The 60 seconds advantage to get sick kids back on track... with a smile! IP : 196.52.84.10
P E M C
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Pediatric Emergency Medicine Course
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Disclaimer Every effort has been made to ensure that the drug doses herein are accurate and in accordance with the standards accepted at the time of publication. However, the user is advised to check the doses carefully. The author shall not be responsible for any error in this publication. Besides, as new research and experience broaden our knowledge, changes in treatment and drug therapy occur. Therefore, the reader is advised to check the product information sheet included in the package of every drug he/she plans to administer to be certain that changes have not been made in the recommended dosage or in the contraindications. This is of particular importance in regard to new or infrequently used drugs. In addition the protocols given in this IP : 196.52.84.10 book are valid at the time of publication and are subject to constant review.
The ‘Pediatric Emergency Medicine Course’— ‘PEMC’. The name and the power point presentations have been legally copyrighted to the Indian Society of Critical Care MedicineChennai Chapter. The name of the course ‘Pediatric Emergency Medicine Course’ or ‘PEMC’ or its contents cannot be used by other individuals or societies in conducting courses of this nature without the written consent of the ISCCM-Chennai Chapter. No unauthorized copying/editing, etc. of the manual or power point presentations from the course material are permitted. Use of the name or course content as mentioned above will imply violation of copyright laws.
The 60 seconds advantage to get sick kids back on track... with a smile! Second Edition IP : 196.52.84.10
Editor Indumathy Santhanam md dch Professor and Head Department of Pediatrics Government Royapettah Hospital Kilpauk Medical College Chennai, Tamil Nadu, India
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P E M C
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Pediatric Emergency Medicine Course
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[email protected] This book has been published in good faith that the contents provided by the contributors contained herein are original, and is intended for educational purposes only. While every effort is made to ensure accuracy of information, the publisher and the editor specifically disclaim any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the contents of this work. If not specifically stated, all figures and tables are courtesy of the editor. Where appropriate, the readers should consult with a specialist or contact the manufacturer of the drug or device. Pediatric Emergency Medicine Course (PEMC) First Edition: 2008 Reprint: 2011 Second Edition: 2013 ISBN 978-93-5090-694-1 Printed at
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Dedicated to IP : 196.52.84.10 The postgraduates and nurses of Institute of Child Health, Madras Medical College, whose disciplined efforts, skills and insights have helped establish the founding principles behind the ‘60 seconds advantage’ in saving lives.
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∫
satyameva jayate nān™taˆ satyena panthā vitato devayānaƒ | yenākramanty™¢ayo hyāptakāmā yatra tat satyasya paramaˆ nidhānam || Truth alone triumphs; not falsehood. Through truth the divine path is spread out by which the sages whose desires have been completely fulfilled, reach where that supreme treasure of Truth resides.
∫
Mundaka Upanishad 3.1.6 circa 2500 BCE
Contributors IP : 196.52.84.10
Editor in Chief Indumathy Santhanam md dch Professor and Head Department of Pediatrics Government Royapettah Hospital Kilpauk Medical College Chennai, Tamil Nadu, India All topics except those from contributors Associate Editor
IP : 196.52.84.10 Jayanthi Ramesh dnb Senior Consultant Kanchi Kamakoti Childs Trust Hospital Chennai, Tamil Nadu, India Procedures
Associate Editor Janani Shankar dnb phD Senior Consultant Kanchi Kamakoti Childs Trust Hospital Chennai, Tamil Nadu, India Procedures
Associate Editor Radhika Raman dnb Senior Consultant Kanchi Kamakoti Childs Trust Hospital Chennai, Tamil Nadu, India Procedures
Associate Editor Shanthi Sangareddi md dch Associate Professor Chinglepet Medical College Chinglepet, Tamil Nadu, India Hypertension DKA Dengue
Associate Editor Thangavelu S md mrcph Senior Consultant Mehtas’ Children’s Hospital Chennai, Tamil Nadu, India Interpretation of Chest Radiographs
Associate Editor Balaji J Assistant Professor Government Dharmapuri Medical College Dharmapuri, Tamil Nadu, India Snake Envenomation
Associate Editor Ramesh Babu B Assistant Professor Government Dharmapuri Medical College Dharmapuri, Tamil Nadu, India Emergency Medications and Equipments
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Guest Editors Mahadevan md Professor and Head Department of Pediatrics Jawaharlal Institute of Postgraduate Medical Education and Research IP : 196.52.84.10 Puducherry, India Envenomation
Suresh Gupta md dch Consultant Pediatrician Pediatric Emergency Department Sir Ganga Ram Hospital New Delhi, India Poisons
Contributors Thanyanat Bunnag md Professor Queen Sirikit National Institute of Child Health Bangkok, Thailand Pra-on Supradish md Queen Sirikit National Institute of Child Health Bangkok, Thailand
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Siripen Kalayanarooj md Queen Sirikit National Institute of Child Health Bangkok, Thailand Dengue Ramesh Menon P Senior Lecturer Department of Pediatrics TD Medical College Alappuzha, Kerala, India Rakesh Lodha Assistant Professor All India Institute of Medical Sciences New Delhi, India Specific Poisons
Pradeep Padmanabhan md msc Assistant Professor Division of Pediatric Emergency Medicine University of Louisville Louisville, KY, USA Pain and Sedation in the ED Jayshree Muralidharan md Additional Professor Department of Pediatric Intensive Care Advance Pediatric Center Postgraduate Institute of Medical Education and Research Chandigarh, India Diabetic Ketoacidosis Yuri Gilhotra Consultant Division of Pediatric Emergency Medicine University of Brisbane Australia Sonia Singh Consultant Division of Pediatric Emergency Medicine University of Pittsburgh USA Severe Traumatic Brain Injury
Contributors
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Student Editorial Committee (Institute of Child Health, Madras Medical College)
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Associate Editor Padmavathy Venkatasubbu dch (2010)
Associate Editor Sangeetha Yoganand md dm (2005)
Associate Editor Rajeshwari Sridharan md (2007)
Associate Editor Kumar N md (2005)
Associate Editor Ramkumar md dm (2007)
Vishwanthan T md (2002)
Prasanna dnb (2002)
Naushad Mallagi dnb (2002)
Jyothsna S dch mrcph (2003)
Jayaprakash mrcph (2003)
Narmada dch dnb mrcph (2003)
Sendhil Kumar KS md (2003)
Shekhar md dch (2004)
Padma dnb (2004)
Priyavardhini md (2005)
Editor in Chief Gunda Srinivas dch (2007)
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Pediatric Emergency Medicine Course (PEMC)
IP : 196.52.84.10 Rajesh Balakrishnan dch (2005)
Srinivas md (2005)
Murali T md (2005)
Sendhilnathan P dch (2006)
Gowrishankar md (2006)
Arun Kumar T md dch (2006)
Kamalkanth dch (2007)
Palani Rajan dch (2007)
Arun Kumar dch (2007)
Susheel Narain dch (2007)
Sujatha md (2007)
Nandini dch dnb (2007)
Shanthakumar md (2007)
Sendhil Kumar md dm (2007)
Mullai Baalaaji md (2008)
Vijaykumar dch (2009)
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Contributors
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IP : 196.52.84.10 Rajitha K dch (2009)
Sugavanesh dch (2009)
Babu Balachandar dch (2009)
Sangeetha dch (2009)
Dhakshayini md (2009)
Sasikala dch (2009)
Jagadeesh A md (2010)
Satya Priya dch (2010)
Vidyasagar dch (2010)
Shankar Srinivasan dch (2010)
Jeyanthi md dch (2012)
Gandhi dch (2012)
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Gopinath md (2002) Rajendran md (2003) Sivaraman md (2005) Saravanan K dch (2005) Ramachandran T dch (2007) Capt. Murali md (2008) Santhosh dch (2009) Sweetlin dch (2009) Gokul dch (2012)
Punitha R md (2012)
Uma md dch
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Foreword IP : 196.52.84.10In 2010 India recorded 1.3 million infant deaths—the highest for any country.1 Millennium Development Goal 4 (MDG 4) requires a two-thirds reduction infant mortally rates (IMR) from 1990 levels by 2015.2 It is predicted that, if current rates of decline in IMR continue, India will achieve MDG4 by 2023-2024, however, if the pace slows, it may only be achieved by 2033-2034.1 All too often medical, pediatric and emergency textbooks, courses and research are targeted at developed countries. Unfortunately, those of us working in developing countries, frequently struggle to translate the recommended best practice into our workplaces. In the field of emergency pediatrics in the developing world, our patients are most likely to present with neonatal emergencies or childhood infections2,3 (sometimes complicated by malnutrition, lack of immunizations, Tuberculosis or HIV). Developing world emergency patients frequently present late and in a critical condition. We often have to contend with woefully inadequate staffing, equipment and resources. IPstaff : 196.52.84.10 Our have rarely been trained in the assessment and management of pediatric and neonatal emergencies. In many developing countries prehospital care, transport and emergency medical systems are underdeveloped or absent. For these reasons many courses and much of the research published from developed countries is not directly relevant to the practice of emergency care in poorer parts the world. Therefore, it gives me great pleasure to endorse the second edition of this excellent pediatric emergency textbook catering for the developing world emergency environment. Given that India accounts for 21% of worldwide under-5 deaths4 it is very encouraging to see experts from this country highlighting quality emergency care of children as a crucial part of the solution. The Pediatric Emergency Care Manual has been written by expert pediatric practitioners—who are clearly experienced in high volume, high acuity, low-resource emergency settings. This book is first and foremost a practical manual of “How to manage seriously ill children?” and this is explained in an easy-to-follow clear manner—often with the use of high quality photographs to illustrate techniques. There are also lots of handy tips—my particular favorite being the ‘common errors’ box included at the end of most chapters. These invariably contain the kinds of ‘pearls of wisdom’ only gained through considerable experience and rarely passed on in textbooks. I am especially impressed by the in-depth explanations of underlying mechanisms of disease and pathophysiology. These help the reader to understand in a ‘back to basics’ way what is going on in a patient and help make differential diagnoses. There is also considerable detail and up to date information on key drugs, emergency treatments and essential equipment. If ever there was a time for pediatric emergency knowledge, skills and expertise to be shared, particularly in India and other developing countries, it is now. Books like this will hopefully form part of the armamentaria of practical help for frontline emergency workers in the battle to reduce global child mortality.
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References
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1. Reddy H, Pradhan MR, Ghosh R, Khan Ag. India’s progress towards the Millennium Development Goals 4 and 5 on infant and maternal mortality. WHo South-East Asia Journal of Public Health. 2012;3:279-89. 2. Building a Future for Women and Children: The 2012 Report. Available: http://www.countdown2015mnch.org/reports-andarticles/2012-report. 3. Lozano R, Wang H, Foreman KJ, Rajaratnam JK, Naghavi M, Marcus JR, et al. Progress towards Millennium Development Goals 4 and 5 on maternal and child mortality: an updated systematic analysis. Lancet. 2011;378(9797):1139-65. 4. You D, Jones G, Hill K, Wardlaw T, Chopra M. Levels and trends in child mortality, 1990-2009. The Lancet. 2010; 379(9745):931-3.
Baljit Cheema mbbs mrcpch bsc dtm&h Chair of Pediatric Emergency Care of South Africa (PECSA) Sub-group of Emergency Medicine Society of South Africa (EMSSA) Member and Lead for Standards of Emergency Care Document-Pediatric Emergency Medicine Special Interest Group of the International Federation of Emergency Medicine (IFEM) Pediatric Emergency Specialist, Khayelitsha Hospital, Cape Town and Emergency Medical Service, Western Cape Honorary Senior Lecturer Department of Health IP : 196.52.84.10 Division of Emergency Medicine University of Cape Town South Africa
Preface to the Second Edition IP : 196.52.84.10The long awaited second edition of the Pediatric Emergency Medicine Course (PEMC)
manual is here. A veritable atlas of resuscitation, it has the largest number of photographs taken before, during and after resuscitation! It explains how the pediatric assessment triangle has been modified to help take therapeutic decisions. Current evidence-based guidelines have been incorporated such that safer and more effective treatments are employed during resuscitation. What’s more! For the first time evidence from our own patients has been used to teach how to save life in the initial minutes. Since 2008, the Pediatric Emergency Medicine Course (PEMC) has achieved several milestones to its credit. In 2010, the Vice Chancellor, Dr Myilvahanan Natarajan ms mch phd and the senate of the Tamil Nadu Dr MGR Medical University, Tamil Nadu, India, passed a resolution making PEMC mandatory for interns (PEMC for house officers) passing out from all medical colleges in Tamil Nadu state. To ensure that thisIPwas implemented, Dr Srilakshmi dch phd, Head, Curriculum Development, Tamil Nadu Dr MGR Medical University, : 196.52.84.10 undertook the task of organizing the ‘train the trainers’ program for Professors and Assistant Professors from all its medical colleges. Her concerted efforts made the PEMC for house officers a reality. In 2011, at the executive committee meeting of the Society of Trauma and Emergency Pediatrics, decision was taken to endorse the PEMC. Earlier in 2006, the PEMC had been copyrighted to the Indian Society of Critical Care Medicine— Chennai Chapter. In 2011, on the eve of the National Assembly of Pediatric Emergency Medicine (NAPEM-2011), the first PEMC-instructor course was conducted. Over 40 instructors from different parts of the country participated. Meanwhile, the PEMC continued to gain in popularity and more than 100 courses were conducted in different parts of the country viz Hyderabad, Kakinada, Thiruvananthapuram, Bengaluru, Agartala, Kolkata and Chennai. The PEMC also went overseas and was conducted in Sydney as part of the Pediatric Critical Care—Pre-congress workshop in 2011. In 2012, the Indian Academy of Pediatrics—Tamil Nadu State Branch under the Presidency of Dr Sivaprakasam, resolved to conduct the course (PEMC for Practitioners) in every district. In 2013, it was conducted as part of the pre-congress workshop of the national Indian Academy of Pediatrics (IAP) Congress, PEDICON at Kolkata. The lessons learnt have now become the core curriculum of the postdoctoral PEM fellowship conducted under the auspices of the Tamil Nadu Dr MGR Medical University. Dr Jeyachandran md dch, Dr P Ramachandran md dch and Dr M Kannaki md dch (Directors of the Institute of Child Health, Madras Medical College), facilitated establishing the fellowship program at this hospital.
Indumathy Santhanam
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Preface to the First Edition IP : 196.52.84.10
“Excellence in specialized pediatric emergency care to get kids back on track”
Few situations in a pediatrician’s practice evoke the anxiety and panic which accompanies the management of an acutely ill child. The Pediatric Emergency Medicine Course (PEMC) offers a structured approach to handle the crisis using a time sensitive, goal directed approach during the initial “golden hour” of critical illness. Conceived by Dr S Krishnan, a pilot course was conducted in 1999 with the collaboration of the emergency and intensive care physicians of the Kanchi Kamakoti Childs Trust Hospital and the Institute of Child Health, Madras Medical College, under the suspices of the Indian Society of Critical Care Medicine (ISCCM)—Chennai Chapter. Since then the content of the course has undergone tremendous changes as international resuscitation guidelines evolved providing better standards of care. In 2006, this course was formally copyrighted to the ISCCM, Chennai Chapter. At the 5th National Pediatric Critical Care Conference, executive body meeting of the Indian Academy of Pediatrics, Critical Care Chapter held at Surat in October 2003, it was suggested the PEMC manual be re-written with evidence-based IP : 196.52.84.10 guidelines. This was not easy. Most resuscitation guidelines are based on work published in Western centers. Do these protocols work for us? Evidence is sparse in the Indian context! Using international guidelines as a prototype, protocols were modified to suit realities of a large volume Emergency Department of a public children’s hospital with little access to resources and advanced technology. Surprisingly, implementation of these modified protocols over the last ten years resulted in mortality rates to levels almost on par with developed nations in life-threatening pediatric emergencies. This is of special relevance in our country, where the vast majority of critically ill children, do not have access to appropriate prehospital emergency medical services, specialist retrieval teams and advanced intensive care facilities. Where critical care often evokes thoughts of advanced technology involving expensive resources this message is of paramount importance. Emergency medicine also involves the ability to take quick and accurate decisions in life-threatening pediatric emergencies. To assist novice residents to take acceptable lines of action quickly in critical illnesses, this manual elucidates a structured method of fitting the findings of the cardiopulmonary assessment into the pediatric assessment triangle, understanding the physiological status and making the optimal therapeutic decisions in the first hour of resuscitation in the absence of biochemical or radiological support. While academicians may feel that the methods published in this manual may not have been validated in other centers, this approach has dramatically improved survival at the Emergency Department (ED) of the Institute of Child Health, which receives and resuscitates the largest volume of pediatric emergencies in the planet!
Indumathy Santhanam
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Acknowledgments IP : 196.52.84.10Successful achievement of therapeutic goals in resuscitation is based on coordinated team efforts. Many of the milestones
of the Pediatric Emergency Medicine Course (PEMC) have been achieved by the combined effort of a hugely talented team. Dr Jayanthi, convenor for the PEMC and south zone coordinator for the BLS, has been a bulwark of strength and integrity on which this course has grown. Dr Shanthi, an active PEMC instructor and former south zone convenor for the PALS, is known for her tremendous commitment for teaching pediatric emergency medicine to young doctors at the bed side. Dr Janani, the former National convenor of the PALS and team leader par excellence is the dynamic force behind this course. Dr Radhika, the South zone convenor of the PALS and coordinator for the BLS is also known for her passion for training doctors in CPR. Under the banner of the Indian Academy of Paediatrics, Tamil Nadu State Branch, Dr Thangavelu, Dr P Ramachandran and Dr Poovazhagi some of the finest intensive care teachers of Tamil Nadu state have taken key messages of this course to the far nook and corners of every district. I thank Dr Suresh Gupta, President and Founding Member of the Society of Trauma and Emergency Pediatrics, and Dr Mahadevan, Professor and Head, Department of Pediatrics, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India for editing the section on poisons and envenomation. I also thank, Professor P Arasar IP : 196.52.84.10 Seeralar, Dr Ramesh Babu, Dr J Balaji, Dr Gowrishankar, Dr Gandhi, Dr Punitha, Dr Vijaykumar, Dr Sasikala, Dr Uma and Dr Ashok of the Department of Pediatrics, Government Dharmapuri Medical College, Dharmapuri, Tamil Nadu, India for adopting these methods in their practice. By enthusiastically implementing these protocols, they were able to demonstrate ‘zero’ mortality during the dengue and scrub typhus epidemic in a rural district known for female infanticide and high infant mortality rates. The concepts that have been taught over many years at the PED of the Institute of Child Health, Madras Medical College were translated on to paper by the creative efforts of Dr Gunda Srinivas. His generosity in sharing his collection of photos and films have greatly enhanced the quality of this manual. Special thanks to Dr Padmavathy, Dr Sangeetha and Dr Rajeshwari for their amazing editorial inputs! I also thank Dr S Thangavelu, Former Professor In-Charge of the Pediatric Intensive Care Unit at ICH, for promptly sending his entire database of valuable clinical material. I am grateful to Dr Bunnag and his team, Dr Padmanaban, Dr Yuri, Dr Sonia, Dr Rakesh Lodha, Dr Ramesh Menon, Dr Jayshree Muralidaran, Dr Balaji and Dr Ramesh Babu for their contributions. It was providence that came to our aid when Dr Marianne Gausche Hill, [the force behind the Advanced Pediatric Life Support (APLS) course] offered to write the prologue and Dr Baljit Cheema, member of the International Federation of Emergency Medicine, the foreword for this manual. I am deeply indebted to them. Words cannot express how grateful I am to all the parents who entrusted their most precious possession to our care and who stood by us as we resuscitated, taught and documented the treatment given to their children. I thank all these parents for permitting us to use photographs taken during resuscitation for educational purposes. I am grateful to my teachers, Dr Elizabeth John md, Dr L Subramanium md and Dr Muralinath md for teaching us the principles of interpreting radiographs in acutely ill children. Many key points have been expounded in this manual. I remember with gratitude Dr Suchitra Ranjith, Dr Soonu Udani, Dr B Ramachandran, Dr P Ramachandran and Dr Indira Jayakumar who made the first edition a great success with their contributions.
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This course owes a great deal to the management of the Kanchi Kamakoti Childs Trust Hospital for providing us with their hospitality and venue to conduct this course. My special thanks to my family. I would not have come this far without the support and encouragement of my husband, Dr Ramesh Dorairajan, my daughter Dr Varshini Ramesh, my parents, Subhashini, Selvan JP and Kicchamma. I would like to thank for the support extended by Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director) and Mr Tarun Duneja (Director-Publishing) and his associates, Ms Seema Dogra (Cover Designer) of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, and I also thank Mr Jayanandan, Mr Mukherjee and IP : 196.52.84.10 Ms Sajini (Bengaluru Branch) and her team, for their tireless efforts in making this edition a unique one.
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Contents IP : 196.52.84.10
Section I
Recognition of Critical Illness
1. Recognition of Early Signs of Critical Illness in the Outpatient Department
Section II
2. 3. 4. 5.
Airway
Basic Airway Management Pharmacologically Assisted Intubation (PAI) in the PED Assessment and Management of the Difficult Airway Flow Inflating Ventilation Device: Non-invasive CPAP in Settings without Immediate Access to Mechanical Ventilation
IP : 196.52.84.10 Section III
Section IV
Section V
Breathing ---------------- 77 ---------------- 84 ---------------- 95
Circulation
10. General Approach to the Management of Shock 11. Intraosseous Access 12. Vasoactive Drugs in the ED 13. Approach to Acute Diarrhea and Shock in the ED 14. Cardiogenic Shock 15. Septic Shock 16. Approach to Recognition and Management of Dengue in the ED 17. Anaphylaxis 18. Cyanotic Spell 19. Hypertensive Emergencies
Section VI
20. Approach to Decreased Level of Consciousness 21. Status Epilepticus
---------------- 53
---------------- 61
7. Approach to Respiratory Distress 8. Management of an Asthmatic Exacerbation 9. Pulse Oximeter
---------------- 25 ---------------- 30 ---------------- 44
Approach to Stridor
6. Stridor
----------------- 3
-------------- 101 ---------------114 ---------------119 -------------- 129 -------------- 134 -------------- 143 -------------- 158 -------------- 170 -------------- 174 -------------- 179
Disability -------------- 187 -------------- 198
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Section VII
Envenomation
22. Scorpion Sting 23. Snake Bite Envenomation
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-------------- 217 -------------- 225
Section VIII
Poisoning
24. Poisoning: General Approach 25. Specific Poisons
-------------- 239 -------------- 247
Section IX
Trauma
26. Approach to Traumatic Brain Injury (TBI) 27. Approach to Polytrauma
Section X
-------------- 265 -------------- 281
Environmental Injury
28. Burns IP : 196.52.84.10 29. Electrical Injury 30. Submersion Injury
Section XI
31. 32. 33. 34. 35.
Special Topics
Gastrointestinal Bleeding Interpretation of Chest X-rays in Critically Ill Children Procedural Sedation and Management of Pain in Children Diabetic Ketoacidosis Setting up Pediatric Resuscitation and Emergency Services
Section XII
36. 37. 38. 39. 40. 41.
-------------- 291 -------------- 296 -------------- 299
Nebulizer Therapy Needle Thoracocentesis and Thoracostomy Pericardiocentesis Cannulation of External Jugular Vein Foley Catheter Insertion Spinal Stabilization
------------------------------------------------------------------
305 312 335 344 355
-------------------------------------------------------------------------------
367 370 375 378 380 382
Procedures
Appendices
Appendices 1 to 13
389-405
Epilogue
407
Index
409
Abbreviations IP : 196.52.84.10ALI
- Acute lung injury - Altered level of consciousness - Acute laryngotracheobronchitis - Advanced pediatric life support - Acute respiratory distress syndrome - Blood brain barrier - Backwards, upwards, rightward cricoid pressure - Bag valve mask BVM CBF - Cerebral blood flow - Cannot intubate cannot ventilate CICV CPAP - Continuous positive airway pressure - Cerebral perfusion pressure CPP IP : 196.52.84.10 CPR - Cardiopulmonary resuscitation CRT - Capillary refilling time CSE - Convulsive status epilepticus DEM - Dolls eye movement DHF - Dengue hemorrhagic fever - Disseminated intravascular coagulation DIC DKA - Diabetic ketoacidosis - Displacement obstruction DOPE pneumothorax equipment failure DSS - Dengue shock syndrome EOM - External ocular movement - End tidal carbon dioxide ETCO2 ET - Endotracheal tube - Focused abdominal sonogram for FAST trauma FB - Foreign body FRC - Functional residual capacity GCS - Glasgow coma score GERD - Gastroesophageal reflux disease - Glucose normal saline GNS GTCs - Generalized tonic-clonic convulsions - Intracranial pressure ICP JR - Jackson-Rees LOC - Loss of consciousness LMA - Laryngeal mask airway - Mean arterial pressure MAP MDI - Metered dose inhaler MODS - Multiorgan dysfunction syndrome MVA - Motor vehicle accidents
ALOC ALTB APLS ARDS BBB BURP
- Minute volume - N-acetyl cysteine - Nonconvulsive status epilepticus - Norepinephrine - Nasogastric tube - Noninvasive positive pressure ventilation NMB - Neuromuscular blocking agent OPC - Organophosphorus compound OPD - Outpatient Department OR - Operating room - Pharmacologically assisted intubation PAI - Pediatric advanced life support PALS PAM - Pralidoxime PAT - Pediatric assessment triangle PBF - Pulmonary blood flow PCR - Polymerase chain reaction - Pediatric emergency department PED PE - Pulmonary edema PEEP - Positive end expiratory pressure PEFR - Peak expiratory flow rate PEGLEC - Polyethylene glycol with electrolytes - Pupils equal and reactive to light PERL PRES - Posterior reversible encephalopathic syndrome RPA - Retropharyngeal abscess RSI - Rapid sequence intubation PT - Prothrombin time SABA - Short acting beta agonist SCIWORA - Spinal cord injury without radiological abnormality SE - Status epilepticus SIRS - Systemic inflammatory response syndrome SVR - Systemic vascular resistance TBI - Traumatic brain injury TV - Tidal volume WBCT - Whole blood clotting time WBI - Whole bowel irrigation - World Health Organization WHO WOB - Work of breathing
MV NAC NCSE NE NGT NIPPV
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Prologue IP : 196.52.84.10
April 19, 2013 To, Indumathi Santhanam md IP : 196.52.84.10 Professor and Head Department of Pediatrics Government Royapettah Hospital Kilpauk Medical College Chennai, Tamil Nadu, India Dear Dr Santhanam I want to congratulate you, as editor, your contributors and publisher M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India for the production of the Second Edition of the Pediatric Emergency Medicine Course (PEMC) manual. It is designed and was first published in 2008, to be a manual for an educational course bearing its name and implemented throughout India since 1999; yet its scope goes beyond a course manual. This comprehensive and well-illustrated manual covers information vital to the care of critically ill and injured children and includes chapters on the following topic areas: Recognition of Critical Illness, Management of the Airway, Approach to Stridor, Respiratory Distress and Respiratory Failure, Shock, Diarrhea and Dehydration, Alteration of Mental Status, Envenomation, Poisonings, Traumatic Injury including Severe Traumatic Brain Injury, Orthopedic Trauma, and Environmental Emergencies. It also has a chapter dedicated to Radiology in the Emergency Department (ED), Pain and Sedation, Setting up Pediatric Emergency Medical Services in Rural Hospitals, and a section on Critical Procedures in Pediatric Emergency Care. It is a perfect reference for pediatric residents, pediatricians, and other medical care providers caring for children in emergency settings. This manual is based on the experiences of a physician practicing at a large volume pediatric emergency department at The Institute of Child Health, Madras Medical College, Chennai, Tamil Nadu, India, who resuscitate nearly 13,000 seriously ill children and neonates every year, and see nearly 750,000 pediatric outpatient visits. This manual provides sorely needed education for physicians caring for children in rural and resource poor environments, as well as physicians with access to more sophisticated medical resources. This is an amazing manual—I reviewed the Pediatric Assessment Triangle (PAT) and I think your modification is brilliant—the original PAT may be too simplistic but there is something to be said for simplicity—I love all your features and the algorithms at the end.
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Pediatric Emergency Medicine Course (PEMC)
The manual incorporates a number of special features that provides the learner with tools to rapidly assess and treat critically ill and injured children. Each chapter presents case scenario pertinent to the topic area, such as a child in respiratory distress, then proceeds through a systematic discussion of the rapid assessment of that patient using a tool based on a similar tool used in the United States for the rapid assessment of children, the Pediatric Assessment Triangle (PAT). The method described includes evaluation of appearance, airway and breathing, and circulation, which when combined together can create a picture of the physiologic status of the child and will drive management priorities including the rapid initiation of life-saving treatment. Besides Case Scenarios and use of a Rapid Assessment Tool, other features include IP : 196.52.84.10 Call Outs that provide key clinical pearls for the learner to better understand either the pathophysiology or the treatment plan. At the end of each chapter are Key Points which emphasizes important concepts that should not be forgotten in the care of children in emergency settings, Common Errors that describe important pitfalls to avoid in the care of children with a particular life-threatening condition highlighted in the chapter, and finally a Protocol is provided at the end of the chapter to serve as a quick reference guide which could be posted for pediatric emergency care providers to manage children with potentially life-threatening conditions. This manual appropriately highlights some of the serious illnesses occurring in children in the subcontinent of India, including acute diarrheal illness and hypovolemic shock. Given that there are over 450,000 cases of diarrheal disease worldwide and that 22% of deaths due to this disease occur in India, it is critical that emergency care providers recognize early signs of dehydration and hypovolemic shock and have a management plan to rapidly treat these infants and children. Recognition and management of septic shock, dengue shock syndrome and specific poisons and envenomations that are endemic in India are also discussed. Finally the manual highlights the assessment and treatment of the mortal conditions that affect children worldwide including respiratory failure, status epilepticus, burns, submersion injury, and traumatic IP : 196.52.84.10 brain injury. This comprehensive manual is a must read for any physician caring for children worldwide. With many physicians and nongovernmental organizations reaching out to provide medical care all over the world, it can be a valuable resource for these providers caring for children in many parts of the world. As the world of medicine continues to ‘go global’ this manual can serve as an important reference for physicians who may not frequently encounter some of these conditions in their home country. I applaud your efforts in educating emergency caregivers in the rapid assessment and resuscitation of children in India. This manual could be used by emergency care providers worldwide for improving the education of the physicians who are caring for critically ill and injured children in emergency settings. In summary, the Pediatric Emergency Medicine Course (PEMC) manual is comprehensive, easy-to-read, full of vital clinical information and pearls and, probably most importantly, it provides an organized approach for the pediatric emergency care provider from assessment through management. With algorithms for care at the end, it provides a means for rapid review of important concepts in the management of critically ill and injured children. Bravo, Dr Santhanam and best wishes with this important publication.
Marianne Gausche-Hill md facep faap Professor of Clinical Medicine, David Geffen School of Medicine at UCLA Vice Chair and Chief of the Division of Pediatric Emergency Medicine Director of EMS and Pediatric Emergency Medicine Fellowships Harbor-UCLA Medical Center, Department of Emergency Medicine Torrance, California, USA
Section I
Recognition of Critical Illness IP : 196.52.84.10
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Recognition of Early Signs IP : 196.52.84.10 of Critical Illness in the Out Patient Department
Figure 1.1: Long queues waiting at the OPD of a medical college affiliated, public children’s hospital in Southern India
Learning Objectives 1. Triage questions that help recognize early hypoxia, shock and myocardial dysfunction in children presenting with ‘minor symptoms’ to the out patient department (OPD). 2. Differentiate seizures from posturing secondary to hypoxia and shock.
Early recognition of critical illness, is perhaps the most important link in the chain of survival. Delayed recognition, late referral and failure to provide effective prehospital resuscitation were some of the reasons for children reaching our hospital with respiratory failure and shock.1 This is highlighted by the fact that children who presented late to the emergency service with respiratory failure and shock had increased risk of mortality.1 More recently features of pulmonary edema, myocardial dysfunction and non-convulsive status epilepticus2 were also associated with increased risk of hospital mortality. This chapter discusses, how to pick up early signs of serious illness in a large volume PED (Figure 1.1) and avoid the consequences of prolonged hypoxia and shock on the heart, lung and brain.
3. The modified cardiopulmonary cerebral assessment and pediatric assessment triangle. 4. Using the modified pediatric assessment triangle to recognize cardiogenic shock, non-convulsive status epilepticus or raised intracranial pressure (ICP) in addition to respiratory failure and shock within the first minute of arrival.
ASSESSMENT OF APpEARANCE BASED ON THE AVPU SCALE An acute fall in mental status is one of the earliest symptoms of hypoxia and shock. The severity of altered level of consciousness (ALOC) or ‘appearance’ may be evaluated rapidly using the alert, voice responsive, pain responsive, unresponsive (AVPU) scale.3
Ù In a large volume pediatric emergency department (PED), symptoms of ALOC such as incessant cry, lethargy, excessive sleepiness have been useful in recognizing hypoxia and shock.4 ●● Incessant cry, a seemingly innocuous symptom emerged as the most ominous of all the presenting symptoms in a cohort of shocked children.5
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Section I n Recognition of Critical Illness
●● ‘Drowsiness’ in the background of fever, diarrhea or breathlessness may be missed by the physician, since a drowsy child could briefly wake up and appear alert, IP : 196.52.84.10 while he is being assessed. ●● Unresponsiveness can be considered as ‘sleeping’ by parents and not brought to the attention of the ED personnel in a busy OPD.
Alert (A)
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Caveat: An early sign of critical illness, incessant cry is often dismissed as normal. Since crying is precipitated by either undressing or stranger distress, it should be identified even as the child is waiting in queue. History of incessant crying must be confirmed by the mother. The best opportunity to recognize critical illness is to observe ‘appearance’ before being formally evaluated or touched by the physician. As seen in Figure 1.2, alteration in mental status is ideally evaluated, whilst children wait in queue.
Figure 1.3: This infant was brought by his mother for diarrhea and fever. Since he was alert and playing he was triaged as normal and referred to the oral rehydration therapy (ORT) cell.
Alertness is evaluated based on age appropriate interaction of a child with his parents and environment (Figure 1.3).
Responsive to Voice (V) Recognition of drop in mental status to ‘responsive to voice’ is a challenge in all age groups. Most infants will initiate crying when put down and will stop crying immediately when picked up and held.
Figure 1.2: This figure shows a healthcare worker scanning children as they wait in queue
All too often, the physician seated in a busy OPD, can miss early fall in mental status. It is worthwhile to remember that a mother knows her child best. If she reports that her child is ‘not as usual’ then it is best to triage her child as hypoxic or shocked even if her child appears to be alert.
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Perform a detailed cardiopulmonary cerebral assessment for any child who’s mother reports ‘not as usual’, ‘more sleepy’, even, if he looks ‘normal’.
Crying has frequently been thought of as attachment behavior caused by an infant’s need to cling to its caregiver. If an infant with ‘minor symptoms’, continues to cry despite being carried and cuddled, evaluate and treat fever, pain, dehydration, wet nappy, etc. If crying does not resolve, categorize as responsive to voice and perform the rapid cardiopulmonary cerebral assessment.
Responsive to Painful Stimulus (P) Acute onset of posturing or failure to respond to the mother is alarming. Such children must be rushed directly into the ED. Sudden flexor or extensor stiffening associated with an upward gaze or hypotonia in a neurologically normal child may be secondary to respiratory failure and shock due to sepsis, hypovolemia, near fatal asthma, etc. Refer Protocol 1.1: PEMC approach: Recognition of relative bradypnea and relative bradycardia; Protocol 1.2: PEMC approach: Recognition of severity of illness on arrival to the ED, and also Figures 1.4 to 1.7.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
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Figure 1.4: A 3-year-old asthmatic girl was brought to the OPD with history of increasing breathlessness and incessant cry since early morning. She was triaged as having a near fatal attack of asthma, since she was sleepy with features of respiratory failure. Note her tone and posture as she lies floppily on her mother’s lap.
A weak cry and loss of eye contact in infants more than 2 months of age are early ominous signs of cerebral hypoperfusion. In older children lethargy, inability to sit, stand or walk, agitation, fighting the oxygen mask and confusion alternating with drowsiness herald brain hypoperfusion.
Ù Inability to recognize the mother or a vacant look is an ominous sign.
Figure 1.5: A 11-month baby was brought to the OPD for acute onset of respiratory distress and fever. Since the morning he had been crying incessantly and was not recognizing his mother. Enroute to the hospital he developed posturing. This baby presented with airway instability, RR > 80/min, grunt, abdominal respiration, tachycardia, muffled heart sounds, decompensated shock and increased liver span. Note the vacant upward gaze of the infant. His saturation was < 92%.
Figure 1.6: This infant also presented with odd squirming, wriggling movements of the limbs, which vary from the classical tonic-clonic components of status epilepticus. Features of severe cardiopulmonary failure help differentiate convulsive status epilepticus from posturing secondary to hypoxia and shock.
Febrile infants who present with squirming movements and upward gaze are often inappropriately referred or treated as atypical febrile fits.
Ù
Control the urge to administer anticonvulsants.
Figure 1.7: Hypoxia, shock and myocardial function improved following fluids, inotropes and elective intubation. Administration of anticonvulsants would have aggravated cardiorespiratory failure precipitating cardiac arrest.
1. Confirm history to find out whether the child is having a tonic-clonic movement or posturing. 2. Ask targeted questions to find out whether the child had fall in mental status such as lethargy or incessant crying prior to the onset of abnormal movements.
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Section I n Recognition of Critical Illness
3. Perform the rapid cardiopulmonary cerebral assessment. 4. Correct hypoxia and Reassess; a clearer picture IPshock. : 196.52.84.10 may emerge to guide therapy. A neurologically normal child developing difficulty in sitting or standing without support or being carried into the hospital, is indicative of critical illness (Figures 1.7 to 1.10). Children who are normal will not voluntarily lie unattended (when parents leave their line of vision). Hence, older children with fever, vomiting, etc. who lie quietly (do not protest) in their parents absence should also be subjected to a more detailed assessment (Figure 1.8).
Figure 1.9: Fluids were interrupted, inotrope initiated and intubation was performed using ketamine, atropine and suxamethonium. Crepitations resolved, saturations improved to 100% and the hepatomegaly resolved. Further fluid boluses were continued till therapeutic goals of shock were achieved. Thirst for water is another ominous symptom in older children presenting with respiratory distress and shock. Failure to recognize this ‘red flag’ symptom and aggressively resuscitate has often resulted in cardiac arrest!
Figure 1.8: A 6-year-old girl, with fever and first episode of acute respiratory distress was carried into the OPD. Since she was unable to maintain her usual tone and posture, she was triaged into the PED. She presented with impending respiratory failure and shock. At 40 mL/kg, she developed grunt, abdominal respiration, SaO2 of 90% and hepatomegaly, but shock persisted.
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Febrile children who are abusive or are inappropriately rude to the physician or their parents should also be assessed in greater detail. Thirst for water is another ominous symptom in older children presenting with respiratory distress and shock. Failure to recognize this ‘red flag’ symptom and aggressively resuscitate has often resulted in cardiac arrest! Acute onset of altered behavior, incoherent speech, agitation or fighting the mask in older children with additional history of fever, trauma, diarrhea, etc. may also suggest a serious drop in mental status.
Figure 1.10: Note the alert, smiling child in comparison with herself in Figure 1.8. Early recognition of ALOC secondary to hypoxia and shock and early goal-directed management were responsible for her neurologically intact survival.
Ù Restlessness and talking unintelligibly at any age is indicative of severe hypoxia or shock.6 • The verbal score is 2 (GCS). • Consider deep unconsciousness. • Failure to aggressively resuscitate these kids could result in rapid deterioration and cardiac arrest!
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
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●● Occasionally, acute posturing and abnormal eye movements (oculogyric crisis) occur due to an over dose of phenothiazine group of drugs. Negative ‘triage questions’ and normal ABCs in an alert child are diagnostic of acute phenothiazine toxicity. ●● History of fever, breathlessness (due to varied etiologies), acute watery diarrhea, etc. followed by progressive LOC and posturing is suggestive of very severe hypoxia and shock.
Breathlessness Figure 1.11: This picture shows a 7-year-old child with shock fighting the oxygen mask. It is an ominous sign indicative of severe hypoxia especially in older children, who are aware that an oxygen mask is not a noxious intervention. Fighting the mask, however is normal in infants and toddlers if the other parts of the pediatric assessment triangle are normal.
Breathlessness is the commonest symptom for which an acutely ill child is brought to the PED (Figure 1.12).
Unresponsiveness (U) Unresponsiveness, whilst not difficult to triage, is often a diagnostic challenge to novice pediatricians manning the ED. ●● Sudden unresponsiveness in the absence of precipitating events in a previously normal child or a child with seizure disorder is suggestive of non-convulsive status epilepticus (NCSE). ●● Failure to regain baseline consciousness after a brief generalized tonic-clonic seizure is also suggestive of NCSE.
Ù All abnormal movements in unresponsive children are not seizures. Upward gaze with extensor stiffening or flexor spasm of limbs can occur due to hypoxia and shock. This clinical presentation must be differentiated from convulsive status epilepticus. A targeted history and rapid cardiopulmonary cerebral assessment (protocol I) are essential to guide management. Inadvertent administration of anticonvulsant drugs for posturing secondary to severe hypoxia or/and shock can be lethal. On the contrary, administration of anticonvulsant drugs is life saving in NCSE.
Figure 1.12: This figure shows why children presenting with severe shock may also have respiratory distress.
Bronchiolitis, pneumonia and asthma are well known etiologies of acute respiratory distress. However, a significant number of shocked children who present to the ED, have breathlessness due to pulmonary edema2 (Figure 1.11). Severe insults such as sepsis, anaphylaxis, status epilepticus, scorpion sting, submersion injury, perinatal depression can directly affect the heart, systemic and pulmonary vasculature. ●● Vasodilation and capillary leak leads to loss of fluids. Loss exceeding 25% of effective circulating volume, results in shock.
