruction in plain X-ray Dilated small bowel loops >3 cm Multiple air fluid levels in erect X-ray Paucity of air in the colon. 25. Gilroy Bevan triad of adhesive pain is Pain may get aggravated or relieved on change of posture Pain in the region of old abdominal scar Tenderness is elicited by pressure over the scar.

Reason of life is destiny of unknown; and desire of life

C. Misnomers in Surgery 1. White bile: It is neither white nor bile. It is opalescent. It contains mucous. It signifies severe obstructive jaundice due to which secretion of bile from liver is stopped. Mucous is derived from biliary tree lining. 2. Mycotic aneurysm: It is not due to fungal infection. It is due to bacterial infection. 3. Lateral aberrant thyroid: It is not an aberrant thyroid. It is secondaries in neck lymph node from occult primary in the thyroid, i.e. papillary carcinoma thyroid. 4. Adenolymphoma of parotid gland: It is not lymphoma. It is a benign tumour of the parotid. It never turns into malignancy. 5. Pretibial myxoedema: It is not seen in myxoedema. It is seen in thyrotoxicosis. 6. Sternomastoid tumour: It is not a tumour. It is due to birth trauma which causes organised haematoma in sternomastoid muscle. 7. Dissecting aneurysm: It is aortic dissection, not dissecting aneurysm. 8. Malignant hydatid: It is not malignant. It is due to Echinococcus alveolaris. It behaves like a malignant condition. 9. Malignant exophthalmos: It is due to primary thyrotoxicosis. It is not a malignant condition. 10. Spina ventosa: It is tuberculous dactylitis. It is not related to spine. 11. Mycosis fungoides: It is cutaneous “T” cell lymphoma. It is not due to fungal infection. 12. Hypernephroma: It is renal cell carcinoma. It is not above the kidney. 13. Hepatoma: It is hepatocellular carcinoma. It is not benign tumour. 14. Melanoma: It is melanocarcinoma. It is not benign. 15. Surgical ganglion: It is arising from the synovial sheath. It is not from nerve ganglion. 16. Brain fungus: It is not a fungal infection. It is seen in cranial injury wherein due to injury brain protrudes out of the wound as fungus. 17. Cock’s peculiar tumour: It is not a tumour. It is ulcerated sebaceous cyst. It mimics SCC of skin. 18. Pott’s puffy tumour: It is not a tumour. It is osteomyelitis of the frontal bone with cellulitis of the frontal region of the scalp. It may spread intracranially through emissary veins which endangers the life of the patient. 19. Tumour alba: It is tuberculosis of synovial sheath of knee joint. 20. Umbilical adenoma: It is not a tumour. It is prolapse of mucosa of cutaneous end of vitello-intestinal duct 21. Madelung’s deformity: It is not associated with any of the conditions in the lung. It is a congenital subluxation or dislocation of the lower end of the ulna, from malformation of the bones. 22. Ray fungus: Actinomycoses, a bacteria infection. 23. Malignant pustule: Anthrax infection. 24. Malignant oedema: Gas gangrene. 25. Juvenile melanoma: It is not a melanoma. It is benign SPITZ naevus. 26. Hydrocele of the neck: It is cystic hygroma 27. Kuttner tumour: It is chronic sclerosing sialadenitis of submandibular salivary gland. 28.  Aneurysmal bone cyst: It is not related to artery. It is expanding lesion in the bone containing blood mixed fluid of unknown aetiology. 29.  Hairy leucoplakia: It is hairy leucoplakia with white confluent patches of fluffy / hairy hyperkeratotic thickening almost always situated in the lateral border of the tongue. It is not hair in tongue; not related hair diseases; not structurally hair component.

D. Triangles in Surgery 1. Hesselbach’s triangle: The medial border of the triangle is formed by the rectus sheath, superolateral border by the inferior epigastric artery, inferior border by the inguinal ligament. Importance: Helps in differentiating direct from indirect hernias. 2. Bryant’s triangle: Patient lies in supine position, three lines are drawn, one from the anterior superior iliac spine vertically down to the bed; another from the tip of the greater tronchanter to join the first line at the right angles; third line from anterior superior iliac spine to the tip of the greater tronchanter—this forms a triangle. Importance: Diminution in the length of the second line indicates upward displacement of the greater trochanter. Third (oblique) helps determine the anteroposterior displacement of the greater tronchanter. 3. Triangle of Doom: Bounded by the ductus deferens medially, spermatic vessels laterally in the male and the apex of the triangle is at the level of internal inguinal ring. Importance: External iliac artery and vein, femoral nerve are located in the triangle and so stapling is avoided in this triangle while doing laparoscopic preperitoneal repair for hernia. 4. Calot’s triangle: Formed medially by the common hepatic artery, laterally by the cystic duct and the apex is formed by the junction of the cystic and the hepatic ducts. Base is formed by the cystic artery. Importance: Cystic lymph node of ’Lund’ is present in the fork created by the junction of the cystic and common hepatic artery. 5. Anal triangle and urogenital triangle: A transverse line joining the anterior parts of the ischial tuberosities and passing immediately anterior to the anus divides the perineum into two triangles, anal and urogenital triangle. Anal triangle contains the termination of the anal canal in the median plane and an ischiorectal fossa on each side. Importance: Both the perineal and ischiorectal spaces in the anal triangle are common sites of abscess. 6. Femoral triangle: It is triangular depression on the front of the upper one-third of the thigh below the inguinal ligament, bounded medially by the medial border of adductor longus, laterally by the medial border of sartorius, apex is formed by the meeting point of the medial and lateral boundaries. Importance: Femoral vein in this site is most suitable for intravenous injection in the infants; femoral artery pulsations are an important aid for clinicians (in diagnosing peripheral vascular disease). 7. Lumbar triangle: a. Inferior lumbar triangle of Petit—bounded by the crest of ilium below, external oblique laterally and medially by the latissimus dorsi. Importance: Most primary lumbar hernia occur through this triangle. b. Superior lumbar triangle of Grynfelt—bounded by the 12th rib above, medially by the sacrospinalis and laterally by the posterior border of the inferior oblique. Importance: Grynfelt hernia appears through superior lumbar triangle. 8. Triangle of auscultation: This is a small triangular interval bounded medially by the lateral border of the trapezius, laterally by the medial border of the scapula and inferiorly by the upper border of latissimus dorsi. Floor of the triangle is formed by the 7th rib, 6th and 7th intercostal spaces and rhomboids minor. Importance: This is the only part of the back which is not covered with muscles. Respiratory sounds are better heard with a stethoscope here than that heard elsewhere in the back. On the left side, the cardiac end of the stomach lies deep to this triangle and in days before X-rays were discovered, sounds of swallowed liquids were auscultated over this triangle. 9. Simon‘s triangle: Bounded anteriorly by the recurrent laryngeal nerve, posteriorly by the common carotid artery and base is formed by the inferior thyroid artery. Importance: Aids in identification of the recurrent laryngeal nerve. 10. Lumbosacral triangle of Marcille: It is a triangular interval on each side of the body of the 5th lumbar vertebra, bounded medially by the body of the 5th lumbar vertebra, laterally by the medial border of the psoas muscle, apex by the junction of the psoas major muscle and the body of the 5th lumbar vertebra. Base is formed by the upper surface of the ala of the sacrum and floor by the transverse process of the 5th lumbar vertebra and the iliolumbar ligament. Importance: Ureter crosses the common iliac vessels at the lateral angle of the triangle. 11. Retromolar trigone: Base overlies the ascending ramus of the mandible from the last molar, apex terminates at the maxillary tuberosity, laterally continuous with the buccal mucosa and medially blends with the anterior tonsillar pillar. Importance: Common site for oral malignancy. 12. Sherren’s triangle: Bounded by the umbilicus, symphysis pubis and the anterior superior iliac spine. Importance: Indicates the area of hyperaesthesia in an acute episode of appendicitis. 13. Scalene triangle: Bounded by scalenus anticus anteriorly, scalenus medius posteriorly and first rib inferiorly. Importance: Subclavian artery and trunks of the brachial plexus pass through the scalene triangle where they may be compressed causing thoracic outlet syndrome.