8
Section I n Recognition of Critical Illness
●● Capillary leak also occurs in the pulmonary capillaries. Increased pulmonary vascular permeability leads to pulmonaryIP edema, also known as acute lung : 196.52.84.10 injury (ALI). ●● Severe insults (hypoxia, prolonged shock, venom, etc.) can lead to acute myocardial dysfunction. The resultant hydrostatic pulmonary edema can present as respiratory distress.
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Triage Questions
1. Mother can provide information of early hypoxia and shock for children presenting with fever, acute diarrhea, asthmatic exacerbations or focus of infection. • Is the child more tired, sleepy than usual? • Is he as usual or not? • Does the child cry inconsolably (in younger infants)? 2. Mother can also help us find out whether her child with sepsis, diarrhea, scorpion envenomation, seizures, etc. has developed features of pulmonary edema. • Has the child developed respiratory distress? • Is it the first episode (not since birth or episodic)?
Ù The three components of the PAT, appearance, breathing (evaluation of the airway is included in breathing) and circulation is depicted as 3 separate colored triangles. The arrows within the 3 triangles indicate the need to reassess systematically the response of interventions on the ABCs. Each assessment is ideally performed in less than 60 seconds (Figure 1.24).
Assessment of airway Crying or vocalization indicates that the airway is patent. Harsh inspiratory sounds suggests stridor secondary to structural airway obstruction. ‘Snoring’ in an unresponsive child indicates that the airway is obstructed by secretions or falling back of tongue. Unresponsive children presenting with stridor must be evaluated on the resuscitation trolley.7
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Presume that the airway is unmaintainable in children who are unconscious or posturing. The patency of the airway is maintained by the normal tone of the palatopharyngeal muscles and tongue. Loss of
tone of these muscles in unresponsive victims result in airway obstruction. ●● Neurogenic or functional stridor should be recognized early. The airway is positioned using the head tilt- chin lift maneuver. ●● If trauma is suspected in the unresponsive child, jaw thrust maneuver must be employed to open the airway. ●● Crying children or children with suspected ‘structural’ airway compromise should be evaluated in their parent’s lap.
Assessment of Breathing Oxygen must be administered simultaneously as the assessment is being performed. ●● Use a flow-inflating ventilation device (refer Chapter 5), if respiratory distress is identified (with the exception of asthma). ●● Use non-rebreathing mask, if effortless tachypnea is noted. ●● Simultaneously, place the hand on the chest and count respiratory rate for 6 seconds and multiply by 10. ●● Check the vital signs chart for age-related ranges. ●● Note whether respiratory rates for age are increased, decreased or normal. Vital signs for each age group must be displayed in the ED. Refer protocol 1.1.
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• If respiratory rates appear to fall within the normal range for age, but is associated with an unstable airway, shock and unresponsiveness, recognize respiratory failure. Initiate bag-valve-mask ventilation, whilst, the next responder continues to perform the remaining part of the cardiopulmonary cerebral assessment. • As the respiratory rate is being counted, look for grunt, retractions and whether respiration is thoracic or abdominothoracic. • Grunt and abdominothoracic respiration are ominous signs of impending respiratory failure.3 Respiratory effort offers information, as to whether the child has respiratory distress or respiratory failure. ●● Auscultate infra-axillary regions on both sides. ●● Listen for air entry, wheeze and crepitations. ●● Evaluate color by comparing the palm of the physician with that of the child’s sole (Figure 1.13).
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
●● Pallor, dusky hue, ashen, mottling is documented as abnormal.
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●● However, tachycardia may persist when atropine is used for intubating children in shock.5 ●● Other causes of persistent tachycardia are fever, anxiety, pain and systemic inflammatory response syndrome (SIRS).3,9 ●● In addition, tachycardia may be the only sign of ongoing seizure activity in a paralyzed and sedated child with shock. ●● Heart rates greater than 220 beats/minute in infants and 180 beats/minute in children warrant urgent evaluation and treatment.3 An electrocardiography (ECG) may be necessary, because the pulse oximeter may be unreliable in identifying supraventricular tachycardia.
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Figure 1.13: It is not uncommon for the color to be noted as normal in shocked children. The difference may be apparent only when comparing with the ‘normal’ color of the physician.
Assessment of circulation Heart Rate Assess heart rate for 6 seconds and multiply by 10. Simultaneously, check the vital signs chart to determine whether tachycardic, bradycardic or normal for age (Figure 1.14).
A heart rate that is relatively normal for age despite the presence of severe respiratory distress or failure and shock (relative bradycardia) is an ominous sign. These children have exhausted their physiological compensatory mechanisms and are at risk for abrupt deterioration and arrest. ●● Other causes of relative bradycardia in children presenting with shock are raised intracranial pressure,10,11 hypothermia, hypokalemia (often noted in diarrheal dehydration and severe malnutrition complicating septic shock), dengue shock syndrome12 and drugs such as digoxin and beta blockers.
Perfusion Comparison of Pulses Central pulse (femoral) is felt by placing the index finger of one hand snugly into the inguinal region. It is compared with the dorsalis pedis, which is felt by simultaneously placing three fingers perpendicularly on the dorsum of the foot.
Figure 1.14: Assessment of heart rate. Note that the physician is holding the airway as he evaluates the heart rate.
●● Tachycardia is the earliest compensatory response to decreased stroke volume or hypoxemia. ●● Young infants and neonates, however, may respond with paradoxical bradycardia.3 ●● Normalization of heart rate is one of the most reliable signs of shock resolution.8
●● Weak or absent distal pulses is caused by peripheral vasoconstriction, while absent distal pulses suggest decompensated shock. ●● Loss of central pulses is a premorbid sign requiring very rapid intervention.7 ●● Bounding central and distal pulses in association with tachypnea, tachycardia and altered mental status suggest the presence of a hyperdynamic circulation with low systemic vascular resistance. ●● Vasodilatory shock is identified when diastolic pressure is lower than 50% of systolic blood pressure.15 ●● If dorsalis is not felt, do not report as ‘normal’ peripheral pulse based on the posterior tibial (Figure 1.15).
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Section I n Recognition of Critical Illness
Core-peripheral Temperature Gap Assess core-peripheral temperature gap by comparing simultaneously, the temperature of the trunk with that of peripheries using the dorsal surface of both hands (gloves need not be removed to evaluate this variable) (Figure 1.16).
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Figure 1.15: Comparison of central and peripheral pulses is shown in this picture. Since interpretation of this sign is not easy, it needs experience to feel and compare the femoral and dorsalis pedis in infants. Occasionally, difficult to feel central pulses with palpable dorsalis pedis in a neonate presenting with cardiogenic shock harbingers coarctation of aorta with a patent ductus arteriosus.
Reassuring one’s self that the child is not shocked based on the presence of the posterior tibial pulse in the absence of the dorsalis pedis has often resulted in failing to pick up hypotensive shock. [Caution: The dorsalis pedis artery may be absent in 12% of normal individuals (Sarrafian’s anatomy of the foot and ankle by Armen S Kelikian)].
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History of early LOC, abnormal cardiopulmonary cerebral assessment, palpable posterior tibial with difficult to feel dorsalis pedis: Recognize shock. Table 1.1: Comparison of femorals and dorsalis pedis Femorals
Dorsalis pedis
+++1 +++1
++3 +++4
+++1
+5
< 40 mm Hg
Normal Bounding (vasodilation) Shock
++
0
Not recordable
Hypotension
2
6
Pulse pressure 30–40 mm Hg > 40 mm Hg
Inference
1: Easy to feel femorals. 2: Difficult to feel femorals. 3: Easy to feel dorsalis pedis. 4: Dorsalis pedis as well felt as femoral pulse. 5: Dorsalis pedis just felt. 6: Dorsalis pedis not felt.
Figure 1.16: Note that the dorsal surface of one hand is placed over the trunk of the infant, while the dorsal surface of the other hand slides over the thigh, leg and foot to compare the difference in temperature between the center and peripheries. If warm or cool throughout, it could signal warm or cold shock in children when other parts of the PAT are abnormal.
●● When cardiac output falls, cooling of the skin begins peripherally in the fingers and toes and extends proximally towards the trunk. A core/toe temperature difference of more than 2ºC is a sign of poor perfusion.
Capillary Refill Time (CRT) It is well known that poor peripheral perfusion may result from cool environmental temperatures in very young infants3 and hence, in very young age groups, this sign may have limited utility for both the recognition of shock and monitoring response to therapy. Other therapeutic goals such as normalization of mental status, respiratory rates and heart rates for age may be more reliable when evaluating for shock resolution in this age group. Conversely, early alterations in extremity perfusion are more reliable in older children, where the baseline mental status may appear to be relatively well preserved despite circulatory compromise.
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Avoid diagnosing shock based on prolongation of CRT in the absence of significant history and other features of shock.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
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ic anemia and congenital heart diseases with shunt lesions. Accurate blood pressure measurement requires the use of an appropriate sized cuff covering at least 75%–80% of the upper arm. Normal blood pressure readings should be displayed in the ED. Age-associated blood pressure cuffs should be used to record this vital sign (Figure 1.18). Table 1.2: Hypotension based on Emergency Cardiovascular Care Guidelines 2000 is characterized by the following limits of systolic blood pressure (SBP)
Figures 1.17A and B: The capillary refill time (CRT) is assessed by lifting the extremity slightly above the level of the heart and applying enough pressure to blanch the skin. Normal time taken for refilling of the blanched area is 2 seconds or less. A prolonged CRT may be seen in shock, rising fever and cold ambient temperature. It is also influenced by lighting and age.3
Blood Pressure Blood pressure (Table 1.2) may be preserved in early shock due to the compensatory increase in systemic vascular resistance (SVR). In young children, increase in vasomotor tone results in BP that is in the higher range for age. Under these circumstances, as therapeutic goals of shock are achieved, blood pressures may decrease to the normal range for age. In vasodilatory shock states, low SVR results in widening of pulse pressure. This is characterized by a diastolic BP that is less than or equal to half of the systolic BP. In these children, pulse pressure narrows with resolution of shock. Wide pulse pressures may also be noted in children with neurogenic and anaphylactic shock, as well as chron-
Age
SBP
Term newborn (0–28 days)
< 60 mm Hg
For infant < 12 months
< 70 mm Hg
1–10 years
< 70 + (2 × age)
> 10 years
< 90 mm Hg
Figure 1.18: Different sizes of BP cuffs used in children. Use of inappropriate large cuffs in small children will result in the recording low BP and vice versa.
Systolic blood pressure: Interpretation of systolic blood pressure in children with shock: ●● High in shock (normal response). ●● Normal range (relative hypotension). ●● Hypotension (can progress to imminent arrest in minutes). Diastolic blood pressure13: As mentioned earlier, diastolic pressures less than 50% of systolic pressure harbinger vasodilatory shock when associated with altered mental status, abnormal respiratory rates, work of breathing, tachycardia, warm, pink peripheries, bounding pulses and rapid CRT.
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Section I n Recognition of Critical Illness
●● Mean arterial pressure (MAP) is calculated as the sum of the diastolic pressure and one-third pulse pressure. A value less than 65 mm is considered as hypotension. IP Hg : 196.52.84.10 ●● Conventionally, documentation of systolic pressure is given importance. Early warm shock could be missed, if diastolic pressure and MAP are not noted.
Liver Span Measure liver span during the assessment of circulation. It is helpful in assessing and monitoring the severity of myocardial dysfunction.5
●● If the liver span is increased in children presenting with respiratory distress, it is probable that myocardial dysfunction is the causative factor. ●● A normal liver span on the other hand points to primary lung pathology as causative of respiratory distress.
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Alteration in liver span following each bolus of fluid, intubation or inotrope infusion helps to decide whether myocardial dysfunction is improving or not. Thus assessment of liver span is a simple method of assessing myocardial dysfunction in settings without access to invasive monitoring.
Disability Assessment Neurological assessment is an integral part of evaluation of a child with hypoxia, shock and seizure activity and may provide clues to the underlying etiology and response to therapy. When examining for pupillary response, simultaneously, look at the position of eyes. Is it conjugating or mid-position? Note for presence of abnormal ocular movements. Abnormal ocular movements in a child presenting with an exacerbation of asthma is suggestive of a near fatal attack. Identification of this sign in a child with respiratory failure and shock due to bronchiolitis suggests the need to aggressively resuscitate hypoxia. Indeed, eye signs in children presenting with severe cardiopulmonary failure in the absence of seizure history, has been associated with increased risk of mortality.14
Figures 1.19A and B: A. Marking lower border of liver; B. Measuring the liver span. Assessment of liver span helps in the evaluation of myocardial dysfunction in critical illness.
●● The upper border is identified by percussion and the lower border by palpation (Figures 1.19A and B). Using a pen, both borders are marked and the total span is measured and documented. ●● These measurements are compared with normal values displayed in the ED.
●● Conjugate eye deviation, nystagmus or eyelid twitch indicate presence of NCSE or severe hypoxic ischemic insult to the brain (Figures 1.20A to C). Other gaze abnormalities, which may mimic non-convulsive status epilepticus are upward gaze and roving nystagmus. Continuous epileptiform electroencephalogram (EEG) abnormalities have been noted in comatose adults with severe metabolic or anoxic encephalopathies.15 ●● Avoid rushing to administer anticonvulsants. ●● The importance of early recognition and simultaneous management of status epilepticus (convulsive and nonconvulsive) is important in ensuring successful outcomes in shock.8
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
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Management of eye signs of non-convulsive status epilepticus (NCSE) is based on the history. If history is suggestive of GTCS, the NCSE is probably due to ongoing seizure activity, administer anticonvulsants. If on the contrary, altered mental status follows acute diarrhea, fever, breathlessness, scorpion sting, etc. the eye signs denote the severity of the shock and hypoxia.
Pupillary Examination (Figures 1.21 and 1.22)
Figure 1.21: Pupillary examination is also performed to assess briskness of response and inequality
Unequal pupils may often be noted from increased intracranial pressure or non-convulsive status. Pupils provide important information regarding response to therapy and normalization of abnormal pupillary size, reaction or symmetry indicates resolution of cerebral hypoxia-ischemia.
Figures 1.20A to C: Conjugate deviation in a child presenting with profound shock and posturing. The dolls eye movement is being performed in the figures. Usually, the deviation persists during the side-to-side movement performed for eliciting the DEM (Courtesy: Dr Gunda Srinivas).
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Do not forget to look at eye position and eye movements during rapid cardiopulmonary cerebral assessment.
Figure 1.22: Unequal pupils. Examination of the pupils can help pick up a wide variety of other unexpected conditions such as coloboma, xerophthalmia, etc. in seriously ill children (Courtesy: Dr Gunda Srinivas).
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Section I n Recognition of Critical Illness
●● Resuscitation from shock due to intracranial infections or head trauma will be incomplete if intracranial hypertension is not simultaneously identified and treated. IP : 196.52.84.10
Interpretation of PAT ●● As the rapid cardiopulmonary cerebral assessment is being performed, simultaneously the heart rates, respiratory rates, BP and liver span should be verified with the normal values for age. ●● The variables are interpreted as normal for age, increased or decreased based on the other parts of the PAT.16 This helps to determine the physiological status and guide therapy. ●● No single variable should be taken in isolation. All sides of the PAT16 should be compromised to recognize respiratory failure or shock. ●● Decreased mental status, respiratory compromise, alteration in heart rates and alteration in skin perfusion suggestive of warm or cold shock with or without fall in blood pressure should be taken together in the recognition of critical illness.
PHYSIOLOGICAL STATUS and appropriate interventions Determine physiological status as Airway/Breathing/Circulation/Disability: Separate therapeutic interventions are necessary for each of the parameters (Figure 1.24).
Airway ●● If stable or obstructed: No positioning is needed. ●● If airway is unstable or unmaintainable: Open the airway using the head tilt-chin lift maneuver (jaw thrust if head trauma is suspected).
Breathing ●● If effortless tachypnea: Provide O2 via the non-rebreathing mask. ●● If respiratory distress or impending respiratory failure: Provide O2 using the Jackson-Rees circuit. ●● If apnea: Suction oropharynx, decompress stomach with appropriate sized nasogastric tube and initiate bag-valve-mask ventilation.
Circulation ●● If bradycardia: Initiate chest compressions. ●● If tachypneic, tachycardic and shocked, without hepatomegaly: Administer 20 mL/kg over 20 minutes. ●● If respiratory distress, tachycardia, shocked with or without hepatomegaly: Administer smaller boluses of 5–10 mL/kg over 5–10 minutes. ●● If BP low: Use pull-push method for administering fluids until BP normalizes (Plan intubation and epinephrine infusion). ●● If pulse pressure wide, MAP < 65 mm Hg: Plan large volumes of fluids.
Disability ●● If child having altered level of consciousness: Correct hypoxia and shock and then reassess. ●● If NCSE/CSE: Treat seizure activity as discussed in Chapter 21. ●● If raised ICP: Treat ICP as discussed in Chapter 20.
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Figure 1.23: The Broselow tape
Often children who are critically ill cannot be weighed conventionally, for such children Broselow tape is useful to calculate approximate weight based on length of the child (Figure 1.23).
Repeat cardiopulmonary cerebral assessment after administration of fluid bolus, anticonvulsant, intubation, etc. and determine the new physiological status. Intervene appropriately for each of the parameters viz ABCDs (Figure 1.24). Uncompromising standards are needed in terms of accuracy, speed and skill in performing rapid cardiopulmonary
Figure 1.24: Pediatric Assessment Triangle (PAT) to enable recognition of severity and decision making in seriously ill children in the emergency setting
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(Modified from Dieckmann RA, Brownstein D, Gausche-Hill M. The Pediatric Assessment Triangle–a novel approach for the rapid evaluation of children. Pediatr Emerg Care. 2010 Apr;26(4):312-15)
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
15
16
Section I n Recognition of Critical Illness
cerebral assessment and its interpretation in critical illness. Refer Figure 1.25.
IP : 196.52.84.10 Accurate documentation of clinical findings is crucial following each intervention (Table 1.1 and 1.2). Refer Figure 1.26A and B. Stringent precautions need to be taken since error or negligence on the part of the physician could be fatal to children whose care depends so heavily on clinical assessment.
Key Points
common errors
Figure 1.25: This picture shows a very young infant making eye contact with his happy mother following successful shock resuscitation. His response to his mother, suggests neurologically intact survival.
ü
1. The two steps for early recognition of serious illness in children presenting with ‘minor’ symptoms are: a. Asking the 2 triage questions and b. Performing a meticulous rapid cardiopulmonary cerebral assessment. 2. Recognition based on OBVIOUS drop in consciousness can result in poor outcomes. 3. Consider the possibility of pulmonary edema when children in shock present with respiratory distress due to non-lung etiologies.
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1. Recognizing serious illness only when the ‘consciousness’ drops profoundly. 2. Referring the febrile child with acute onset posturing to the neurologist or to the psychiatrist for agitated behavior. 3. Administration of higher antibiotics for a febrile child with altered mental status without evaluating or managing coexisting shock. 4. Administration of sedatives for infants with incessant cry without ruling out hypoxia and shock.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
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Figure 1.26A: Pediatric emergency case record: front page (assessment part)
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Section I n Recognition of Critical Illness
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Figure 1.26B: Pediatric emergency case record: back page (monitoring and reassessment part) Note: Refer appendix for sample documentation of Pediatric Emergency Case Record
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
Protocol 1.1: PEMC approach: Recognition of relative bradypnea and relative bradycardia
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Section I n Recognition of Critical Illness
Protocol 1.2: PEMC approach: Recognition of severity of illness on arrival to the ED
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Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
References 1. Santhanam Indumathy, Pai M, Kasthuri KR, et al. MortalIPthe : 196.52.84.10 ity after admission in pediatric emergency department: A prospective study from a referral children’s hospital in Southern India. Pediatr Crit Care Med. 2002;3:358-363. 2. Santhanam I, et al. Implementation of Pediatric Emergency Medicine Course Guidelines (PEMC). Impact on mortality in critically ill children presenting to a large volume PED of an academic children’s hospital in India. Pediatr Crit Care Med. 2011;(12):3. 3. Zaritsky AL, Nadkarni VM, Hickey RW, et al. Recognition of respiratory failure and shock. Textbook of Pediatric Advanced Life Support. Dallas TX: American Heart Association; 2002. 36:97-98. 4. Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the emergency department. Pediatr Emerg Care. 2008;24:647-55. 5. Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the emergency department. Pediatr Crit Care Med. 2007;Suppl Vol 8, No 3:A17. (Paper presented at the 5th Pediatric Critical Care Congress June 24th 2007, Geneva). 6. Kirkham FJ, Newton CR, Whitehouse W. Paediatric coma scales. Dev Med Child Neuro. 2008;50:267-74. 7. Santhanam I, Ranjit S, Kissoon N. Management of shock in the emergency department. Minerva Pediatr. 2009;61:01-15. 8. Dellinger RP, Mitchell M, Carlet JM, et al. Surviving Sepsis Campaign: International guidelines for manage-
9.
10.
11.
12.
13.
14.
15. 16.
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ment of severe sepsis and septic shock. Crit Care Med. 2008;36(1):296-327. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6:02-08. Pollard AJ, Britto J, Nadel S, et al. Emergency management of meningococcal disease. Arch Dis Child. 1999;80:29096. Pollard AJ, Nadel S, Ninis N, et al. Emergency management of meningococcal disease: eight years on. Arch Dis Child. 2007;92:283-86. Ranjit S, Kissoon N, Ghandhi D, et al. Early differentiation between dengue and septic shock by comparison of admission hemodynamic, clinical and laboratory variables: a pilot study. Pediatr Emerg Care. 2006;23:368-75. L. Chameides, R. Samson, Schexnayder SM, et al. Pediatric Advanced Life Support. American Heart Association; 2011. pp. 72. Santhanam I, Padma V, Murali T, et al. Predictors of mortality of serious sepsis. Proceedings of the 1st European congress on Pediatric Resuscitation and Emergency Medicine (PREM). May 2nd, 3rd 2013:Ghent, Belgium. Jordan KG. Non-convulsive status epilepticus in acute brain injury. J Clin Neurophysiol. 1999;16:332-40. Dieckmann RA, Brownstein D, Gausche-Hill M. The Pediatric Assessment Triangle–a novel approach for the rapid evaluation of children. Pediatr Emerg Care. 2010 Apr;26(4):312-15).
Section II
Airway
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Basic Airway Management
Figure 2.1: Effective bag-valve-mask ventilation technique is key to successful resuscitation (Courtesy: Dr Gunda Srinivas).
Learning Objectives 1. Why the emergency physician must master the skills of bag-valve-mask ventilation? 2. Selection of the appropriate sized self-inflating bag-valve-mask device for resuscitation.
INTRODUCTION Expertise in basic airway maneuvers initially, followed by pharmacologically assisted tracheal intubation are core skills essential in resuscitation care. The pediatric airway differs in many ways from the adult airway. A relatively large tongue, makes visualization of the larynx difficult, with little space for maneuvering the laryngoscope and even less space for passage of the tube. Reduced tone of the pharyngeal muscles can also predispose to airway obstruction. The small, narrow, fragile and horizontally placed epiglottis makes visualization of the vocal cords difficult. The anterior placement of the larynx aggravates the difficulty in visualization. The short trachea predisposes to intubation of the right main bronchus. The cricoid ring (the narrowest portion of the airway), is at increased risk of trauma during tube insertion. For all the reasons mentioned above, the first responder in the PED, (usually a novice resident) may find intubating
3. EC-clamp: Pearls and pitfalls. 4. Precautions taken during bag-valve-mask ventilation.
a child difficult. In fact, level I evidence supports the use of bag-valve-mask versus tracheal intubation in the prehospital setting. Survival and neurological outcomes were same, whether intubation was performed or mask ventilation was provided before reaching the PED.1
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Bag-valve-mask ventilation is recommended over tracheal intubation for ventilatory support in the out-of hospital setting.1 This is also true in PEDs manned by novice physicians where intubation skills may not be available 24 × 7.
Bag-valve-mask Ventilation Self-inflating bag-valve-mask devices are used to initiate respiratory support in apneic children. It is designed to de-
26
Section II n Airway
liver positive pressure breaths when compressed. Key to successful bag-valve-mask ventilation is the technique of applying an airtight sealIP(Figure 2.1). : 196.52.84.10 ●● Selection of the appropriate sized bag is the first step to successful resuscitation. ●● A mask that extends from bridge of nose to chin must be selected. The correct fitting mask is crucial for a tight seal. ●● Insert NGT and decompress stomach contents prior to initiating bag-valve-mask ventilation. ●● The self-inflating bag-valve-mask device cannot be used to deliver oxygen to the spontaneously breathing child.2
Figure 2.2: Which sized bag would you choose, when a 3-month-old infant presents with respiratory failure due to probable pneumonia? Answer: The largest size bag in this picture. The 250 mL bag is used for preterm neonates. 450–750 mL bag is recommended for resuscitating the term neonate in labor ward settings (lung parenchyma may not have sustained damage immediately after birth).
Age appropriate sizes of bags are available for the different age groups (Figure 2.2). 450–750 mL bags are recommended for resuscitating term newborns and infants. Conventionally, larger bags (1–1.5 liters) are recommended exclusively for adults. In reality, however, 450–750 mL bag-valve-mask devices are often insufficient in ventilating young infants presenting with respiratory failure.
tion of critically ill children on arrival into the ED. Use the largest sized bags in any child beyond the newborn period. “Regardless of the size of the bag, caution should be taken to use the force and tidal volume to make the chest just visibly rise.”3
Figure 2.3: This neonate who presented with respiratory failure to the ED had severe pulmonary edema and shock due to sepsis. He needed a 1 liter bag and minimal hyperextention at neck to ensure adequate chest rise and improvement in oxygen saturation.
●● Prior to initiating BVM ventilation, suction the oropharynx using a large bore Yankauer suction catheter. ●● The Yankauer catheter has a wide bore tip that aids in clearing large volume vomitus and food particles rapidly. ●● Avoid stimulation of the posterior pharynx during suctioning by turning the head to one side. This simple maneuver prevents vagal-induced bradycardia. ●● Simultaneously, empty stomach contents. ●● Rapidly introduce a large bore nasogastric tube and decompress the stomach by connecting the tip to the suction apparatus (Figure 2.4).
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Most infants and children who require respiratory support on arrival in to the ED, have abnormal lung parenchyma. Chest compliance is poor and immense effort is often needed to provide effective ventilation and normalize oxygen saturation (Figure 2.3). The largest bags (at least 1 liter) are needed to provide effective chest rise. Smaller bags or ‘pediatric bags’, i.e. 450–750 mL are not sufficient for providing bag-valve-mask (BVM) ventilaFigure 2.4: Gastric decompression via NGT
Chapter 2 n Basic Airway Management
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●● In small infants neonates, the nasogastric tube should be aspirated using a syringe.
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Suctioning pressure should not exceed 100 mm Hg in young infants and 300 mm Hg in older children. ●● Avoid suction, if the child is having active gastrointestinal bleed. ●● Tie a collection bag to the nasogastric tube to avoid spillage of gastric contents.
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Vomiting of gastric contents secondary to gastric distension during bag-valve-mask ventilation, could result in disastrous consequences during resuscitation. One nurse should be assigned to the left of the airway manager exclusively for suctioning (Figure 2.5).
Figure 2.5: Additional precautions during bag-valve-mask ventilation—nasogastric tube should be inserted prior to initiating BVM ventilation. Oropharyngeal secretions should also be suctioned simultaneously. One nurse should be assigned exclusively for suctioning since frequent suctioning may be needed. Suctioning is performed by turning the child’s head to one side to avoid stimulation of the posterior pharynx and causing vagal-induced bradycardia.
Figure 2.6 Inappropriate EC-clamp: Avoid encircling the top of the mask and pressing it down. Airtight seal will not be possible and BVM ventilation may be ineffective.
Figure 2.7 Inappropriate EC-clamp: Avoid standing and bagging, failure to support one’s elbows can kink the neck and obstruct the airway. Standing can also strain the back of the airway manager.
Effective BVM technique may look apparently easy. However, several potentially difficult steps are needed to provide adequate ventilation. Separate and position the individual digits (index, middle and ring finger) over the bony part of the mentum, ramus and angle of mandible respectively. Avoid compressing the soft tissues in the midline. Care is taken to ensure that the fingers providing the E-clamp are as far away from the midline as possible.
Figure 2.8 Inappropriate EC-clamp: Avoid bunching the fingers used for provision of C-clamp.
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Section II n Airway
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Figure 2.9 Double EC-clamp: Often provision of effective BVM ventilation may need two persons. One person provides the double EC-clamp. The second person pumps the bag, while giving additional pressure on the mask to prevent air leak.
The commonest cause for ineffective BVM technique stems from failure to provide an airtight seal of the mask. The nasogastric tube emerging from the rim can thwart attempts to make the seal airtight.
Figure 2.10 Appropriate EC-clamp: The airway manager should sit and support his elbows, while performing BVM ventilation. Fingers providing C-clamp should encircle the rim of the mask. Effort is taken to prevent air leak at the site of exit of the NGT. Fingers providing E-clamp should be flexed at the MP joints to hook and lift the jaw. The middle fingers is at the mentum, the ring finger at the ramus and the little finger at the angle of the jaw.
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The correct EC-clamp technique (not easy) is the important first step (Figures 2.5–2.11). The E-clamp is provided using the middle, ring and little fingers each of which are positioned on the mentum, ramus and the angle of the mandible. The tip of these fingers should indent the soft tissue along the bony rim of the mandible. The E-clamp acts as a bucket handle to lift the jaw to meet the C-clamp such that the seal is airtight. The C-clamp is provided using the thumb and index finger to encircle the mask along its rim. The elbow of the hand holding the EC-clamp should be placed on the resuscitation trolley. The ‘V’ position of the elbow automatically ensures that airway patency is maintained (‘head tilt, chin lift’).
Ù Ensure that the elbow is at a lower level than the ECclamp to avoid compromise of the airway.
Avoid standing and bagging when the elbow gets positioned above the EC-clamp (refer Figure 2.7).
Figure 2.11 Inappropriate technique: Mask ventilating children presenting with respiratory failure, needs immense effort to move the chest. Avoid pumping the bag from below.
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Ability to bag-valve-mask effectively is the foundation for advanced airway skills.4 The EC-clamp will be effective if the following precautions are taken: ●● Fingers (E-clamp) should not be bunched together. ●● Fingers providing the E-clamp should be flexed at both the metacarpal joints thus avoiding soft tissue obstruction.
Chapter 2 n Basic Airway Management
●● Elbows must be supported on the resuscitation trolley whilst the thenar eminence is used to tilt the fore head ensuring the head tilt maneuver. IP : 196.52.84.10 ●● Standing may lead to improper positioning and kinking of the neck. ●● Avoid using bag-valve-masks without the reservoir. ●● Lack of oxygen reservoir or a leaking reservoir, will prevent the provision of 100% oxygen to the child with apnea. The brain suffers hypoxic injury when oxygen deprivation lasts for more than 5 minutes. Hypoxic encephalopathy, can result in permanent crippling neurological handicap. Preventing hypoxia-induced brain damage is one of the prime responsibilities of the ED physician. Recognizing respiratory failure and initiating effective bag-valve-mask ventilation can not only improve survival, but also ensure neurologically intact survival. Anticipation of respiratory arrest is key to successful resuscitation. Flying, to the airway end of the resuscitation trolley when, an unresponsive child is being rushed gives a 2 second advantage in initiating bag-valve-mask ventilation. Recognizing apnea and initiating effective bag-valvemask ventilation early can not only reduce mortality, but also ensure neurologically intact survival.
Key Points
ü
1. Recognizing respiratory failure and providing effective bag-valve-mask ventilation is the most important responsibility of the emergency physician or nurse. 2. Initiation of bag-valve-mask ventilation is the appropriate first maneuver for a child presenting with respiratory arrest.
common errors
29
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1. Rushing to intubate before preoxygenating (mask ventilation). 2. Selection of smaller sized bags. 3. Standing and bending, while initiating mask ventilation. 4. Not decompressing the stomach prior to mask ventilation. 5. Failure to recognize the sound of air leak during mask ventilation. 6. Failure to recognize that the reservoir is not distended (oxygen tube is not connected to the bag). 7. Failure to use a bag-valve-mask device with the oxygen reservoir. Lack of the latter can reduce oxygen delivery up to 40% to the apneic child. 8. Failure to occlude the pop-off valve in the older child.
References 1. M Gausche, MD Roger J. Lewis, et al. Effect of Out-ofHospital Pediatric Endotracheal Intubation on Survival and Neurological Outcome A Controlled. Clinical Trial JAMA. 2000;283(6):783-90.doi:10.1001/jama.283.6.783. 2. Carter BG, Fairbank B, Tibbals J, et al. Oxygen delivery using self-inflating resuscitation bags. Pediatr Crit Care Med. 2005;6:125-28. 3. Ralston M, Hazinski MF, Zaritsky AL, et al. Textbook of Pediatric Advanced Life Support, American Heart Association. 2006-2007. 4. Benger J, Nolan J, Clancy M. Basic airway management techniques. Emergency Airway Management. Cambridge: Cambridge University Press; 2008. pp. 27-40.
Pharmacologically Assisted Intubation (PAI) in the PED IP : 196.52.84.10
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Figure 3.1: Sequential steps of PAI
Learning Objectives 1. Anatomy of “why intubation is challenging in children?” 2. Case scenarios illustrating indications for intubation using the pediatric assessment triangle.
INTRODUCTION More than a decade ago, virtually all ‘outside the operation room’ intubations were performed when children presented with imminent arrest. Currently however, anesthetic drugs have enabled elective intubation in spontaneously breathing critically ill children. Profoundly deranged physiology, severe metabolic dysfunction, absence of nil per oral precautions, incomplete information from parents, unanticipated difficult airway situations, presence of distraught parents and the responsibility of concurrently resuscitating other sicker babies can often make intubation a challenge in the ED setting (Figure 3.1). Smaller-sized vocal cords, positioning of glottis at C1-4, leafy shaped, floppy epiglottis and a large occiput make intubation difficult in young children. Infants also have a very compliant rib cage, where the inward recoil is greater than the outward recoil. The soft
3. Hazards of intubating children without using drugs for sedation or paralysis. 4. Pharmacologically assisted intubation (PAI): Protocol used in a large volume PED. rib cage and poorly maintained negative intrathoracic pressure result in lower functional residual capacity (FRC) in infants. In addition to the lower FRC (due to causes mentioned above), higher BMR, higher O2 consumption and greater CO2 production make infants more prone to desaturation when they slip into respiratory failure. Upper airway muscles are also more sensitive to the effects of anesthetic agents with a greater predisposition to collapse. Controversy exists in several areas of RSI1, including use of atropine as an adjunct for children, the role of Lidocaine as premedication, the role of a ‘de-fasciculating’ dose of a non-depolarizing paralytic agent, relative contraindications for the use of succinylcholine, methods of preoxygenation and the need to use cricoid pressure. However, this chapter is based on the experience of a large volume PED.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
Indications for Intubation A 6-month-old infant has been having acute watery di196.52.84.10 arrhea and vomiting IP for: the past 2 days. He had not been responsive to his mother since the evening. For the past ½ hour he had been ‘mouth breathing’.
Figure 3.2 Physiological status: Imminent arrest
Imminent arrest is the most well-known indication for urgent intubation. Airway protective reflexes are absent and vocal cords are not responsive. In these situations, BVM is initiated and intubation performed without resorting to anesthetic drugs (Figure 3.2).
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citation for respiratory failure due to severe parenchymal lung disease (Figure 3.3). A 9-year-old boy is referred for snake envenomation. Even as he is being evaluated, he develops bilateral ptosis and apnea.
Figure 3.4 Physiological status: Respiratory failure due to respiratory muscle paralysis
After provision of basic airway management, he needs to be intubated and ventilated for respiratory failure secondary to neuromuscular paralysis (Figure 3.4).
A 1-year-old child is being treated for cellulitis over the right upper limb. She has been crying inconsolably since the morning.
A 5-year-old child is being provided BVM ventilation for respiratory arrest secondary to convulsive status epilepticus. She continues to convulse despite 2 doses of Lorazepam and loading dose of Phenytoin. Is there a need to intubate this child (Figure 3.5)?
Figure 3.3 Physiological status: Sepsis with cardiogenic shock
Figure 3.5 Physiological status: Refractory status epilepticus
This child has presented with respiratory failure either due to, cardiogenic or non-cardiogenic pulmonary edema. In addition, she also has vasodilatory shock with low mean arterial pressure secondary to severe sepsis. She will eventually need elective intubation after the initial fluid resus-
Provision of prolonged mask ventilation cannot be sustained. This child’s seizures have been refractory to the initial drugs. Administration of further anticonvulsant drugs is an indication for elective intubation using anesthetic agents (Figure 3.5).
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Section II n Airway
A 2-year-old child is rushed into the ED after he develops stridor, respiratory distress following intravenous contrast administration the radiology department. IP in : 196.52.84.10
lent intubating conditions 60 seconds after administration of anesthetic drugs. Excellent intubating conditions are defined as complete jaw relaxation, open immobile vocal cords with absence of coughing, bucking and diaphragmatic movement in response to intubation. It is implemented in a logical sequence and comprises of several coordinated steps. The pharmacologically assisted intubation (PAI) described in this manual deviates from the classical RSI.
Pharmacologically Assisted Intubation Unlike, pharmacologically facilitated intubation2, which is described as ‘sedation only protocol’, we made the following modifications: Figure 3.6 Physiological status: Obstructed airway and hypotensive shock secondary to anaphylaxis
Obstruction to the airway secondary to anaphylaxis fa cial trauma, epiglottitis, can often worsen. In these clinical scenarios elective intubation is advisable (Figure 3.6).
HAZARDS OF INTUBATION Direct laryngoscopy activates airway protective responses by stimulating the glossopharyngeal nerve above the epiglottis and the vagus nerve below it. Gagging, coughing, apnea, laryngospasm and bronchospasm are some of the noxious respiratory responses. Hypertension and tachycardia in older children and bradycardia in children less than 5 years occur due to stimulation of the sympathetic and parasympathetic nervous system. Furthermore, difficulty in visualizing the glottis, often results in prolonged manipulation of the airway resulting in worsening of hypoxia and hypercapnia. This in turn could trigger cardiac arrest in the seriously ill child. Airway trauma, breakage of teeth and bleeding are other hazards when electively intubating a struggling child. RSI facilitates airway visualization with the use of drugs that cause muscle relaxation, control agitation, control seizures and blunt the gag and cough reflexes. Use of premedications minimizes the risk of autonomic-induced cardiovascular complications such as bradycardia during emergency intubation. RSI is defined as “the simultaneous administration of a sedative (induction agent) and a neuromuscular blocking agent for the purpose of intubation”. RSI produces excel-
1. Sedative and paralytic agents were used to assist intubation. 2. To avoid aspiration of stomach contents during intubation, the stomach was decompressed. 3. Children were preoxygenated using the bag-valvemask technique after paralysis, until saturations were maintained at 100%. Steps 2 and 3 were deemed mandatory to avoid cardiac arrest from occurring in children presenting with profound hypoxia and shock. Cricoid pressure was applied during intubation not to prevent regurgitation, but to enable visualization of the vocal cords.
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Nasotracheal Intubation (NTI) Securing the airway via the the orotracheal route is faster and is therefore preferred in ED settings.
1. History and evaluation of the patient. 2. Preparation: a. Gastric decompression. b. Preoxygenation of patient: 3–5 minutes. c. Equipment and staff. d. Medications. 3. Administration of premedication. 4. Administration of sedation. 5. Cricoid pressure and ventilation. 6. Administration of neuromuscular blockage. 7. Postintubation documentation and monitoring. 8. Continuous sedation and paralysis.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
HISTORY AND EVALUATION OF PATIENT Coordinated preparation is essential for success in perIP : 196.52.84.10 forming pharmacologically assisted intubation. Rigorous assessment of the airway before administration of paralytic agents is an essential first step.
HAZARDS OF ANESTHETIC DRUGS IN THE PED Use of paralytic drugs, in children who are difficult to intubate could result in tragic outcomes. In these children whose respiratory efforts have been eliminated, gas exchange will not occur when intubation fails. Bag-valvemask ventilation may also become impossible, since tone of the oropharyngeal muscles and ligaments are lost. The ED physicians nightmare of ‘cannot intubate, cannot ventilate’ can occur.
Problems in Intubation Characteristics that contribute to causing difficulty in visualizing the glottis or introducing the tracheal tube are:
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●● ●● ●● ●● ●● ●● ●● ●●
Evidence of facial and neck trauma. Micrognathia or mandibular hypoplasia. Low-set ears. Dysmorphic facial features. Limited mouth opening, small mouth. High-arched palate. Large tongue. Loose teeth, prominent upper incisors with overriding maxilla. ●● Stridor due to structural abnormality of the airway. ●● Mallampati class III and IV (rarely assessed in the emergency setting).
AMPLE History is Obtained Before Intubation History should be brief objective and cover the following issues represented by the acronym AMPLE, a mnemonic to facilitate intubation: ●● ●● ●● ●● ●●
A = M = P = L = E =
Allergies. Medications. Past history. Liquids and last meal. Events leading to the need for intubation.
Table 3.1: Airway equipment to be prepared prior to intubation (SOAPME) Suction Oxygen source
Yankauer suction catheter ●● Cylinder or central oxygen should be connected to the bag-valve-mask device ●● Sufficiency of oxygen verified by demonstration of filling up of the O2 reservoir of the bag-valve-mask device
Airway equipment ●● Bag-valve-mask device
●● 750 mL, 1,000 mL
●● Non-rebreathing mask ●● Jackson-Rees circuit, Bain circuit Age appropriate endotracheal tubes
●● Uncuffed tube: 4+ (age in years/4) ●● Cuffed tube: 3+ (age in years/4) ●● Prepare 1/2 size smaller and larger
Appropriate sized laryngoscope
Appropriate sized oral airway Tincture benzoin soaked cotton Plaster for securing tube Pharmacology
Monitoring Equipment
●● Up to 2 years: Straight blade ●● 2 years to adolescence: Curved blade (Size of curved blade: Measure from mouth to thyroid prominence (refer Figure 3.11) ●● Flange to tip is measured from angle of jaw to angle of lip ●● Adhesive applied above the upper and below the lower lip prior to sticking plaster ●● Cut as ‘trouser legs’ (refer Figure 3.10) Drugs must be constituted and labeled before use ●● Premedication agents: Atropine, Lidocaine ●● Induction agents: Thiopental, Ketamine ●● Neuromuscular blocking agents: Suxamethonium, Vecuronium, Rocuronium ●● Pulse oximeter ●● Cardiorespiratory monitor ●● ETCO2 monitor
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Section II n Airway
Preparation of Patient Refer Table (SOAPME) 3.1.
IP : 196.52.84.10 Nasogastric Tube Insertion If the child presents with respiratory failure, a nasogastric tube (NGT) is introduced and stomach contents are rapidly decompressed by connecting the NGT to the suction apparatus. Simultaneously, bag-valve-mask ventilation is initiated as shown in this picture (Figure 3.8).
Preoxygenate for 3–5 minutes using a non-rebreathing mask or flow inflating ventilation device (refer Chapter 5). This ensures that alveolar nitrogen is replaced by oxygen. Children need this additional oxygen to remain saturated for the 2–3 minutes of pharmacologically induced apnea prior to intubation.
Due to the inherent risk of regurgitation of stomach contents, the NGT is not introduced prior to intubation in the classical RSI technique. In the PAI, the NGT must be introduced as soon as the decision to intubate is taken since children presenting to the ED seldom present with empty stomach.
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Failure to decompress stomach contents prior to bagvalve-mask ventilation can irrevocably damage lung parenchyma by aspiration of stomach contents and worsens hypoxia precipitating CARDIAC ARREST. If the child struggles or gags, introduce the NGT after a sedative agent has been given.
Preoxygenation of Patient
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The spontaneously breathing patient should be preoxygenated with supplemental oxygen (Figures 3.7 and 3.8).
Figure 3.8: A modification of the classical RSI, introduction of the NGT and decompression has been safely employed to prevent aspiration during mask ventilation in a large number of pharmacologically assisted intubations in a busy PED.3 This picture also shows two lines secured prior to RSI: An intraosseous line (secured on arrival in view of severe shock) for inotrope infusion and one intravenous lines for administration of anesthetic drugs, fluids, etc.
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Figure 3.7: The airway being positioned and oxygen is provided using a Jackson-Rees circuit. Note that the NGT has been inserted prior to administration of anesthetic agents.
Secure 2 intravenous lines prior to intubation One line is dedicated for inotrope infusion Most critically ill children requiring intubation in ED settings have shock. Since sedatives tend to lower systemic vascular resistance and the application of positive pressure concurrently decreases preload, shock could worsen immediately after intubation and assisted ventilation. An additional bolus, is recommended postintubation. The second line is dedicated for administration for anesthetic drugs.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
Avoid having a single intravenous line during PAI. Dependence on a single line with its risk of ‘getting IP :be196.52.84.10 blocked or bulged’ could dangerous when anesthetic drugs are being administered in the hypoxic or shocked child!
Positioning
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●● The right-sided nurse assists the airway manager by handing her the laryngoscope, tracheal tube and helps to secure the tube. ●● The nurse to the left of the airway manager is responsible for suctioning. She operates the electrical and vacuum suction simultaneously.
Preparation of Airway Tray (Figures 3.10, 3.11)
The external auditory meatus is aligned with the anterior border of the shoulder such that the oropharynx is in line with the laryngopharynx. This is accomplished by placing a towel or folded cloth under the shoulder. In older children where occiput is not as prominent as in infants, the cloth is placed under the head to ensure alignment (Figure 3.9).
Figure 3.9: Positioning of airway
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Figure 3.10: 1. Appropriate sized oropharyngeal airways. 2. Anesthetic drugs; 3. Tracheal tubes (calculated size for age as per the PALS guidelines, with half size greater and half size less for age); 4. Appropriate sized bag-valve-mask device; 5. Elastoplast (cut up to one third like trouser legs); 6. Cotton with tincture benzoin; 7. Age appropriate laryngoscopes; 8. Towels for positioning the airway; 9. O2 tubings.
Proper positioning is one of the most crucial aspects of visualizing the glottis. A few moments spent in confirming alignment can mean a difference between success and failure in intubation.
Preparation of Staff Ideally, securing the airway using neuromuscular blockade agents in critically ill children, requires a trained team comprising of at least two physicians and three nurses. ●● The airway manager (team leader) calls out instructions and should be the only voice heard. ●● A trained nurse is dedicated for application of cricoid pressure in the older child. ●● The second physician is assigned the responsibility of performing the cardiopulmonary assessment following intubation.
Figure 3.11: The appropriate sized laryngoscopic blade is selected by matching the blade with the distance between angle of mouth and thyroid prominence as shown in this picture (Courtesy: Dr Mullai Baalaaji).
36
Section II n Airway
Medications: Choice of Drugs Table 3.2: Anesthetic agents of choice
IP : 196.52.84.10
Physiological status
Anesthetic agents
Shock without raised intracranial pressure
Atropine, Ketamine and Succinylcholine
Shock with raised intracranial pressure
Lidocaine, with or without Atropine, Thiopental 2 mg/kg, Vecuronium
Raised intracranial pressure without shock
Lidocaine, Atropine, Thiopental 5 mg/kg and Vecuronium
The drug names are called out immediately after being administrated to avoid confusion, e.g. ‘ketamine given!’ ‘vecoronium given!’
Sequence of Intubation (Figures 3.12 to 3.18) The following intubation sequence (steps 3, 4, 5, 6) from start to finish has been captured over a period of 5 minutes.
Sellick’s Maneuver4 Though not recommended, after administration of induction agent, cricoid pressure may be applied to enable visualization of the glottis. Since the breadth of the cricothyroid membrane admits tip of nail in young children, the finger providing Sellick’s pressure should be held perpendicular to the surface of the neck.
Figure 3.12: Majority of children requiring intubation in the ED are hypoxic on arrival. After administration of premedication and sedative agent as shown in this figure, cricoid pressure is applied. Neuromuscular blocking (NMB) agent is administered and bag-valve-mask is initiated to improve oxygen saturation. Failure to provide bag-valve-mask ventilation after administration of NMB agent, could result in worsening of hypoxia leading to cardiac arrest in children presenting to the emergency department with profound hypoxia and shock (Note the timings on photos).
Ù Caution: The routine use of cricoid pressure application to prevent aspiration during endotracheal intubation in children is no longer recommended. If the cricoid pressure interferes with ventilation or the speed or ease of intubation, it should be discontinued. In small infants and neonates, the intubator can apply pressure over the cricoid to help visualize the glottis using the tip of his/her little finger. The hand holding the laryngoscope can be used for this purpose.
Ù
Excessive cricoid pressure can distort the airway preventing visualization of the glottis.
Ù
Vomiting during intubation is one of the dreaded com plications. Quickly release cricoid pressure, turn the head to one side and rapidly suction and clear the airway.
Figure 3.13: Tube insertion: When the drugs have been given and the child’s saturations are optimal, the mouth is opened and the laryngoscope is introduced. The blade is used to push the tongue to the left side. Simultaneously, the tip is placed in the vallecula (curved Macintosh blade) or tip of epiglottis (if straight Miller blade) is used. The tracheal tube is introduced into the glottis under vision.
The airway physician, receives the larygnoscope handle in his left hand, with the blade pointing down. The blade is inserted from the right side of the mouth and is used to
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
37
move the tongue to the left. The tip of the laryngoscope is used to hold the tip of the epiglottis.
196.52.84.10 The tube is held in IP the :right hand and inserted into the glottis up to the vocal cord mark using the right hand.
Ù Caution: Introduction of the blade beyond the base of the tongue is the commonest error made by novice physicians resulting in esophageal intubation.
Postintubation Management
Ù A common misconception amongst novice airway managers is that the ‘job is done after intubation’. Fixing the tube is as important as intubation!
Confirmation of Tube Position Tube position is usually confirmed by auscultating over the right and left infraclavicular areas, right and left infraaxillary areas and over the stomach.
Ù
It is mandatory to verify whether the tube is in the trachea and not in the stomach or in the right main bronchus.
Figure 3.14: Postintubation management: Confirmation of tube position prior to fixation of tube: This picture shows how the tracheal tube is held steady by the airway manager soon after intubation. It is held at the corner of the mouth using the thumb and the index finger between the inner and outer aspect of the cheek. Note that tube position is being confirmed by the 5-point auscultation.
Auscultation for air-entry and normal pulse oximetry readings are insufficient to confirm tube placement. Air-entry may be reported as ‘equally heard’ even if the tube had been wrongly placed in the esophagus. In these patients, saturations can remain 100% secondary to effective preoxygenation. Failure in heart rate improvement, persistence of cyanosis, hepatomegaly, fall in BP, etc. can herald a wrongly placed tube.
Ù
To confirm tube position, perform the complete cardiopulmonary cerebral assessment. Check pulse oximetry and ETCO2 if available. Shock can worsen following intubation and positive pressure ventilation. Venous return falls, leading to fall in cardiac output. The rapid cardiopulmonary cerebral assessment helps to recognize whether shock is persistent or worsening.
Figure 3.15: This picture shows how auscultation over the stomach is being performed during the 5-point auscultation as the tracheal tube is being secured
Condensation of vapor in the tube, bilateral chest rise, improvement in heart rate if bradycardic, improvement in color, stabilization of BP, normalization of saturations to 100%, briskly responding pupils suggest that the intubation process was successful. Liver span normalizes as myocardial function improves.
38
Section II n Airway
If breath sounds are absent on the left side, the tube is most likely inserted into the right main bronchus. The tube is repositioned by pulling tube and fixing at the approIP the : 196.52.84.10 priate length. The depth of the tube can be estimated by multiplying the tube size into three. The tip of the tube ideally must lie at the carina. When the tube is in position, care must be taken to fix it securely such that it does not slip.
Figure 3.18: Endotracheal tube is fixed securely and the child is being ventilated with self-inflating BVM device bag
DOCUMENTATION AND MONITORING AFTER INTUBATION Drugs, their dosages, size of the tube, length at which it was fixed, cardiopulmonary response of the patient to intubation and complications which occurred during the procedure should be documented (Table 3.3). Figure 3.16: Method of fixation of tracheal tube: Tube is fixed as shown in the figure, after applying tincture benzoin as adhesive using 2 bits of plaster cut into ‘trouser legs’. One half of the trouser leg is fixed along the lower lip and the other strip is coiled around the tube.
The following monitoring equipment and personnel must be available during intubation. ●● Pulse oximeter. ●● ECG monitor. ●● Non-invasive BP monitor. ●● End tidal carbon dioxide monitor. Delegate one team member to assess tube position, hemodynamic status and monitor the monitors.
INTUBATION IN ED SETTINGS: CHALLENGES
Figure 3.17: This is repeated for the second piece of plaster on the upper lip as shown in the next picture
Following intubation, the 5-point auscultation, is used to check tube position. Auscultation is performed over the right infraclavicular region, then over the left infraclavicular, right infra-axillary, left infra-axillary areas and over the stomach. Next, HR, color, CRT, pulses, core-peripheral temperature gap, BP, liver span and pupils are examined sequentially.
Pharmacologically assisted intubation involves use of anesthetic drugs commonly used in the OR. Children for whom elective intubation is planned, are advised ‘nil per oral’ 6 hours prior to surgery. Surgery is often canceled if minor illnesses are identified during evaluation for anesthetic fitness. Besides, if intubation is difficult following after induction, the anesthetist has the option of postponing surgery to another day. ●● On the contrary, critically ill children are presumed to have ‘full stomach’. ●● They are being intubated for severe hemodynamic instability. ●● Unlike, intubations performed in the OT, emergency intubations are performed in full view of anxious and often grief stricken parents.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
●● ‘Need to ventilate cannot intubate’ after neuromuscular blockade is perhaps the most anxiety provoking situation for the ED physician. IP : 196.52.84.10 ●● Postponing intubation to a later date is not an option in the ED.
Caution Intubation using anesthetic drugs is hazardous when undertaken by physicians who are not trained in the OT under the guidance of anesthetists. The key to successful intubation is the ability to perform effective bag-valve-mask ventilation, have thorough knowledge of anesthetic drugs and should have performed several intubations using ‘sedation only’ protocol. Intubation using paralytic agents in the ED requires enormous dedication, expertise and team work for successful outcomes. Drawing up appropriate medications and assigning tasks to all personnel assisting in the procedure should be seamlessly performed.
Ù
In the Indian context, majority of children reaching the ED are in respiratory failure with severe hypoxia on arrival. Under these circumstances, preoxygenation with nonrebreathing mask prior to intubation seems in-sufficient to improve oxygen reserves. It appears safer to provide positive pressure ventilation after administration of neuromuscular blockade. This practice, prevents deterioration to cardiac arrest during during intubation in the hemodynamically compromised child. To avoid, gastric distension and aspiration, a nasogastric tube is introduced to rapidly remove gastric contents. This modified technique employing preoxygenation using bag-valve-mask after paralysis and NGT decom pression has not resulted in mishaps in a large volume PED. No child desaturated during intubation attempts.4
Medications Atropine Pediatric Emergency Medicine Committee of the American College of Emergency Physicians5 recommends atropine for RSI in children younger than 1 year, for older children (1–5 years) receiving succinylcholine and adolescents receiving a second dose of succinylcholine. The recommended atropine dose is 0.02 mg/kg in children with
39
a minimum dose of 0.1 mg (lesser dose causes paradoxical bradycardia). Atropine also blocks secretions induced by succinylcholine and ketamine. Studies have shown that use of atropine is unnecessary when performing RSI in pediatric patients in the ED. However, this evidence lacks statistical power and further studies are needed.6
Lidocaine7,8 Lidocaine is advocated as pretreatment in the management of children with risk of raised intracranial pressure. It is useful in attenuating the rise in ICP caused by reflex sympathetic response to laryngoscopy. It is administered prior to succinylcholine (1.5 mg/kg intravenously) to avoid drug-induced rise in ICP. Use of lidocaine should be avoided in patients with bradyarrhythmia, hypotension and in those allergic to amides. RSI medications, are divided into induction and paralytic agents. Development of pulmonary edema, hypotension, imminent arrest, raised ICP, respiratory failure and refractory status epilepticus are the commonest indications for intubation in the ED.
Induction Agents Induction agents are primarily administered to sedate prior to paralyzing. Commonly used induction agents are: Midazolam, Thiopental, Ketamine, Fentanyl, Etomidate
Midazolam Midazolam, a sedative and hypnotic agent, is also useful in controlling convulsions. A frequently used induction agent, it causes respiratory depression and hypotension.
Ù
Midazolam should be avoided in children presenting with hypotensive shock.
Thiopental Thiopental an ultrashort acting barbiturate, acts by inhibiting the GABA receptor complex. It causes a dose-dependent decrease in cerebral metabolic oxygen consumption, cerebral blood flow and ICP. It also maintains cerebral perfusion pressure. Thus, its cerebroprotective effect is useful
40
Section II n Airway
in clinical scenarios complicated by cerebral edema and status epilepticus. Unfortunately, its myocardial depressant effect results in hypotension. It is therefore the drug IP : 196.52.84.10 of choice in head trauma and central nervous system infections and contraindicated in hypotensive shock.
Ketamine Ketamine is a dissociative amnestic agent, which causes the peculiar sensation of the mind being separated from the body. It belongs to the phencyclidine group of drugs. Ketamine stimulates norepinephrine release in those patients with adequate presynaptic stores and is associated with less cardiovascular depression than barbiturates or Benzodiazepines. Hence, it is useful in maintaining blood pressure in shocked children and has been recommended as an induction agent for children with septic shock.7 Infants and the chronically ill may have inadequate norepinephrine stores; in this setting ketamine’s direct myocardial depressant action may become apparent. Low-dose fentanyl may be considered for the induction of hemodynamically unstable septic patients. It also causes tachycardia, which helps to block the bradycardia caused by laryngoscopic manipulation of the upper airway. Bronchodilation secondary to beta 2 adrenergic stimulation is another beneficial effect, making ketamine the induction agent of choice in asthma. Ketamine increases intracranial and intraocular pressure. Consequently, it is contraindicated in head injury, meningoencephalitis and glaucoma. It also increases salivation and emergence reactions consisting of visual and auditory hallucinations. Atropine, counteracts salivation and midazolam lessens hallucinations when ketamine9 is used as an induction agent. Laryngospasm, another side effect of ketamine is countered by the use of a neuromuscular blockade agent given sequentially after ketamine.
Ù
Caution: • Ketamine could worsen hypotension and precipitate cardiac arrest in children presenting with decompensated shock secondary to chronic myocardial dysfunction. Avoid ketamine in children presenting with severe congestive heart failure and shock. •
In children being intubated for upper airway obstruction (where paralytic agents are contraindicated), ketamine may be contraindicated due to its inherent risk of laryngospasm.
Fentanyl Fentanyl, an opioid agent, reduces the cardiovascular side effects of laryngoscopy and intubation. It is 100 times more potent than morphine in its analgesic effect and helps to attenuate the hypertensive effects of intubation rendering it useful in raised ICP. Since, its sedative effect is not adequate, it is often combined with a benzodiazepine. The combination however, could cause profound cardiovascular compromise and troublesome apnea.
Ù
Chest wall rigidity and bradycardia are precipitated when fentanyl is administered rapidly.
Etomidate Etomidate is an imidazole hypnotic agent, which does not cause either hypotension or raised intracranial tension. It causes adrenal suppression and therefore is avoided in septic shock (relative adrenal insufficiency). At the time of writing this manual it is not currently available for wide spread use in our country.
Neuromuscular Blockade Agents Succinylcholine Succinylcholine remains the most preferred neuromuscular blocking agent for RSI in the ED. It owes its popularity to its rapid onset of action with shortest duration of paralysis. Despite its long list of complications, it creates excellent intubating conditions more reliable than Rocuronium.10 It is available as a 20 mg/mL solution. It rapidly loses potency after one month if stored in room temperature. The dose requirement is increased by 50% if defasciculating doses are used. When given through the intramuscular route, onset is delayed and the duration of action is approximately 20 minutes. Transient increase in heart rate is often noted. Bradycardia can also occur, but is countered by atropine (premedication agent). The most devastating arrhythmias are caused by hyperkalemia, which can lead to cardiac arrest. Conditions, which predispose to hyperkalemia are extensive burns, severe trauma, myopathies and muscle necrosis. The period of greatest risk of hypokalemia varies between 2 days and 6 months after the onset of these comorbidities. If ECG changes of hyperkalemia are noted, NMB should be avoided. Rise in intracranial pressure and intraocular
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
41
pressure has been attributed to the use of succinylcholine. Hence this drug is withheld in children with risk of ICP and glaucoma. In general, are less intense in IP fasciculations : 196.52.84.10 children than in adults. The routine use of defasciculation doses of succinylcholine in the ED is controversial.8
cally difficult and intellectually challenging procedure performed on critically ill children in ED settings. If performed successfully, the outcomes can be extraordinarily gratifying.
Vecuronium, Pancuronium and Rocuronium
1. Preoxygenate on arrival and insert NGT. 2. Initiate inotrope. 3. Preparation—O2, suction, IV access, tubes, tapes, drugs, equipment. 4. Premedicate. 5. Put to sleep. 6. Position the patient. 7. Pressure on cricoid. 8. Paralysis. 9. Preoxygenate using bag-valve-mask device. 10. Place the tube and check position. 11. Prevent dislodgement during transport.
Vecuronium, pancuronium and rocuronium are the commonly used non-depolarizing agents. These drugs act by binding to the neuromuscular receptor causing blockade, but no depolarization. All act less quickly and last much longer than succinylcholine. Amongst these drugs, rocuronium has the fastest onset of action (60–90 seconds) with duration of action of approximately 30–40 minutes. Pancuronium has the slowest onset and longest duration of action lasting up to 60–90 minutes. Though the side effects described for succinylcholine do not exist in this group of drugs, the longer duration of action delays recovery. Difficulty in securing the airway would be hazardous under these circumstances.
Failed Intubation ●● Intubate within the time taken for you to breathe out! (20–30 seconds). ●● Avoid making more than 2 attempts if unsuccessful on the first attempt. When patient is paralyzed and the ET tube cannot be placed, the first option is to ventilate the child using a bagvalve-mask device until the return of spontaneous respiration. This technique can be employed until expert help arrives (Refer to Chapter 4 on Assessment and Management of the Difficult Airway). Pharmacologically assisted intubation, in the hemodynamically unstable child, is perhaps the most techni-
Key Points11
common errors
ü
û
1. Failure to adequately preoxygenate prior to intubation. 2. Failure to position the child such that the oropharynx and laryngopharynx are not in the same straight line. 3. Inserting the laryngoscope into the esophagus. 4. Failure to confirm tube position by performing the complete cardiopulmonary cerebral assessment. 5. Failure to initiate an inotrope prior to administration of anesthetic agents. 6. Failure to hold the ET tube, until it is secured. 7. Failure to anticipate that shock can worsen after intubation.
42
Section II n Airway
Table 3.3: Drugs for rapid sequence induction Drugs
Dose
Route
Duration
IP : 196.52.84.10
Premedications
Side Effects
Comments
Atropine
0.01 mg–0.02 mg/kg Min: 0.1 mg Max: 1 mg IM dose: 0.02 mg/kg
IV IM
> 30 min
Paradoxical bradycardia can occur with doses < 0.1 mg
a. Inhibits bradycardic response to hypoxia b. Dilates the pupil but will not fix it c. Recommended when ketamine and/or succinylcholine is being used d. Used for intubating children < 4 years e. Used in intubating children with bradycardia
Glycopyrrolate
0.005–0.01 mg/kg Max: 0.2 mg
IV
> 30 min
Tachycardia Dry Mouth
a. Inhibits bradycardic response to hypoxia b. Dilates the pupil, but will not fix it c. Has less tachycardia compared to atropine
2–4 ug/kg
IV, IM
1–2 h
Respiratory depression, hypotension, chest wall rigidity and bradycardia can occur when given rapidly
a. Less histamine release associated hypotension than with other opioids b. May elevate ICP c. Movement disorders can occur with prolonged use
Narcotic agents Fentanyl citrate
Sedative hypnotics agents Midazolam
0.1–0.2 mg/kg Max: 4 mg
IV, IM
30–60 min Respiratory depression and hypotension
a. Potentiates respiratory depressive effects of narcotics and barbiturates
Diazepam
0.1–0.2 mg/kg Max: 4 mg
IV
30–90 min Hypotension
b. No analgesic properties
Thiopentone
2–4 mg/kg
IV
5–10 min
Negative inotropic effects hypotension
a. Ultrashort-acting barbiturate b. Decreases cerebral metabolic rate and ICP c. Potentiates respiratory depressive effects of narcotics and benzodiazepines d. No analgesic properties
Propofol
2 mg/kg (up to 3 mg/kg in young children)
IV
3–5 min
Hypotension in children with relative hypovolemia, pain on injection
a. On prolonged infusion can caused propofol infusion syndrome b. Potentiates respiratory depression c. No analgesic properties d. Highly lipid soluble with short duration of action e. Less likely to increase airway reactivity
Myocardial and CNS depression with high doses. Seizures can occur with repeated doses
Decreases ICP Hypotension less common
Anesthetic agents Lidocaine
1–2 mg/kg
IV
= 30 min
Ketamine
1–4 mg/kg
IV, IM
30–60 min Increased ICP and BP increased secretions and laryngospasm hallucinations and emergence reactions
Dissociative anesthetic agents No to limited respiratory depression, bronchodilator
Contd...
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED
43
Contd... Drugs
Dose
Route
Duration
IP : 196.52.84.10
Side Effects
Comments
Muscle fasiculations, rise in intraocular, intracranial intragastric pressure, life-threatening hyperkalemia, hypertension
Depolarizing muscle relaxant with rapid onset and short duration of action; Avoid in renal failure, burns or hyperkalemic states; Consider nondepolarizing agent in children < 5 years of age Do not use for maintenance of paralysis
Neuromuscular blocking agents Succinylcholine
IV: 1–1.5 mg/kg for children IV: 2 mg/kg for infants IM: Double the dose for IV
IV, IM
3–5 min
Vecuronium
0.1–0.2 mg/kg
IV, IM
30–90 min Minimal cardiovascular side effects
Non-depolarizing agent acting within 2–3 minutes and having longer duration of respiratory paralysis compared to succinylcholine (caution if intubation is difficult in the ED)
Rocuronium
0.6–1.2 mg/kg
IV
30–60 min Minimal cardiovascular side effects
Non-depolarizing agent that has a rapid onset of action equaling succinyl choline
REFERENCES 1. Audrey Zelicof-Paul, et al. Controversies in rapid sequence intubation in children. Curr Opin Pediatr. 2005;17:355-62. 2. SE Mace. Challenges and Advances in Intubation: Rapid Sequence Intubation Emerg Med Clin N Am; 2008 1043– 1068 doi:10.1016/j.emc.2008.10.002. 3. Preethi V, Venkatesh P, I Santhanam, P Jeyachandran, Profile of rapid sequence intubation in the PED of an academic children’s hospital in S.India- A pilot study. Proceedings of the National Assembly on Pediatric Emergency Medicine, 2012. 4. Ellis DY, Harris T, Zideman D.H.Cricoid pressure in emergency department rapid sequence tracheal intubations: a risk-benefit analysis. Ann Emerg Med. 2007;50(6):65365. 5. ACEP Policy Statement. Rapid-sequence intubation. Approved by ACEP Board of Directors – 2006, www. ACEP.org. 6. A. Bean. Atropine. Re-evaluating its use during pediatric RSI. Emerg Med J. 2007;24(5):361-62. doi: 10.1136/ emj.2007.048512.
7. Salhi B, Stettner E. In defense of the use of lidocaine in rapid sequence intubation. Mower III WR, Knopp RK, (Ed). Clinical controversies: lidocaine administration before rapid sequence intubation in patients with traumatic brain injuries. Ann Emerg Med. 2007;49(1):84-86. 8. Vaillancourt C. Kapur AK. Opposition to the use of lidocaine in rapid sequence intubation. Mower III WR, Knopp RK, Ed. Clinical controversies lidocaine administration before rapid sequence intubation in patients with traumatic brain injuries. Ann Emerg Med. 2007;(1):86-87. 9. Wathen JE, Roback MG, Mackenzie T, et al. Does midazolam alter the clinical effects of intravenous ketamine sedation in children? A double-blind, randomized, controlled, emergency department trial. Ann Emerg Med. 2000;36:579-88. 10. Perry J, Lee J, Sillberg VAH, et al. Rocuronium versus succinylcholine for rapid sequence induction intubation. (database online) Cochrane Database Syst Rev. (2): 2008;CD002788. 11. www.vdh.virginia.gov/OEMS/files page /symposium/2010. Presentations/PREP-1013. PDF.
Assessment and Management of the Difficult Airway IP : 196.52.84.10
4
Figure 4.1: Spectrum of difficult airway (Courtesy: Dr Thangavelu S and Dr Gunda Srinivas).
Learning Objectives 1. Defining a ‘Difficult airway’. 2. How do we recognize the red flag signs of airway difficulty?
Introduction Being confronted with a need to intubate a child presenting with respiratory failure and not being able to do so is every ED physician’s nightmare (Figure 4.1).
Difficult airway In most instances, securing the airway of a child, will be straightforward if the clinician is skilled and the airway anatomy is normal. A difficult airway can result from a variety of anatomical or clinical conditions.
Difficult airway can be recognized: 1. On arrival—when the child reaches may have spontaneous breathing or in respiratory arrest. 2. During BVM ventilation—before or after a paralyzing agent has been administered. 3. During laryngoscopy. 4. During tracheal intubation.
3. A modified ‘Difficult airway protocol’. 4. Laryngeal mask airway (LMA). 5. Difficult airway equipment. In many instances, difficult bag-valve-mask ventilation or intubation can be predicted. Ability to recognize a difficult airway, helps to plan on an alternative method if one technique fails. To avoid a potentially life-threatening ‘cannot ventilate, cannot intubate’ situation, a ‘difficult airway’ algorithm must be available.
Preparation ●● If a difficult airway is suspected following focussed history and physical examination and the child is not in cardiopulmonary failure, notify subspecialty teams from critical care, otolaryngology or pulmonology who are skilled in flexible or rigid bronchoscopy.
Ù
Do not meddle with a difficult airway. Call for ENT physician’s or anesthesiologist’s help. ●● Difficult intubation equipment should ideally be readily available in one location in addition to standard intubation equipment.
Chapter 4 n Assessment and Management of the Difficult Airway
It is very rare that a surgical cricothyrotomy will be needed to perform in children and it should be avoided at all costs in the ED. TheIPintubator should be familiar with : 196.52.84.10 specialized airway equipment (Box 4.1).
STEP 1 Recognize ‘Red flag’ signs during Airway assessment STEP 2 Ensure oxygenation
Box 4.1: Difficult airway kit3 ●● Bag-valve-mask (various sizes) ●● Guedel airways (various sizes) ●● Nasopharyngeal airways (various sizes) ●● Laryngeal mask airways (various sizes) ●● Laryngoscope blades (straight, curved, McKoy) Magill forceps ●● Gum elastic bougie ●● Needle cricothyrotomy set (14G cannula, 5 mL syringe, 3.0 ETT adapter) ●● Surgical cricothyrotomy set ●● Jet ventilation set (high pressure oxygen tubing, 3-way tap) Optional: ●● Intubating laryngeal mask ●● Light wand ●● Fiberoptic laryngoscope bronchoscope ●● Video laryngoscope
More specialized equipments such as intubating laryngeal mask, light wand or fiberoptic intubating laryngoscope may be helpful only if the intubator be familiar with their use.4
Step 1: Recognize ‘Red Flag’ Signs During Airway Assessment Emergent airway management often includes the ability to take a comprehensive history and perform a thorough physical exam. Clinical examination, provides clues that can predict potentially ‘difficult to intubate’ airway. ‘Red flags’ for a potentially difficult airway include: ●● Young age (infant or neonate). ●● History of trauma (including facial, laryngeal or tracheal trauma or trauma with possible cervical spine involvement). ●● Inhalational injury. ●● Acute infectious disease such as epiglottitis. ●● History consistent with foreign body aspiration. ●● Known difficult airway from prior intubation. ●● Congenital craniofacial abnormalities: – Micrognathia, large tongue and short neck. ●● Stridor. ●● Drooling. ●● Obesity. ●● Significant scoliosis.2
45
Position the airway Open the airway Suction Flow inflating device if spontaneously breathing, or BVM ventilation in respiratory failure If BVM is difficult, 1. Reposition 2. Consider airway obstruction such as FB 3. Jaw thrust 4. Two-person technique 5. Introduce oropharyngeal/nasopharyngeal airway STEP 3 Laryngoscopy and Intubation Difficult laryngoscopy 1. Reposition 2. Change blade 3. Cricoid pressure 4. BURP 5. Bimanual laryngoscopy Difficult tracheal intubation 1. Change ETT (0.5 mm smaller, cuffed over uncuffed when choosing a smaller size (ETT) 2. Laryngospasm STEP 4 Supraglottic airway devices/difficult airway adjuncts— Laryngeal Mask Airway STEP 5 Equipments used to intubate difficult airways like Bougie, videoscopy, etc. by airway experts (ENT or anesthetists). STEP 6 Surgical airway Cricothyrotomy
Figure 4.2: Difficult airway algorithm
Recommendations for the management of the difficult pediatric airway have been proposed, but the technique used depends on the skill of the intubator.5
46
Section II n Airway
Step 2: Ensure Oxygenation 1. Provide high concentration oxygen using a flow inflatIP :(refer 196.52.84.10 ing ventilation device Chapter 5) in a spontaneously breathing child with airway obstruction. 2. Initiate bag-valve-mask ventilation, if the child presents with respiratory failure or has not recovered from paralysis. Oxygen flow should be enough to keep the reservoir inflated throughout the respiratory cycle. 3. Constantly, ensure that the oxygen saturation is greater than 95% (one member in team should be delegated the responsibility of informing the airway manager when the saturations drop to 92%).
Ù
Bag-valve-mask ventilation could be difficult when oral or posterior pharyngeal structures crowd the airway. Large tongue, tonsils, or adenoids, or a ‘floppy’ larynx can all obstruct the airway. If bag-valve-mask ventilation is difficult: ●● Reposition the airway by manipulating—head tilt-chin lift maneuver/jaw thrust technique. ●● Release cricoid pressure, if ventilation is difficult in paralysed child.5 ●● Use nasopharyngeal or oropharyngeal airways to improve airway patency. Measure the distance between tip of nose and tragus and cut a 3.5 sized endotracheal (ET) tube to fashion a nasopharyngeal airway. Attach an adaptor to the cut end of tube (to avoid slippage into the air passage). ●● Two persons can be delegated to ventilate, one to hold the mask using both hands and the other to pump the bag. This technique will be needed in high-pressure bag-valve-mask ventilation in obese patients or in patients with low chest wall compliance (refer Figure 21.1, Chapter on status epilepticus). Adequacy of bag-valve-mask ventilation is assessed by following methods: 1. Degree of chest rise and fall. 2. Improvement of heart rate if bradycardic, color and oxygen saturation. ●● If oxygenation and ventilation can be provided, by effective bag-valve-mask ventilation, continue to do so until help arrives. ●● If effective bag-valve-mask ventilation is possible, intubation may not be so difficult. ●● Call for expert help to intubate (ENT physicians or anesthetists) at the earliest.
●● Avoid manipulation of the airway if more than two attempts had been made and earlier attempts had failed. ●● If saturations cannot be maintained despite effective bag-valve-mask ventilation, plan to insert the laryngeal-mark airway (LMA).
Ù
Patients need oxygen not tube.5
Difficult tracheal intubation can be divided into problems with laryngoscopy and problems with intubation.
Step 3: Laryngoscopy and Intubation
Ù
Difficult laryngoscopy most commonly results from improper head positioning along the frontal plane. 1. Reposition. ●● Reposition airway, such that the external auditory meatus and anterior edge of the shoulder are in the same straight line or position where chest rise is maximal during bag-valve-mask ventilation. ●● Extend or flex the neck to improve the intubator’s view of the vocal cords. ●● Place a towel under the shoulder blades of infants or neonates. This allows for better alignment of the oral/pharyngeal/and laryngeal axes. ●● Place a towel under the head for adolescents to achieve the same. ●● Apply backwards, upwards, rightward cricoid pressure (‘BURP’). The anteriorly placed infant larynx may be better visualized with external laryngeal manipulation. 2. Change the technique of inserting the laryngoscope. ●● Insert the laryngoscope into the right side of the mouth and actively ‘sweep' the tongue out of the intubator's line of vision. Oropharyngeal crowding is normal in neonates due to their relatively large tongue. 3. Intubating medications. ●● Use lower doses of intubating medications, if difficulty is anticipated.
Chapter 4 n Assessment and Management of the Difficult Airway
●● Use sedatives with caution, since these drugs can cause hypotension and can convert a difficult airway into an obstructed airway. IP : 196.52.84.10 ●● Give half the dose initially followed by another half dose if airway and breathing can be supported by bag-valve-mask ventilation. ●● Consider use of atropine to avoid vagal-induced bradycardia during laryngoscopy, though evidence for this practice is equivocal.6 ●● Use muscle relaxants judiciously in upper airway obstruction. ●● Avoid muscle relaxant, if bag-mask-valve ventilation is ineffective. ●● Rapidly transport to the operating room for inhalational induction, if child presents with stridor and respiratory failure to the ED.
47
5. Change the airway manager If the airway manager, is unable to intubate after 2 attempts, ideally, assistance must be sought from a more skilled person (Figures 4.2 to 4.5). Continue to initiate bag-valve-mask ventilation and wait until a more experienced airway physician arrives. This could be an anesthetist, ENT surgeon’s or ED or intensive care physician.
Ù
Patients do not die from failure to intubate. They die from failure to STOP trying to intubate.5
4. Intubation. Difficult tracheal intubation could result from several problems. Small endotracheal tubes are compliant leading to difficulty in negotiating the acute angle of an anteriorly placed pediatric larynx.
Ù
Use an introducer, bent into a ‘hockey-stick’ . The small size of the newborn’s mouth causes difficulty in visualizing the vocal cords, when introducing the endotracheal tube (mentioned earlier).
Figure 4.3: Note the abscess on the back can prevent visualization of the glottis. Though the neck appears hyperextended, optimal airway alignment was possible based on the position, which ensured maximum chest rise, improvement in heart rate, perfusion and SaO2.
Ù
Insert the endotracheal tube from the right-hand corner of the mouth with the plane of insertion at 90° from the plane of the cord visualizing. Difficulty may be encountered, when advancing the endotracheal tube beyond the vocal cords. This results from the narrowing of the pediatric airway at the cricoid ring or could be the result of a pathological subglottic process.
Ù
Use 0.5 mm smaller internal diameter of the endotracheal tube appropriate for the age. Cuffed tubes may be preferred over uncuffed, while using ET tubes smaller than appropriate for age to avoid air leak for effective ventilation. ●● Stop intubation attempts and reoxygenate (continue bag-valve-mask ventilation) if saturations drop.
Figure 4.4: Note the airway manager manipulating the airway using the little finger. Also note the airway nurse on the right hand side of the intubator providing lip retraction whilst the airway nurse on the left side is poised with a suction catheter. Ability to anticipate the needs of the airway manager and assist in the intubation process, is one of the most important skills of the airway nurse.
48
Section II n Airway
Choice of appropriate LMA is based on the patient's weight are listed in Table 4.1.7
IP : 196.52.84.10
Table 4.1: Selection of LMA LMA size
Figure 4.5: The airway manager is holding the tube against the inner aspect of the cheek, while tube position is being checked prior to fixing the tube.
Step 4: Failed Intubation Laryngeal Mask Airway (LMA)
Patient size
Max cuff volume (mL)
1
< 5 kg
4
1.5
5–10 kg
7
2
10–20 kg
10
2.5
20–30 kg
14
3
30–50 kg
20
1. Lubricate the posterior surface of the LMA with a water soluble lubricant. 2. Place an inflation syringe in the cuff valve and deflate the cuff completely for insertion, making sure that the leading tip is not folded backwards. 3. Hold the LMA close to the cuff using a pencil grip (Figure 4.7).
The LMA is a small inflatable mask, attached to tubing with an universal adapter. It is designed to sit in the oropharynx with the tip in the hypopharynx and the base at the epiglottis. With the cuff inflated, the laryngeal mask creates a seal around the supraglottic area, allowing air flow between the tubing and trachea (Figure 4.6).
Ù
If despite all the maneuvers mentioned above, intubation has failed and saturations are dropping, resort to LMA. Laryngeal mask airway is a rescue device in a ‘cannot intubate cannot ventilate’ (CICV) situation.
Figure 4.6: Parts of laryngeal mask airway (LMA).
Figure 4.7: Technique of insertion
4. Place the head and neck in the sniffing position. Open the mouth, while lifting the chin forward (Figure 4.8).
Figure 4.8: Technique of insertion (Contd...)
Chapter 4 n Assessment and Management of the Difficult Airway
49
5. To facilitate LMA introduction into the oral cavity, gently press the middle finger down on the jaw (Figure 4.8). IP : 196.52.84.10 6. Simultaneously, press the LMA against the hard palate and guide it along the posterior oropharynx until the operator feels firm resistance. The opening of the cuff faces towards the tongue. This method prevents folding up of the epiglottis (Figures 4.9 and 4.10). Ensure that the patient is fully unconscious when inserting the LMA. Often, the partially conscious victim may inadvertently bite the finger of the rescuer as he inserts it in this manner. Figure 4.11: LMA inserted.
8. Gently maintain cranial pressure with the non-dominant hand, while removing the index finger (Figure 4.12).
Figure 4.9: Technique of insertion (Contd...)
Figure 4.12: Stabilization of LMA.
Figure 4.10: Technique of insertion (Contd...)
7. Maintaining pressure with the finger on the tube in the cranial direction, advance the mask until definite resistance is felt at the base of the hypopharynx. Note the flexion of the wrist (Figure 4.11).
9. Inflate the cuff using an air filled syringe until the pilot balloon gets filled up. The laryngeal mask may be observed to ‘rise up' slightly out of the oropharynx (Figure 4.13). 10. Fix the LMA in the midline with dynaplast tape around the tube. Also insert a roll of gauze on either side of the LMA to avoid biting the tube. The laryngeal mask does not prevent reflux and aspiration of gastric contents. It is not helpful with glottic or subglottic pathology and cannot be used to deliver high pressure ventilation (laryngeal mask seal pressure is ~25 mm H2O).
50
Section II n Airway
IP : 196.52.84.10
Figure 4.14: Bougie Figure 4.13: Cuff being inflated.
Complications of LMA insertion: ●● Partial airway obstruction by the epiglottis. ●● Loss of adequate seal with patient movement. ●● Air leak during positive pressure ventilation. ●● Poor tolerance of the LMA, if airway protective reflexes are intact or recovering.
Step 5: Airway Experts Bougie8 (Figure 4.14) ●● The Bougie is a straight, semirigid stylet-like device with a bent tip that can be used when intubation is (or is predicted to be) difficult. ●● When vocal cords cannot be visualized due to extreme anterior positioning, the bougie can be inserted blindly above the epiglottis. ●● Confirmation of insertion into the trachea occurs, when the bougie can be felt to ‘hop' along the tracheal rings as it is advanced. ●● Introduce an endotracheal tube over the bougie into the trachea and remove the bougie (Figure 4.15). ●● The Bougie is an important part of the armamentarium of the anesthetist. If in need, do not hesitate to call for expert help.
Videoscopic Techniques8 A variety of fiberoptic and videoscopic devices facilitate intubation in difficult airway scenarios, where direct laryngoscopic visualization of the laryngeal opening is not possible. Practice and familiarity are needed to make use of these devices.
Figure. 4.15: Endotracheal tube introduced over bougie.