Dead men are always good men !!

E. Drugs at a Glance Remember how much you do not know. Do not pour strange medicines into your patients. —William Osler, 1903

ANTIBACTERIALS It seems likely that in the next few years a combination of antibiotics with different antibacterial spectra will furnish a “cribrum therapeuticum” from which fewer and fewer infecting bacteria will escape. —Alexander Fleming, 1946

SULFONAMIDES They act by inhibiting folic acid synthetase which converts PABA to folic acid. Side effects: Intolerance, crystalluria, agranulocytosis, goitre, neuritis, jaundice. Drugs Sulfadiazine: 1 gm 6th hourly. Sulfamethizole: 200 mg 6th hourly. Sulfadimidine: 1 gm 6th hourly. Sulphamethoxazole: Sulfaguanidine: 3 gm 6th hourly. Sulfamethoxale: 1 gm 6th hourly. Used in meningitis, UTI, chancroid, trachoma, ulcerative colitis, toxoplasma, Bacillary dysentery. Silver sulphadiazine cream 1% for burns. Sulphacetamide as ophthalmic solution. Cotrimoxazole: Combination of trimethoprim and sulfamethoxazole in a ratio of 1 : 5 in different strengths Trimethoprim inhibits dihydrofolate reductase enzyme which converts dihydrofolate into tetrahydrofolate. It has got synergistic action with sulphamethoxazole. It is used as BID dose in typhoid, plague, UTI, prostatitis. Side effects: Severe skin reactions, megaloblastic anaemia.

QUINOLONES They act by interfering with the synthesis of DNA. They are useful against gram-negative organisms, enteric fever, respiratory infections, gastroenteritis, urinary infections, tuberculosis. Side effects: Allergic reactions, CNS manifestations, hallucinations, nephritis, arrhythmias. Drugs Nalidixic acid 1 gm 6th hourly. Norfloxacin 400 mg BD for 10 days. Ciprofloxacin 500 mg BD for 10–14 days. Pefloxacin 400 mg BD. Ofloxacin 200 mg OD or BD for 10–14 days. Lomefloxacin 400 mg OD. Sparfloxacin 200 mg BD. Levofloxacin 500 mg OD for 7–14 days. Gatifloxacin 200 mg OD.

PENICILLIN It acts by interfering with the cell wall synthesis of bacteria. Used in Streptococcus, Pneumococcus, Meningococcus and gonococcal infections, syphilis, tetanus, gas gangrene, actinomycosis, plague. It is also used as prophylaxis in rheumatic fever. It is used in pelvic infections, lymphoedema. Side-effects: Anaphylaxis, serum sickness, Jerisch-Herxheimer reaction.

Drugs at a Glance Drugs: Benzyl penicillin. 4–10 lakhs 4th or 6th hourly intravenously after test dose. Procaine-penicillin 4–10 lakhs IM after test dose OD for 7–14 days. Benzathine penicillin 12–24 lakhs deep IM into the buttocks after test dose once in 3 weeks.

AMPICILLIN/AMOXYCILLIN/TALAMPICILLIN/PIVAMPICILLIN Used in respiratory infections, meningitis, endocarditis, cutaneous infections. It is not useful in penicillin-resistant staphylococci infections. Dose: 500 mg 6th hourly.

METHICILLIN

It is a penicillin group of antibiotic which is used in penicillin resistant staphylococcal infections. Dose: 1-2 gm. IM 6th hourly. 1 gm in 5–10 ml normal saline can be used as intrapleural or intra-articular therapy.

CLOXACILLIN/DICLOXACILLIN/FLUCLOXACILLIN These drugs are used in penicillin resistant staphylococcal infections. Dose: 500 mg 6th hourly.

CARBENICILLIN/TICARCILLIN It is used in septicaemias, urinary tract infections mainly due to Pseudomonas and Proteus infections. Dose: 1 gm 6th hourly IV.

PIPERACILLIN/AZOCILLIN/MEZLOCILLIN It is active against Pseudomonas. Dose: 2 gm 4th–6th hourly.

CLAVULANIC ACID It is a beta lactamase inhibitor used against beta lactamase producing bacteria. It is used along with amoxycillin/ticarcillin/ampicillin.

SULBACTUM It is a beta lactamase inhibitor. It is combined with ampicillin.

TAZOBACTUM It is a beta lactamase inhibitor combined with piperacillin.

CARBAPENEM/IMIPENEM/MEROPENEM These are bactericidal beta lactam antibiotic. They are used in septicaemia, Pseudomonas, Klebsiella and Proteus infections.

LINCOMYCIN/CLINDAMYCIN They act on bacterial ribosomal RNA. Side effect: Pseudomembranous colitis. Dose: 500 mg tds.

VANCOMYCIN/TEICOPLANIN It inhibits cell wall synthesis. Side effects: Nephritis, ototoxicity. Used in pseudomembranous colitis. Dose: 500 mg 6th hourly IV.

He is the best physician who knows the worthlessness of many medicines.—Benjamin Frunklin

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SRB's Manual of Surgery CEPHALOSPORINS They are bactericidal. They inhibit bacterial cell wall synthesis. Useful in most of the bacterial infections. Side effects: Anaphylaxis, Hepatotoxicity, Nephrotoxicity. Ist Generation

IInd Generation

Cephalexin 500 mg TDS oral. Cephadroxyl 500 mg BD oral. Cephadrine 250 mg QID oral. Cephazolin 1 gm BD IV. Cephalothin 2 gm 6th hourly. Cepharin 2 gm 6th hourly.

Cefuroxime 500 mg BD oral. Cefaclor 500 mg 8th hourly. Cefamandone 2 gm 6th hourly. Cefoxitin 2 gm 8th hourly. Cefonicid 2 gm 6th hourly. Ceforanide 2 gm 12th hourly.

IIIrd Generation

IVth Generation

Cefetoxime 1 gm 6th or 8th hourly. Ceftriaxone 1 gm 12th hourly. Ceftizoxime 2 gm 8th hourly. Ceftazidime 2 gm 8th hourly. Cefaperazone 2 gm 12th hourly. Cefixime 200 mg BD orally.

Cefepime 200 mg BD orally. Cefpodoxime 200 mg BD orally.

MACROLIDES They act by inhibiting protein synthesis and also by blocking ribosomal activity. Side effects: Allergic reactions, gastric irritation, cholestasis. Uses: Respiratory infections, skin infections. Drugs: Erythromycin: 500 mg QID. Roxithromycin: 150 mg BD. Azhithromycin 500 mg OD before food for 3 days. Clarithromycin 500 mg BD. It is also used as anti-Helicobacter pylori in treating duodenal ulcer. Spiramycin 1–5 millions BD.

AMINOGLYCOSIDES They block the RNA-ribosome combination and also inhibits the enzymes involved in Krebs’ cycle. Side effects: Ototoxicity (vestibular), nephrotoxicity. Aminoglycoside will not get absorbed through the GIT because of high pH. So they are given either IM or IV. As bowel antiseptic they can be given orally. Drugs: 1. Streptomycin: 0.75 gm IM OD for 3 months. Used in tuberculosis, plague, chancroid, granuloma inguinale, brucellosis, respiratory infections, gut sterilisation during large bowel preparation. 2. Kanamycin: 1.5 gm/day. It is more cochlear toxic. 3. Gentamicin: 80 mg BD IM or IV. 1 mg/kg body weight. Antipseudomonal drug. 4. Tobramycin 5 mg/kg body weight. More effective against Pseudomonas than gentamicin. 5. Amikacin 250 mg BD IM/IV. 15 mg/kg body weight. 6. Netilmycin: 3–6 mg/kg body weight. 7. Neomycin 1 gm 6th hourly. Mainly used in hepatic failure and in gut sterilisation. 8. Framycetin as 0.5% ointment. 9. Paromomycin: 2 gm QID. Used in amoebic dysentery.