Fiberoptic scopes may be broadly classified into two groups: 1. Flexible devices. 2. Rigid and semirigid devices. This device permits indirect visualization of the glottis through an image transmitted via fiberoptic bundles. The fiberoptic bundles are aligned with a non-malleable blade or stylet with a J-shape or L-shape, allowing the physician to see around the corner. Examples of rigid devices include the bullard laryngoscope (ACMI Corp, Southborough, Mass); the Upshers cope F2 (Mercury Medical, Clearwater, Fla) and the WuScope (mercury medical). Readers should familiarize themselves with the advantages and disadvantages of each of these instruments and techniques.8 The use of these devices however, is beyond the scope of this manual.
Chapter 4 n Assessment and Management of the Difficult Airway
51
Step 6: Surgical Airway—Cricothyrotomy (Rarely Needed) IP : 196.52.84.10
This method should be reserved as a last resort. A hazardous procedure, needle cricothyroidectomy should not be undertaken lightly. Consider needle cricothyrotomy, if upper airway obstruction is proximal to the glottic opening and other measures of securing the airway have failed. 1. Equipment necessary for the procedure includes: • 14 gauge intravenous cannula. • 3.0 size endotracheal tube adapter. • 5 mL syringe. 2. Position child supine by extending the head and placing a towel under the shoulders. 3. If cricothyroid membrane is palpable, cannula should be inserted at this point. 4. If cricothyroid membrane is not palpable as in young infants, palpate and immobilize the trachea. 5. Advance cannula to which syringe is attached into the tracheal lumen at a 30° angle until air is aspirated. 6. Fix the 3.0 endotracheal tube adapter to the hub of the cannula and initiate bag ventilation. 7. Transtracheal jet ventilation should be used with extreme caution. It should only be used when a pressure release valve is attached to the system (such as a 3-way tap) to prevent excessive air flow and barotrauma. Complications include bleeding, subcutaneous emphysema and failure to adequately oxygenate.
Ù
Surgical cricothyrotomy is discouraged in young children (< 10 years) due to the low likelihood of success and high complication rate in the emergency setting.6 Documentation should focus on the following:
i. Difficulties encountered during intubation. ii. Methods used to secure the airway. The sight of recovered child with their parents after successful resuscitation in the ER is always a satisfying experience. Refer Figure 4.16
Figure 4.16: The happy mother and her newborn 4 days following resuscitation (same new born managed in 4.3–4.5).
Key Points
ü
1. Practice of protocols for the management of the difficult airway is necessary. 2. Effective bag-valve-mask ventilation is the most important technique in the management of the difficult pediatric airway. 3. Repositioning is the most effective means of providing adequate bag-valve-mask ventilation. 4. The laryngeal mask may be a life-saving device in event of failed intubation, desaturation and inability to bag-valve-mask ventilate. 5. Fiberoptic techniques are useful for visualization and should also be practiced. 6. Surgical techniques such as needle cricothyrotomy are rarely necessary.
common errors
û
1. Failure to recognize ‘red flag’ signs of difficult airway. 2. Failure to call for expert help. 3. Making multiple attempts despite repeated failure. 4. Failure to oxygenate between attempts. 5. Failure to respond urgently to fall in saturations to 92%.
52
Section II n Airway
References 1. The American Society of Anesthesiologists Task Force: : 196.52.84.10 Practice guidelines IP for management of the difficult airway. Anesthesiology. 2003;98:1267-277. 2. Murphy MF, Walls RM. Identification of the difficult and failed airway. In: Walls RM, Murphy M, Luten RC (Eds). Manual of Emergency Airway Management. Philadelphia. PP. P. Lippincott Williams and Wilkins; 2008;82. 3. Preece R. Guidelines for difficult airway equipment in emergency departments. Emerg Med J. 2006;3:230. 4. Walker R, Ellwood J. The Management of difficult intubation in children. Pediatr Anes th. 2009;19:77-87.
5. Benger J. Nolan J, Clancy M. Emergency Airway Management. London: Cambridge University Press; 2009: pg 81. 6. Weiss M, Dullenkopf A, Fischer JE, et al. European Paediatric Endotracheal Intubation Study Group. Prospective randomized controlled multi-centre trial of cuffed or uncuffed endotracheal tubes in small children. Br J Anaes. 2009;103(6):867-73. 7. http://www.lmana.com/faqs.php#faq03 8. Levin R, Kissoon N, Froese N. Fibreoptic and videoscopic indirect intubation techniques for intubation in children. Pediatr Emerg Care. 2009;25(7):479. 9. Cote C, C Hartnick. Pediatric trans-tracheal and cricothyrotomy devices for emergency use: which are appropriate for infants and children? Pediatr Anaes th. 2009;19:66-76.
Flow Inflating Ventilation Device: IP : 196.52.84.10 Non-invasive CPAP in Settings Without Immediate Access to Mechanical Ventilation
5
Figure 5.1: Flow inflating ventilation device, a boon in the ED management of acute pulmonary edema and shock
Learning Objectives 1. CPAP and its benefits in the management of acute pulmonary edema during shock resuscitation. 2. Parts of the flow inflation ventilation device (Jackson-Rees/Pediatric Bain circuit).
INTRODUCTION A large number of seriously ill children reach our hospitals with respiratory distress or failure, have features of acute pulmonary edema or cardiac dysfunction (Figure 5.1).
Ù
Hypoxic and shocked children due to various etiologies often present with pulmonary edema due to cardiac dysfunction or acute lung injury. Under these circumstances, the flow inflating ventilation device, which provides continuous positive airway pressure in spontaneously breathing patients, appears to be a boon in the initial management of these children in settings without immediate access to mechanical ventilation. However, the use of NIPPV for pediatric patients in emergency situations is not well established and a recent Cochrane review notes the lack of well-designed and con-
3. Pearls and pitfalls when using this device. 4. Evidence supporting the use of non-invasive positive pressure ventilation (NIPPV).
trolled studies to support the use of non-invasive respiratory support in children.1
PHYSIOLOGY Functional residual capacity (FRC) is the volume of gas remaining in the lungs during normal expiration. Diseased lungs with atelectasis have reduced FRC. Consequently, blood is shunted to the heart without oxygenation (intrapulmonary shunting). Lung compliance decreases, while airway resistance increases. A combination of these factors result in increased work of breathing. Application of continuous positive airway pressure (CPAP) improves FRC, thereby alleviating intrapulmonary shunting and increasing oxygenation. Lung compliance becomes better, airway resistance falls and work of breathing is reduced (Figures 5.2 to 5.5).
54
Section II n Airway
IP : 196.52.84.10
Figure 5.2: Parts of the flow inflating ventilation device (Jackson-Rees circuit)
Under-ventilated alveoli open up (recruitment) as FRC improves. Perfusion to the newly recruited alveoli takes place, thereby improving oxygenation. In acute cardiogenic PE, CPAP reduces left ventricular transmural pressure. This is the main mechanism by which CPAP improves oxygenation in cardiogenic PE. CPAP increases intrathoracic pressure. Consequently, preload and afterload falls leading to improvement in cardiac output and PE.
Figure 5.3: This infant is being manually ventilated in the ED following intubation using the flow inflating ventilation device. Inotrope and catecholamine infusions are on flow during fluid resuscitation of myocardial dysfunction and shock.
Figure 5.4: Parts of the flow inflating ventilation device continued...
Chapter 5 n Flow Inflating Ventilation Device: Non-invasive CPAP in Settings Without Immediate Access to Mechanical Ventilation
IP : 196.52.84.10
55
analysis12-16 in adult patients. Compared to administration of oxygen alone, application of CPAP reduces the need for intubation, as well as risk of mortality. ●● Non-invasive application of continuous positive airway pressure, using the flow inflation ventilation device during fluid resuscitation of septic shock has shown a significant drop in hospital mortality.17
Technique: How to Use the Jackson-Rees Circuit?
Figure 5.5: Note that the child is being given an inotrope infusion and is being monitored with a pulse oximeter. The bag- valve-mask is available close at hand.
Children presenting with respiratory distress often, also have auto-PEEP or dynamic hyperinflation. Normally, upper airway pressure is higher than the positive end expiratory pressure at the alveoli for inspiratory gas flow to occur. Inspiratory muscles, have to work harder to drop alveolar pressure from its baseline positive end expiratory value to less than upper airway pressure (normally 0) before inspiratory gas flow occurs. This is termed ‘threshold work’. By increasing airway pressure, CPAP reduces the work required to initiate inspiratory flow. The beneficial effects of reducing the work of breathing are improvement in respiratory rates and a fall in PaCO2. For this reason, provision of CPAP is considered to provide ventilatory support. Refer Figure 5.6 for mechanism of working of JR circuit.
Ù
The flow inflating ventilation device has dual benefits; delivery of 100% oxygen with the benefits of continuous positive airway pressure. ●● Use of non-invasive positive pressure ventilation in acute cardiogenic pulmonary edema has been supported by randomized controlled trials (RCTs)2-11 and meta-
1. Ensure that airway is spontaneously maintainable and apply the face mask, such that it fits with an airtight seal (Figure 5.4). 2. The person holding the mask should ensure that the reservoir remains inflated at all times. 3. A severely hypoxic child will tend to fight the mask. Hold the mask firmly in position. Tolerance improves as hypoxia resolves. Until then, the child may need to be restrained or cajoled by his mother. 4. Monitor using a pulse oximeter and cardiac monitor. 5. Avoid closing the expiratory pressure valve. Insufficient venting of exhaled gas will cause both volume and pressure to increase within the system. This would prevent expiration and increase intrathoracic pressure. The latter, may lead to barotrauma or aggravate ICP in children with cerebral edema. The latter may lead to barotrauma in the lung and aggravate ICP in children with cerebral edema. 6. Inadequate oxygen flow Inadequate flow of O2 results in failure to flush out CO2. The resultant rebreathing leads to hypercarbia. The latter can cause increase in cerebral blood flow, ICP and predisposition to cardiac arrhythmias.
Ù
If the reservoir over-distends, check whether the pressure release valve is closed or the flow of gas has become excessive.
Figure 5.6: Mechanism of working of Jackson-Rees circuit
56
Section II n Airway
7. Avoid using the JR circuit in an apneic child Assisted ventilation for the non-intubated child, is best provided using theIPself-inflating bag-valve-mask de: 196.52.84.10 vice. 8. Use age appropriate reservoirs When smaller reservoirs are used in older children, hypoxia can worsen or not improve. Use of larger reservoirs and circuits increase dead space ventilation and predispose to respiratory fatigue in young infants. 9. Continue to use the flow inflating ventilation device, until respiratory distress and shock resolves. Parents and attendants must be taught to hold the mask under supervision in centers where healthcare providers are not available round the clock. 10. JR circuit is contraindicated if level of consciousness drops profoundly. Development of hypotonia or posturing or seizure activity are indications for intubation. 11. Worsening of irritability, inconsolable cry and posturing may be noted in some children when applying the Jackson-Rees circuit. As respiratory distress and shock resolve, tolerance improves.
Key Points
ü
1. Use the flow inflating ventilation device to provide O2 to all critically ill children presenting with respiratory distress and shock. 2. Flow inflating ventilation device is useful to provide O2 for children presenting with acute cardiogenic shock due to various etiologies such as scorpion sting, sepsis, submersion injury, etc.
common errors
û
1. Use of flow inflating device in apneic children (bagvalve-mask preferred). 2. Inappropriate sized reservoir. 3. Complete closure of pressure release valve.
REFERENCES 1. Shah PS, Ohlsson A, Shah JP. Continuous negative extrathoracic pressure or continuous positive airway pressure for acute hypoxemic respiratory failure in children. Cochrane Database Syst Rev. 2008;1:CD003699. 2. Mehta S, Jay GD, Woolard RH, et al. Randomized prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med. 1997;25:620-28.
3. Nava S, Carbone G, Di Battista N, et al. Noninvasive ventilation in cardiogenic pulmonary edema. A multicenter, randomized trial. Am J Respir Crit Care Med. 2003;168:1-6. 4. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med. 1991;325:1825-830. 5. Lin M, Yang YF, Chiang HT, et al. Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema: short-term results and long-term follow-up. Chest. 1995;107:1379-386. 6. Pang D, Keenan SP, Cook DJ, et al. The effect of positive airway pressure on mortality and the need for intubation in cardiogenic pulmonary edema. Chest. 1998;114:1185192. 7. Park M, Sangean MC, Volpe Mde S, et al. Randomized, prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway Pressure by face mask in acute cardiogenic pulmonary edema. Crit Care Med. 2004;32:2407-415. 8. Crane SD, Elliott MW, Gilligan P, et al. Randomised controlled comparison of continuous positive airways pressure, bilevel non-invasive ventilation, and standard treatment in emergency department patients with acute cardiogenic pulmonary oedema. Emerg Med J. 2004;21:155-61. 9. Bellone A, Monari A, Cortellaro F, et al. Myocardial infarction rate in acute pulmonary edema: noninvasive pressure support ventilation versus continuous positive airway pressure. Crit Care Med. 2004;32:1860-865. 10. Bellone A, Vettorello M, Monari A, et al. Non-invasive pressure support ventilation versus continuous positive airway pressure in acute hypercapnic pulmonary edema. Intensive Care Med. 2005;31:807-11. 11. Giacomini M, Iapichino G, Cigada M, et al. Short-term noninvasive pressure support ventilation prevents ICU admittance in patients with acute cardiogenic pulmonary edema. Chest. 2003;123:2057-061. 12. Masip J, Roque M, Sanchez B, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. Systematic review and meta-analysis. JAMA. 2005;294:3124-130. 13. Ho KM, Wong K. A comparison of continuous and bilevel positive airway pressure non-invasive ventilation in-patients with acute cardiogenic pulmonary edema: a metaanalysis. Crit Care. 2006;10:R49. 14. Collins SP, MielniczukLM, Whittingham HA, et al. The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: a systematic review. Ann Emerg Med. 2006;48:260-69. 15. Winck JC, Azevedo LF, Costa-Pereira A, et al. Efficacy and safety of non-invasive ventilation in the treatment of acute cardiogenic pulmonary edema: a systematic review and meta-analysis. Crit Care. 2006;10:R69.
Chapter 5 n Flow Inflating Ventilation Device: Non-invasive CPAP in Settings Without Immediate Access to Mechanical Ventilation
16. Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of noninvasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary edema: a IP 2006;367:1155-163. : 196.52.84.10 meta-analysis. Lancet. 17. Ferrari G, Olliveri F, De Filippi G, et al. Non-invasive positive airway pressare and risk of myocardial infarctio in acute cardiogenic pulmonary edema: continuous posi-
57
tive airway pressure versus non-invasive positive pressure ventilation. Chest. 2007;132:1804-809. 18. Santhanam I, Padma V, Murali T, et al. Predictors of mortality of children presenting with severe sepsis. Proceedings from the first European congress on Pediatric resuscitation and emergency medicine, Ghent. May 2013.
Section III
Approach to Stridor IP : 196.52.84.10
IP : 196.52.84.10
6
IP : 196.52.84.10
Stridor
Figure 6.1: A child being resuscitated for acute laryngotracheobronchitis in the PED (Courtesy: Dr Gunda Srinivas)
Learning Objectives 1. Highlight the importance of recognizing supraglottic stridor. 2. Precautions taken during assessment and management. 3. Establish etiology.
INTRODUCTION The presentation of stridor with impending respiratory failure, is an ED physician’s nightmare (Figure 6.1). To avoid the dreaded complication of complete airway obstruction, a swift, systemic, protocol based approach is mandatory.
PATHOPHYSIOLOGY The upper airway begins at the nose and extends up to the main bronchi. Stridor, a high pitched sound of respiration is a sign of partial obstruction of any part of the upper airway. The effect of upper airway obstruction can be explained by the ‘venturi effect’. Pressure exerted on a partially closed tube of gas, is equal in all directions except during linear movement of air. The linear flow of air creates an additional pressure in the forward direction within the tube, resulting in a fall in pressure along the lateral wall. Hence, during inspiration, the airway has a tendency to collapse.
4. Evidence and treatment is based on etiology. 5. Establish severity using the rapid cardiopulmonary cerebral assessment and pediatric assessment triangle. 6. Management based on severity and etiology. Different parts of the airway are more collapsible than others. Anatomically, the upper airway is divided into supraglottic, glottic and subglottic regions. The vocal cords, glottis or trachea (good cartilaginous support) are less collapsible than the supraglottis region. The lack of cartilaginous support, enhances the tendency for complete collapse when airway obstruction occurs due to supraglottic pathologies. This risk is aggravated in young children where the subglottic airway is smaller and even more compliant (supporting cartilage less developed than in the adult).
Ù Supraglottis can easily become obstructed by mucus, blood, pus, edema, active constriction, external compression or pressure differences created during spontaneous respiratory effort in the presence of airway obstruction.
62
Section III n Approach to Stridor
Even minimal mucosal edema can significantly reduce the diameter of the pediatric airway and increase resistance to airflow and work of breathing.
Ù Crying can
IP : 196.52.84.10
aggravate hypoxia by increasing air turbulence in the obstructed airway. All precautions should be taken to prevent a child with stridor from crying.
GENERAL APPROACH 1. Avoid the following maneuvers in children presenting with stridor. ●● Do not separate the child from his mother. Examine and manage the child on his mother’s lap. ●● Avoid changing the position of comfort, which the child has adopted. Do not make an alert or agitated child with stridor, lie down on the resuscitation trolley or bed. It could precipitate complete airway obstruction. ●● Avoid forcing an oxygen mask on a screaming child. Without separating the child from his mother, help the mother to administer oxygen in a non-threatening manner. 2. Ascertain the severity of the lesion based on the physiological status. ●● Perform the rapid cardiopulmonary cerebral assessment. It helps to quickly determine whether the airway obstruction can be handled in the ED or in the OT. 3. Simultaneously, obtain a focused history to establish the anatomical site of obstruction. The ‘5A’s approach helps to identify the level of lesion. ●● Age: What is the age of the child? ●● Acuity: Is the presentation, hyperacute, acute, chronic or acute on chronic? ●● Acoustics: Is the stridor harsh or soft. ●● Associated symptoms: Is stridor associated with fever, dysphagia or drooling? ●● What is the quality of voice (hoarse or muffled)? ●● Aggravating factors?
lapsible due to lack of cartilaginous support. The presence of multiple tissue planes in this region encourages rapid spread of infection especially in infancy. In addition, in children less than 2 years of age, the retropharyngeal space contains lymph nodes that serve as a nidus for the formation of abscess. As the nodes atrophy, the risk of abscess formation becomes much less. Obstruction at the supraglottis, i.e. above the level of the esophagus, as in epiglottitis or retropharyngeal abscess causes pooling of saliva. The latter leads to: 1. Soft stridor (may not be reported by the mother, but identified by the ER physician). 2. Drooling and dysphagia. 3. Muffling of voice (‘hot potato voice’). 4. Ineffective cough.
Glottis The glottic and subglottic region extends from the vocal cords to the trachea before entering the thoracic cage. Since the cricoid cartilage and tracheal cartilaginous rings surround majority of its length, this section of the airway is not as collapsible as the supraglottis. The commonest causes of obstruction at this site are inflammation and edema due to acute laryngotracheobronchitis (ALTB). 1. Hoarse voice. 2. The harsh stridor may occur in either the inspiratory or expiratory phase or occasionally both phases of respiration (biphasic). The latter is due to minimal alterations in the size and shape of the airway obstruction during both phases of respiration. 3. Brassy cough. 4. Drooling and dysphagia are not characteristic features of glottic obstruction unless the obstruction is large enough to compress the esophagus.
Intrathoracic
Supraglottis
The intrathoracic airway comprises of the trachea and the main stem bronchus. Intrathoracic airway obstruction causes stridor that is loudest during expiration. Increase in intrathoracic pressure during expiration, causes collapse of the airway. During inspiration, the intrathoracic pressure falls. As a result, the obstructed thoracic airway expands leading to a quieter sound.
The supraglottis extends between the nose and the vocal cords. As mentioned earlier, it is easily distensible and col-
Congenital malformations of the airway are the commonest causes of obstruction within the thorax.
SITE OF OBSTRUCTION
Chapter 6 n Stridor
ETIOLOGY OF OBSTRUCTION 1. Age at which stridor presents helps in recognizing IP : 196.52.84.10 etiology. ●● Stridor in young infants is more likely due to a congenital problem. Older children (1–4 year) are more likely to have an infectious etiology or foreign body aspiration. ●● Unusual in infants younger than 6 months, croup reaches its peak incidence during the second year of life.1 Around 6 years of age, a child's airway is similar to that of an adult and the effect of mucosal edema becomes minimal. ●● Epiglottitis, historically peaks at 3 years of age. More recently, its presentation has shifted to older children and adults.2 ●● Retropharyngeal abscess is most commonly seen in infants and children up to age 4 years.2 Infections of the nasopharynx, paranasal sinuses or middle ear can extend up to lymph nodes located in the space between the posterior pharyngeal wall and the prevertebral fascia. Since these retropharyngeal nodes atrophy beyond 4 years of age, retropharyngeal abscesses are common under this age. ●● From 6 months to 6 years of age, children tend to explore their environment, increasing the risk of foreign body aspiration. Stridor due to aspiration of a foreign body is most common in children aged between 1 and 3 years. ●● The incidence of peritonsillar abscess peaks at 10 years. ●● Past history of intubation or birth injury suggest vocal cord paralysis or laryngotracheal stenosis. 2. Acoustics of the stridor often help in identification of the level of airway obstruction. ●● An inspiratory soft stridor suggests supraglottic pathology. ●● A harsh inspiratory or a biphasic stridor is suggestive of either a glottic or subglottic lesion. ●● Expiratory stridor is more in favor of an intrathoracic lesion. 3. Acuity or rapidity of onset. ●● Hyperacute onset of stridor should arouse suspicion of FB aspiration. ●● Children with an anaphylactic response will present with acute stridor, wheeze, hypotensive shock and rashes within 5 minutes of contact with the allergen.
63
●● Epiglottitis develops over a few hours after onset of symptoms. 4. Associated symptoms. ●● High grade fever indicates bacterial etiology, e.g. epiglottitis, retropharyngeal abscess or tracheitis. ●● Low-grade fever could be associated with ALTB (Box 6.1). ●● Non-infectious causes such as FB aspiration or congenital causes are characterized by absence of fever. ●● Drooling, dysphagia and a ‘hot potato voice’ indicate that the obstruction is at the level of the supraglottis. ●● Barking cough, brassy voice along with stridor is commonly due to croup. ●● Restriction of neck movements is diagnostic of retropharyngeal abscess. ●● Children with stridor due to epiglottitis, diphtheria, retropharyngeal abscess appear toxic, hyperalert and maintain a tripod position. ●● A weak cry is associated with laryngeal anomaly or neuromuscular disorders. ●● Hemangiomas elsewhere in the body of a child with stridor, suggest that the obstruction to the airway, is due to a hemangioma in the subglottic region. ●● Respiratory rates are usually normal or mildly elevated. Head bobbing, retractions and use of accessory muscles indicate impending respiratory failure. ●● Sternal retractions in the young infant or neonate suggest the presence of an airway obstruction, even, if the stridor is not clearly audible. ●● Acute viral croup, follows a protracted prodromal period of cough and rhinorrhea. ●● Bacterial tracheitis and retropharyngeal abscess may be preceded by a viral upper respiratory infection. 5. Factors which aggravate or make the stridor louder! ●● Crying: Laryngomalacia, subglottic hemangioma. ●● Choking: Tracheoesophageal fistula, FB. ●● Supine position: Laryngomalacia, macroglossia, micrognathia. ●● Virtually all children presenting with acute stridor and respiratory distress, (except ALTB and angioedema) should be evaluated and managed in the OT by ENT specialists or anesthetists.
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If airway obstruction is associated with respiratory failure, call for ENT help. Urgent intubation must be performed in the ED by airway experts.
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Section III n Approach to Stridor
Case Scenario 1 A toddler presented with 1 day history of fever, stridor IP : 196.52.84.10 and swelling in front of the neck (Figures 6.2 to 6.8).
Figure 6.4: Case progression: As oxygen and fluids were being given, the child’s mental status deteriorated. His assessment was as follows:
Figure 6.2: Swelling in front of the neck
Figure 6.5 Physiological status: Unmaintainable airway with respiratory failure, compensated shock and coma.
Intervention Figure 6.3 Physiological status: Structural stridor with impending respiratory failure, compensated shock and altered mental status
Intervention ●● A: Child was seated in his mother’s lap. ●● B: Oxygen was given by his mother in a non-threatening manner. ●● C: Vascular access was secured and 10 mL/kg of NS was started over 20 minutes. ●● ENT specialist and the pediatric surgeon were called for help immediately.
●● A: Airway was positioned using the head tilt-chin lift maneuver (Figure 6.4). ●● B: Oxygen was given via the Jackson-Rees Circuit. ●● C: Dopamine was initiated at 10 μg/kg/minute. ●● The surgeon performed diagnostic aspiration (thick pus was aspirated). ●● Airway tray was ordered. ●● Fentanyl and atropine were ordered ●● Ketamine was avoided for its risk of laryngospasm. ●● Succinylcholine, was also avoided since paralysis would have deprived the child of his respiratory effort where difficulty was anticipated during intubation.
Chapter 6 n Stridor
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Figure 6.6: The child continued to worsen and developed apnea. Figure 6.8: This picture shows a neurologically normal child who was briefly ventilated. Complete drainage of the abscess was performed in the intensive care unit. Box 6.1: Etiology of stridor
Figure 6.7 Physiological status: Airway intubated, assisted ventilation, hypotensive shock with low MAP.
Intervention ●● A: Laryngoscopic evaluation showed a smooth globular swelling with no anatomical landmarks to guide intubation. Viz: epiglottis, arytenoid folds or vocal cords were not visible. ●● B: Bag-valve-mask ventilation was initiated. Chest rise was adequate and saturation improved to 100%. ●● Successfully intubated on the 6th attempt using a 3.5 mm tube. Each attempt was preceded by preoxygenating with bag-valve-mask ventilation, such that SaO2 was > 95%. ●● C: 80 mL/kg NS, dopamine and norepinephrine infusions were needed to resolve warm shock with low MAP. ●● The first dose of antibiotic was also administered. ●● Hypoglycemia was ruled out. GNS with KCl was initiated at maintenance rates.
Infectious 1. ALTB (classical croup) 2. Acute epiglottitis 3. Bacterial tracheitis 4. Retropharyngeal abscess Non-infectious 1. Congenital malformations obstructing the airway 2. Spasmodic croup 3. Foreign body obstruction 4. Angioedema 5. Laryngomalacia 6. Laryngeal papilloma 7. Hypocalcemia 8. Vocal cord paralysis
Acute Laryngotracheal Bronchitis (Box 6.1) A careful history and physical exam is mandatory to confirm diagnosis and simultaneously, rule out FB aspiration or epiglottitis. Most children present with acute onset barking cough, stridor and chest wall in drawing.3,4 It is preceded by a prodrome of cough, cold and low-grade fever. Typically, the illness lasts for 3–7 days. As the obstruction worsens, the child becomes increasingly tachypneic with distress of variable severity. Tachycardia is noted when the child becomes hypoxia. Severe airway obstruction is associated with pulsus paradoxus. Rarely, progressive increase in the work of breathing leads to respiratory failure, characterized by severe chest retractions, decrease in breath sounds and oxygen saturation. Increasing cyanosis along with
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Section III n Approach to Stridor
change in mental status indicate need for intubation. Some children with ALTB may develop secondary bacterial tracheitis. IP : 196.52.84.10
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Tachycardia indicates hypoxia. Peripheral perfusion is usually normal, but can be compromised in severe hypoxia.
CASE SCENARIO 2 A 1-year-old child presents with barking cough and inspiratory stridor. His mother reports that her son has been coughing for a week (Figure 6.9).
Epinephrine is the drug of choice. Due to its non-selective α-adrenergic and β-agonistic action, it relieves mucosal edema and improves breathing mechanics. In most children, one dose is adequate, although it may be repeated after 4–6 hours. The Cochrane review5 concluded that nebulized epinephrine, both racemic and L-isomeric preparation caused reduction of croup symptoms within 30 minutes after treatment and improved stridor related respiratory distress. Ideally, both pulse oximetry and ECG monitoring should be available during epinephrine nebulization.
Glucocorticoids6-15 Glucocorticoids reduce upper airway swelling leading to significant improvement in croup symptoms. Their onset of action occurs within 1 hour after administration. Action is delayed when compared with inhaled epinephrine. Peak effect is noted, 6–12 hours after administration. A recent cochrane review further confirmed that, glucocorticoids are effective in improving severity of croup, decreasing the number of return visits, readmissions and length of stay in hospital. Dexamethasone rapidly improves stridor, decreases hospital stay and reduces the need for intubation. Figure 6.9 Physiological status: Stridor due to glottic edema with respiratory distress and tachycardia. Perfusion, BP and mental status is normal.
The history is suggestive of croup.
Treatment ●● Administer ‘blow-by’ oxygen through a plastic hose with its end held within a few centimeters of the child’s nose and mouth.
Epinephrine ●● Add, 0.5 mg/kg up to a maximum of 5 mg epinephrine (1:1,000) to 2–3 mL of NS into the nebulizing chamber. Nebulize through oxygen. ●● Observe the child for recurrence for at least 2 hours after nebulization. ●● Less than 4 years—2.5 mL. ●● More than 4 years—5 mL.
●● Administer 0.6 mg/kg/dose IM, IV or oral (maximum 10 mg). An oral dose of 0.15 mg/kg is also effective. Onset of action occurs within 1–2 hours. ●● A single dose is generally sufficient in most children for prompt and sustained improvement. If necessary, the steroid dose may be repeated after 12–24 hours. ●● No significant differences have been noted between the use of prednisolone (1 mg/kg/dose) and dexamethasone (dose at either 0.15 or 0.6 mg/kg) in the treatment of children with mild to moderate croup.
Budesonide Nebulized budesonide has a rapid effect. High-dose nebulized budesonide seems as effective as either oral or intramuscular dexamethasone in the treatment of mild to moderate croup. ●● Dose: Nebulized budesonide 2–4 mg irrespective of age.
Chapter 6 n Stridor
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Analgesics
Clinical Features
Analgesics provide some degree of comfort by reducing IP : 196.52.84.10 fever and pain.
It presents with an acute onset of fever, irritability, throat pain, difficulty in swallowing and drooling of saliva. Respiratory failure may follow rapidly (progression is in hours).
Antitussives and Decongestants
The child has a toxic appearance and adopts position of comfort by sitting with chin up, mouth open and tongue hanging out. Due to inability to swallow saliva, voice becomes muffled viz ‘hot potato voice’. Supraglottic stridor is soft and needs a high index of suspicion to identify.
No experimental studies have been published regarding the potential benefit of antitussives or decongestants in children with croup. There is no rational basis for their use.
Antibiotics No role for antibiotics in the management of croup. Rarely, it may be used when bacterial superinfection is suspected.
Heliox Helium-oxygen mixture 60:40 or 70:30 acts by promoting laminar gas flow in the obstructed airway. This therapeutic modality is not yet widely available in our country.
Diagnosis ●● Croup is diagnosed clinically. CXR is not useful in the diagnosis of croup. X-rays are ordered only if other causes are being considered. Lateral neck films may be indicated, if retropharyngeal abscess is a possibility. A chest film is helpful to rule out pneumonia or aspiration of a radiopaque foreign body. ●● The classic radiographic ‘steeple sign’ or ‘pencil point’ sign (narrowing of the tracheal shadow) may be unreliable for diagnosing or excluding croup. ●● There is no role for routine blood tests. ●● The need for tracheal intubation in ALTB is extremely rare and is indicated only when the obstruction is wors ens and respiratory failure is imminent. ●● A smaller sized tracheal tube should be used and needs to be retained in situ for 3–5 days.
Acute Epiglottitis ●● Acute epiglottitis occurs due to bacterial cellulitis of the supraglottic structures, notably epiglottis and aryepiglottic folds. Rapid inflammatory swelling of these tissues can obstruct the airway. Almost 80%–90% of affected children will require early and elective intubation. Haemophilus influenzae type b is the most common causative organism.
When epiglottitis is suspected ●● Avoid examining the oropharynx in the ED. ●● Avoid separating the child from his parents. ●● Avoid forcing him to lie down for examination, X-ray or during shift to the OT. ●● Allow him to assume ‘position of comfort’.
Stridor with Respiratory Distress ●● Instruct parents to carry their child in the sitting position to the OT. ●● Organize a physician who can effectively bag-valvemask ventilate the child, if he deteriorates during transfer. ●● Airway should be secured in the OT by pediatric anesthesiologist and otolaryngologist in attendance.
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Making a child with stridor, lie down is dangerous. It can convert a partial obstruction to complete obstruction. An X-ray neck is not usually informative. A thick, thumb like epiglottis is suggestive of epiglottitis.
Stridor with Respiratory Failure ●● Bag-valve-mask ventilation till help arrives. ●● Prepare for emergency airway management. ●● Call for help (anesthetist and otolaryngologist). Diagnosis is made by direct laryngoscopic visualiza tion. Epiglottitis is diagnosed when a large, swollen, cherry like epiglottis is found with erythema and swelling of the arytenoids and aryepiglottic folds. The examination should be done in the OT with experienced personnel. If epiglottitis is suspected, culture of the epiglottic surface is taken and the child intubated with a tracheal tube one size smaller than calculated for the age. Blood culture is taken and appropriate IV antibiotic (ceftriaxone, cefotaxime or
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Section III n Approach to Stridor
amoxiclav) is started. The tracheal tube should remain in situ for 48–72 hours.
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IP : 196.52.84.10
Avoid direct laryngoscopic examination in the ED. Laryngoscopic evaluation of an obstructed airway in an alert child could convert a difficult airway into an impossible one!
Bacterial Tracheitis Usually follows viral ALTB and is caused by Staphylococcus aureus; rarely by H. influenza and Group A, B hemolytic Streptococcus. Age: 6 months to 8 years. The initial croup-like symptoms are associated with high fever, toxic appearance and increasing respiratory distress. Difficulty in swallowing and drooling is not common. Direct laryngoscopy reveals pus in the glottic region. Bronchoscopy may also reveal the presence of pus, sloughing of tracheal mucosa and a pseudomembrane formation in the subglottic region.
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Bacterial tracheitis is suspected when croup does not subside and child becomes febrile, ill and toxic.
Treatment ●● Shift to OT for early intubation. ●● Plan for frequent and meticulous suctioning. ●● Administer appropriate antistaphylococcal antibiotics.
Retropharyngeal Abscess Retropharyngeal abscess (RPA) is a potentially, serious deep space neck infection. Complications include, airway compromise, invasion of contiguous structures and sepsis. Suppuration, occurs in the potential space between the pos terior pharyngeal wall and prevertebral fascia. Causative organisms: Group A, B-hemolytic Streptococcus, oral an aerobes, Staphylococcus aureus.
Clinical Features16 Fever, dysphagia, drooling, muffled voice, noisy breathing, respiratory distress, toxic appearance and neck stiffness. ●● Children prefer to keep their neck in the neutral position with limitation of neck extension and flexion.
●● Most use eye movements to look up. The head is maintained in the stationary position. ●● Some children present with torticollis. ●● Examination of the oropharynx reveals a bulging of both posterior pharyngeal wall and soft palate. A lateral X-ray pharynx shows, soft tissue swelling, which is more than half the width of the adjacent vertebral body. Occasionally an air fluid level may be seen. CT scan is useful to distinguish patients with RPA from those with retropharyngeal cellulitis.
Treatment Most patients with retropharyngeal cellulitis and some with RPA can be treated successfully without surgery. If surgical drainage of the abscess is planned, intubation is needed to avoid aspiration of pus in the OR. ●● Administer intravenous antibiotics (penicillinase-resis tant penicillins, amoxiclav). ●● Monitor closely if surgical drainage and intubation have been performed.
Spasmodic Croup Acute attacks of stridor occurring at nights and subsiding in a short time characterize spasmodic croup. It tends to recur in subsequent nights. Age: 1–3 years. Symptoms are similar to croup, but features of infection (URI or fever) are absent. The child is usually awakened from sleep with a stridor and onset of a harsh, barking, metallic cough. Acute vocal cord abductor spasm triggered by viral, allergy, gastroesphageal reflux or psychogenic factors have been postulated as causative. Treatment: Taking the child into the cool night air may stop the stridor. If the stridor persists, ●● Humidified air through nebulizer. ●● Nebulized epinephrine.
Foreign Body (FB) Obstruction Sudden attack of respiratory symptoms, such as cough, choking, gagging or cyanosis in a previously normal child should arouse suspicion of FB aspiration. Symptoms depend on the location of the FB. Laryngeal/tracheal FB may present with croupy cough resembling ALTB. Varying degrees of stridor, wheeze, chest retraction, hypoxia and cyanosis may also be seen. The clinical features may change
Chapter 6 n Stridor
69
if the FB migrates. An esophageal FB can compromise the airway if it is impacted high up or has been retained for a long time.
FB Obstruction in the ED
Diagnosis is based on a high index of suspicion, history, neck X-ray and flexible fiber optic bronchoscopy.
A 1-year-old male child was rushed by his mother for aspirating a fish. He had been splashing water in the bucket of water freshly drawn from the well by his mother (Figures 6.11 and 6.12).
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Treatment
CASE SCENARIO 3
●● Provide supplemental oxygen, while allowing the child to maintain position of comfort in the mother's lap, ●● Avoid noxious stimuli. ●● Plan elective airway evaluation and removal using rigid, open tube bronchoscopy in the OT.
Acute FB Obstruction in the Prehospital Setting (Figures 6.10A and B) ●● Children < 1 year: 5 back blows followed by 5 chest thrusts. Figure 6.11: Fish which was removed later in the hospital
Figure 6.12 Physiological status: Alert child with stridor and respiratory distress. The normal heart rate suggests, that this child is not hypoxic.
●● Call ENT specialists and transfer to the OT for removal of FB.
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Figures 6.10A and B: Heimlich maneuver to dislodge foreign body in infants. Remove FB, if visualized. Avoid blind finger sweep.
●● Children > 1 year: Repetitive abdominal thrusts or Heimlich maneuver.
Examination of the throat in an alert child to remove the FB causing stridor in the ER can precipitate cardiac arrest.
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Section III n Approach to Stridor
CASE SCENARIO 4 A 2-year-old male child was rushed into ER by the parIP : 196.52.84.10 ents who found him unresponsive while playing. Some parts of a toy were found missing (Figure 6.13).
No specific treatment is required. Super added viral infection could worsen obstruction resulting in the need for intubation.
Laryngeal Papilloma This is the commonest benign tumor of the larynx occurring in childhood. It causes an acute onset of stridor and dysphonia. Recurrent episodes are common and lethal airway obstruction resulting in death is not uncommon. Treatment: surgical removal.
Hypocalcemia
Figure 6.13 Physiological status: Airway un-maintainable and obstructed, respiratory failure, bradycardia, hypotensive shock with altered mental status.
●● Initiate bag-valve-mask ventilation, chest compressions, injection epinephrine 1.2 mL (1:10,000) IV. ●● Urgently call for ENT assistance.
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An unstable airway, bradypnea, tachycardia or bradycardia, cyanosis and deteriorating mental status are indicative that urgent resuscitative efforts are needed in the ER. ●● Preoxygenate prior to intubation attempts. ●● Avoid paralytic agents during intubation. ●● Removal of foreign body may be attempted after intubation. ●● During the process of intubation, if it is not possible to remove the FB in the ER, attempt to dislodge it into the main stem bronchus. This will at least ensure that half of respiratory tree is freed for ventilation. Follow-up bronchoscopy may be performed later for removal of FB.
Laryngomalacia (Congenital Laryngeal Stridor) Intermittent stridor and chest retractions occur from 2–6 weeks of age. Symptoms peak at 3–5 months, but most resolve spontaneously by 10 months.
Hypocalcemia presents with intermittent stridor, hypocalcemic tetany, seizures and cardiac failure. The child appears normal between the episodes of stridor. Serum calcium < 7 mg/dL or ionized calcium < 1 mmol/dL is diagnostic. CXR may show signs of rickets, cardiomegaly and pulmonary congestion.
Treatment ●● Maintain airway patency. Dose: IV calcium gluconate at 0.5 mL/kg slowly followed by a maintenance dose are therapeutic. Rate of administration: 0.5–1 mL/kg not exceeding 0.1 mL/kg/minute.
Vocal Cord Paralysis Bilateral abductor palsy occurs due to the abnormal medial position of the vocal cords. It results in severe stridor and respiratory distress. Bilateral abductor palsy causes apho nia with little respiratory distress.
Diagnosis ●● Long duration of stridor, older children, (not within the age group for developing ALTB), absence of fever, poor response to nebulized epinephrine and persistence of stridor are clues to recognition of vocal cord paralysis. ●● Laryngoscopy is confirmatory.
Treatment ●● Supportive. ●● Temporary intubation. ●● Rarely surgery.
Chapter 6 n Stridor
Neurogenic Stridor The child is brought with the history of profound fall in 196.52.84.10 mental status, seizuresIPor: posturing. Noisy breathing of stridor is not the reason for bringing the child to the ED. In the critically ill unresponsive child, the airway is unmaintainable. Airway protective reflexes are absent and the tongue falls back obstructing the airway. ●● Intubation is recommended using ICP precautions in the ED. Refer Protocol 6.1.
Key Points
4. If stridor with respiratory failure is recognized in the ED, initiate bag-mask ventilation and call for urgent ENT help. 5. Avoid paralytic agents while attempting to intubate a child with structural obstruction. 6. Intubation in the ED is mandatory in the management of neurogenic stridor. 7. Etiology of stridor is made from history and not from radiographs.
common errors
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1. Determining anatomic level of obstruction enables appropriate management. 2. Assessment of severity helps decide whether the child needs respiratory support in the ED or can wait to be shifted to the OT for definitive care. 3. Use of pulse oximeter to diagnose respiratory failure not reliable.
71
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1. Attempting to perform laryngoscopic examination in an alert child with stridor in the ED. 2. Separating the stridorous child and his mother and placing him on the couch for examination. 3. Administering nebulized epinephrine for all etiologies of stridor. 4. Not taking a focussed history and not performing a rapid clinical exam to establish etiology.