TETRACYCLINES They are bacteriostatic. They act by inhibiting enzyme system, protein synthesis and ribosomal activity. Side effects: Hepatic dysfunction, gastric irritation, permanent yellow staining of teeth, suppresses the bone growth. Uses: Plague, cholera, sexually transmitted diseases like syphilis, gonorrhoea, chancroid, actinomycosis. It is also used to identify malignant cells as brilliant yellow fluorescence under UV light after giving tetracycline for 5 days. Dose: 500 mg QID. Doxycycline: 100 mg OD/BD for 10–14 days.

Drugs at a Glance CHLORAMPHENICOL / THIAMPHENICOL It interferes with protein synthesis. Side effects: Bone marrow suppression, Grey-baby syndrome, liver damage. Uses: Typhoid fever, meningitis, plague. Dose: 2 gm/day.

DRUGS FOR TUBERCULOSIS RIFAMPICIN: It inhibits DNA-dependent RNA polymerase. It is bactericidal. Side effects: Hepatotoxicity, orange-red coloured urine, flu-like syndrome. Uses: Tuberculosis. Other uses: Leprosy, Meningococcal carrier, brucellosis, mycetoma, Q-fever, Legionella, Chlamydia. Dose: 450–600 mg/day (OD) before food. RIFABUTIN: 150 mg/day. ISONICOTINIC ACID HYDRAZINE (INH): It inhibits the synthesis of phospholipid synthesis of cell wall of bacteria. It is bactericidal. Side effects: Intolerance, Neuritis, Hepatitis. It crosses the blood-brain barrier and placenta. Dose: 300 mg orally OD. ETHAMBUTOL: It is bacteriostatic. Side effects: Gastric intolerance, retrobulbar neuritis (green colour vision is defective). It crosses the blood-brain barrier and concentrates in CSF. Dose: 25 mg/kg body weight. 800 mg OD after food. PYRAZINAMIDE: It is bactericidal. It acts on dormant bacteria, bacteria inside the macrophages and caseating material. Side effects: Hepatotoxicity, hyperuricaemia, photosensitivity. Dose: 1.5 gm OD after food or 750 mg BD after food for 2 months. MORPHAZINAMIDE: 3 gm/day. STREPTOMYCIN. CYCLOSERINE: 2 gm daily. It is a reserve drug. VIOMYCIN: 1 gm twice a week. IM. It is used in multi-drug-resistant tuberculosis. AMIKACIN/KANAMYCIN. CAPREOMYCIN. PAS: Para-amino salicylic acid: It interferes with PABA metabolism of the bacteria.   Side effects: GIT intolerance, hepatotoxicity, blood abnormalities. ETHIONAMIDE and PROTHIONAMIDE. CLARITHROMYCIN. AZHITHROMYCIN.

ANTIAMOEBIC DRUGS DEHYDROEMETINE: It acts on the trophozoite. But not on the cyst. It is used for extra-intestinal amoebiasis. Side effects: Myocarditis, myalgia. Dose: 60 mg deep IM OD for 10 days given under monitor. DIIDOHYDROXYQUINOLINE: 2 gm/day. It is more useful against trophozoites. IDOCHLOROHYDROXYQUINOLINE: 0.75 gm/day. It is more useful in cyst passers. CHLOROQUINE: Used for only extra-intestinal amoebiasis. 500 mg BD for 2 days. 250 mg BD up to 3 weeks. METRONIDAZOLE: 400–800 mg tds for 10 days. Or 500 mg (1 mg/ml) tid IV. It is used for intestinal and extra-intestinal amoebiasis.

Abilities not used are abilities wasted.

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SRB's Manual of Surgery TINIDAZOLE: 300–600 mg tid for 3–5 days. SECNIDAZOLE: 2 gm single dose after food for intestinal amoebiasis. 2 gm OD for 5 days. ORNIDAZOLE: DILOXANIDE FUROATE: 500 mg tid for 10 days. Used in cyst passers and chronic carriers. TETRACYCLINES: 2 gm/day for 10 days. It is used only as an adjuvant drug.

IMPORTANT ANTIHELMINTHICS PIPERAZINE CITRATE: Dose: 5 gm single dose. 1 ml = 150 mg. Used for Ascariasis. Side effects: Cerebellar ataxia, vertigo, convulsion. TETRAMISOLE: 150 mg for adult, 50 mg for children. Used in ascariasis and ankylostomiasis. MEBENDAZOLE: 100 mg BD for 3 days. 600 mg tid for 21 days. Used in Ascariasis, Ankylostomiasis, Trichuris trichura, hydatid cyst. ALBENDAZOLE: 400 mg single dose. PRAZIQUANTEL: 500 mg tid for 15 days. THIABENDAZOLE: 25 mg/kg for 3 days. PYRANTEL PALMOATE: 11 mg/kg. 15 ml. (1 ml = 50 mg). LUCANTHONE 1 gm tid for 3 days. HYCANTHONE 4 mg/kg orally for 4 days. Used in S. haematobium, S. mansoni. METRIFONATE: 7.5 mg/kg for 3 days. NIRIDAZOLE: 25 mg/kg. Used in schistosomiasis. ANTIMONY COMPOUNDS: Given intramuscularly. Used in S. haematobium and leishmaniasis. DIETHYL CARBAMAZINE CITRATE (DEC): 100 mg tid for 21 days. Used in Filariasis, tropical eosinophilia, larva migrans. LEVAMISOLE: 150 mg OD. Used in ascariasis, hookworms, strongyloidosis, as immunomodulator in cancer.

ANTICOAGULANTS HEPARIN: 10,000 units IV and later 5,000 subcutaneously 8th hourly. Uses: DVT, pulmonary embolism, DVT prophylaxis. Heparin therapy should be monitored by partial thromboplastin time (PTT). Side effects: Haemorrhage, alopecia. Protamine sulphate neutralizes the action of heparin. It is given IV slowly. Dose should not exceed 50 mg. LOW MOLECULAR WEIGHT HEPARINS: It has got longer duration of action. Monitoring is not required. Given as once a day regime. Dalteparin 2500–10, 000 IV- SC/IV. Enoxaparin: 40 mg SC. Parnaparin. Fraxiparin. WARFARIN SODIUM: It is an oral anticoagulant. It is monitored using prothrombin time. Available as 5 mg tablets. Dose: 10 mg OD. It causes haemorrhage and drug interactions.