Protocol 6.1: PEMC approach: Management of stridor in the emergency department
72 Section III n Approach to Stridor
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Chapter 6 n Stridor
REFERENCES 1. Geelhoed GC. Croup. Pediatr Pulmonol. 1997;23 (5):70IP : 196.52.84.10 374. 2. Cordle RJ, Relich NC. Pediatrics: Upper respiratory emergencies. In: Tintinalli JE, Kelen GD, Stapczynski JS (Eds). Emergency Medicine: A Comprehensive Study Guide. 5th edition. New York, NY: McGraw-Hill Health Professions Division; 2000. pp. 384-91.doi:10.1056/NEJMep072022. 3. Bjornson CL, Johnson DW. ‘Croup’. The Lancet. 2008; (371)329-339, DOI:10. 1016/S0140-6736(08)60170-1. 4. Cherry JD. Clinical Practice. Croup. N Engl J Med. 2008;358:384-391. 5. Bjornson C, Durec T, Vandermeer B, et al. “Nebulized epinephrine for croup in children,” Cochrane Database of Systematic Reviews, no. 3, Article ID CD006619, 2007. 6. Luria JW, Gonzalez-Del-Rey JA, DiGiulio GA, et al. “Effectiveness of oral or nebulized dexamethasone for children with mild croup,” Archives of Pediatrics and Adolescent Medicine. 2001;155(12):1340-345. 7. Rittichier KK, Ledwith CA. “Out-patient treatment of moderate croup with dexamethasone: intramuscular versus oral dosing.” Pediatrics. 2000;106(6)1344-348. 8. Cetinkaya F, Tufekci BS, Kutluk G. “A comparison of nebulized budesonide, intramuscular and oral dexamethasone for treatment of croup.” International Journal of Pediatric Otorhinolaryngology. 2004;68(4): 453-56. 9. Johnson DW, Jacobson S, Edney PC, et al. “A comparison of nebulized budesonide, intramuscular dexamethasone,
10.
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12.
13.
14.
15.
16.
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and placebo for moderately severe croup.” The New England Journal of Medicine. 1998;339(8):498-503. Klassen TP, Craig WR, Moher D, et al. “Nebulized budesonide and oral dexamethasone for treatment of croup: a randomized controlled trial.” Journal of the American Medical Association. 1998;279(20):1629-632. Klassen TP, Watters LK, Feldman ME, et al. “The efficacy of nebulized budesonide in dexamethasone-treated outpatients with croup.” Pediatrics. 1996;97(4):463-66. Geelhoed GC. “Budesonide offers no advantage when added to oral dexamethasone in the treatment of croup.” Pediatric Emergency Care. 2005;21(6):359-62. Chub-Uppakarn S, Sangsupawanich P. “A randomized comparison of dexamethasone 0.15 mg/kg versus 0.6 mg/ kg for the treatment of moderate to severe croup.” International Journal of Pediatric Otorhinolaryngology. 2007;71(3)473-77. Geelhoed GC, Macdonald WB. “Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg.” Pediatric Pulmonology. 1995;20(6):362-68. Fifoot AA, Ting JYS. “Comparison between single-dose oral prednisolone and oral dexamethasone in the treatment of croup: a randomized, double-blinded clinical trial.” Emergency Medicine Australasia. 2007;19(1)51-8. Craig FW Schunk JE. Retropharyngeal abscess in children: clinical presentation, utility of Imaging and current management. Pediatrics. 2003;111:1394-398.
Breathing
Section IV
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Approach to Respiratory Distress
7
Figure 7.1: Most commonly seen condition in children viz respiratory distress can have varying etiologies, systematic approach often reveals the etiology (Courtesy: Dr Thangavelu S, Dr Gunda Srinivas).
Learning Objectives 1. Approach to respiratory distress using a stepwise structured history. 2. Using the modified rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle to recognize severity of respiratory distress.
INTRODUCTION Breathlessness is the commonest cause for referral to the PED. This chapter will discuss a simple approach to recognition and management of a very common pediatric emergency. Refer Figure 7.1.
PATHOPHYSIOLOGY
3. Classification of breathing patterns to determine the physiological status.
counter airway resistance, increases turbulence of air flow further worsening hypoxia. ●● Crying or agitation can also aggravate hypoxia.
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Maneuvers such as provision of oxygen, performance of rapid cardiopulmonary cerebral assessment, connecting to the pulse oximeter or securing an IV access may aggravate the hypoxia in the sick child.
The unique anatomic and physiologic characteristics of the respiratory tract in children and infants make them vulnerable to respiratory failure and hypoxia.
CASE SCENARIO
●● The pediatric airway is narrower than the adult. Consequently, pathological processes that cause narrowing of the airway could result in an exponential increase in airway resistance increasing the risk of hypoxia (Figure 7.2). In addition, respiratory efforts generated to
A 4-year-old boy with episodic breathlessness is brought into the PED, with an acute exacerbation of asthma. He has no fever, but has become too dyspneic to speak or feed. He has also become lethargic and unable to walk into the hospital (Figure 7.3).
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Section IV n Breathing
Evaluation of the respiratory rate and work of breathing IP : 196.52.84.10
Figure 7.2: Note that this boy with respiratory distress is looking sleepy and is not able to maintain an upright posture. He is profoundly hypoxic.
Normal breathing is quiet and is accomplished with mini mal work of the respiratory muscles. The normal respiratory rate in the neonate is rapid. As the child grows older, the respiratory rates fall. However, tidal volume or the vol ume of each breath per kilogram of body weight remains fairly constant throughout life. Adequacy of tidal volume is clinically evaluated by observing chest wall excursion and auscultating the lung fields. Parenchymal lung diseases or shock lead to an increase in minute ventilation (MV = TV × RR). As respiratory rates increase, the tidal volume falls, i.e. each breath becomes shallow.
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Roughly, doubling of normal (low normal range) respiratory rates for age should be interpreted as respiratory failure.
CLASSIFICATION OF ABNORMAL RESPIRATION ●● ●● ●● ●● ●●
Effortless tachypnea. Respiratory distress. Respiratory distress with features of respiratory failure. Relative bradypnea. Apnea.
Effortless Tachypnea Figure 7.3 Physiological status: Life-threatening asthma with shock.
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To avoid precipitating hypoxia consequent to crying or agitation, children with respiratory distress or impending respiratory failure should not be separated from their mother. ●● It is preferable, that on arrival and during subsequent management, children with respiratory distress remain seated in their mother’s lap. ●● The mother should be taught to administer oxygen by holding the rebreathing mask or flow inflating ventilation device in a non-threatening manner. ●● Infants who cry and resist the mask can be adminis tered oxygen via a tube held close to the nose.
Tachypnea occurs due to a variety of causes: Hypoxia, hypercarbia, shock, metabolic acidosis, pain, anxiety and central nervous system pathologies in comatose children. ●● Effortless tachypnea or quiet tachypnea is defined as increased respiratory rates without increased work of breathing. ●● Hypoxia and shock due to various etiologies result in decreased availability of oxygen at the cellular level. Anerobic metabolism supervenes, leading to lactic acidosis. The latter triggers the respiratory centers. Respiratory rates increase in an attempt to maintain a normal pH.
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Lung parenchyma is normal in children presenting with effortless tachypnea.
Chapter 7 n Approach to Respiratory Distress
79
Respiratory Distress
Relative Bradypnea
Respiratory distress is characterized by tachypnea and inIP :Increased 196.52.84.10 creased work of breathing. airway resistance and decreased chest and lung compliances in pathological conditions would require a greater pressure to inflate the lung to the same lung volume. This imposes a greater workload on the respiratory muscles and increases the oxygen cost of breathing. When the oxygen supply-demand balance to the respiratory muscles is disturbed, respiratory failure may ensue because of muscle fatigue.
Slowing of respiratory rates indicate respiratory muscle fatigue. Inability of young infants to sustain prolonged respiratory distress, result in early fatigue and respiratory failure.
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Abnormal lungs due to alveolar edema, pneumonia, bronchospasm, bronchiolitis, etc. result in recruitment of the accessory muscles of respiration. Retractions of the intercostal, subcostal, sternal and supraclavicular muscles indicate that the underlying lung is diseased. In young infants, severe respiratory compromise can result in nasal flare and head bobbing with each breath.
Respiratory Failure It is characterized by inadequate oxygenation, ventilation or both. It may be functionally defined as a clinical state that requires intervention to prevent respiratory or cardiac arrest. ●● Recognition of respiratory failure is based on the clinical features (discussed below) and not on blood gas analysis. Deterioration in respiratory function or imminent respiratory arrest should be anticipated in infants or children who demonstrate any of the following signs: ●● Inadequate respiratory rate or gasping respiration. ●● Inadequate effort or chest excursion with diminished peripheral breath sounds. ●● Grunting respirations. ●● Abdominal or see-saw respiration. ●● Decreased level of consciousness or response to pain; poor skeletal muscle tone or cyanosis.
Ù Due to high metabolic rates, the child has a higher
oxygen demand than the adult. Oxygen consumption is 6–8 mL/kg in children as compared to 3–4 mL/kg in the adults. Consequently, when a child develops alveolar hypoventilation or apnea, hypoxemia develops more rapidly.
Slowing of respiratory rates with reduced work of breathing is not as easy to identify as respiratory distress. The profound fall in mental status, hypotonia and poor color suggest that the child is slipping into respiratory failure.
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The ‘normal respiratory rate for age', in association with profound alteration of mental status, grunt, abdominal respirations, cyanosis, tachycardia, bradycardia and shock indicate that respiration is failing. Unless recognized and managed in the ED, respiratory arrest may supervene.
Abdominal Respiration The ribs and the costal cartilage in the infant are soft and compliant resulting in failure to support the lungs or keep them adequately expanded. Hence, when the airways become obstructed, active inspiration causes paradoxical intercostal retractions rather than chest and lung expansion. The tidal volume becomes dependent on the movement of the diaphragm and functional residual capacity falls. When diaphragmatic movement is impeded by gastric distension or increased intrathoracic pressure such as asthma or bronchiolitis, respiration can become further compromised. Fatigued intercostal muscles also lead to abdominal respiration.
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See-saw or abdominal respiration indicate respiratory muscle fatigue and impending respiratory failure.
Grunting An ominous sign, grunt is indicative of impending respiratory failure. It is produced by premature closure of the glottis at the end of expiration in order to generate positive end-expiratory pressure in an effort to improve the FiO2. Grunting helps to keep the alveoli patent and improve the functional residual capacity.
80
Section IV n Breathing
Cyanosis Is a late and ominous sign, representing inadequate oxyIP : 196.52.84.10 genation within the pulmonary bed or poor oxygen delivery by the cardiovascular system.
Alteration in Mental Status Incessant, inconsolable cry, failure to recognize the mother, sleepiness or posturing in the young infant with respiratory distress, indicate varying severity of hypoxia. Fighting the oxygen mask, combativeness and diaphoresis also suggest severe hypoxia and imminent respiratory failure. Somnolence and obtundation occurs as hypercarbia supervenes. Tachycardia is an early sign of hypoxia in a child with respiratory distress. A fall in the heart rate to the ‘normal range’ or ‘relative bradycardia’ is ominous indicating that respiratory failure is imminent. Relative bradycardia can be recognized when associated with signs of poor perfusion with profound alteration in mental status and abnormality in tone and posture.
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Avoid rushing to take an X-ray as the first intervention in a child presenting with respiratory distress or respiratory failure.
Step 1 Targeted history to identify etiology.
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Duration of respiratory distress offers many clues to the possible etiology. ●● Hours (hyperacute) suggests that aspiration could be the cause of respiratory distress. ●● Days (acute) indicates that the presence of an infective lung disease, e.g. pneumonia, empyema, bronchilitis, etc. ●● Respiratory distress in months or since birth (chronic) implies that the possible etiology is cardiac or less commonly chronic lung disease. ●● Episodic breathlessness with symptom-free periods, points towards asthma. Rarely, recurrent aspiration syndromes can present with episodic respiratory distress. Unlike asthmatic children, the latter is often associated with failure to thrive or developmental delay.
●● Acute first episode of respiratory distress, associated with history of fever and non-lung foci of sepsis suggests the possibility of acute cardiogenic pulmonary edema.
Step 2 Targeted history to identify hypoxia or shock. ●● Ask mother, for history suggestive of altered mental status in any child presenting with respiratory distress. If she denies fall in mental status, the child is unlikely to have respiratory failure. ●● History of talking or taking feeds could be misleading. Mother is the best judge. If she reports: ‘Not as usual’, lethargic, ‘sleepier than usual’, recognize early hypoxia or shock.
Step 3 Targeted history of fever suggests infective causes for respiratory distress. Example: Pneumonia, bronchiolitis.
Step 4 Perform the rapid cardiopulmonary cerebral assessment. a. Does this child have respiratory distress or respiratory failure?
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Classifying whether respiratory distress or respiratory failure whilst taking history on arrival helps initiate bagvalve-mask ventilation if needed. If ‘BRADYPNEIC’, further assessment, should be continued by the next responder. b. Does this child have shock or not?
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It is not uncommon for shock to coexist in hypoxic children. Early and aggressive fluid resuscitation of shock is mandatory for early resolution of hypoxia. Respiratory distress and shock viz cardiogenic shock may mimic asthma or bronchiolitis! When respiratory distress and shock are noted in children presenting with ‘non-lung etiologies’ such as scorpion sting, septic foci, acute diarrhea, submersion injury, hypoxic ischemic encephalopathies, etc. suspect the presence of pulmonary edema due to cardiac dysfunction or acute lung injury.
Chapter 7 n Approach to Respiratory Distress
c. Does this child have cardiogenic shock or not?
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IP :gallop, 196.52.84.10 Muffled heart sounds, relative bradycardia, low BP, low MAP are signs of myocardial dysfunction. Examination of the liver span in a child with respiratory distress often provides valuable information on cardiac function. Since a pushed down liver could erroneously suggest hepatomegaly, emphasis is laid in assessment of the span. Assessment of the liver span during the cardiopulmonary assessment helps to find out whether respiratory distress is due to respiratory or cardiac causes. Chronic respiratory distress associated with increased liver span, points towards a structural heart disease with cardiac failure. Acute respiratory distress with increased liver span could occur due to cardiac failure or cardiogenic shock secondary to myocarditis or severe sepsis. d. Does this child have severe hypoxia or shock as evidenced by features of non-convulsive status epilepticus?
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Nystagmus, conjugate deviation or eyelid twitch or a combination of signs, which signal severe hypoxia in young children and infants with respiratory distress indicate NCSE (avoid treating with anticonvulsants). ●● Increased respiratory rates without increased work of breathing (quiet tachypnea), point towards a non-car diorespiratory etiologies such as acidosis secondary to DKA, hypovolemic shock, etc. ●● Comatose children present with altered breathing patterns secondary to neurogenic etiologies.
MANAGEMENT BASED ON ETIOLOGY Aspiration Hyperacute respiratory distress: Treatment is focused on correction of hypoxia and shock (refer Chapter 6).
Pneumonia Acute first episode of breathlessness with high grade: Whilst correcting hypoxia and shock, administer the first dose of antibiotic in the ED.
81
Bronchiolitis Acute first episode breathlessness with wheeze in young healthy infants, presenting with low-grade fever and prodrome is suggestive of bronchiolitis. ●● Provide O2 using the JR circuit. ●● Correct shock if identified (usually 20–30 mL/kg may be needed unless the infant shows signs of SIRS with septic shock). ●● Nebulize with hypertonic saline. ●● Epinephrine nebulization 0.1 mL/kg (1:1,000) in 4 mL of normal saline has also been recommended. Monitor ECG for cardiac arrhythmias.
Septic Cardiogenic Shock First episode respiratory distress with or without hepatomegaly due to acute pulmonary edema (refer Chapter 15). ●● Provide oxygen through flow inflating ventilation device. ●● Administer smaller aliquots of fluids. ●● Initiate early inotrope infusion and perform early intu bation if needed. ●● Administer 1st dose of antibiotic.
Asthma
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Episodic breathlessness in healthy children more than 2 years of age is probably asthma. ●● Grade severity and implement treatment as per asthma management guidelines (refer Chapter 8).
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Caution: Avoid treating all children with respiratory distress and wheeze as asthma. Acute cardiogenic or noncardiogenic pulmonary edema could mimic asthma. Avoid rushing to diagnose asthma in infants less than 2 years of age. Other causes of acute or chronic respiratory distress, which mimic asthma such as congenital heart diseases , cystic fibrosis, etc. should not be misdiagnosed as asthma. A suggested approach to child more than 1 month presenting with respiratory distress in the ED is shown in Protocol 7.1.
82
Section IV n Breathing
Key Points
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1. Avoid separating mother and child during assessment IP : 196.52.84.10 of a child presenting with respiratory distress. 2. Teach mother to hold the oxygen mask in a nonthreatening manner. 3. Focused history with emphasis on duration provides clues to the possible etiology. 4. A focused history also helps recognize early signs of hypoxia in a child presenting with respiratory distress. 5. Recognize myocardial dysfunction or acute lung injury when respiratory distress occurs in children presenting with ‘non-lung’ etiologies. 6. Rapid cardiopulmonary assessment, which incor porates assessment of liver span helps to recognize whether respiratory distress is due to respiratory or cardiac causes.
common errors
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1. Diagnosing asthma in all children presenting with the respiratory distress and wheeze. 2. Nebulization of all children and infants presenting with respiratory distress without considering etiology. 3. Failure to recognize the need to assess liver span in children presenting with respiratory distress. 4. Failure to anticipate that acute pulmonary edema due to acute lung injury or acute myocardial dysfunction could present as respiratory distress secondary to severe hypoxic insults. 5. Failure to provide CPAP for children presenting with pulmonary edema and shock. 6. Believing that diagnosis of respiratory failure is dependent on laboratory investigations and not on clinical features on arrival into the ED.
PE, pulmonary edema; CLD, chronic lung disease; CHD, congenital heart disease; DCM, dilated cardiomyopathy; CCF, congestive cardiac failure.
Protocol 7.1: PEMC approach: Respiratory distress
Chapter 7 n Approach to Respiratory Distress
IP : 196.52.84.10 83
8
Management of an Asthmatic Exacerbation IP : 196.52.84.10
Figure 8.1: Systematic approach, repeated rapid cardiopulmonary assessments lead to dramatic improvement in acutely ill asthmatic kids. A child with near fatal attack of asthma being successfully resuscitated with subcutaneous epinephrine.
Learning Objectives 1. Using the rapid cardiopulmonary cerebral assessment and PAT to identify severity and response to therapy.
2. Pearls and pitfalls in salbutamol nebulization. 3. Evidence-based management of acute exacerbation of asthma.
INTRODUCTION
Appearance
The management of acute exacerbation of asthma in the ED, has been based on the recommendations of the National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma (Summary Report 2007) and the British Thoracic Society, Scottish Intercollegiate Guidelines Network: British Guideline on the Management of Asthma, June 2009.
●● Obtundation, impaired alertness, incessant cry, exhaustion, diaphoresis, agitation, not tolerating the oxygen mask, confusion or combativeness are signs suggestive of profound hypoxia viz near fatal exacerbation of asthma. ●● Floppiness and inability to maintain posture correlate clinically with hypercarbia.1
The PEMC approach, employs the rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle to recognize severity of the asthmatic exacerbation and use these guidelines to manage appropriately (refer Figure 8.1). Severity is scored as follows: Refer Protocol 8.1. ●● ●● ●● ●●
Moderate asthma. Acute severe asthma. Life-threatening asthma. Near fatal asthma.
Breathing Respiratory rates: ●● > 30/min in children more than 5 years. ●● > 50/min in children between 2 and 5 years. ●● > 60/min in 2 years in an asthmatic child suggest acute exacerbation of asthma.2 ●● Reduced respiratory rate for age (bradypnea), grunt, head bobbing, nasal flare, use of accessory muscles and abdominal or paradoxical chest wall movements
Chapter 8 n Management of an Asthmatic Exacerbation
are more ominous and indicate impending respiratory failure. ●● Other signs of a near attack include diminished IP :fatal 196.52.84.10 air-entry, absence of wheeze due to severe bronchos pasm (silent chest) and or saturation < 92% in room air. Serial pulse oximetry measurements have been found useful in assessing the severity of exacerbation and evaluating improvement with treatment (Evidence B).
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Though low oxygen saturation is helpful in recognizing severity, normal oxygen saturations does not rule out a severe asthmatic exacerbation.3
Circulation ●● Tachycardia denotes early hypoxia. ●● Relative bradycardia is suggestive of very severe hypoxia. ●● Very high heart rates should prompt evaluation for the presence of coexisting shock. Normalization of heart rate during bronchodilatory intervention is a reassuring sign of improvement. On the other hand, increasing heart rates during inhalation therapy indicate the presence of other causes of respiratory distress mimicking asthma.
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Cyanosis is a late sign of severe exacerbation. Shock often complicates near fatal attacks of asthma. Severe hypoxia, insensible water loss due to respiratory distress, vomiting, refusal of feeds during the exacerbation and coexisting sepsis may increase the need for fluids during resuscitation.
ASTHMA MIMICS It is not uncommon for central airway obstruction to be misdiagnosed as asthma. Upper airway foreign bodies, epiglottitis, structural diseases of the larynx, vocal cord dysfunction and tracheal narrowing could mimic asthma. Dysphonia, inspiratory stridor, wheezing loudest over the central airway are some of the clues, which help differentiate these causes from asthma. Diagnosis of asthma in toddlers and infants is unusual. Intermittent wheezing attacks may be due to recurrent viral infections. Recurrent aspiration leading to pneumonitis,
85
pneumonia, bronchiolitis, tracheobronchomalacia, cystic fibrosis and congenital anomalies could present with recurrent wheeze and respiratory distress. Response to short-acting bronchodilator agent (SABA) is often inconsistent in these children
Investigations: Role in Resuscitation of Asthmatic Exacerbations ●● Chest radiographs are not routinely indicated in an asthmatic child. They are ordered if there is failure to improve or deterioration occurs during the management of life-threatening or near fatal asthmatic exacerbation.
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When deterioration occurs during salbutamol nebuliza tion, the respiratory distress and wheeze is more likely due to non-asthmatic causes. ●● Arterial blood gas (ABG) measurements are also not routinely indicated and do not give additional useful information. ●● In the early phase of an asthmatic exacerbation, the partialpressure of carbon dioxide (PaCO2) is low. ●● A normal PaCO2 is indicative of severe respiratory distress and a rise in PaCO2 is a sign that respiratory collapse is imminent.
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“Treat the patient and not the numbers”.1 Blood gas analysis may be performed only when the child has respiratory failure requiring intubation despite initial management in the emergency department.1
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Assessment of severity is the first step in the management of acute asthma. The exacerbation is classified as moderate, acute severe, life-threatening or near fatal attack. Based on the severity of the attack, the appropriate bronchodilatory therapy is initiated (Protocol 8.1).
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Repeated assessment is recommended after each intervention (bronchodilator) (Evidence A).
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Section IV n Breathing
●● Each therapeutic intervention should be followed by the rapid cardiopulmonary cerebral assessment to determine whether theIPchild had improved, deteriorated : 196.52.84.10 or remained status quo. ●● This helps to decide the next step in the treatment. ●● If oxygen, fluids, the first inhalational dose of salbutamol/ipratropium and subcutaneous epinephrine have resulted in improvement in a child presenting with near fatal asthma, the subsequent dose of epinephrine may be withheld. However, if he remains in the same physiological status, epinephrine may be repeated along with the next inhalation of salbutamol and ipratropium bromide.
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A structured approach using a proforma is the most important determinant of a successful outcome in the ED.
Case scenario A 3-year-old asthmatic child is brought to the ED after his usual home treatment failed to give relief. He is too dyspneic to speak or feed. He has diaphoresis his assessment is as follows (Figures 8.2 and 8.3).
Figure 8.3 Near fatal asthma: Child in respiratory distress with grunting, progressive fall in mental status, loss of tone, evidence of shock, agitation, fighting the mask, cyanosis diaphoresis.
●● Supplemental oxygen through a tight fitting face mask or a non-rebreathing bag or a nasal cannulae at flow rates sufficient to maintain saturations > 92% should be provided (Class A evidence). ●● Oxygen and inhalational therapy should be provided in a non-threatening manner with the child seated comfortably on the mother’s lap. ●● Separation of child from his mother is contraindicated, since agitation and crying could worsen hypoxia. ●● Besides, mother’s help is crucial for holding the nebulizer mask. She is the most sensitive ‘monitor’ during nebulization of a hypoxic child and is the first to alert emergency personnel if sudden deterioration occurs during nebulization. While assessment is being performed, a brief, focused history is taken. A more detailed history, complete physical examination and laboratory studies should be performed only after initial therapy has been completed (Evidence D).
Figure 8.2: Note the diaphoresis, loss of tone and failure of the pulse oximeter to pick up oxygen saturation in this child with a near fatal attack of asthma. Children, often resent the face mask. The apparent tolerance to the nebulizer mask suggests significant drop in level of consciousness due to severe hypoxia. Also, note that this child with an asthmatic exacerbation appears well nourished. For less known reasons, asthma does not seem common in malnourished kids.
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Short-acting beta 2-agonist treatment is recommended for all patients (Evidence A).1,2,3,4,5
Nebulizer Therapy ●● Administer salbutamol by nebulizer, driven by oxygen if the asthmatic exacerbation is severe.
Chapter 8 n Management of an Asthmatic Exacerbation
●● 2.5 mg of salbutamol (nebulizer solution) is diluted in 3–4 mL of normal saline. It should not be diluted using distilled water. IP : 196.52.84.10 It would seem intuitive to dose salbutamol, based on the child’s weight. However, a fixed amount of drug is added to the nebulizing chamber (independent of the child’s age or weight). The patient’s minute ventilation regulates the amount deposited in the lungs. Thus, a 12-year-old child (due to the greater minute ventilation) will deposit a larger amount of drug in the lungs, than a 12-month-old infant. Other factors which limit drug delivery in the young child are smaller airways, shorter inspiratory times and lack of cooperation. Furthermore 90% of the drug is wasted to the atmosphere. In the small volume nebulizer, drug delivery is maximal when the volume of solution is 3–4 mL and the flow rates are set at 6–8 mL/min. The nebulizer with a mouth piece is superior to face mask since nasal deposition is minimized. Children with severe asthma who do not respond to the initial salbutamol dose should be treated aggressively with higher and more frequent doses. Drug dosing is individualized according to severity and the subsequent doses are based on the patient's response.
ADVERSE EFFECTS OF NEBULIZED SALBUTAMOL IN HYPOXIC CHILDREN Brochospasm causes alveolar hypoxia which results in pulmonary vasoconstriction. This protective reflex phenomenon, diverts blood to better ventilated parts of the lung thus maintaining the ventilation perfusion ratio. Salbutamol prevents this beneficial reflex phenomena by inhibiting the hypoxia-induced pulmonary vasoconstriction resulting in pulmonary vasodilation. The latter leads to increased blood flow to the hypoxic alveolus aggravating the ventilation-perfusion mismatch worsening hypoxia in the already compromised child. It is not uncommon for a hypoxic child to deteriorate during salbutamol nebulizer therapy (refer Figures 8.4 to 8.8). Close physician monitoring is essential during nebulization. Nebulization of salbutamol should be performed through high flow oxygen. Pulse oximetry and resuscitation equipment should also be close at hand when nebulizing a child with life-threatening or near fatal asthma. Prefilled epinephrine syringe (0.1 mL/kg of 1:10,000) must also be available close at hand.
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Caution
Figure 8.4 Hazards of salbutamol nebulization: In asthma, bronchospasm causes reduction in oxygen within the alveoli. This leads to hypoxia-induced pulmonary vasoconstriction diverting blood to the better ventilated alveoli. In hypoxic asthmatics, salbutamol inhibits hypoxia-induced vasoconstriction resulting in pulmonary vasodilation, which further aggravates hypoxia!
Figure 8.5 Hazards of salbutamol nebulization: In children, presenting with respiratory distress and wheeze due to alveolar causes, salbutamol has no beneficial effects. In hypoxic children, salbutamol, will inhibit the reflex pulmonary vasoconstriction causing pulmonary vasodialation and increase blood supply to the hypoxic alveoli. The latter could aggravate hypoxia due to ventilation perfusion mismatch and can precipitate cardiac arrest!
Alveolar pathologies can also present with respiratory distress and wheeze, e.g. pneumonia, pulmonary edema.
Figure 8.6: This asthmatic child, referred from the asthma clinic for a near fatal attack of asthma was being nebulized. During her third nebulization, she suddenly deteriorated and progressed to severe respiratory failure needing ventilation.
88
Section IV n Breathing
●● Salbutamol nebulization unmasks or worsens hypoxia in hypoxic asthmatics and can even precipitate cardiac arrest (Figure 8.6)!4IP : 196.52.84.10 ●● If deterioration is profound, stop nebulization and reconsider the diagnosis. All that wheezes is not asthma!
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Nebulization of salbutamol is one of the commonest interventions in seriously ill children presenting with respiratory distress. It is also one of the most hazardous interventions in hypoxic children presenting with respiratory distress (Figure 8.8).
Figure 8.8: A well-child and happy mother. Though asthmatic, this episode of respiratory distress was secondary to pneumonia. The catastrophic deterioration during nebulization was a complication of salbutamol nebulization. Consider nonasthmatic cause of respiratory distress, if sudden worsening occurs during nebulization.
Ipratropium Bromide
Figure 8.7: This picture shows her following emergency intubation and ventilation after deterioration during her nebulization. This particular episode of respiratory distress was secondary to pneumonia and not due to asthma. Hence, for sudden deterioration during salbutamol even in asthma stop nebulization, reconsider etiology.
Intermittent Versus Continuous Nebulization with Salbutamol ●● 2.5–5 mg of salbutamol nebulization is repeated every 20–30 minutes. ●● Continuous nebulization entails that 10–20 mg is added to the chamber and administered over 1 hour. The onset of action for SABAs is less than 5 minutes; repetitive administration produces incremental bronchodilation. Continuous administration of SABA may be more effective in more severely obstructed patients. However, this should be performed under very close supervision.
Ipratropium bromide (IB), an anticholinergic derivative competes with the acetylcholinesterase at the M3 musca rinic receptor attenuating the neural signal for bronchoconstriction, thus leading to relaxation of airway smooth muscle. It also relieves mucosal edema and secretions. Contractility of the smooth muscle lining the large and medium sized airways is under parasympathetic neural control and is activated by acetylcholine (ACh) release. ●● The larger airways are constricted in life-threatening asthma resulting in greater benefits with the use of IB. ●● Respiratory viruses trigger asthmatic exacerbations by increasing parasympathetic activity of the airways viz bronchospasm and airway secretions. Inhaled IB has been found to be more beneficial in pediatric asthma triggered by viral upper respiratory tract infection (URTI). ●● High doses of racemic SABA contain an S-isomer, which increases intracellular concentration of free calcium in the smooth muscles of the airways. The latter provokes bronchoconstriction. Concomitant use of IB, when high doses of salbutamol are being used abolishes this response. ●● A multidose regimen showed statistically significant improvement in lung function and clinical asthma score.
Chapter 8 n Management of an Asthmatic Exacerbation
The quaternary ammonium compound, which forms part of this drug makes it lipid insoluble preventing its systemic absorption. LessIP than 1% is systemically absorbed, : 196.52.84.10 making it one of the safest bronchodilator drugs used in the management of acute asthma. Therapeutic response occurs within 3–30 minutes after being given. The peak effect occurs at around 90 minutes and remains effective up to 6 hours after nebulization. ●● Administer 250–500 µg via nebulizer through oxygen. ●● Repeat every 20–30 min for 3 doses (maximum of 1,500 µg) in the first hour along with intermittent aerosolized SABA. ●● Repeat as needed up to the first 3 hours during the initial management of severe exacerbations.
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Inhaled ipratropium bromide is recommended for ED management of life-threatening or near fatal asthma. (Evidence A).6
Corticosteroids The early use of steroids, speed the resolution of airflow obstruction, reduces need for hospitalization and prevents relapse of the asthma exacerbation. All steroid preparations are equally efficacious in so far as anti-inflammatory effects are concerned. ●● Intravenous hydrocortisone (4 mg/kg and repeated 4th hourly) is administered only when oral medications are not tolerated.
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Oral prednisolone is given at the dose of: – 10 mg in infants < 2 years – 20 mg stat in children between 2 and 5 years – 30–40 mg > 5 years early in the management of asthma. The dose is repeated if the child vomits the medication. Steroids may be given for 3–5 days and tapered depending on the response to treatment. Currently, there is insufficient evidence to support the use of inhaled corticosteroids in the management of acute asthma exacerbation in the ED. Hence, inhaled steroids are not initiated in preference to oral steroids (Evidence B). Steroids may be given 5–10 days following discharge to prevent early relapse.
89
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Parenteral steroids are recommended in the management of asthma exacerbations (Evidence A).
Subcutaneous Adrenaline ●● Severely ill children have poor inspiratory flow due to decreased tidal volume. Low tidal volume limits delivery of inhaled salbutamol to the terminal airways. This subset of children benefit from urgent subcutaneous administration of beta-2 agonists. ●● The ILCOR guidelines 2005 suggested that in near fatal attacks of asthma, where tidal volume is reduced, bolus doses of epinephrine or terbutaline may be used as an initial therapy and repeated every 20 minutes up to a maximum of 3 doses based on the response of the patient in life-threatening asthma. ●● Dilute 1 mL adrenaline in 9 mL of NS (1:10,000). ●● Administer 0.1 mL/kg of 1:10,000 solution subcutaneously. Widely available, subcutaneous adrenaline has been safe in children and does have a role in near fatal asthma not responding to more conventional therapies. However, it is a non-selective adrenergic drug with side effects such as tachycardia, arrhythmias, hypertension, etc.
Magnesium Sulfate7,8 Many patients, who present for assessment and treatment to the ED with an asthmatic exacerbation may not benefit from early treatment with magnesium sulfate. The NHLBI guidelines recommend that for severe ex acerbations, unresponsive to the initial treatments listed above, a single dose of intravenous magnesium may be considered (Evidence B). In patients with severe acute asthma, magnesium sulfate appears to improve pulmonary function and reduce hospital admissions. ●● Magnesium sulfate is infused slowly in the dose of 25– 100 mg/kg/dose (maximum of 2 g) as a single dose. A relatively safe drug, it is useful in children presenting with severe tachycardia complicating life-threatening asthma. It is also believed to decrease the need for intubation.
Aminophylline
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The NHLBI guidelines do not recommend the use of methylxanthines (Evidence A).
90
Section IV n Breathing
Conversely, the British Thoracic Guidelines suggest that aminophylline may be useful in near fatal asthma not responding to maximalIPdoses of bronchodilators and ste : 196.52.84.10 roids. In settings, where access to mechanical ventilation is limited, this drug has been useful in reducing ICU admis sion and fatality in asthma-induced respiratory failure.
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Aminophylline is not recommended in mild and moderate asthma. Its troublesome side effects far outweigh its bronchodilatory effects. ●● 5 mg/kg loading dose is given as an infusion over 20 minutes followed by a continuous infusion at 1mg/ kg/h. ●● The loading dose is avoided in children, who have been on chronic theophylline therapy or have received a prehospital intramuscular dose of deriphyllin. ●● ECG monitoring is recommended during aminophylline infusion.
Intravenous Salbutamol ●● Intravenous (IV) salbutamol (15 mg/kg) is reserved for those children for whom the drug cannot be reliably administered through the nebulizer unit. ●● Continuous IV infusion of beta 2 agonist is not superior to maximal inhaled dose. ●● Hypoxia occurring due to the salbutamol-induced V/Q mismatch is more severe with IV beta-2 agonist infusion than the inhaled route. ●● In addition, there is a greater risk of arrhythmias making ECG monitoring mandatory during therapy. Any intravenous therapy in asthma requires continuous ECG monitoring.
●● However, it is not uncommon for young children with life-threatening asthma to present with shock. These children often require large volumes in our setting to attain therapeutic goals of hypoxia and shock resolution. Perhaps, the increased fluid requirement, may be secondary to late referral, refusal of feeds, vomiting and coexisting sepsis or dengue. There may be a drop in serum potassium levels secondary to use of SABA, theophylline, steroids and epinephrine. Consequently, potassium should be monitored closely in children with refractory asthma.
PEF Monitoring9 ●● If peak expiratory flow rate (PEFR) is less than 33%, it is suggestive of acute severe asthma. ●● PEFR less than 60% of the child’s best or predicted values, is indicative of life-threatening asthma. Monitoring asthma based on PEFR is useful for children older than 5 years of age. In children less than 5 years, this maneuver can aggravate hypoxia by causing dynamic airway collapse. Unfortunately, this may not always be possible in busy ED, which prevents its wide spread use in the Indian scenario.
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The expert panel report 3 has given recommendations for the following interventions in the management of acute asthma in the ED.
Intravenous Fluids
●● Antibiotics are not recommended during the ED treatment of acute asthma exacerbations (Evidence B) unless evidence of bacterial sepsis is available. ●● Mucolytics are not recommended (Evidence C). ●● Sedation: Anxiolytic and hypnotic drugs are contraindicated in severely ill asthma patients, because of their respiratory depressant effect (Evidence D).
Aggressive hydration is not recommended for older children, but may be indicated for young children (Evidence D).
Indications for intubation is based on clinical judgment (Evidence D). Absolute indications for intubation and mechanical ventilation are minimal and include:
●● Correct dehydration since it could cause reduction in ciliary activity and mucus plugging. ●● In the absence of dehydration, fluids are administered cautiously at two-thirds maintenance due to the risk of SIADH induced by pulmonary edema.
●● Apnea and coma. ●● Fatigue, with poor respiratory effort. ●● Imminent arrest and arrhythmias.
Other Therapies
Since intubation is difficult in patients who have asthma, it should be performed by a physician, who has extensive
Chapter 8 n Management of an Asthmatic Exacerbation
experience in intubation and airway management in the ED. Ketamine usage for premedication prior to intubation, have not shown clinical Ideally, even without inIPbenefit. : 196.52.84.10 tubation, patients who have not been improving satisfactorily or deteriorating despite aggressive bronchodilatory therapy in the ED should be transferred into the ICU.
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●● The spacer should be washed periodically with detergent to reduce the electrostatic and enhance delivery. Refer Table 8.1.
Discharge An asthmatic exacerbation is considered a failure of preventive therapy and discharge plans should take into account the following: ●● Motivate the parents and the child to take regular inhaler therapy. ●● Consider use of steroid inhalers. ●● Explain the use of these devices with a detailed written asthma plan and the need for regular follow-up. ●● Advise regarding the need to seek urgent help, if there is exacerbation of asthma. ●● Arrange for care in the asthma clinic.
Figure 8.9: Child using MDI with spacer and mask
METERED DOSE INHALER AND SPACER ●● Inhaled salbutamol provides the most rapid relief and is the initial bronchodilator of choice. It may be administered through metered dose inhalers (MDI) with spacers or small volume nebulizers. MDI + spacer are the preferred option in mild to moderate asthmatic exacerbation associated with normal tidal breathing. ●● The spacer, acts as a reservoir for the aerosol, resulting in greater drug delivery to the airways and less wastage to the atmosphere. Since this MDI with spacer, also reduces the amount of drug deposited in the oropharynx, it reduces systemic absorption and unwanted side effects such as tachycardia and hypoxia (Figure 8.9). ●● 6–8 puffs of B2 agonist using MDI and spacer can provide a dose of 2.5 mg. A reasonable starting dose may be one half puff/kg with a maximum of 10 puffs (OR). ●● 2.5 mg of salbutamol via small volume nebulizer. ●● Mild attacks: 2–4 puffs may be sufficient, while in severe attacks 10 puffs may be needed. ●● In children less than 4 years of age, face masks connected to the mouth piece of the spacer are necessary. ●● In children older than 4 years of age, mouth pieces connected directly to the spacer are preferable. ●● Eight breaths are needed per actuation to completely empty the spacer.
Key Points
ü
1. Recognize asthma since “all that wheezes is not asthma”. 2. Salbutamol can precipitate cardiac arrest in hypoxic children with respiratory distress and wheeze secondary to non-asthmatic etiologies. 3. Determine severity of the asthmatic exacerbation on arrival. 4. Salbutamol can worsen hypoxia in near fatal attacks of asthma. 5. Every intervention should be followed by a rapid cardiopulmonary assessment to determine the next step in the protocol.
common errors
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1. Nebulization using the electrical nebulizer and not through high flow oxygen. 2. Nebulization of child with respiratory distress due to pneumonia or cardiac failure. 3. Continuing to treat based on initial assessment of severity, without reassessment. 4. Failure to recognize shock and manage appropriately. 5. Failure to monitor and document during resuscitation of hypoxic asthma. 6. Failure to treat until resolution of therapeutic goals of hypoxia, bronchospasm and shock in the ED.
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Table 8.1: Drugs used for asthmatic exacerbation in the ED Drugs 1.
Salbutamol
2.
Route
Dose
IP Nebulized : 196.52.84.10 0.05–0.1 mg/kg for three
Side effects
Remarks
doses. Continuous dose: 0.15–0.45 mg/kg/h Max: 20 mg/h
Tremors, nausea, tachycardia, blood pressure instability, cardiac arrhythmias, myocardial instability
Hypokalemia occurs with continuous nebulization. Prolongation of QTc interval. Unmasks or worsens hypoxia in hypoxic asthmatics.
Ipratropium bromide Nebulized
250–500 µg Q4–6 hourly
Rarely mydriasis and blurred vision
Peak response develops after 30–90 min.
3.
Hydrocortisone
IV
2–4 mg/kg Q6 hourly
Hypertension, hyperglycemia, mood disorders, gastritis
Always give H2 receptor blocker as prophylaxis against gastritis and perforation. Short course for 5–7 day. After the acute course is over, can be changed to oral.
4.
Methylprednisolone
IV
0.5–1 mg/kg/dose Q6 hourly
Hypertension, hyperglycemia, mood disorders, gastritis
Always give H2 blocker as prophylaxis for gastritis and to prevent perforation. Short course for 5–7 day. After the acute course is over can be changed to oral.
5.