Drugs at a Glance OTHER DRUGS xx VITAMIN K: 10 mg OD IM for 3–5 days. It is used in bleeding disorders, Vitamin K deficiencies in children, liver disorders. xx ERYTHROPOIETIN: 500 IU/kg thrice a week. It is used in chronic renal failure. xx BROMOCRIPTINE: Dose: 20 mg/day. It is used to suppress lactation, galactorrhoea, hyperprolactinaemia, parkinsonism, acromegaly. xx CLOMIPHENE CITRATE: Used in infertility. Dose: 50 mg for 5 days from 5th day of menstruation. xx OCTREOTIDE: 0.1 mg BD. Used after pancreatic surgeries in haematemesis, gut endocrine tumours. xx VASOPRESSIN: 20 IU IV/SC. Used in bleeding oesophageal varices. DESMOPRESSIN 4 microgram/day-SC-IV-NASAL SPRAY. TERLIPRESSIN: 2 mg IV. xx L-THYROXINE: 25, 50, 100, 200 microgram tablets. Uses: Myxoedema, cretinism for maintenance therapy after total thyroidectomy, as suppressive therapy in papillary carcinoma thyroid (300 µgm) in physiological goitre, in dyshormonogenesis. xx ANTITHYROID DRUGS: Side effects: Agranulocytosis and alopecia. CARBIMAZOLE: 5–20 mg daily exactly 8th hourly. METHIMAZOLE: 5–20 mg daily. PROPYLTHIOURACIL: 600 mg tid. Used in pregnancy and children. xx DANAZOL: It is used in fibrocystic disease of breast, gynaecomastia, mastalgia, infertility, precocious puberty. Dose: 800 mg OD. xx ANTACIDS: Aluminium hydroxide, magnesium trisilicate, sodium bicarbonate. Dose is variable. xx CARBENOXOLONE: 100 mg tid. It is used in peptic ulcer. It causes water and sodium retention, hypokalaemia. xx H2 RECEPTOR BLOCKERS: Used in peptic ulcer. Cimetidine 1000 mg/day. Ranitidine 150 mg BD or 300 mg at bed time. Injection ranitidine 50 mg IV 6th–8th hourly. Famotidine: 40 mg OD. Roxatidine 75 mg OD. Nizatidine. xx PROTON PUMP INHIBITORS: Used in peptic ulcer. Omeprazole: 20 mg OD/BD 1 hour before food. Lanzoprazole: 30 mg OD before food. Esomeprazole 40 mg OD. Pantoprazole 40 mg OD before food. xx PIRENZEPINE: 50 mg BD. Used in peptic ulcer. xx BISMUTH COLLOIDS: Used in peptic ulcer. It is also anti-Helicobacter pylori. It stains the oral mucosa. xx SUCRALFATE: Used in peptic ulcer. Dose: 1 gm tid. xx ONDANSETRON: 8 mg BD. Orally or IV. It is used to prevent vomiting before starting chemotherapy. xx LAXATIVES: Castor oil: 16 ml HS. Phenolphthalein 300 mg HS. Bisacodyl 5 mg orally. HS or 100 mg as rectal suppositories. Isabgol as bulk laxative. 15 mg HS. Liquid paraffin: 30 ml HS. xx ANTIDIARRHOEAL: Bismuth kaolin. Diphenoxylate, atropine. Loperamide 2–4 mg 8th hourly or as required up to maximum of 16 mg/day dose. xx PROKINETIC DRUGS: Metoclopramide: Used in vomiting, dyspepsia, hiccough. It causes extra-pyramidal reactions. Domperidone: Dose: 10 mg tid before food. It does not cause extra-pyramidal reaction as it does not cross the blood-brain barrier. Cisapride: 10–40 mg/day before food. It can cause cardiac arrhythmias. Mosapride. xx POTASSIUM: It should be given only in IV drip slowly. IV Bolus should not be given. 2 mEq/ml. Dose: 20–40 m equivalents. IV should be given under ECG monitoring. xx SODIUM BICARBONATE: 7.5% w/v in correction of acidosis.

It seems likely that in the next few years a combination of antibiotics with different antibacterial spectra will furnish a “cribrum therapeuticum” from which fewer and fewer infecting bacteria will escape. —Alexander Fleming

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Appendix

URINE

Important Laboratory Values

Specific gravity: Normal: 1.010 to 1.025. Low: less than 1.010. High: more than 1.025. Fixed: 1.010 to 1.014. Reaction: Acidic with a pH of 6.0. Colour: Clear and amber coloured. Parameter

Values

Aldosterone Nitrogen Amylase Calcium Catecholamines Copper Creatinine Creatinine clearance Estrogens 17–hydroxy corticosteroids 5–HIAA 17–ketosteroids Magnesium Metanephrines Urine osmolarity Phosphorus Porphyrins   Coprophyrin   Uroporphyrin Potassium Protein Sodium Urobilinogen VMA

2–10 μg/day 0.4–1.0 gm/day 30–250 Somogyi units/hour