Adrenaline
SC
0.1 mL/kg (1:10,000)
Tachycardia, hypertension
Administered in near fatal asthma
6.
Terbutaline
IV
Loading dose: 10 µg/kg over 10 min Infusion: 0.1 µg/kg/min 0.01 mg/kg dose for 3 doses q20 min
Same as salbutamol but more pronounced
Subcutaneous doses can be tried before giving IV infusion. Adrenaline can be used as the other alternative.
7.
Aminophyline
IV
Loading dose: 5 mg/kg/ dose Over 20 min < 6 month: 0.5 mg/kg/h 6–1 year: 0.85–1 mg/kg/h 1–9 year: 1 mg/kg/h > 9 year: 0.75 mg/kg/h
Nausea, vomiting, fever, dyskinesia, seizures and death
Extremely narrow therapeutic index. Decrease dose in patients with hepatic and cardiovascular dysfunction.
8.
Magnesium sulfate
IV
25–50 mg/kg/dose over 20–30 min
Hypotension, nausea, flushing arrhythmias, muscle weakness, areflexia and respiratory depression
No role for repeat doses or continuous infusion.
9.
Ketamine
IV, IM
Loading dose: 2 mg/kg Infusion: 1–2 mg/kg/h
Sialorrhea and increased airway secretions (can be offset with atropine) Dissociative anesthesia (can be offset with sedative)
Used as an adjunct for intubating patients with asthma. Monitor for increase in ICP, metabolic rate, BP and heart rate.
SC
Protocol 8.1: PEMC approach: Management of acute exacerbation of asthma
Chapter 8 n Management of an Asthmatic Exacerbation
IP : 196.52.84.10 93
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References 1. Circulation: Journal of the American Heart Association IPAugust : 196.52.84.10 2005; Vol 102. No 8. (Part 8.) 2. Thorax: Journal of the British Thoracic Society 2003:58 (suppl I Annex 6.) 3. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma (Summary Report 2007) In: Busse W, ed. J Allergy Immunol. 2007; 120 (5): S 94-138. National Institute of Health ----National Heart Lung and Blood Institute. 4. British Thoracic Society, Scottish Intercollegiate Guidelines Network: British Guideline on the Management of Asthma- June 2009.
5. Scarfone, et al. Beta-2 agonists in acute asthma: The evolving state of the art. Ped Emer Care. Dec 2002;18:442-48. 6. Dotson K, Dallman M, Bowman M, Titus. MO Ipratropium Bromide for acute asthma exacerbation Ped Emer Care. 2009;25(10)687-92. 7. Cheuk D K L, Chau T C H, Lee S L A meta analysis on intra venous magnesium sulphate for treating acute asthma Arch Dis Child. 2005;90:74-77. 8. Rowe BH, Bretzlaff J, Bourdon C, Bota G, Blitz S, Camargo CA. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department (Review). The Cochrane Library 2009. 9. Gorelick M.H et al, Difficulty in obtaining Peak Expiratory Flow Measurements in Children with Acute Asthma. Ped Emerg Care. Jan 2004:20(1):22-26.
9
IP : 196.52.84.10
Pulse Oximeter
Figure 9.1: Different equipments used for pulse oximetry and cardiorespiratory monitoring
Learning Objectives 1. How does the pulse oximeter work?
2. Pearls and pitfalls in pulse oximetry.
INTRODUCTION Considered as the ‘5th vital parameter’, the pulse oximeter helps to determine the oxygen content of hemoglobin (SpO2) using a finger probe (Figure 9.1). It works by utilizing selective wavelengths of light. Having understood the significance of pulse oximetry as a component of clinical assessment and decision-making in young infants and children, pulse oximeters have been made available even in the Primary Health Centers. Figure 9.2: Photodetector picks up R/IR light source.
Principle Oxygenated hemoglobin absorbs infrared light and allows red light to pass through. Deoxygenated (or reduced) hemoglobin absorbs red light and allows infrared light to pass through. Red light is within the 600–750 nm wavelength light band, (Figure 9.2) while the infrared band lies within the 850–1,000 nm wavelength band (Figure 9.3).
The pulse oximeter probe, emits both red and infrared light using LED technology. The light shines through a site with good blood flow. Typical adult/pediatric sites with good blood flow are the finger, toe, pinna (top) or lobe of the ear. Infant sites are the foot, palm, hand, big toe or thumb. Opposite the emitter is a photodetector that receives the light passing through the measuring site.
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Section IV n Breathing
●● The LED emits red light alternatively at two different wavelengths, visible and infrared regions of the electromagnetic spectrum. IP : 196.52.84.10
LIMITATIONS OF PULSE OXIMETER 1. The pulse oximeter picks up late and severe hypoxemia. It fails to pick up early, minimal fall in oxygen levels.
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An oxygen saturation of 90% in the pulse oximeter equates to a blood gas of 60 mm Hg!
Figure 9.3: Wavelength spectrum.
●● These are transmitted through the tissues and adsorbed to different degrees by oxyhemoglobin and deoxyhemoglobin. The arteriolar bed pulsates and absorbs variable amounts of light during systole (peak) and diastole (trough), as blood volume increases and decreases. The ratio of light absorbed at the peak and trough is translated into oxygen saturation measurements. Since peaks occur with each heartbeat or pulse, the term ‘pulse oximetry’ was coined (Figure 9.4).
Figure 9.4: Variable absorption of light.
●● The pulse oximeter provides continuous non-invasive monitoring of oxygenation at the tissue level. ●● Monitoring of oxygen is not affected by skin pigmentation.
2. Fails to detect signals in severe shock. Intense vasoconstriction reduces pulsatile signals to the probe. 3. Does not provide any information on PaCO2: The child may have severe hypercapnea due to alveolar hypoventilation or respiratory failure. If the child is receiving a high concentration of inspired O2, the pulse oximeter will continue to show normal oxygen saturations. 4. Will not show correct values in children with abnormal hemoglobinopathies. 5. Progressively under-reads the saturation as the hemoglobin decreases. However, it is not affected by polycythemia. 6. Unreliable when child has excessive movements such as status epilepticus. 7. May not be accurate in bright extraneous light.
Tips for Use 1. Ensure that the optical components of the sensor are properly aligned. 2. Check adhesive sensor sites every 8 hours and move it to a new site if necessary. 3. Change the site of sensors to a new site at least every 4 hours. 4. Adhesive digit sensors may be reused on the same patient if the adhesive tape attaches without slipping. 5. Replace the sensor whenever the adhesive quality is depleted. 6. Fix the probe in an extremity free of an arterial catheter, blood pressure cuff intravascular infusion line. 7. Clean reusable sensors between patients. 8. Document SpO2 results in the patient's medical record. It should detail the conditions under which readings were obtained viz date, time of measurement, concentration of inspired oxygen concentration and type of oxygen delivery device being used. 9. Cardiopulmonary assessment must be documented along with pulse oximeter reading.
Chapter 9 n Pulse Oximeter
10. The external portion of the monitor should be cleaned according to manufacturer's recommendations. When soiled, it can be a IP source of potentially transmissible : 196.52.84.10 organisms.
Key Points
ü
1. SaO2 of < 92% in room air or with supplemental oxygen, for a child presenting with respiratory distress is suggestive of severe hypoxia. 2. SaO2 < 92% in an intubated child suggests that the oxygen levels in the blood have fallen to 60 mm Hg.
common errors
97
û
1. Failure to immediately respond to a fall in SaO2 < 92% in an intubated child can result in cardiac arrest in minutes. 2. Using the pulse oximeter as the sole method to recognize critical illness! 3. Failing to provide supplemental oxygen to a shocked child because the pulse oximeter is showing normal saturations. 4. Considering that a normal pulse oximeter reading is the only criteria for intubation.
Section V
Circulation IP : 196.52.84.10
IP : 196.52.84.10
10
General Approach to the Management of Shock IP : 196.52.84.10
Figure 10.1: Pull push technique used to administer fluids in a child presenting with respiratory failure and hypotensive shock. Time-sensitive goal-directed therapy results in successful outcomes.
Learning Objectives 1. Pathophysiology of shock. 2. Risks of fluid therapy during shock resuscitation.
INTRODUCTION Early recognition of shock is key to successful resuscitation in critically ill children.1,2 Often, shock results in or coexists with myocardial dysfunction or acute lung injury. Recognition and resuscitation should be directed to restoration of tissue perfusion, normalization of cardiac function and resolution of pulmonary edema. Underlying cause of shock should also be addressed urgently3 (Figure 10.1).
PATHOPHYSIOLOGY Shock results from inadequate delivery of oxygen and nutrients to tissues relative to their metabolic demand. The impaired tissue perfusion and consequent cellular hypoxia results in cellular injury, which in turn causes metabolic derangements and the release of inflammatory mediators. 1. Metabolic derangements: The reduced availability of oxygen also results in glucose being metabolized
3. Pearls and pitfalls in shock management. 4. A modified shock protocol based on ‘small volume or large volume etiologies’. to pyruvate and lactate. This represents an inefficient utilization of substrate with minimal energy production. Although this early injury is often reversible, persistent hypoperfusion leads to cellular injury, which further exacerbates the microcirculatory derangements and maldistribution of blood flow that can further impair perfusion and eventually cause irreversible tissue damage.4 2. Inflammatory mediators: Tissue hypoperfusion activates multiple humoral mediators along with the complement cascade. Activation of the complement cascade results in widespread endothelial injury, systemic leukocyte adhesion, pulmonary alveolar capillary damage, acute respiratory distress syndrome (ARDS) and activation of the coagulation system culminating in disseminated intravascular coagulation and multiorgan failure.4,5 Signs of acute lung injury (respiratory distress) is often an early sign of organ dysfunction in a shocked child compared to DIC, which occurs later.
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IP : 196.52.84.10
Figure 10.2: Rapid compensatory mechanism in shock (Boxed entities are the manifested symptoms clinically). GFR, glomerular filtration rate; RAS, reticular activating system; SVR, systemic vascular resistance; BP, blood pressure.
3. Neurohormonal responses are activated early to preserve adequate tissue perfusion and maintain vital organ function6 (Figure 10.2). However, with further deterioration, these mechanisms can no longer compensate and hypotension, a late sign of shock ensues. 4. Cardiovascular response to shock: Attempts to increase cardiac output is dependent on increase of heart rate and augmentation of stroke volume. Stroke volume has three determinants—the volume of blood present in the ventricle before contraction (preload),
resistance to ventricular ejection (afterload) and myocardial contractility. Autoaugmentation of preload depends on the two-thirds of the total circulating blood volume, which is contained in the small veins. When shock occurs, one of the earliest responses is alphaadrenergic mediated vasoconstriction that diverts this reservoir of blood centrally to improve venous return and ventricular filling. In septic and neurogenic shock venous dilatation rather than vasoconstriction occurs, further accentuating preload deficits and myocardial
Chapter 10 n General Approach to the Management of Shock
dysfunction. Reduction in stroke volume for a given ventricular end-diastolic volume leads to an increase in systemic vascular (SVR), a compensaIP resistance : 196.52.84.10 tory mechanism to augment blood pressure. While an increased SVR is an important compensatory mechanism that helps preserve vital organ perfusion, pathologic increases in afterload can occur in patients with cardiac tamponade, tension pneumothorax and diaphragmatic hernia. Normally, an increase in SVR is an important compensatory mechanism that helps preserve vital organ perfusion. Excessive increase in (SVR) afterload can obstruct cardiac output thereby worsening shock (Refer Chapter on Cardiogenic Shock). Structural obstruction to cardiac output occurs due to cardiac tamponade, tension pneumothorax and diaphragmatic hernia. These conditions can cause profound shock that is refractory to fluids and inotropes. 5. Pulmonary response: Initially, metabolic acidosis induces effortless tachypnea. As the SVR increases, pulmonary vascular resistance also increases resulting in increased minute ventilation. Uncorrected shock can lead to capillary leak and vasodilation in the pulmonary circulation resulting in acute lung injury and acute respiratory distress syndrome (non-cardiogenic pulmonary edema), which manifests clinically as increased work of breathing. Myocardial dysfunction, a precursor or the end result of shock due to a variety of etiologies can also cause respiratory distress due to cardiogenic pulmonary edema. 6. Renal response: Prolonged renal hypoperfusion may result in pre-renal and ultimately acute renal failure. In compensated shock, blood flow is redistributed to the vital organs and oxygen consumption is maintained by an increased extraction of oxygen leading to lower oxygen saturation in venous blood. Oxygen delivery can be calculated by the following formula: Oxygen delivery (DaO2) = Cardiac output (CO) × Arterial Oxygen content (CaO2). CaO2 is the product of the hemoglobin concentration and arterial oxygen concentration. It is calculated by the formula: CaO2 = Hb (g/dL) × 1.39 × SaO2. The normal O2 content of arterial blood is 18– 20 mL/dL and mixed venous blood is 75% saturated. The normal tissue extraction ratio for oxygen is measured with the following formula: Extraction ratio = (CaO2- CvO2)/ CaO2. Oxygen saturation is used as a surrogate to calculate the extraction ratio viz SaO2-SvO2/SaO2. The normal value
103
is about 25%. In shock, low SvO2 in the face of normal arterial oxygen saturation indicates that the tissues are extracting greater than 25% of oxygen from the arterial blood in order to maintain adequate tissue oxygenation because of decreased cardiac output. Ideally, therapy should be targeted towards normalization of SvO2.7 Since monitoring of SvO2 requires intensive care expertise, which is not usually available to staff in the ED, management in the ED should be targeted towards normalization of clinical goals of shock resolution.8 The commonest causes of shock are shown in Box 10.1. Box 10.1: Types of shock Hypovolemic shock (decreased blood volume) Hemorrhage Trauma Surgery Burns Vomiting and diarrhea Severe sepsis Distributive shock (marked vasodilation; also called vasogenic or low resistance shock) Anaphylaxis Severe sepsis Cardiogenic shock (inadequate output due to cardiac dysfunction) Congestive heart failure Myocardial dysfunction Arrhythmias Severe sepsis Obstructive shock (obstruction to blood flow) Tension pneumothorax Diaphragmatic hernia Pulmonary embolism Cardiac tamponade Severe sepsis Dissociative shock Methemoglobinemia Carbon monoxide poisoning
Recognition Early signs of hypoxia or shock are subtle and identifying at risk patients may be challenging.2,9,10 Late shock is easy to recognize, but resuscitation may be futile. Consequently emergency department (ED) staff must be sensitized to situations in which shock may occur. Triage questions, which help recognize shock have already been discussed in Chapter 1.
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If the clinical setting suggests the possibility of shock, IP : 196.52.84.10 then it is best to treat early when signs are subtle rather than waiting for overt signs to develop.9 This is of special relevance in children who may present with non-specific symptoms such as breathlessness, diarrhea and fever, where symptoms may be misinterpreted as benign and their significance dismissed.3 Early recognition of shock has been discussed in Chapter 1.
CASE SCENARIO A neonate was brought into the ED, 3 hours after birth, for the bullous lesions on the skin (Figures 10.3 and 10.4).
Figure 10.3: Anticipation that loss of fluids via the extensive weeping exudative lesions can cause shock along with clinical findings of shock is key to successful resuscitation.
Figure 10.4 Physiological status: Effortless tachypnea, tachycardia, shock with altered mental status.
Airway ●● Airway is patent or maintainable or clear if the infant is crying or vocalizing. If airway is clear: ●● Perform assessment and shock resuscitation, whilst oxygen is being administered. Airway positioning is warranted: ●● If the child is carried into the ED, ‘responsive to pain’, unresponsive or convulsing. ●● Place the child on the resuscitation trolley and open the airway as shown in Figure 10.5.
Breathing ●● Provide oxygen through non-rebreathing mask in older children and oxyhood in young infants presenting with effortless tachypnea.
Figure 10.5: Airway being opened using the head tilt-chin lift maneuver in this unresponsive child with shock. Oxygen is being provided using the non-rebreathing mask. Up to 80%– 90% O2 can be administered using this device in contrast to the nasal cannula, which delivers a maximum of 40% O2 (Courtesy: Dr Mullai Baalaaji).
●● Provide oxygen through flow inflating ventilation device (Jackson-Rees circuit) for children presenting with respiratory distress and shock (Figure 10.6). ●● If apneic, initiate bag-valve-mask ventilation. ●● Call for the intubation tray. Prepare age-appropriate laryngoscopes, tracheal tubes, ties, plaster, tincture benzoin and drugs (Refer Chapter 3 on PAI). ●● However, avoid rushing to intubate. ●● Effective bag-valve-mask ventilation should be continued until IO or IV access is secured.
Chapter 10 n General Approach to the Management of Shock
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Figure 10.6: This picture shows a toddler receiving O2 via a flow inflating ventilation device (Jackson-Rees circuit) during fluid resuscitation for shock with respiratory distress.
●● Consider early intubation in an apneic child with shock, using ketamine, suxamethonium and atropine. ●● If the child is apneic and bradycardic, intubation can be performed without drugs.
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Waiting for confirmatory blood gas analysis to intubate is not recommended when the child presents with respiratory failure. Ketamine11 is the induction agent and atropine the premedication agent of choice. However, in a hypotensive child with chronic congestive cardiac failure ketamine, may worsen cardiac function. A short acting neuromuscular blocker may be used to facilitate intubation.
Figure 10.7: Insert two large bore short-length intravascular catheters. One line is used for fluid resuscitation and medications. The second line is dedicated for inotrope infusion.
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During fluid therapy, watch out for signs of pulmonary edema! Use a CPAP device to reduce risk of intubation in settings with limited access to mechanical ventilators. Initiate inotrope infusion if signs of PE are noted. Continuation of fluids without provision of PEEP or inotropes when signs of PE are noted can result in cardiac arrest.
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Induction agents such as midazolam can worsen hy potension. Avoid midazolam for intubation in hypotensive shock.
Circulation Fluids are the cornerstone of shock therapy. As fluids are being administered to correct hypoperfusion, fluid can leak out of leaky pulmonary capillaries resulting in pulmonary edema. PEEP must be provided during fluid therapy for shocks of all etiologies except hypovolemia.
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Do not forget to position the airway and provide oxygen throughout fluid resuscitation.
Figure 10.8: Intraosseous access is life saving in shock management. After infusing the first 20–40 mL/kg, intravenous access becomes easier. Avoid damage to peripheral veins in the attempt to secure peripheral access in the shocked child.
●● After securing intravenous or intraosseous access, check dextrostix (refer Figures 10.7 to 10.9).
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Section V n Circulation
Speed of Fluid Administration Normotensive Shock IP : 196.52.84.10
●● Infuse 20 mL/kg at the rate of 20 minutes (by gravity)8 if the shocked child presents with effortless tachypnea. ●● Infuse 5–10 mL/kg at 5–10 minutes if he has respiratory distress and shock (pulmonary edema and shock). ●● Hypotensive shock: Use a pull push technique, using a 3-way stopcock and reservoir, if the child presents with hypotensive shock (Figure 10.10).
Figure 10.9: After addressing the ABCs, DEFG: “Do not ever forget glucose”! Correct documented hypoglycemia with 25% dextrose: 2 mL/kg bolus.
What is the best fluid to correct shock? ●● Administer 20 mL/kg Ringer’s lactate or 0.9% normal saline. ●● Isotonic fluids are given to establish euvolemia. RL is preferred for diarrheal losses. NS is preferred in shock due to DKA and severe traumatic brain injury. ●● Avoid dextrose containing fluids to resolve shock. Administration of glucose containing fluids cause cellular dehydration and osmotic diuresis, thus worsening shock. ●● Theoretically, crystalloids are redistributed into the extracellular compartment resulting in an increased risk of tissue edema. It also reduces serum protein concentrations and packed red cell volume.12 Besides, large volumes of normal saline may result in hyperchloremic metabolic acidosis. Alteration in bicarbonate levels may also alter renal function, this being one of the determinants of normal renal blood flow.13,14 ●● In reality, 100–120 mL/kg of NS or RL can be administered in the initial hours of resuscitation without dangerous metabolic consequences. ●● Besides, crystalloids are inexpensive, readily available, can be stored conveniently and are unlikely to transmit infectious agents.
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Colloids such as albumin are expensive, not readily avail able and have not been found beneficial in comparison with isotonic crystalloids.15
Figure 10.10: This picture shows the fluid bolus therapy being initiated using a pull push technique in this infant with hypotension due to hypovolemia complicated by marasmus and severe sepsis. One team member is poised with her hand around the chest to initiate cardiac massage if the need arises.
Hypotension is suggestive of severe myocardial dysfunction and imminent arrest indicating need for early epinephrine infusion, intubation and ventilation (Figure 10.11).
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If the child is maintaining his airway and has spontaneous breathing, fluid boluses are enough to correct shock due to hypovolemia (acute diarrhea). Intubation and epinephrine infusion are rarely needed in hypotensive shock due to hypovolemia. Level 1 evidence8 suggests that pushing large volume fluids in a short span of time (15 minutes to 1 hours) in normotensive shock could precipitate volume overload. The inherent risk of pulmonary edema in the back ground of acute lung injury and the failing heart must always be taken into consideration. Fluids infused by gravity can safely resolve shock without increasing risk of PE or hepatomegaly.
Chapter 10 n General Approach to the Management of Shock
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IP : 196.52.84.10
Figure 10.11: Hypovolemic shock due to loss of fluid from the exposed bowel and viscera
Despite the need for fluids to resolve severe shock, some children may progress to cardiac arrest during fluid administration. Preload unresponsiveness, suggests severe myocardial dysfunction. Underlying comorbidities such as severe malnutrition, anemia, electrolyte disorders can also contribute to the deleterious effects of fluids on a failing heart. How much fluids needed to correct shock? More than 60 mL/kg or less than 20–30 mL/kg?
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As the initial resuscitative steps are being performed, simultaneously evaluate for etiology of shock: Is the shock due to sepsis, hypovolemia or anaphylaxis. Ask for history of: 1. Fever with or without infective focus? 2. Vomiting, diarrhea, abdominal distension, trauma, bleed? 3. Allergen, drugs? ●● If the answer to any of these questions is ‘Yes’ viz sepsis, vomiting, diarrhea, intussusception, peritonitis, burns and polyuria, plan to administer large volumes (Figures 10.11 and 10.12).
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Large volume fluids (up to 120 mL/kg in the initial hours of resuscitation) may be needed to resolve shock due to gastrointestinal losses, abdominal sepsis and warm shock due to severe sepsis.
Figure 10.12: This emergency case record shows how this infant was monitored by performing the rapid cardiopulmonary assessment at the end of each fluid bolus until he achieved all therapeutic goals of shock resolution (refer appendix for sample documented case record in a child with septic shock).
●● If the answer to all three of these questions is negative, then the total volume of fluids needed to resolve shock in the ‘Golden hour’ is probably less than 20–30 mL/kg. Etiologies such as, congenital heart diseases, myocarditis, arrhythmias, near fatal asthma, status epilepticus, envenomation, submersion injury, toxins, DKA, trauma, severe traumatic brain injury, etc. need less than 20–30 mL/kg unless these etiologies are complicated by fluid loss, sepsis or anaphylaxis. What do I look for after each bolus? Perform the rapid cardiopulmonary cerebral assessment and find out whether the child has: ●● Achieved therapeutic goals (signs of shock resolution: Box 10.2). ●● Remained status quo (shock persists but no signs of PE). ●● Deteriorated (shock persists, but signs of pulmonary edema: Box 10.3).
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Caution: Watch out for signs of pulmonary edema and preload unresponsiveness. ●● If signs of PE are not noted, but therapeutic goals have not been attained continue fluid therapy.
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Box 10.2: Therapeutic goals of shock resolution in fluid responsive shock.
IP : 196.52.84.10 Airway: Maintainable airway. Breathing: Normal respiratory rate for age, normal work of breathing, absence of grunt, retractions, abdominal respirations (in the absence of pneumonia, empyema or other foci of sepsis in the lung). Circulation: Normal heart rate for age, easy to feel dorsalis pedis, warm, pink peripheries, CRT < 2 sec, normal range of systolic BP for age with a normal pulse pressure. In vasodilatory or warm shock, wide pulse pressure due to low systemic vascular resistance may be characterized by diastolic BP that is less than or equal to half of the systolic BP. In these children, narrowing of pulse pressure is an additional therapeutic goal. Normal liver span Urine output > 1 mL/kg/h Disability: Return to baseline mental status in the AVPU scale. Eyes mid position with normal extraocular movements in older children or dolls eye movement in very young infants. Pupils, which are equal and are briskly responsive to light. The brisk response to light may be the only indicator of resolution of cerebral hypoxia, hypoperfusion, seizure activity or ICP in a sedated and paralyzed child. Box 10.3: Signs of pulmonary edema8 Airway: Airway instability, froth, new onset cough. Breathing: Decreased or increased respiratory rates requiring respiratory support in the absence of neuromuscular diseases. Onset of grunt, retractions, abdominal respirations, new rales or wheeze, drop in saturations < 92%. Circulation: Bradycardia for age, gallop, hypotension, increase in liver span from baseline, shock not resolving with 60 mL/kg. Disability: Agitation, fighting the mask, combativeness, thirst.
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Achievement of all therapeutic goals of shock is necessary for successful resuscitation of shock.8 What if signs of PE are identified, but shock persists? 1. Interrupt further fluids. 2. Initiate an appropriate inotrope8 (Table 10.1). a. Dopamine, if BP is low normal with warm shock. b. Dobutamine, if BP is high with cool shock. c. Epinephrine, if BP is low. d. Norepinephrine, if systolic BP is in the hypotensive range and diastolic pressure is less than 50% of systolic pressure.
Figure 10.13: This picture shows a young infant with cardiogenic septic shock developing froth during fluid therapy.
3. Provide CPAP using the Jackson-Rees circuit (if not using already) or intubate.8
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When giving the shocked child a sedative or anesthetic agent for intubation, the sympathetic response to stress is removed. It is this response that has been maintaining the heart rate and BP. If the sympathetic drive is removed, HR and BP would drop dangerously leading sudden cardiac arrest during the procedure. Hence, initiation of an appropriate inotrope infusion is MANDATORY to ensure hemodynamic stability during intubation. If features of pulmonary edema and/or hepatomegaly resolve, but shock persists after application of flow inflating ventilation device and initiating the appropriate inotrope, continue administering small boluses of fluids until shock resolves. Refer Figure 10.13.
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If shock is due to ‘large volume etiologies’ such as sepsis, further fluid in aliquots (up to a maximum of 100–120 mL/kg) may be given in the initial hours until shock resolves. Caveat: ‘Small volume etiologies’ causing shock could be complicated by hypovolemia, sepsis or anaphylaxis such as severe diaphoresis in scorpion sting, anaphylactic shock during administration of antisnake venom or acute watery diarrhea in a child presenting with near fatal asthma.
Chapter 10 n General Approach to the Management of Shock
109
Table 10.1: Indications for initiating inotropes, vasopressors and inodilators Drug Dopamine
Indication
Adverse CVS† effects
IPShock : 196.52.84.10 with normal BP and low SVR*
SVT , VPC , VT, ‡
Cardiogenic shock
§
Dose 10 µg/kg/min
Hypertension
Distributive shock Epinephrine
Severe bradycardia with shock
SVT, VPC, VT, ST 0.05–1.0 µg/kg/min elevation, post resuscitation myocardial dysfunction
Pulse-less electrical activity Post cardiopulmonary arrest stabilization, toxic doses of calcium channel antagonists, β-blocking drugs Hypotensive shock of all etiologies
Hypertension
Anaphylactic shock
1–4 µg/kg/min
Dobutamine
Cardiogenic shock with high SVR, cardiac failure
5–20 µg/kg/min
Norepinephrine
Low BP with low SVR
Tachy, brady arrhythmias, hypertension
0.05–1.0 µg/kg/min
Milrinone
Cardiogenic shock with high SVR
Hypotension
50–75 µg/kg over 10–60 minute followed by infusion 0.5–0.75 µg/kg/min
*
SVR, systemic vascular resistance; †CVS, cardiovascular; ‡ SVT, supraventricular tachycardia; §VPC, ventricular premature contractions.
OBSTRUCTIVE SHOCK Tension pneumothorax, massive empyema, cardiac tamponade are some of the causes of obstruction to cardiac output.
●● Catheterize to monitor urine output during shock management (Figure 10.15).
Needle thoracocentesis or pericardiocentesis should be performed to relieve shock (Figure 10.14).
Figure 10.14: Needle thoracocentesis to relieve massive empyema that was obstructing cardic output during shock resuscitation in the PED. Note the large volume purulent material that is being aspirated in the syringe. Obstructive shock will not resolve with fluids, inotropes and intubation.
Figure 10.15: Urine output is decreased or absent in shock and catheterization is recommended for monitoring urine output during resuscitation. Urine output of > 1–2 mL/ kg/h is a reassuring sign of normal renal perfusion in shock in children beyond 1 year of age. Polyuria or anuria may occur as complications of renal impairment in septic shock. Inappropriate polyuria has been noted in patients with severe sepsis and normal baseline renal function.16
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Section V n Circulation
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Non-convulsive status epilepticus (NCSE) signals severe hypoxia and shock: IP : 196.52.84.10
If eye signs are ignored or not recognized generalized tonic-clonic fits supervenes as a preterminal event.
●● On arrival and during every step in the management of shock, examine the eyes for position and movements. Conjugate deviation, nystagmus and eyelid twitch sig nal the coexistence of severe hypoxia and shock.17
How do I ensure a stable metabolic profile during shock resuscitation?
If the child presented to the PED, with the history of generalized tonic-clonic activity, eye signs suggest primary seizure activity needing immediate anticonvulsant drugs. If however, the presenting history was acute diarrhea, fever, breathlessness, submersion, envenomation, etc. and any one sign of NCSE is noted anytime during shock resuscitation, it signals severe cerebral hypoperfusion. It is not uncommon to note these findings during resuscitation of hypotensive shock or cardiac arrest. ●● Initiate an inotrope. ●● Intubate and ventilate.
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Signs of NCSE in a shocked child denote very poor prognosis.
●● Initiate GNS with KCl and administer at maintenance rates for age. Example, 4 mL/kg/hour in infants less than 10 kg. Ensure that the child has voided urine prior to addition of potassium (Figure 10.16). Do not forget to simultaneously treat etiology of shock! ●● Simultaneously, provide appropriate treatment for the etiology of shock (Table 10.2).
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The physiological responses of individual children to shock resuscitation are often variable and unpredictable. Therefore, repeated assessments with continuous, noninvasive monitoring are needed for taking appropriate decisions in the ED. While the protocol for shock management is based on broad guidelines, the treatment often needs to be individualized.
Anticonvulsants Anticonvulsant medications may be hazardous in this situation. ●● During every reassessment do not forget to look for eye signs of NCSE. NCSE is an indication that aggressive management of hypoxia and shock are needed. Resolution of NCSE occurs if hypoxia and shock are corrected. If however, these signs persist, anticonvulsant drugs may be administered very cautiously. ●● Avoid phenytoin, if seizure activity is noted in a child with shock and myocardial dysfunction. Phenytoin has been noted to be hazardous in emergency settings, where seizure activity complicates shock and myocardial depression. ●● If eye signs are not apparent in paralyzed children, tachycardia, not explained by shock or pain relief suggests the coexistence of NCSE.
Figure 10.16: This 36-day-old infant is being managed with the NS boluses, JR circuit, inotrope infusions to combat pulmonary edema and shock in the PED. Maintenance (GNS with KCl) fluids are also being infused at 4 mL/kg/hour throughout resuscitation.
Shock may be precipitated in children by a variety of causes. Early recognition of shock and aggressive early re-
Chapter 10 n General Approach to the Management of Shock
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Table 10.2: Etiologies of shock Etiology
IP : 196.52.84.10 Acute laryngotracheobronchitis upper airway obstruction
Specific management Epinephrine, steroids, call for ENT, anesthetist assistance for securing the airway
Asthma
Bronchodilator therapy, steroids
Anaphylaxis
Early intubation if airway obstruction is anticipated or CPR, epinephrine, steroids, antihistamines, antacids
Sepsis
Antibiotics, source control
Poisons
Elimination, decontamination, antidotes
Envenomation
Antivenom serum
SVT, Arrhythmias
Adenosine, cardioversion
Cardiac tamponade, pneumothorax
Pericardiocentesis, thoracocentesis
Trauma
Control bleed
Seizures
Anticonvulsant therapy
suscitation is likely to yield the most favorable outcomes. Isotonic fluids form the cornerstone of treatment and the amount required for resuscitation is based on etiologies and therapeutic response. After resuscitation has been initiated, targeted history and clinical evaluation must be performed to ascertain the cause of shock. Management of comorbidities such as asthma and seizures should be implemented simultaneously. Inotropes, respiratory support, antibiotics and steroids may also be needed during the management of shock. While the management of shock can be protocol based, the treatment needs to be individualized depending on the suspected etiology and therapeutic response. Management of shock is one of the most labor inten sive protocols. Anticipation of potential side effects of fluids based on the pathophysiology is key to survival. Repeated rapid cardiopulmonary cerebral assessment provides a 60 second advantage in deciding whether to continue the same intervention, stopping or changing tactics. Indeed, “repeated cardiopulmonary assessment of the patient in shock, by a competent observer remains the most effective and sensitive physiologic monitor in the management of shock” (Zimmerman-1999). Refer Protocol 10.1.
KEY POINTS
ü
1. Anticipate shock in the appropriate clinical scenario. 2. Glucose normal saline infusions can worsen shock by causing osmotic diuresis. 3. Volumes greater than 20 mL/kg are needed to correct shock due to hypovolemia, anaphylaxis and sepsis. 4. Avoid volumes greater than 20 mL/kg in shock due to scorpion sting, submersion injury, isolated severe traumatic head injury, asthma, status epilepticus, etc. 5. Reassess at the end of every bolus. 6. Treat until all therapeutic goals of shock are achieved.
COMMON ERRORS
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1. Avoiding administration of fluids for fear of precipitating pulmonary edema. 2. Failure to anticipate that pulmonary edema could occur due to coexisting cardiac dysfunction or leaky pulmonary capillaries. 3. Failure to initiate inotrope and intubate when features of pulmonary edema are noted. 4. Failure to treat until all therapeutic goals of shock are resolved.
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Section V n Circulation
Protocol 10.1: PEMC approach: Management of shock with or without myocardial dysfunction
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Airway and Breathing: 1. Effortless tachypnea and shock: O2 through non-rebreathing mask. 2. Grunt, retractions, abdominal respiration and shock (cardiogenic shock): O2(Jackson-Rees circuit). 3. Bradypnea* and shock (cardiogenic shock)*: Initiate bag-valve-mask ventilation (*plan intubation). Circulation: Secure 2 peripheral IV access, 1. a. Normal BP: Shock with effortless tachypnea: NS/RL 20 mL/kg @ 20 minutes. b. Shock with respiratory distress: 5–10 mL/kg @ 5–10 minutes. 2. Hypotensive/(NCSE signals severe hypoxia/shock): Pull push 20 mL/kg through IV/IO until BP normalizes. Call for epinephrine infusion @ 0.3 µg/kg/min (at any step in protocol) and urgent intubation Disability: GTCS: lorazepam 0.1 mg/kg × 2, levetiracetam 20–30 mg/kg IV (avoid phenytoin in cardiogenic shock) Avoid treating extensor or flexor posturing due to hypoxia/shock/raised ICP as fits Dextrostix: Correct documented hypoglycemia; infuse GNS + KCl at maintenance rate for age.
Chapter 10 n General Approach to the Management of Shock
REFERENCES 1. Han YY, Carcillo JA, et al. Early reversal of pediatric-neoIPcommunity : 196.52.84.10 natal septic shock by physicians is associated with improved outcome. Pediatrics. 2003;112(4):793-99. 2. Ninis N, Phillips C, Bailey L, et al. The role of healthcare delivery on outcome of meningococcal disease in children: case-control study of fatal and non-fatal cases. BMJ. 2005;330(7505):1475. 3. Santhanam I, Ranjit S, Kissoon N: Management of shock in the Emergency Department. Minerva Pediatr. 2009;61:1-15. 4. Deitch EA. Multiple organ failure: Pathophysiology and potential future therapy. Ann Surg. 1992 Aug;216(2):117-34. 5. Maier RV. Approach to a patient in shock Fauci, In Braunwald , Kasper , Hauser, Longo, Jameson, Loscalzo (Eds). Harrisons’ s Principles of Internal Medicine, United States of America: McGraw Hill; pp. 1689-702. 6. Ganong WF. Shock Review of Medical Physiology. Boston: McGraw-Hill; 2005. pp. 636-40. 7. Nadel S, Ranjith S, Kissoon N. Recognition and initial management of shock. Philadelphia Walter Roger’s Textbook of Pediatric Intensive Care. DA Nichols 4th edition (Eds) . Kluwer /Lippincott Williams and Wilkins; 2008. pp. 372-83. 8. Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the emergency department. Pediatr Emerg Care. 2008;24:647-655.
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9. Seear MD, Shock A, Macnab D, et al. Henning (Eds). Care of the Critically ill Child, London, UK 1999; Churchill Livingstone: 1999. pp. 60-67. 10. McQuillan P, Pilkington S, et al. Confidential enquiry into quality of care before admission to intensive care. BMJ. 1998;20;316(7148):1853-58. 11. Reynolds SF, Heffner J, Airway management of the critically Ill patient:*rapid-sequence intubation. Chest. 2005;1 27;1397-412 DOI 10.1378/chest.127.4.1397. 12. Martin GS, Lewis CA. Fluid management in shock. Semin Respir Crit Care Med. 2004;25:683-694. 13. Wilcox CS. Regulation of renal blood flow by plasma chloride. J Clin Invest. 1983;71:726-35. 14. Williams EL, Hildebrand KL, McCormick SA, et al. The effect of intravenous lactated Ringer’s solution versus 0.9% sodium chloride solution on serum osmolality in human volunteers. Anesth Anal. 1999;88:999-1003. 15. Finfer S, Bellomo R, Boyce N. SAFE Study Investigators. A comparison of Albumin and Saline for fluid resuscitation in the intensive care unit. NEJM. 2004;350:2247-256. 16. Cortez A, Zito J, Lucas CE, et al. Mechanism of inappropriate polyuria in septic patients. Arch Surg. 1977;112:471-76. 17. Santhanam I, Padma V, Murali T, et al. Predictors of mortality of children presenting with severe sepsis to the PED. Proceedings of the 1st European Congress of Pediatric Resuscitation and Emergency Medicine (PREM), May 2nd, 3rd 2013:Ghent, Belgium.
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Intraosseous Access
Figure 11.1: Intraosseous access is a life-saving procedure in shock when peripheral IV access is difficult.
Learning Objectives 1. How to organize an intraosseous tray? 2. How to secure an IO access?
Introduction American Heart Association’s resuscitation guidelines state that the intraosseous (IO) route should be the first alternative to difficult or delayed intravenous access.1 This chapter will discuss the preparation of an intraosseous access tray and the method of performing this procedure (Figure 11.1). When used in severely shocked kids, IO access is faster and more easily obtained than other access. Complications are not more than other venous access methods. However, IO access is still under utilized because of lack of awareness, proper training and lack of appropriate equipment.2 The last statement appears to be true in the Indian context as well.
Preparation of an Intraosseous Tray
(Figure 11.2) ●● Sand bag: Used for positioning the limb. ●● Gauze.
3. Pearls and pitfalls in IO access. 4. Evidence supporting intraosseous access in emergency settings. ●● ●● ●● ●●
●●
●● ●● ●● ●● ●● ●●
Betadine, sterile gloves, masks, surgical gowns. Small stainless steel cups. Draping site of insertion. Bone marrow needle (16G, 18G): Easily available and inexpensive, this needle can be safely used to secure IO access. 10 or 20 mL syringes: Ensure that both syringes are filled with NS or RL prior to insertion. Avoid, waiting to fill the syringe after entry. Delay can cause clogging of the needle. Dynaplast: To fix the IO needle. IV infusion set. Normal saline or Ringer’s lactate bottles. 3-way stopcock. Medications. Infusion pumps.
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Use universal aseptic precautions.
Chapter 11 n Intraosseous Access
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How To Secure Intraosseous Access? IP : 196.52.84.10
Figure 11.3 shows the intraosseous access in a secured way. ●● Place a sand bag under the knee (refer Figure 11.4). ●● Slightly abduct and rotate the knee externally. ●● Clean the site of insertion with Betadine-soaked gauze. ●● Identify the tibial tubercle. ●● Then introduce the bone marrow needle with trocar 1 cm below and medial to this anatomic landmark.
Figure 11.2: Organization of the intraosseous tray. 1. Towel roll for support; 2. Stainless steel tray; 3. Tincture Benzoin; 4. Bone marrow needle (16G, 18G) with trocar; 5. Betadine; 6. 2 cups with gauze; 7. Dynaplast (cut to fix the needle); 8. 3-way adapter; 9. Disposable sterile gloves; 10. Saline bottle; 11. 10 mL syringes; 12. Drape; 13. Infusion set. Both items 1 and 2 must be autoclaved and ready for use. Figure 11.4: Positioning and method of insertion of IO needle
Figure 11.3: Intraosseous (IO) access is a rapid, safe and effective route for administration of fluids, epinephrine, anticonvulsants, blood products and inotropes. Onset of action and drug levels reached in the circulation were comparable to venous administration. Administration of a drug should be followed by a 5 mL saline flush to promote entry into the central circulation.
Note that in this picture, the airway has been positioned and bag-valve-mask ventilation is in progress even prior to securing IO access. Oxygen saturation has normalized. Tachycardia is due to shock.
●● The patented intraosseous needle is expensive and not widely available in India. ●● The bone marrow needle on the other hand, is an easily available alternative. ●● Unfortunately, it is not sturdy enough for use in older children. ●● Currently, intraosseous guns are available. – This device has been used in adults and can effortlessly and painlessly penetrate hard bone and enter the marrow space. ●● Ideally, the intraosseous route should NOT be used beyond 24 hours. ●● It is retained until an intravenous access has been secured. ●● Other locations for introduction of IO needle: – Proximal tibia in infants. – Proximal tibia and distal femur in adolescents. – Iliac crest and distal tibia (when conventional sites are unavailable). ●● Technique used in infants is described below: The thumb of the left hand is used to fix the tibial tuberosity to guide insertion of the bone marrow needle.
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Section V n Circulation
Method of Insertion (Figures 11.5A and B)
After Insertion
(Figures 11.6A and B)
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Figures 11.5A and B: The left hand is used to palpate the tibial tubercle and guide insertion of the bone marrow needle 1 cm below and medial to it.
●● Use screwing movements to introduce the bone marrow needle into the tibia. ●● Enter the tibia perpendicular to its shaft. Continue to fix the knee with the left hand. ●● Point away from the growth cartilage ●● Other sites of insertion are lower end of tibia at the malleolus, lower end of femur and ischiorectal spine. ●● Avoid IO access, if the bone above the site of insertion is fractured, infected or the child has osteogenesis imperfecta. The commonest contraindication is however failed IO access. ●● If intraosseous access had been unsuccessful in one limb, make an attempt on the other limb.
Figures 11.6A and B: Introduce the BM needle until a ‘give’ is felt. The needle will stand proud. The trocar is removed. Prior to insertion of bone marrow needle, prefilled syringes should be available. Waiting to fill the syringe after entry will delay infusion and result in clogging of the needle with marrow. Connect the syringe to the bone marrow needle and manually push fluid.
●● Avoid using the same site during second time. ●● Introduce the BM needle until a ‘give’ is felt. The needle will stand proud. ●● Remove the trocar and connect the fluid filled syringe. Prior to insertion of bone marrow needle, prefilled syringes should be available. Waiting to fill the syringe after entry, will delay infusion and result in clogging of the needle with marrow. ●● Connect the syringe to the bone marrow needle and manually push fluid.
Chapter 11 n Intraosseous Access
Pushing Fluids via IO Route (Figure 11.7)
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●● Fix the needle with the other hand. Often, displacement can occur as the syringe is withdrawn. A great deal of effort is needed to push the fluid into the marrow space. ●● Apply tincture benzoin around the site of entry of the IO needle. Encircle the needle with gauze and fix with dynaplast.
Figure 11.7: During bolus therapy, dislodgement can occur resulting in extravasation. To avoid this complication, fix the needle with gauze and dynaplast.
Figure 11.8: A second peripheral IV line is obtained after the first bolus through the IO line
●● Use an infusion pump to continue fluids or infusions. Fluids will not run freely from the intravenous bottle. ●● Attempt to secure IV access after pushing 20–40 mL/kg of fluids. Usually, a second peripheral IV line is obtained after first bolus through the IO line (Figure 11.8). ●● All resuscitation drugs can reach therapeutic levels in blood.
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●● Ceftriaxone, chloramphenicol, phenytoin, tobramycin and vancomycin may result in lower peak serum concentrations. ●● The most common adverse effect seen with IO use, extravasation2, compartment syndrome, osteomyelitis and tibial fracture. These are rare, but have been reported.3
Figure 11.9: IO access may be removed once a peripheral venous access is obtained. In the management of severe shock IO is retained even if a peripheral IV line is obtained later. While, the peripheral IV access is useful for administration of fluid boluses, anesthetic medications, dextrose, etc. during resuscitation, the IO line may be used exclusively for inotrope infusion.
Airway Manager ●● Throughout the procedure, ensure that the airway is opened as shown in the picture and oxygen should be provided (refer Figure 11.9). ●● The bag-valve-mask must be available close at hand. ●● Failure to obtain IV access and need for IO access suggests that the child is in severe shock. Hence, fluid resuscitation can precipitate features of pulmonary edema in the failing heart. ●● The airway manager must watch out for signs of pulmonary edema such as froth, signs of respiratory distress or respiratory failure. ●● Consider the need for intubation and call for an airway tray. ●● Repeat the rapid cardiopulmonary cerebral assessment after every fluid bolus. ●● Depute one team member to keep track of the number of fluid boluses. ●● When disconnecting the syringe from the IO needle, care must be taken to avoid dislodgement of the needle. ●● Look carefully for signs of extravasation. Figure 11.10 shows recovered child after resuscitation.
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Section V n Circulation
common errors IP : 196.52.84.10
Figure 11.10: Intraosseous access is a life-saving intervention. This infant with hydronephrosis and urosepsis presented to the ED with hypotensive shock. He required 120 mL/kg fluid in the initial hours of resuscitation to resolve shock. In this picture, he is responding to the mother after correction of shock (therapeutic goal).
Key Points
ü
1. Prefer to use IO access. Avoid damaging veins, if IV access is not easily available. 2. Follow all drugs with 5–10 mL of NS flush. 3. Early use of IO access prevents damage to the veins. After bolusing 20–40 mL/kg, IV access is easier. 4. Ideally, if 2 separate secure IV access had been obtained, the IO needle should be removed.
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1. Using the blood set needle (which does not have a trocar). 2. Preferring to obtain access using ‘cut down’ technique. 3. Failing to fix during bolus therapy resulting in slippage of the IO needle. 4. Not using screwing movements to enter the marrow space. 5. Connecting the IV bottle directly to the IO needle and expecting it to run as in IV access. 6. Not fixing the IO needle effectively after entering the marrow space.
REFERENCEs 1. R Fowler, JV Gallagher, SM Isaacs, et al. The Role of Intraosseous Vascular Access in the Out-of-Hospital Environment (Resource Document to NAEMSP Position Statement) 2007, (11) 1 , 63-66 (doi:1. 1080/10903120601021036). 2. ML Buck, BS Wiggins, JM Sesler. Intra-osseous drug administration in children and adults during cardiopulmonary resuscitation. Ann Pharmacother. 2007 Oct;41(10):1679-86. 3. Voigt J, Waltzman M, Lottenberg L. Intraosseous vascular access for in-hospital emergency use: a systematic clinical review of the literature and analysis. Pediatr Emerg Care. 2012 Feb;28(2):185-99. doi: 10.1097/ PEC.0b013e3182449edc.
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Vasoactive Drugs in the ED
12
Figure 12.1: Vasoactive medications: The magic drugs to restore hemodynamics
Learning Objectives 1. Case scenarios illustrating the choice of inotropes. 2. Pharmacology of the vasoactive medications.
3. Evidence-based approach for the use of vasoactive medications in ED settings.
INTRODUCTION This chapter will discuss an overview of inotropes and catecholamines in ED settings1 (Figure 12.1).
CASE SCENARIO 1 A febrile 32-day-old infant presented with history of breathlessness and not behaving ‘as usual’. He had an abscess in his arm (Figures 12.2 to 12.4). The rapid cardiopulmonary cerebral assessment reveals. RR: 70/minute, minimal retractions, HR: 200/minute, warm, pink peripheries, well felt peripheral pulses, rapid CRT and normal liver span. His suck and moro are sluggish, eyes are mid-position, DEM is normal. His temperature is 38.5ºC and his capillary blood glucose is 72 mg/dL. He had a large abscess over his left shoulder.
Figure 12.2: Triaged as respiratory distress and shock due to severe sepsis, he receives O2 through the oxyhood and 35 mL of NS (10 mL/kg) as the initial fluid bolus for shock (Note the huge abscess over the left arm). Reassessment is as follows:
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Section V n Circulation
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These effects mentioned above are dose-dependent. Hemodynamic response to dopamine varies from patientto-patient.2–4 While dopamine is the commonest initial drug of choice, age-specific insensitivity to dopamine is a concern in infants less than 6 months.5,6
Figure 12.3 Physiological status: Respiratory failure, wide pulse pressure (warm cardiogenic) shock.
You are planning to intubate. Which vasoactive medication would be appropriate?
Dopamine Dopamine hydrochloride is an endogenous catecholamine and a chemical precursor of norepinephrine (NE). It has both α- and β-receptor stimulating actions. In addition, it also has receptors unique to this group of drugs (DA1, DA2, i.e. dopaminergic receptors). ●● At low infusion rates (5 µg/kg/min), activation of the DA1, DA2 receptors cause relaxation of vascular tone and increase blood flow to the renal, splanchnic, cerebral and coronary vascular beds. ●● At higher infusion rates (10–15 µg/kg/min), Dopamine stimulates the heart, directly through β-adrenergic receptors and indirectly through release of stored NE from the nerve endings. ●● At higher rates (> 15 µg/kg/min), dopamine infusion, causes vasoconstriction through two pathways. Direct stimulation of α-receptors and indirect stimulation through release of stored NE from the nerve endings. In shock secondary to myocardial dysfunction, dopamine improves myocardial contractility. Improved contractility, causes reduction in both preload and afterload. These factors, further increase cardiac output. Coronary perfusion pressure also improves (increasing oxygen supply). In addition, the reduction in heart rate, enhances diastolic coronary perfusion. The increase in oxygen consumption is countered by the improvement in coronary blood flow. The net effect on oxygen delivery is beneficial.
Figure 12.4: This picture shows the same baby being fluid resuscitated after intubation. Dopamine and norepinephrine infusion are on flow and abscess has been drained.
●● Dopamine is initiated and maintained at the rate of 10 μg/kg/minute. Increasing rates of infusion will increase risk of tachyarrhythmias, peripheral vasoconstriction and ischemia.7 ●● Frequent monitoring of the cardiopulmonary response to dopamine infusion is advisable. ●● The onset of action is within 2 minutes, peak 10 minutes and its effects wane within 10 minutes of stopping the infusion. Tapering or stopping dopamine prematurely viz as soon as the child’s cardiopulmonary parameters have stabilized is a common error in the postresuscitative period.
Clinical Role
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Prior to initiating dopamine, volume repletion is mandatory and cardiac rhythm should be normal. In chronic congestive heart failure, depletion of stored NE occurs, resulting in resistance to the effects of dopamine.7
Indications ●● Cardiogenic shock secondary to scorpion sting, status epilepticus, heart disease, perinatal depression, hyaline membrane disease.8
Chapter 12 n Vasoactive Drugs in the ED
●● Cardiogenic shock with vasodilation (warm septic shock), characterized by elevated cardiac output, low systemic vascular resistance and normotension.8 IP : 196.52.84.10
Not Useful ●● Hypotensive shock of any etiology where epinephrine is more appropriate. ●● Primary myocardial disease presenting with hypotensive cardiogenic shock. Dopamine is not preferred, since it aggravates tachyarrhythmias and increases myocardial oxygen consumption thereby worsening of cardiac dysfunction. Dobutamine is the preferred drug in this scenario.
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Preparation and Administration Ideally dopamine should be administered through a central line. However in the ED, it can be initiated through a secure peripheral IV line or intraosseous route18,19 using an infusion pump. Mixing with sodium bicarbonate solutions is avoided.
CASE SCENARIO 2 A 6-week-old baby, being evaluated for congenital heart disease, has had worsening of breathlessness. He has not been able to take his usual feeds at breast since the morning (Figure 12.5).
Adverse Effects ●● Tachycardia, dysrhythmias and hypertension could occur as a result of dopamine infusion. Tachycardia, increases oxygen consumption and shortens diastole (reducing coronary perfusion during diastole). The deleterious effects of dopamine on myocardial oxygen consumption is less than epinephrine, but greater than Dobutamine, Amrinone and Milrinone.9 ●● Dobutamine has also been shown to depress minute ventilation10,11 in response to hypoxia and hypercarbia by as much as 60%. Within the lung, it increases blood flow to the hypoventilated areas worsening hypoxia. ●● Low dose of dopamine does not improve glomerular filtration rate and is not protective to the kidney.12,13 ●● It increases splanchnic oxygen consumption15, adversely affects gastrointestinal motility14,15 with varying effects on the splanchnic circulation16-18.
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Extravasation of dopamine can cause limb ischemia resulting in gangrene of limbs and extensive skin necrosis. Infusion rates as low as 1.5 µg/kg/minute have been known to be associated with limb loss! ●● To prevent this dreaded complication, tight strapping the entire limb must be avoided. ●● The IV line should be checked for free flow. ●● Flushing the inotrope line must be avoided. ●● Extravasation, should be treated with local infiltration with a solution of phentolamine (5 mg in 15 mL of normal saline) using a fine hypodermic needle.
Figure 12.5 Physiological status: Cardiogenic shock due to CHD.
Oxygen is provided through JR circuit and 5 mL/kg of NS is administered over 20 minutes. Reassessment after the bolus shows that BP had improved to 90/60 mm Hg, but the liver span had increased to 8 cm. The intubation tray is being prepared. What inotrope infusion would you order?
Dobutamine21-23 A selective beta-1 adrenergic agent, Dobutamine increases heart rate by stimulating the SA node. It also increases automaticity, conduction velocity and myocardial contractility. Tachycardia and vasodilation also occurs due to its action on the Beta-2 receptors. Due to its alpha-adrenergic blocking activity it can cause cause severe vasodilation (especially in septic shock) and precipitate hypotension. In addition dobutamine also causes pulmonary vasodilation.
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Section V n Circulation
Clinical Role ●● Normotensive cardiogenic shock due to primary myoIP :as196.52.84.10 cardial pathology such myocarditis, rheumatic, congenital heart disease, Kawasaki’s disease, etc. ●● Fluid refractory septic shock when the blood pressure is normal or high. ●● Cardiogenic shock due to severe hypoxia-ischemia of any etilogy.
Administration Therapy is started at the rate of 5–10 µg/kg/minute and titrated based on clinical response of the child. Mixing with sodium bicarbonate solutions should be avoided. The onset of action, duration, peak action and precautions taken for infusion are similar to dopamine.
Figure 12.6: He is bag ventilated and cardiac compressions are initiated. Epinephrine 1.2 mL of 1:10,000 dilution is administered through the intravenous catheter, which had been placed for administration of contrast.
Adverse Effects
Repeat cardiopulmonary assessment after CPR as shown in Figure 12.6.
●● Dobutamine increases myocardial oxygen demand. However, improved cardiac contractility in children with cardiac dysfunction results in enhanced oxygen supply to the heart. ●● Hypotension, hypertension, tachyarrhythmias, VPCs, angina.
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An increase in heart rate without improvement in shock should prompt a reduction in the rate of infusion.
CASE SCENARIO 3 A 2-year-old child was being given contrast intravenously in the radiology department to evaluate a voiding cystourethrogram. He vomits, postures and becomes unresponsive. As he was being rushed into the PED, he developed swelling around the eyes, lips and face. Generalized rashes were also noted. On arrival into the PED, his airway is opened using the head tilt-chin lift maneuver. The airway nurse suctions oropharyngeal secretions, inserts a nasogastric tube (10F) and decompresses stomach by connecting the NGT to a suction apparatus. Simultaneously, the airway manager recognizes that the child is not breathing and initiates bagvalve-mask ventilation. The team member who is assessing HR, starts initiating chest compression. A 3rd team continues assessment...
Figure 12.7: Cardiac compressions are stopped. 240 mL saline is being pushed with a 3-way stopcock.
Reassessment Physiological status: Assisted ventilation, relative bradycardia with hypotensive shock (Figure 12.7). Cardiac compressions were stopped. 240 mL saline is being pushed with a 3-way stopcock. Which vasoactive medication would you start after CPR when heart rate has been established?
Epinephrine A stress hormone, epinephrine has affinity for β-1, 2 and α-receptors (present in both cardiac and vascular smooth muscle). β-adrenergic effects are more pronounced at lower
Chapter 12 n Vasoactive Drugs in the ED
doses, whilst, α-1 adrenergic effects manifest at higher doses.24
IP : 196.52.84.10 Beta-1 adrenergic receptor stimulation increases heart rate, myocardial contractility, automaticity and conduction velocity.
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●● If hypotension persists despite epinephrine bolus injections and fluid administration, initiate epinephrine infusion at the rate of 0.1–1 µg/kg/minute.
Administration
Beta-2 adrenergic receptors stimulation occurs at lower doses resulting in effects similar to β-1 activity. The other effects of β-2 activity are bronchodilation and dilation of the arterioles by decreasing the diastolic BP. SVR decreases and diastolic pressure falls. There is a slight increase in heart rate, cardiac output and systolic BP. The force of contraction also increases. However, the myocardial oxygen consumption is disproportionate to the improvement in myocardial contractility.
It can be safely administered through an intraosseous or peripheral intravenous route using an infusion pump.
Prolonged infusions of high doses can be cardiotoxic and lead to apoptosis.
Metabolic Effects
Epinephrine has been shown to reduce splanchnic blood flow, increase carbon dioxide production in the gastric mucosa and lactate production in the regional and systemic circulation.25,26
Clinical Role ●● Anaphylactic shock. ●● Hypotensive shock of any etiology. ●● Fluid unresponsive, dopamine refractory, hypotensive septic shock.27,28,29 ●● Drug of choice in CPR and postcardiac arrest shock. Dose
Adverse Effects ●● Tachyarrhythmias, such as atrial and ventricular extrasystoles, tachycardias and fibrillation. ●● Hypertension and ischemic changes in the ECG are other dangerous side effects of this drug.
●● Hypokalemia occurs due to β-2 adrenergic receptor stimulation. ●● Hyperglycemia results from α-adrenergic mediated suppression of insulin release. ●● Infiltration into skin and tissues can produce severe vasospasm and tissue injury.
CASE SCENARIO 4 An 8-month-old is being treated for septic shock in the ED. She had received 100 mL/kg isotonic saline and had been intubated. Dopamine had been initiated when her shock was refractory to 60 mL/kg. Her assessment was as follows (Figures 12.8, 12.9 and 12.11).
Anaphylaxis: DEEP IM (avoid subcutaneous route, since it may delay absorption): 0.01 mg/kg (0.1 mL/kg of 1:10,000) every 15 minutes PRN (maximum dose 0.3 mg). IV/IO route: 0.01 mg/kg (0.1 mL/kg of 1:10,000) every 3–5 minutes up to a maximum dose 1 mg, if hypotension is noted. Each bolus of epinephrine must be followed by a saline flush (5 mL of NS), if the drug is administered via the IO route. Cardiac arrest: 0.01 mg/kg (0.1 mL/kg of 1:10,000) via the IO/IV route every 3–5 minutes for a maximum of 1 mg. If heart rate is established, but hypotensive shock is noted initiate epinephrine infusion at the rate of 0.1–1 µg/ kg/minute via a secure peripheral or IO line. ●● If IV/IO access is not immediately available, 10 times the calculated dose for weight may be administered into the endotracheal tube.
Figure 12.8: Note the flushed, bright pink palms and soles of this infant who has received 100 mL/kg fluids and dopamine. These findings should not be misconstrued as normalization of shock. Check her BP with special emphasis on the point of disappearance of the Korotkoff sounds (for diastolic BP).
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Section V n Circulation
IP : 196.52.84.10
kaline solutions. Watch closely for extravasation. The drug effects will cease within 10 minutes of discontinuation of infusion.
CASE SCENARIO 5 A 9-month-old infant presenting with acute cardiogenic shock and a possible diagnosis of myocarditis has been fluid resuscitated, intubated and is having dobutamine administered at the rate of 10 µg/kg/min. The current cardiopulmonary status shows the following (Figure 12.10)
Figure 12.9 Physiological status: Fluid unresponsive, dopamine refractory hypotensive vasodilatory shock with low mean arterial pressure of 40 mm Hg.
Which vasoactive medication should be initiated now?
Norepinephrine32-37 This endogenous catecholamine is a potent alpha-1 adren ergic receptor agonist with some β agonist activity. Predominantly a vasoconstrictor, it increases systolic, diastolic and pulse pressures with minimal effects on cardiac output and heart rate. This latter effect makes it a useful catecholamine in children with tachycardia. Improvement in cardiac output has been attributed to better coronary perfusion pressures. Several studies have demonstrated that norepinephrine normalized hemodynamic parameters, reestablished urine output, decreased serum creatinine and increased creatinine clearance in high output, low systemic vascular resistance septic shock.
Clinical Role ●● Hypotensive warm shock not responding to intravascular volume repletion and dopamine infusion. In this scenario, NE infusion increases SVR, BP and urine output without significantly elevating the heart rate.16 ●● Other indications for NE are vasodilator ingestion and CNS depressant intoxication where shock is characterized by low SVR and hypotension. ●● Adverse effects are similar to other vasoactive medications. However, bradycardia is an unusual complication of norepinephrine infusion. ●● Dose: 0.1–2 µg/kg/minute (titrate based on repeated cardiopulmonary assessment. Avoid mixing with al-
Figure 12.10 Physiological status: Refractory cardiogenic shock with high BP.
What would be the appropriate drug in this setting?
Bipyridines These agents increase the levels of cAMP by inhibiting its breakdown in the cardiac myocyte and vascular smooth muscle.39 These properties result in increased myocardial contractility and vasodilatation. In addition, it also improves diastolic relaxation (lusitropy), thus reducing preload, after load and systemic vascular resistance. PDI have long half-lives ranging from 0.5 hour i.e Milrinone and 4 hours viz Amrinone. Unlike catecholamines, PDI are rec ommended for cold shock with normal or high MAP40,41 a clinical scenario often encountered in catecholamine refractory low cardiac output and high vascular resistance states and after initiation of epinephrine, where blood pressure is increased, but the other therapeutic goals of shock are not achieved. The main concerns of the PDI are related to their propensity to cause hypotension in volume depleted patients, accumulation in renal failure and occurrence of thrombocytopenia with prolonged infusions.
Chapter 12 n Vasoactive Drugs in the ED
Clinical Role ●● Catecholamine resistant cold septic shock with normal IP : 196.52.84.10 or increased blood pressure. ●● Catecholamine resistant shock complicated by severe tachyarrhythmias.
125
Ù
Placement of an arterial catheter for intra-arterial pressure monitoring is mandatory during administration of this drug. Since invasive monitoring is fraught with complications in shocky children, its use in the ED is limited.
Adverse Effects
Vasopressin
Amrinone can aggravate myocardial ischemia and cause supraventricular and ventricular ectopy. Rapid infusions of amrinone and milrinone during loading may produce hypotension, which is aggravated by volume depletion. Amrinone also produces reversible dose-dependent thrombocytopenia.
Vasopressin is released in response to increased plasma osmolality, hypoxia or shock. It acts on the V1 receptor in the vascular smooth muscle to produce vasoconstriction and the V2 receptors, which mediate water reabsorption in the renal collecting ducts. A few case studies have shown its usefulness in norepinephrine unresponsive warm shock.41 However, data is limited in the use of vasopressin in children42 and there is little evidence to support its use as rescue therapy in catecholamine resistant shock.43 Besides, children with septic shock have been shown to have high levels of vasopressin.44,45
Administration Amrinone and milrinone are formulated in a manner similar to dopamine and dobutamine. Amrinone is not compatible with dextrose containing solutions unlike milrinone, which is compatible with dextrose containing solutions. ●● Amrinone is administered as a loading dose of 1–2 mg/ kg over 30–60 minutes. The infusion ranges from 5–10 µg/kg/minute. Caution should be taken to correct intravascular volume depletion, since this group of drugs can cause profound hypotension. Dose adjustment needs to be made in children with renal failure.
Indications ●● Hypotensive, warm septic shock refractory to fluid, Dopamine and norepinephrine infusion.
Key Points
1. Initiate the appropriate inotrope when signs of pulmonary edema are noted or when shock is refractory to fluids. 2. Choose the appropriate inotrope based on blood pressure. 3. Epinephrine is the only agent, which can be initiated simultaneously with fluids even before establishing euvolemia in hypotensive shock.
common errors
Figure 12.11: Neurologically intact survival of a child with septic shock. Timing and use of the ‘best’ vasoactive medication is crucial for successful outcomes (Same child as managed in Figure 12.8).
ü
û
1. Stepping up the dopamine infusion from 10 µg/kg/ min to 20 µg/kg/min in refractory shock. 2. Combining dopamine and dobutamine in the same syringe. 3. Initiating inotropic agents prior to correction of hypovolemia. 4. Failing to initiate an appropriate inotrope.
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Table 12.1: Preparation and infusion rates of commonly used vasoactive agents in the ED Rule (add to 100 mL) Rule of 3 (add to 50 mL) IPof:6196.52.84.10
Rate of administration: 10 mL/h
Epinephrine
0.6 × body weight mg
0.3 × body weight mg
1 µg/kg/min
0.1–1.0 µg/kg/min
Norepinephrine
0.6 × body weight mg
0.3 × body weight mg
1 µg/kg/min
0.1–1.0 µg/kg/min
Dopamine
6 × body weight mg
3 × body weight mg
10 µg/kg/min
5–10 µg/kg/min
Dobutamine
6 × body weight mg
3 × body weight mg
10 µg/kg/min
5–10 µg/kg/min
Name of drug
Dose
Table 12.2: Indications for initiating inotropes, vasopressors and inodilators Drug Dopamine
Indication
Adverse CVS† effects
Shock with normal BP and low SVR*
SVT ‡,VPC§, VT,
Cardiogenic shock
Hypertension
Dose 10 µg/kg/min
Distributive shock Epinephrine
Severe bradycardia with shock
SVT,VPC, VT, 0.05–1.0 µg/kg/min ST elevation, postresuscitation myocardial dysfunction
Pulseless electrical activity Postcardiopulmonary arrest stabilization, toxic doses of calcium channel antagonists, β-blocking drugs Hypotensive shock of all etiologies
Hypertension
Anaphylactic shock
1–4 µg/kg/min
Dobutamine
Cardiogenic shock with high SVR, cardiac failure
5–20 µg/kg/min
Norepinephrine
Low BP with low SVR
Tachy, brady arrhythmias, hypertension
0.05–1.0 µg/kg/min
Milrinone
Cardiogenic shock with high SVR
Hypotension
50–75 µg/kg over 10–60 minute followed by infusion 0.5–0.75 µg/kg/min
*
SVR, systemic vascular resistance; †CVS, cardiovascular; ‡ SVT, supraventricular tachycardia; §VPC, ventricular premature contractions.
References 1. Overgaard CB, Davik V. Ionotropes and Vasopessors. Review of physiology and clinical use in cardiovascular disease. Circulation. 2008;118:1047-56. 2. Allen E, et al. Alterations in dopamine clearance and catechol O- methyl- transferase activity by dopamine infusions in children. Crit Care Med. 1997;25. 3. Notterman DA, et al. Dopamine clearance in critically ill infants and children effects of age and organ system dysfunction. Clin Pharmacol Ther. 1990;48:138.
4. Zaritsky A, Lotze A, Stull R, et al. Steady state dopamine clearance in critically ill infants and children. Crit Care Med. 1988;16:217-90. 5. Padbury JF, Agata Y, Baylen BG, et al. Dopamine pharmacokinetics in critically ill newborn infants. J Pediatr. 1987;110:293-98. 6. Padbury JF, Agata Y, Baylen BG, et al. Pharmacokinetics of dopamine in critically ill newborn infant. J Pediatric.1990; 117:472-76. 7. Ralston M, Hazinski MF, Zaritsky AL, et al. Textbook of Pediatric Advanced Life Support, American Heart Association. 2007.
Chapter 12 n Vasoactive Drugs in the ED
8. Dellinger RP, Mitchell M, Carlet JM, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock. Crit Care Med. IP : 196.52.84.10 2008;36(1):296-327. 9. Regnier B, Safran D, Carlet J, et al. Comparative hemodynamics of dopamine and dobutamine in septic shock. Intensive Care Med. 1979;5:115-20. 10. Jardin F, Gurdjian F, Desfonds P, et al. Effects of dopamine on intra-pulmonary shunt fraction and oxygen transport in severe sepsis with circulatory and respiratory failure. Crit Care Med. 1979;7:273-77. 11. Vane de Borne P, Oren R, Somers V. Dopamine depresses minute ventilation in patients with heart failure. Circulation. 1998;98:126-31. 12. Denton MD, Chertow GM, Brady HR. Renal –dose Dopamine for the treatment of acute renal failure: scientific rationale, experimental studies and clinical trials. Kidney Int. 1996;50:4-14. 13. Bellomo R, Chapman M, Finfer S, et al. Low dose dopamine in patients with early renal dysfunction: A placebo controlled randomized trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical trial group. Lancet 2000;356:2139-43. 14. Jakob SM, Ruokonen E, Takala J. Effects of dopamine on systemic and regional blood flow and metabolism in septic and cardiac surgery patients. Shock. 2002;18:8-13. 15. Meier-Hellman A, Bredle DL, et al. The effect of low dose dopamine on splanchnic blood flow and oxygen uptake in patients with septic shock. Intensive Care Med. 1997;23:3137. 16. De Backer D, Creteur J, Silva E, et al. Effects of dopamine, norepinephrine and epinephrine on the splanchnic circulation in septic shock: which is best? Crit Care Med.2003;31:1659-667. 17. Ruokonen E, Takala J, Kari A, et al. Regional blood flow and oxygen transport in septic shock. Crit Care Med. 1993;21:1296-1303. 18. Neviere R, Mathieu D, Chagnon JL, et al. The contrasting effects of dobutamine and dopamine on gastric mucosal perfusion in septic patients. Am J Respir. Crit Care Med. 1996;154:1684-88. 19. Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the emergency department. Pediatr Emerg Care. 2008;24:647-55. 20. Orlowski JP, Porembka DT, Gallagher JM. Comparison study of intra-osseous, central intravenous and peripheral intravenous infusions of emergency drugs. Am J Dis Child. 1990;144:112.
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21. Sharanz D, Stopfkuchen H, Jungst BK, et al. Hemodynamic effects of Dobutamine in children with cardiac failure. Eur J Pediatr. 1982;139:4-7. 22. Majerus TC, et al. Dobutamine: Ten years later, Pharmacotherapy. 1989;9:245. 23. Berg RA, et al. Dobutamine pharmacokinetics and pharmacodynamics in normal children and adolescents. J Pharmacol Exp Ther. 1993;265:1232. 24. Habib DM, et al. Dobutamine pharmacokinetics and pharmacodynamics in pediatric intensive care patients. Crit Care Med. 1992;20:601. 25. Fisher DG, Shwartz PH, Davis AL. Pharmacokinetics of exogenous epinephrine in critically ill children. Crit Care Med. 1993;21:111 26. Meier-Hellman A, Reinhart K, Bredle DC. Epinephrine impairs splanchnic perfusion in septic shock. Crit Care Med. 1997;25:399-404. 27. Levy B, Bollaert FE, Charpentier C, et al. Comparison of nor-epinephrine and dobutamine to epinephrine for hemodynamics, lactate metabolism, and gastric tonometric variables in septic shock. Intensive Care Med. 1997;23:282287. 28. Bollaert FE, Baeur P, Audibert, et al. Effects of epinephrine on hemodynamics and oxygen metabolism in dopamine resistant shock. Chest. 1990;98:949-53. 29. Wilson W, Lipman J, Scribante J, et al. Septic shock: Does adrenaline have a role as a frontline inotropic agent in septic shock? Anaesth Intensive Care. 1992;21:70-77. 30. Moran JL, et al. Epinephrine as an inotropic agent in septic shock: a dose profile analysis, Crit Care Med. 1993;21(1):70. 31. Brown C, et al. A comparison of standard-dose and high dose epinephrine in cardiac arrest outside the hospital. N Engl J Med. 1992;327(15):1051. 32. Dieckman R, Vardis R. High dose epinephrine in pediatric out of- hospital cardiopulmonary arrest. Pediatrics. 1995; 95:901. 33. Desjars P, Pinaud M, Potel G, et al. A re-appraisal of norepinephrine therapy in human septic shock. Crit Care Med. 1987;15:134-37. 34. Desjars P, Pinaud M, Bugnon D, et al. Nor-epinephrine therapy has no deleterious renal effects in human septic shock. Crit Care Med 1989;17:426-29. 35. Hesselvik JF, Brodin B. Low dose norepinephrine in patients with septic shock and oliguria: Effects of after load, urine flow and oxygen transport. Crit Care Med. 1989;17: 179.
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36. Martin C, et al. Renal effects of nor-epinephrine used to treat septic shock patients. Crit Care Med. 1990;18:282. 37. Martin C, Papazian L, Perrin G, et al. Nor-epinephrine or IP : 196.52.84.10 dopamine for the treatment of hyper-dynamic septic shock? Chest. 1993;103:1826-31. 38. Martin C, et al. Effects of norepinephrine on right ventricular function in septic shock patients. Intensive Care Med. 1994;20:444. 39. Richard J Beale, Steven M Hollenberg, Jean Louis Vincent, et al. “Vasopressor and inotropic support in septic shock: An evidence based review”. Surviving Sepsis Campaign Guidelines. Crit Care Med. 2004;Vol 32: No.11 (Suppl). 40. Barton P, Garcia J, Kouat HA, et al. Hemodynamic effects of IV milrinone lactate in pediatric patients with septic shock. Chest. 1996;109:1302-12.
41. Choong K, Kissoon N. Vasopressin in pediatric shock and cardiac arrest. Ped Crit Med. 2008;9:372-379 42. Mayer S, Gortner L, McGuire W, et al. Vasopressin in catecholamine refractory shock in children. Anesthesia. 2008;63:228-234. 43. Leclerc F, Walter-Nicolet E, Leteurtre S, et al. Admission plasma vasopressin levels in children with meningococcal septic shock. Intensive Care Med. 2003;29:1339-44. 44. Lodha R, Vivekanandhan S, Sarthi M. Serial circulating vasopressin levels in children with septic shock. Pediatr Crit Care Med. 2006;7:220-224. 45. Vasudevan A, Lodha R, Kabra SK. Vasopressin infusion in children with catecholamine-resistant septic shock. Acta Pediatrica. 2005;94:380-83(d).
Approach to Acute Diarrhea and Shock in the ED IP : 196.52.84.10
13
Figure 13.1: Severe dehydration responds dramatically to IV fluid therapy (Courtesy: Dr Mullai Baalaaji and Dr Gunda Srinivas)
Learning Objectives 1. Recognition of severity of dehydration and shock using the modified rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle.
2. How fluids are administered using the pull push technique? 3. Recognition of coexisting septic shock in a child presenting with diarrhea and hypovolemic shock.
INTRODUCTION
CASE SCENARIO
Acute diarrhea with or without shock is the commonest emergency encountered in day to day practice (Figure 13.1). This chapter is predominantly based on the WHO recommendations—20051 for the management of acute diarrhea.
A 10-year-old girl is rushed into the ED following several episodes of diarrhea and vomiting. She is drowsy.
The PEMC approach helps the novice physician to identify the severity of fluid loss using the rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle and match fluid resuscitation. This approach also emphasizes that altered mental status (lethargy), in the background of severe dehydration may be secondary to hypovolemic shock. This observation is based on the fact that loss exceeding 25% of effective circulating volume leads to decreased cerebral perfusion and fall in level of consciousness. Severe dehydration is attributed to loss of 10% circulating volume. However, altered mental status in children with severe dehydration may also result from dyselectrolytemia or hypoglycemia.
Figure 13.2: Note the sunken eyes in this child, who presented with hypovolemic shock. Two intravenous lines have been secured. Pull push technique is being used to administer RL boluses (Note O2 being given through NRM and BP cuff tied for BP monitoring) (Courtesy: Dr Gunda Srinivas).
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Section V n Circulation
IP : 196.52.84.10
Figure 13.3 Physiological status: Airway stable/effortless tachypnea/hypotensive shock/with altered mental status and severe dehydration.
Figure 13.4: The 3-way stopcock is turned to close the patient end and facilitate withdrawal of fluid from the reservoir (Courtesy: Dr Gunda Srinivas).
Management (Figure 13.2 to 13.8) ●● Provide oxygen using the non-rebreathing mask. ●● Secure 2 IV lines and infuse RL 20 mL/kg using pushpull technique. ●● Until BP normalizes for age. ●● Remember systolic BP less than or equal to 90 mm Hg should be considered as hypotension in children aged 10 years or more. ●● Check Dextrostix and correct documented hypoglycemia. ●● Repeat rapid cardiopulmonary cerebral assessment after every fluid bolus. ●● Send blood for electrolytes, urea, creatinine. ●● Avoid antibiotics, since most diarrheal episodes are secondary to viral infections. ●● If acute gastroenteritis is due to giardiasis or the child is having dysentery or less than 6 months of age or has systemic illness or has proven or suspicion of shigellosis.
Ù
Cholera: Oral Doxycycline Dose: 4–5 years 100 mg stat, 2–4 years: 50 mg stat single dose. Shigellosis: Ciprofloxacin Dose: 1 month to 18 years 20 mg/kg (max 750 mg) twice daily. Giardiasis: Oral Metronidazole 1–3 years : 500 mg OD for 3 days 3–7 years : 600–800 mg OD for 3 days Child 7–10 years : 1 g OD for 3 days 10–18 years : 2 g OD for 3 days.
. Figure 13.5: The 3-way stopcock is now turned such that fluids can be pushed into the intravenous line (Courtesy: Dr Gunda Srinivas).
The pull push method described above is one of the fastest methods of administering large volumes of fluids in the shortest period of time. Dedicate one team member to: ●● Keep track of the number of boluses that are being administered. ●● Perform the rapid cardiopulmonary cerebral assessment after each intervention. ●● Document the findings and response to treatment.
Ù
Do not stop fluid boluses on the basis of normalization of BP. All the therapeutic goals should be achieved. If shock persists, plan to continue fluid therapy. Dehydration may persist after shock correction.
Chapter 13 n Approach to Acute Diarrhea and Shock in the ED
CASE SCENARIO CONTINUED Following three rapid boluses of 20 mL/kg, her repeat IP : 196.52.84.10 assessment was as follows:
131
●● Discontinue oxygen therapy. ●● If the patient can drink, begin giving oral rehydration salts (ORS) solution by mouth. Children > 1 year ●● 30 mL/kg as rapidly as possible (within 30 minutes); then 70 mL/kg in the next 2 hours. Children < 1 year ●● 30 mL/kg in the 1st hour; then. ●● 70 mL/kg in the next 5 hours.
CASE SCENARIO CONTINUED Following RL 100 mL/kg over 6 hours, her repeat assess ment revealed.
Figure 13.6 Physiological status: Airway stable/tachypnea/ tachycardia with normotensive shock with severe dehydration.
Management ●● Continue O2 administration using the non-rebreathing mask. ●● Infuse RL 20 mL/kg over 20 minutes.
CASE SCENARIO CONTINUED Following the 4th bolus of 20 mL/kg, her repeat as sessment revealed.
Figure 13.8 Physiological status: Cardiopulmonary cerebral status is normal, tachycardia has also resolved. She has features of ‘some dehydration’.
●● Advice ORS 75 mL/kg for 4 hours and review. ●● ORS ad lib in the older child. ●● When hydration becomes normal: Advice ORS 10 mL/ kg for every loose stool.
CONTRAINDICATIONS TO ORAL REHYDRATION ●● ●● ●● ●● Figure 13.7 Physiological status: Airway stable/breathing normal/shock has resolved, but she has dehydration as evidenced by sunken eyes and loss of skin turgor. Persistent tachycardia is a sign of dehydration, since shock as resolved.
Signs of shock. Ileus or intestinal obstruction (proven or suspected). Comatose or unconscious. Unable to tolerate oral/NGT rehydration (persistent vomiting). ●● Often, children presenting with hypovolemic shock have elevated renal parameters due to prerenal failure. Decision to withhold fluids will have disastrous consequences.
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Section V n Circulation
Refer Protocol 13.1.
common errors
Ù
IP : 196.52.84.10 Correct shock and re-evaluate renal parameters in previously normal children. Key Points
ü
1. Repeat cardiopulmonary cerebral assessment after every fluid order. Recurrence of diarrheal episodes and vomiting can alter the physiological status. 2. Attempt to shift the pediatric assessment triangle from hypotensive shock to the normal triangle. 3. Inotropes and intubation are rarely needed in the management of uncomplicated hypovolemic shock. 4. Evidence of warm shock (wide pulse pressure), tachycardia and tachypnea fulfilling the SIRS criteria, in a dehydrated child should alert the to the possibility of coexisting GI sepsis. Evidence of respiratory distress in a shocked child with diarrhea, but without respiratory symptoms is hallmark of cardiogenic or non-cardiogenic pulmonary edema in GI sepsis.
û
1. Failure to recognize shock and treat as severe dehydration! 2. Failure to anticipate that hypovolemic shock may coexist with septic shock secondary to GI sepsis. 3. Initiating dopamine for shock persisting after administration of 60 mL/kg of fluids. 4. Using GNS or other glucose containing fluids to correct shock. 5. Withholding fluids in shocked children in view of elevated urea and creatinine. 6. Failure to correct metabolic abnormalities after resolving shock and dehydration. 7. Failure to anticipate that failure in improvement in tone and posture after correction of shock could be due to persistent hypokalemia.
REFERENCE 1. “The Treatment Of Diarrhea, A manual for physicians and other senior health workers”: WHO-2005.
Protocol 13.1: PEMC approach: Recognition of the severity of dehydration and presence of septic shock in children presenting with diarrhea
Chapter 13 n Approach to Acute Diarrhea and Shock in the ED
IP : 196.52.84.10 133
14
IP : 196.52.84.10
Cardiogenic Shock
Figure 14.1: Rapid IV adenosine can reverse certain arrhythmias in seconds (Courtesy: Dr Gunda Srinivas, Dr Bhushan Chavan).
Learning Objectives 1. Using the pediatric assessment triangle to recognize cardiogenic shock.
2. Management of cardiogenic shock in the ED.
Introduction
PATHOPHYSIOLOGY
Cardiogenic shock is a hemodynamic state wherein, prima ry myocardial dysfunction is responsible for the failure of the cardiovascular system to meet metabolic demands of tissues.
Depressed myocardial contractility causes a reduction in stroke volume and cardiac output leading to tissue hypoperfusion. The ensuing metabolic acidosis further impairs myocardial function. Other causative factors of myocar dial dysfunction are myocardial depressant factor (found in severe sepsis), myocardial edema, adrenergic receptor dysfunction, impaired sarcolemmic calcium flux and re duced coronary blood flow.2
Structural heart disease, arrhythmias or myocarditis are well known causes of cardiogenic shock (Figure 14.1).
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Surprisingly, cardiogenic shock has been more commonly noted in children presenting with shock due to severe sepsis, scorpion envenomation, established status epilepticus, submersion injury, etc. Probably, failure to provide appropriate prehospital resuscitation and delay in recognition of early signs of hypoxia and shock are the other causes contributing to cardiogenic shock in our setting.1
Myocardial dysfunction may be systolic or diastolic. Diastolic dysfunction occurs due to inadequate myocar dial relaxation. The latter results in increased end diastolic pressure for a given end diastolic volume.3 The increased left ventricular pressure is transmitted to the lungs causing pulmonary edema. Similarly, systolic dysfunction causes an increase in end systolic volume for a given pressure leading to a fall in the stroke volume.
Chapter 14 n Cardiogenic Shock
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In the failing heart, however, both systolic and diastolic dysfunction, coexist. Consequently, cardiac output falls and pulmonary congestion occurs. At the cellular level, IP : 196.52.84.10 lactate levels increases and central venous (superior vena cava) oxygen saturation (SvcO2) falls. SvcO2 saturations could fall to less than 20% of the arterial oxygen satura tion. Ideally, management is aimed at maintaining SvcO2 above 70%.4 In cardiogenic shock, as in other types of shock, com pensatory neurohormonal responses increase systemic vascular resistance. Activation of adrenergic receptors, heightened renin-angiotension response, increased stimu lation of endothelin are some of the factors that increase systemic vascular resistance. As opposed to hypovolemic shock, these compensa tory responses have a deleterious effect on the failing heart (Figures 14.2 and 14.3). As cardiac output (COP) decreases, systemic vascular resistance (SVR) progressively increases, increasing the afterload effect on the heart.
Ù
The failing heart has to work harder against more pressure.
Figure 14.2: This picture shows the physiological mechanisms that help to maintain cardiac output when myocardial contractility fails.
Worsening myocardial pump failure, decreasing stroke volume and increasing afterload leads to a vicious cycle. Whilst, in cardiogenic shock secondary to myocarditis or structural heart disease, the preload may be adequate or increased. Cardiogenic shock due to sepsis is characterized by massive deficits in circulating blood volume. Causes of cardiogenic shock are shown in Box 14.1.
Figure 14.3: Increase in systemic vascular resistance (a physiological response) can be counterproductive in a child with myocardial dysfunction resulting in a further fall in cardiac output. Box 14.1: Common causes of cardiogenic shock in children2 1. Heart rate abnormalities Supraventricular tachycardia Ventricular dysrhythmias Bradycardia 2. Congenital heart disease 3. Cardiomyopathy 4. Myocarditis 5. Hypoxic ischemic events Cardiac arrest Prolonged hypoxia and shock due to various etiologies Anomalous left coronary artery from the pulmonary artery (ALCAPA) Kawasaki’s disease Excessive catecholamine state Cardiopulmonary bypass 6. Sepsis Viral Bacterial 7. Metabolic Hypoglycemia Acidosis Hypocalcemia Hypothermia 8. Mechanical Cardiac tamponade 9. Others Burns Anaphylaxis Envenomations Toxic reactions (penicillins, anthracyclines) Submersion injury
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Section V n Circulation
case SCENARIO
INTERVENTIONS IN THE ED
A previously healthy, 65-day-old baby, is brought with IP : 196.52.84.10 history of breathlessness for a week. He has had no fever or cough. He was not responding to his mother. Temperature is 38.5°C. SaO2: 92%, ECG monitor shows ST segment depression with ventricular premature contractions (Figures 14.4 and 14.5).
Goals 1. Minimize myocardial oxygen demand. 2. Maximise myocardial performance. 3. Correct metabolic abnormalities.
Minimize Myocardial Oxygen Demand Airway Provide oxygen using the flow inflating ventilation device. Continuous positive airway pressure ventilation using a flow inflating ventilation device improves outcomes in acute cardiogenic pulmonary edema.
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If signs of PE and hepatomegaly do not resolve with application of CPAP and inotropes, plan elective intubation and ventilation.
Figure 14.4: Froth in the mouth and in the nasogastric tube (Courtesy: Dr Gunda Srinivas).
Elective, early intubation and mechanical ventilation will decrease the oxygen consumption of the respiratory muscles, thus diverting blood supply to the vital organs. Mechanical ventilation also improves the FRC thereby decreasing intrapulmonary shunting and improving oxy genation. As hypoxia within the alveoli improves, pul monary vascular resistance (PVR) falls. As a result, right ventricular (RV) performance improves. Ventilation also decreases the afterload on the failing heart (remember increased afterload acts as a villain to the failing heart), thus improving cardiac output.5
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Caution During Intubation Use sedating and muscle relaxing agents that do not aggravate shock. Figure 14.5 Physiological status: Impending respiratory failure with hypotensive cardiogenic shock and non-convulsive status epilepticus (secondary to severe hypoxia and shock).
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Consider early cardiogenic shock whenever a child with shock presents with respiratory distress or respiratory failure. Bradycardia, muffled heart sounds, gallop, hepatomegaly and hypotension are late signs of cardiac dysfunction.
Ketamine is the ideal drug for intubating a child presenting with acute cardiogenic shock in the ED. Avoid ketamine in cardiogenic shock due to chronic heart failure. Its nega tive inotropic effect could precipitate cardiac arrest during intubation.
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Whenever sedative drugs are being considered for intubating a child with acute cardiogenic shock, an inotrope infusion must be initiated prior to intubation.
Chapter 14 n Cardiogenic Shock
137
Table 14.1: Maintenance of fluid requirements (Holliday and Segar, 1957) Body weight < 10 kg
Volume/amount in 24 hour
IP : 196.52.84.10 100 mL/kg
Volume per hour 4 mL/kg/h
11–20 kg
1,000 mL + 50 mL/kg for each kg >10 kg
40 mL/h + 2 mL/kg/h for each kg >10 kg
> 20 kg
1,500 mL + 20 mL/kg for each kg > 20 kg
60 mL/h + 1 mL/kg/h for each kg > 20 kg
Note: Maximum fluid rate 100 mL/h. Reduce maintenance fluids to two third, if history of structural heart disease, arrhythmias, cardiomyopathies, etc.
Intubation for child with cardiogenic shock without the aid of inotropes or anesthetic drugs could precipitate car diac arrest Refer Table 14.1 for fluid requirement.
Maximize Myocardial Performance
Precautions taken during intubation of a hypotensive child with cardiogenic shock.
Administer 5–10 mL/kg of normal saline (NS) or Ringer’s lactate (RL) up to a maximum of 20 mL/kg in cardiogenic shock due to non-sepsis etiologies.
●● Order an Epinephrine infusion prior to intubation. ●● Dedicate one team member to initiate chest compres sion if heart rate begins to fall. ●● Initiate chest compressions when there is a significant fall of heart rate from baseline (e.g. fall from baseline HR of 170/min–100/min). Do not wait for heart rate to fall to less than 60/min.
Maintain Normal Temperature Resuscitate young infants under a warmer. ●● Hypothermia increases vasoconstriction and worsens the afterload effect on the heart. ●● Use Paracetamol suppository to reduce temperature (15 mg/kg every 6 hourly). ●● Hyperthermia increases metabolic demand and oxygen consumption.
Sedation Administer morphine 0.1 mg/kg and midazolam 0.1 mg/kg (slow IV), if the child has been intubated. Agitation and restlessness will increase oxygen demand and systemic vascular resistance. Both factors could stress the failing heart.
Ù
Avoid sedative drugs in restless, agitated children with cardiogenic shock who have not been intubated.
Maintain Hematocrit Transfuse 5–10 mL/kg of fresh PRBCs if hemoglobin is less than 10 g/dL. The oxygen carrying capacity of blood should be opti mized by maintaining the hematocrit at 35%–40%.6
Optimize Preload
Intravascular volume is characteristically normal or in creased in cardiogenic shock due to many etiologies.
Ù
Administer 5–10 mL/kg aliquots up to a maximum of 60–120 mL/kg in cardiogenic shock due to sepsis. In cardiogenic shock due to sepsis, intravascular vol ume (preload) is significantly reduced. Large volume flu ids are needed to optimize preload and improve myocar dial dysfunction. 1. Hypovolemia could complicate cardiogenic shock of all etiologies. 2. Check history of vomiting, poor intake, severe diapho resis, sepsis and anaphylaxis in all children presenting with shock.
Ù
Caution: Fluids can be dangerous if child has undiagnosed or untreated structural heart disease. To avoid fatal errors ask whether history of respiratory distress is truly acute or ‘acute on chronic’. During fluid therapy, if signs of pulmonary edema (intuba tion triggers) are noted: ●● Stop bolus therapy. ●● Initiate inotrope infusion. ●● Perform intubation. Diuretics are contraindicated in the presence of shock.
Ù
Cautious diuresis may be implemented in the intensive care unit (ICU) after correction of shock.
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Following intubation, if features of pulmonary edema IP : 196.52.84.10 and hepatomegaly resolve, but shock persists, ask three questions. • Is the cardiogenic shock due to sepsis, anaphylaxis or hypovolemia? • If yes to any of the three questions, continue smaller aliqouts, until therapeutic goals of shock are achieved. • If pulmonary edema or hepatomegaly worsen, further fluid therapy is contraindicated even if shock persists.
Afterload Reduction Clinically, if cardiogenic shock persists despite establish ing euvolemia and inotropes, management should focus on reducing after load. Sedation and pain relief (discussed earlier).
Improve Myocardial Contractility 1. Correct rhythm disturbances (refer Pediatric Advanced Life Support PALS algorithm). 2. Initiate inotropes (discussed in the Chapter on Vasoac tive Medications). 3. Correct metabolic disturbances such as hypoglycemia, hypocalcemia, acidosis, hypokalemia.
Correct Metabolic Abnormalities Maintain Euglycemia Correct documented hypoglycemia with 2 mL/kg of 25% dextrose.
Ù
Initiate GNS infusion to which potassium chloride (KCl) has been added at recommended maintenance rates after establishing urine output. Initiate maintenance fluids at two third of calculated volumes, if the etiology of cardiogenic shock is CHD, RHD, myocarditis or cardiomyopathy.
Ù
Ionized calcium level less than 0.9 mmol/L. Administer calcium gluconate (9 mg elemental calcium per mL). Dose: 1 mL/kg (100 mg/kg) diluted 1:1 with normal saline over 10 minutes. Rate of administration: 1 mL/minute, slow IV bolus under cardiac monitoring. Follow-up with 150–200 mg/kg/24 hour of calcium to maintain ionized calcium > 0.9 mmol/L.
Hypokalemia Suspect hypokalemia if large volume gastrointestinal (GI) losses complicate cardiogenic shock. Clinically hypokalemia may be suspected when brady cardia is not associated with other features of imminent ar rest. Other clues include, persistence of hypotonia despite correction of shock. 1 mL of KCl = 2 mEq/mL of potassium Up to a maximum of 40 mEq/L can be added to the maintenance fluid and infused via the peripheral IV line.
Ù
If higher concentrations of KCl need to be infused, central venous access should be the route of administration.
Metabolic Acidosis Correction of acidosis improves myocardial performance, decreases systemic and pulmonary vascular resistance and decreases the need for increased respiratory effort. A base deficit of > 10 mEq in cardiogenic shock is associated with poor outcome. ●● After intubation and ventilation, if pH < 7.2 or a base deficit of more than 6 mEq administer sodium bicar bonate IV bolus at 1–2 mEq/kg body weight (dilute in equal amount of 5% D and infuse over 30 minutes. ●● Monitor for hypernatremia and hyperosmolality.
Hypocalcemia
Drug Therapy
Suspect hypocalcemia if cardiogenic shock is associated with rachitic rosary, wide open anterior fontanel (AF), poor dentition, widening of malleolus, Harrison sulcus with or without history of seizures or stridor.
Refer to Chapter 12 on Vasoactive Medications. The effects of inotropes vary from patient-to-patient and hour-to-hour.
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Chapter 14 n Cardiogenic Shock
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Initiate the following inotropes if signs of pulmonary IP fluid : 196.52.84.10 edema are noted during resuscitation of shock. 1. Dobutamine when blood pressure is normal or high with cool shock. 2. Epinephrine preferred in cardiogenic shock presenting with hypotension, muffling of heart sounds, gallop or chronic heart failure due to structural heart disease. Therapy must be continuously tailored to patient’s re sponse. Inotropes initiated at rates greater than 10 µg/kg/ minute increases both myocardial oxygen consumption and systemic vascular resistance. When cardiogenic shock does not respond to inotropes, afterload reducing agents will improve myocardial perfor mance. Refer Chapter on Vasoactive Medications. ●● Vasodilators may be safely used with invasive moni toring. Hence, they are not employed in ED settings. ●● Combination of vasodilators and inotropes often bring about an improvement in hemodynamic status not achieved by either drug alone. ●● The vasodilators commonly used in cardiogenic shock are phosphodiesterase (PDE) III inhibitors, sodium ni troprusside and nitroglycerine. These drugs should not be used as first-line therapy to reverse shock. Factors that increase SVR such as hypothermia, acido sis, hypoxia, pain and anxiety should also be treated simul taneously. Refer Protocol 14.1.
Antibiotics If sepsis is suspected administer 3rd generation Cephalosporins (Ceftriaxone 100 mg/kg) empirically, after collecting blood and body fluids for culture. ●● If focus of sepsis is obvious, administer the first dose of appropriate antibiotics (e.g. Azithromycin, Doxycy cline for rickettsia).
Monitoring Perform the rapid cardiopulmonary cerebral assess ment frequently during vasoactive drug therapy. Bedside limited echocardiography by the emergency physician (BLEEP) accurately determines diminished car diac function, mechanical compromise of the heart and hypovolemia in the shocked patient7 (Table 14.2). It helps to assess systolic and diastolic function, cardiac output, in ferior vena cava diameter in relation with respiration8,9 and volume status. Table14.2: ECHO findings in shock End-systolic volume
End-diastolic volume
Fractional shortening or ejection fraction
Shock
Very low
Low
High
Hypovolemic shock
High
High
Low
Cardiogenic shock
Very low
Normal or high
High
Distributive shock
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Plan surgery for surgically correctable lesions.
INVESTIGATIONS 1. Chest X-ray usually reveals cardiomegaly and pulmo nary congestion. 2. Serum electrolytes, calcium, arterial blood gases (ABG), renal function test (RFT), liver function test (LFT). 3. ECG helps to recognize dysrhythmias. 4. Complete blood count, sepsis screen and serology for dengue, rickettsia, leptospirosis, typhoid etc. Body fluids and urine for culture. 5. Evaluate hormonal levels such as TSH, ACTH, PTH if deficiency is suspected.
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Key Points
ü
IP : 196.52.84.10 1. High index of suspicion needed to recognize acute cardiogenic shock following a wide variety of hypoxic insults. 2. Check list history of chronic respiratory distress to identify underlying structural heart disease. 3. Position airway and provide 100% oxygen using the flow inflating ventilation device throughout resuscitation of acute cardiogenic shock. 4. Rule out history of chronic respiratory distress to check for underlying structural heart disease. 5. Maintain airway and provide highest concentration of oxygen using the flow inflating ventilation device. 6. Perform early intubation using RSI and guarantee ventilatory support. 7. Dobutamine is the inotrope of choice in normotensive cardiogenic shock.
common errors
û
1. Failing to identify acute cardiogenic shock, in shocked children presenting with respiratory distress or failure. 2. Not check-listing for coexisting cardiac disease. 3. Mistaking acute cardiogenic shock for an asthmatic exacerbation and nebulizing with salbutamol. 4. Failure to use afterload reducing agents after stabilizing BP. 5. Using furosemide in the ED to treat pulmonary edema in children with cardiogenic shock. 6. Withholding fluids in cardiogenic shock due to sepsis. 7. Failing to establish euvolemia prior to initiating dopamine or dobutamine. 8. Failing to correct rhythm disturbances. 9. Not monitoring and managing serum potassium and calcium deficits.
Chapter 14 n Cardiogenic Shock
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Protocol Protocal 14.1: PEMC approach: Recognition and management of cardiogenic shock
IPdistress : 196.52.84.10 History of respiratory following submersion, perinatal depression, envenomation, severe sepsis, prolonged seizures, airway obstruction, toxins, cardiac diseases, etc.
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References 1. Santhanam I, et al. Implementation of Pediatric Emergency IP : 196.52.84.10 Medicine Course Guidelines (PEMC). Impact on mortal ity in critically ill children presenting to a large volume PED of an academic children’s hospital in India. Pediat Crit Care Med. 2011.(12):3 (Paper presented at the 6th Pediatric Critical Care Congress March 13th–17th 2011, Sydney. 2. Califf RM, Bengtson JR. Cardiogenic shock. N Engl J Med. 1994;330:1724-730. 3. Arques S, Ambrosi P, Gelisse R, et al. Prevalence of angio graphic coronary artery disease in patients hospitalized for acute diastolic heart failure without clinical and electrocar diographic evidence of myocardial ischemia on admission. Am J Cardiol. 2004;94:133-35. 4. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-377.
5. Fuhrman and Zimmerman. Pediatric Critical Care, 3rd edition. Lincoln Smith, Lynn Hernan Chapter 27; Shock states. 6. Nelson. Textbook of Pediatrics, 19th edition; Chapter 462 Red blood cell transfusions and erythropoietin therapy. 7. Field LC, Guldan GJ III and Finley AC, et al. Echocardiog raphy in the intensive care unit. Semin Cardiothorac Vasc Anesth. 2011;15:25. 8. Charron C, Caille V, Jardin F, et al. Echocardiographic measurement of fluid responsiveness. Curr Opin Crit Care. 2006 Jun;12(3):249-54. 9. Feissel M, Michard F, Faller JP, et al. The respiratory varia tion in inferior vena cava diameter as a guide to fluid ther apy. Intensive Care Med. 2004 Sep;30(9):1834-837. Epub 2004 Mar 25.
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Septic Shock
Figure 15.1: Focus of infection must be detected and treated along with hemodynamic interventions for complete recovery
Learning Objectives 1. Recognition of shock, pulmonary edema and cardiovascular dysfunction and non-convulsive status epilepticus in febrile children using the pediatric assessment triangle and the rapid cardiopulmonary cerebral assessment.
2. Fluid resuscitation of septic shock until clinical therapeutic goals of shock resolution are attained in a time sensitive manner. 3. Recognition and management of pulmonary edema during fluid resuscitation. 4. Modified septic shock protocol for settings with limited access to mechanical ventilation.
INTRODUCTION
PATHoPHYSIOLOGY
In India, fever and infections are the leading cause for visits to the OPD, whilst, the commonest cause of hospital mortality is serious sepsis (Figure 15.1).
Local and systemic inflammatory response occurs when microbes traverse the epithelial and tissue barriers. This response to microbial invasion is known as ‘systemic inflammatory response syndrome’ (SIRS).
Fifty percent of deaths due to serious sepsis in developing countries occurred within the first 24 hours and these deaths were a result of shock.1 This chapter describes an ED protocol that made a dramatic impact on hospital mortality in severe sepsis. Developed from the findings of a prospective randomized controlled study on fluid resuscitation of septic shock, it teaches how to resuscitate shocked children prone for pulmonary edema.2
Sepsis is diagnosed when SIRS occurs in association with suspected, proven or obvious infection.
It also teaches how the pediatric assessment triangle can be used to recognize severe sepsis.
Severe sepsis is diagnosed, when sepsis is associated with dysfunction of organs distant from the site of infection.5
Fever (> 38.5ºC) or hypothermia (< 36.5ºC), tachypnea (respiratory rates > 2 SD above normal) and tachycardia (heart rate > 2 SD above normal) are the cardinal clinical signs of SIRS. Leukocytosis, leukopenia and band count more than 10% are the other features of SIRS.3,4
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It is interesting to note that microbial invasion from the site of infection into the blood stream does not cause dysfunction of distant organs. On the contrary, microbes cause IP : 196.52.84.10 organ damage by stimulating the inflammatory cascade, leading to excessive release of inflammatory mediators in susceptible individuals. The latter causes acute lung injury in addition to dysfunction of other organs (MODS).5 Kids presenting with septic shock are very likely to have features of ALI and MODS. The International Sepsis Definitions Conference defined organ dysfunction based on the laboratory variables shown in the Table 15.1. In many low and middle income countries, laboratory facilities may not be available at the time of entry into the hospital, thereby delaying recognition and resuscitation.
Ù Respiratory distress due to ALI is characterized by features of severe sepsis and shock.5 If triage questions are positive, perform the rapid cardiopulmonary cerebral assessment to ascertain whether the child is presenting with SIRS, sepsis, or serious sepsis within the 1st minute of arrival (Figure 15.2). The pediatric assessment triangle is used to diagnose serious sepsis in children presenting with temperature > 38°C or < 36°C, suspected, proven or visually seen focus of infection (Figure 15.2).
This chapter discusses a modified guidelines to recognize severe sepsis in children presenting with fever and foci.
Ù
Triage Questions
Ask the following triage questions to mothers bringing children to the OPD with fever with or without focus of infection. 1. History of incessant cry, lethargy, more sleepy than usual, ‘not as usual’ or posturing? Which help to detect abrupt changes in mental status. 2. History of breathlessness in children presenting with altered mental status and perfusion defects? Which help to recognize pulmonary edema. Foci of sepsis outside the lung such as diarrhea, urinary tract infections, malaria in shocked children are clues to recognizing acute lung injury or cardiac dysfunction.
Figure 15.2 Physiological status: Respiratory distress or failure with tachycardia, shock with or without myocardial dysfunction, ALOC with or without NCSE.
The pathophysiology of shock in severe sepsis is multifactorial.6
Table 15.1: Definitions of SIRS and different degrees of severity of sepsis3,4 Condition
Description
SIRS
Two or more of the following conditions: temperature > 38.5°C or < 35.0°C; heart rate of > 90 beats/min; respiratory rate of > 20 breaths/min or PaCO2 of < 32 mm Hg and WBC count of > 12,000 cells/mL, < 4,000 cells/ mL or > 10% immature (band) forms
Sepsis
SIRS in response to documented infection (culture or gram stain of blood, sputum, urine, or normally sterile body fluid positive for pathogenic microorganism or focus of infection identified by visual inspection, e.g. ruptured bowel with free air or bowel contents found in abdomen at surgery, wound with purulent discharge)
Severe sepsis
Sepsis and at least one of the following signs of organ hypoperfusion or organ dysfunction: areas of mottled skin; capillary refilling of ≥ 3 s; urinary output of < 0.5 mL/kg for at least 1 hour or renal replacement therapy; lactate > 2 mmol/L; abrupt change in mental status or abnormal EEG findings; platelet count of < 100,000 cells/mL or disseminated intravascular coagulation; acute lung injury/ARDS and cardiac dysfunction (echocardiography)
Chapter 15 n Septic Shock
●● Hypovolemia : Venodilation, capillary leak. ●● Cardiogenic : Decreased myocardial contractility. ●● Obstructive : Increased pulmonary vascular resisIP : 196.52.84.10 tance. ●● Distributive : Maldistribution, hypoperfusion. ●● Cytotoxic : Cellular inability to utilize oxygen despite adequate supply.
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Case scenario A 1 month infant presented with history of fever, abdominal distension and vomiting for 1 day. She had been grunting since morning (Figures 15.3–15.21).
Principles which assist in the management Septic shock is characterized by decreased systemic vascu lar resistance (vasodilation) and increased cardiac index.7 Transient intrinsic depression of left ventricular perfor mance is also a feature of severe sepsis (cardiac function normalizes within 10 days after the onset of septic shock).7 In addition, several studies have shown clear evidence of transient intrinsic depression of left ventricular performance (cardiac function normalizes within 10 days after the onset of septic shock).8 Pulmonary hydrostatic pressure secondary to sepsis-induced cardiac dysfunction rises, driving the plasma ultrafiltrate to cross the pulmonary capillary membrane into the interstitium. Simultaneously, permeability changes in the pulmonary capillary membrane8 lead to non-cardiogenic pulmonary edema or ALI.8
Figure 15.3: Note the tense abdominal distension and bilious aspirate in this infant with shock. He is being given boluses for correction of shock on arrival into the ED, while awaiting surgical opinion.
Large volumes of fluids are needed to resuscitate chil dren with septic shock. Elevation in circulating blood vol ume and subsequent increase in intravascular pressure can worsen alveolar fluid collection and deoxygenation.9
Ù
Pulmonary edema (PE) is an inherent complication of severe sepsis. Therapy to correct shock can also aggravate PE. Despite the risk of PE, it is important to fluid resuscitate shock, in order to maximize patient outcomes. Positive end-expiratory pressure (PEEP), an important strategy in the management of acute PE, improves oxygenation by increasing mean alveolar pressure, opening collapsed alveoli and reducing repetitive opening and closure of alveoli during the respiratory cycle. Providing PEEP however, is a challenge in settings with limited access to mechanical ventilation.2 Restriction of fluids to avoid the risk of PE is lethal.10 Administration of fluids without provision of PEEP can also increase the risk of mortality in resource limited settings.11
Figure 15.4 Physiological status: Maintainable airway with effortless tachypnea, cardiogenic shock (warm shock), low mean arterial pressure (MAP: 40 mm Hg) with non-convulsive status epilepticus.
Airway and Breathing ●● Provide oxygen through the non-rebreathing mask or hood if the child with shock has effortless tachypnea. ●● Even if the airway appears maintainable on arrival, watch out for signs of deterioration. Neonates and young infants can quietly slip into apnea as shock is being resuscitated.
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●● Initiate bag-valve-mask ventilation if child presents with bradypnea. ●● During shock resucitation, consider intubation if the airway becomes unmaintainable or signs of respiratory failure, bradycardia, hypotension, unresponsiveness or signs of non-convulsive or convulsive status epilepticus are noted (Figure 15.6).
Figure 15.5: The airway is being positioned as oxygen is being provided using the non-rebreathing mask. Note that the bagvalve-mask device is available at the head end of the infant (for immediate access) in anticipation of the adverse effects of fluid administration.
●● Administer oxygen through flow inflating ventilation device (Jackson-Rees circuit), if the child has respira tory distress and shock (Figure 15.5).
Figure 15.7: This infant with cellulitis was presented with bradypnea and shock. On arrival he was ventilated using bagvalve-mask device as vascular access was being obtained.
Respiratory distress leads to a 10 fold increase in blood supply to the diaphragm.12 Diversion of blood supply away from the muscles of respiration to the vital regions could be enhanced by paralysis, sedation and mechanical ventilation. ●● Intubation should not be delayed till the child is moribund.12
Ù
Figure 15.6: This child presented with unmaintainable airway, respiratory failure, tachycardia, shock and unresponsiveness. The airway being positioned and provision of oxygen using the Jackson-Rees circuit. Note the lines drawn to mark the liver span.
Ù
When respiratory distress or failure due to acute cardiogenic shock is anticipated or being treated, the flow-inflating ventilation bag may be a more appropriate device to deliver oxygen. The Jackson-Rees or pediatric Bain circuit can be used to tide over acute pulmonary edema during fluid therapy in settings without immediate access to mechanical ventilation.
Despite lack of postresuscitation mechanical ventilatory facilities, intubation and manual ventilation offers a 50% chance of survival to children who need it, while failure to intubate would mean certain death.2
Circulation Secure two intravenous lines simultaneously on arrival. ●● If IV access is not immediately available, intraosseous (IO) line should be urgently secured. ●● Obtaining intravenous access is key to survival. ●● Remember every device you insert will breach the natural body defences your patient has against infection. ●● Protect your patient: Use skin prep and aseptic technique. ●● Protect yourself: Adopt universal precautions.
Chapter 15 n Septic Shock
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Figure 15.8: Throughout fluid resuscitation, ensure that the airway is positioned and oxygen is provided. The airway manager must be alert to the possibility of developing respiratory distress or failure secondary to pulmonary edema.
Occasionally, during ongoing resuscitation, with secure IV lines, sudden cardiovascular collapse can occur. The previously functioning IV lines tend to ‘back up’. In these children, urgent intraosseous access during resuscitation is life saving.
Hypotensive shock Hypotensive shock suggests the presence of significant myocardial dysfunction. It can progress to cardiac arrest within minutes! The following unique steps are taken during resuscitation of hypotensive shock: ●● Assign one physician exclusively for managing the airway, even if breathing or oxygen saturations look normal. ●● He should be prepared to initiate bag-mask ventilation. Due to the propensity for the child to develop cardiac arrest, the airway manager should be prepared to initiate bag-mask ventilation. ●● Call for airway tray. ●● If IV access is not available, double the dose of ketamine, atropine and succinylcholine can be administered through the intramuscular route. ●● Secure intravenous or intraosseous access urgently. ●● Administer 1st bolus using pull push technique till the blood pressure improves to the normal range.
Ù
Resuscitation of hypotensive shock needs a large team of trained rescuers.
Figure 15.9: Pull push technique needs a 3-way stopcock to help draw fluids from the reservoir and push into the patient. Coordination is needed to close the reservoir line, while pushing fluids into the patient’s line.
●● Administer small boluses of 5–10 mL/kg cautiously, with frequent assessments.
Ù
Fluids could precipitate or worsen bradycardia in the failing heart. ●● Assign one responder to initiate chest compressions during fluid resuscitation, especially when intubation is in progress (Figure 15.9). ●● Order for epinephrine infusion simultaneously and initiate at 0.3–1 µg/kg/minute. ●● Ensure that age appropriate bolus doses of epinephrine (0.1 mL/kg of 1:10,000) are available close at hand.
Figure 15.10: This infant presented with respiratory failure and hypotensive shock. The airway manager is bagging, the bolus is being given. One rescuer is poised for initiating chest compression.
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Unlike Dopamine, Dobutamine, etc. which should be initiated after establishing euvolemia, epinephrine infusion may be started along fluids. It should be on flow IP with : 196.52.84.10 during both fluid resuscitation and intubation. Even if BP normalizes, epinephrine should not be discontinued. ●● If BP increases to higher than normal range, with tachycardia, taper adrenaline infusion to minimal rates. ●● Do not stop adrenaline despite high normal range of BP in the initial hours of resuscitation of hypotensive shock.
Figure 15.11: BP normalized in this hypotensive infant. Epinephrine was tapered and continued in lower doses. Dopamine had also been initiated once BP had stabilized.
Ù
Recent hypotension suggests severe myocardial dys function and response to therapy does not mean that it has resolved completely. Management of hypotensive shock is one of the most challenging situations in the ED. Survival in hypotensive shock could be greatly improved with availability of advanced postresuscitative intensive care.
Normotensive shock2 Speed of Fluid Administration Fluids should be administered in aliquots of 20 mL/kg over 20 minutes (Level I). Administration of large volumes (60 mL/kg over 15 min)13 can result in life-threatening pulmonary edema with increased need for intubation. If the initial assessment suggests pulmonary edema or respiratory distress and shock, plan to administer small aliquots of fluid 5–10 mL/kg over 5–10 minutes.
●● If initial assessment suggests effortless tachypnea with shock, viz the increased respiratory rate is secondary to metabolic acidosis and lung parenchyma is normal, administer 20 mL/kg over 20 minutes.2
Ù
Fluid boluses should be directed towards achievement of clinical therapeutic goals of shock resolution. Discontinuing fluid therapy based on achievement of some and not all the goals could result in inadequate resuscitation.9
Following each bolus
Figure 15.12: Assessment of heart rate for 6 seconds.
Step 1 Open the airway using the head tilt-chin lift maneuver in children, who are responsive to pain or unresponsive simultaneously. Step 2 Count respiratory rates for 6 seconds and multiply by 10. i. Assess whether the respiratory rate is increased, decreased or normal for age. ●● If apnea or bradypnea is identified, rapidly initiate bag-valve-mask ventilation and the next responder assesses the heart rate. ●● If not apneic, check for grunt, retractions and pattern of breathing whilst evaluating the respiratory rate. ●● Auscultate the infra-axillary areas and listen for added sounds. ●● All three lobes of the lung are represented in the infra-axillary region, which makes it an ideal point for rapid auscultation.
Chapter 15 n Septic Shock
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Figure 15.13: This picture shows the airway being positioned and oxygen being provided using the JR circuit. The assessor is evaluating the pulses after the heart rate.
Figure 15.14: This picture shows the child being reassessed after intubation.
Step 7 ii. Count heart rate for 6 seconds and multiply by 10. Assess, whether the heart rate is increased, decreased or normal for age. While counting, evaluate for presence of gallop or whether the heart sounds are muffled (difficult to hear). ●● If bradycardic, the second responder initiates chest compression. ●● If not, continue to evaluate the peripheral perfusion, liver span and the BP. ●● Check whether the BP is normal or decreased for age. ●● Check whether the liver span has regressed to normal for age or increased. iii. Look at eye position, check for abnormal movements and evaluate the pupils for response to light. Step 3 Document the clinical variables immediately.
Check whether each individual components of the airway, breathing, circulation and disability have improved, deteriorated or remained status quo. Re-evaluate the cardiopulmonary cerebral assessment and re-establish the physiological status. Step 8 Initiate the next therapeutic intervention until therapeutic goals of shock, pulmonary edema, cardiac dysfunction and seizures are achieved.
therapeutic goals of shock resolution (Table 15.2) Table 15.2: Therapeutic goals of shock resolution2 Goals
Features
Airway
Crying, verbalization in children, who have not been intubated
Interpret the physiological status after verifying normal values for age.
Breathing
RR (normal for age), absence of grunt, retractions, normal thoracic respirations, no added sounds
Step 5
Circulation
HR (normal for age), pulses +++/++, CRT < 2, warm peripheries, pink, liver span (normal for age), BP: normal for age, with normal pulse pressure, urine output > 1mL/kg/h
Disability
Alert, normal tone and posture, eyes midposition, normal extraocular movements in children, who were not intubated. Pupils are equal and reacting to light
Step 4
Initiate appropriate intervention to the individual components of the ABCDs simultaneously. Step 6 Repeat this assessment either as soon as the therapeutic intervention is completed or after allowing time for drug to act (e.g. fluid bolus, intubation, initiating inotrope therapy or administration of an anticonvulsant).
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Airway
Peripheral Perfusion
Crying or vocalalization suggests a maintainable airIP : 196.52.84.10 way.
●● Normalization of peripheral pulses, color, capillary re fill time and core peripheral temperature gap.
●● As hypoxia and shock resolve, improvement in the cerebral perfusion results in return of mental status and stabilization of the airway. ●● Development of new cough, froth or stridor during fluid resuscitation indicates the development of pulmonary edema (see the end of Chapter for protocol when intubation triggers are noted).
During fluid resuscitation, cool septic shock often changes to warm septic shock before complete resolution. This change is heralded by warm, pink peripheries with well felt pulses and rapid capillary refill time (all signs mimic return of normal perfusion).
Breathing Normalization of respiratory rates to age appropriate ranges. ●● Restoration of normal perfusion results in resolution of metabolic acidosis and reduction of respiratory rates to the normal range. Normalization of work of breathing ●● Fluid bolus therapy can resolve grunt, retractions, abdominal respiration and crepitations. ●● Fluid therapy not only improves perfusion, but also corrects myocardial dysfunction secondary to preload deficits. ●● Resolution of acute cardiogenic pulmonary edema results in normalization of the work of breathing.
Circulation Normalization of heart rate is one of the most reliable signs of shock resolution.13
Ù
Antipyretic measures, antiseizure medications, pain relief, abscess drainage and mother’s close proximity can often help in achievement of normal range of heart rate in the appropriate clinical scenarios. ●● Heart rate, which falls within the normal range for age, in children with respiratory distress or impending respiratory failure and shock is an ominous sign. These children are at risk of profound deterioration (imminent arrest). ●● Muffling should disappear and the heart sounds should be well heard. Gallop should also resolve.
Figure 15.15: The flushed bright pink color is commonly construed as normalization of circulation. If this finding is associated with respiratory distress, tachycardia, wide pulse pressure and altered mental status as in this child, consider progression from cool shock to warm septic shock during fluid resuscitation.
●● When these parameters are noted, counter check BP and find out whether the pulse pressure is normal or wide (diastole < 50% of systole is clue to the diagnosis of vasodilatory shock).
Ù
Wide pulse pressure, in association with respiratory distress and altered mental status is suggestive of vasodilatory shock. Normalization of blood pressure with normal pulse pressure. ●● Blood pressure in young children and infants with shock is often higher than normal. As shock begins to respond to therapy, the blood pressures drops to the normal range for age. ●● Whilst the resolution of hypotensive shock is based on improvement in systolic blood pressure for age, diastolic pressure should also improve such that it is greater than 50% of systolic pressure.
Chapter 15 n Septic Shock
Ù Avoid stopping resuscitation when peripheries become IP : 196.52.84.10 warm and pink, pulses become well felt and CRT < 2 seconds. Check the other parts of the pediatric assessment triangle. If child remains in altered mental status, has respiratory distress, with or without hepatomegaly and BP is associated with wide pulse pressure, continue fluid resuscitation.
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Disability
Ù
Normalization of mental status to base line is one of the most important goals of shock resolution.
Resolution of Hepatomegaly
●● Fluid responsive shock is characterized by resolution of incessant cry, lethargy and posturing resulting in consolable cry, playfulness and normal sleep. ●● Consolable cry as a therapeutic goal of fluid responsive shock is recognized when fluid therapy and monitoring is performed with the child in his mother’s arms.
●● Normalization of liver span for age is suggestive of resolution of myocardial dysfunction.
Resolution of eye signs of non-convulsive status epilepticus.
Regression of liver span is often noted during bolus therapy, inotrope infusion and following intubation.
Urine Output ●● Urine output greater than 1 mL/kg/h in children beyond 1 year of age and greater than 1.5 mL/kg/h in infants suggests normal renal perfusion. ●● Urine output of less than 1 mL/kg/h during resuscita tion is an ominous sign of refractory shock. ●● However, it may fail to provide information, when polyuria or anuria occurs as complications of renal dis eases with septic shock.
●● It is not uncommon to encounter eye signs of non-convulsive status epilepticus on arrival or during resuscitation of hypoxia or shock due to severe sepsis. ●● Successful resuscitation of fluid responsive shock is associated with return of eyes to mid position and normal extraocular movements. ●● Examine eyes for lateral conjugate deviation, eyelid twitch and/or nystagmus following each intervention during resuscitation.
Ù
The importance of early recognition and simultaneous management of convulsive and non-convulsive status epilepticus cannot be understated in ensuring successful outcomes in septic shock. ●● Persistence of posturing after achieving therapeutic goals of shock resolution associated with abnormal patterns of respiration, bradycardia, high BP, abnormal pupillary response and defective doll’s eye movement suggest the presence of raised intracranial pressure (ICP).
Ù
Resuscitation of shock due to intracranial infections would be incomplete, if raised ICP is not simultaneously identified and treated in the initial hours of management. Figure 15.16: This picture shows catheterization for monitoring urine output in fluid unresponsive, inotrope responsive shock in settings without access to central venous pressure monitoring. This variable can occasionally be inaccurate in assessing renal perfusion pressure, when underlying renal disease exists as in this child with hematuria and pyuria.
●● Clinical signs suggestive of myocardial dysfunction or pulmonary edema on arrival or its development during fluid therapy should be anticipated. If signs of pulmonary edema (intubation triggers) (Figure 15.6) are noted during fluid therapy, further fluid administration is interrupted briefly.
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Stomach contents should be emptied rapidly, if intubation is being considered. 3. Initiate an appropriate inotrope. 4. Consider intubation.
Figure 15.17: Note the froth within the mask. On identification of this sign of PE, further fluids were interrupted, inotrope initiated and CPAP device was used to provide O2.
Inotrope/CPAP/Intubation Triggers
2
Ù
●● Provide O2 using the flow inflating ventilation device if not being used already. If the child is unable to protect the airway, unresponsive, having evidence of NSCE or convulsive SE or signs of imminent arrest consider intubation. ●● After initiating inotrope and CPAP, or inotrope and intubation, perform the rapid cardiopulmonary cerebral assessment. If signs of PE and hepatomegaly have resolved and shock persists: ●● Continue to provide CPAP via mask (non-invasively) or after intubation using the Jackson-Rees circuit throughout fluid therapy. ●● Ensure that an inotrope infusion is also on flow throughout fluid therapy.
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Development of pulmonary edema makes intubation a challenge. Froth, that is noted during the fluid resuscitation (Figure 15.9) predicts increased risk of mortality.
Figure 15.18: Signs of pulmonary edema and cardiac dysfunction.
●● Other intubation triggers: seizures not resolving with 2 doses of Benzodiazepine, features of raised ICP. During bolus therapy, if any one or a cluster of signs of deterioration, viz pulmonary edema are identified: 1. Interrupt fluid boluses briefly.
Ù
Continuation of fluid therapy when signs of PE have developed suggests the need for inotropes and provision of PEEP. Failure to do so could precipitate cardiac arrest. 2. Insert a nasogastric tube and decompress stomach contents.
Figure 15.19: Note the development of froth during fluid therapy both in the mouth and in the nasogastric tube (Courtesy: Dr Gunda Srinivas).
●● Continue smaller and slower fluid boluses until signs of shock and pulmonary edema have resolved.
Chapter 15 n Septic Shock
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Following intubation if oxygen saturations drop below IP : 196.52.84.10 92%, ‘DOPE’ should be ruled out to avoid lethal consequences. In vasodilatory shock in severe sepsis, it is not uncommon for recurrence of pulmonary edema.
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Source Control ●● Obvious foci of sepsis should be drained even as resuscitation is in progress. If focus of sepsis is inaccessible, the child is shifted to the OR at the earliest after stabilization. Avoid transferring to the ICU or ward without draining the focus of sepsis.
●● Development of froth, crepts, desaturation, gallop, muffling of heart sound, fall in mean arterial pressure, increase in liver span, suggests the development of fluid refractory, dopamine unresponsive shock. ●● Add norepinephrine infusion at the rate of 0.3 µg/kg/ minute and titrate up to 0.5 µg/kg/minute. ●● Continue smaller and slower fluid boluses until signs of shock and pulmonary edema have resolved.
Figure 15.20: Crossing limits to save lives: This infant shown above received up to 250 mL/kg during the initial 24 hours to attain therapeutic goals of shock resolution. He developed PE and cardiac dysfunction, was intubated and needed dopamine and norepinephrine before he achieved all therapeutic goals (Courtesy: Dr Gunda Srinivas).
Treatment and Prevention of Hypoglycemia ●● Correct documented hypoglycemia with 2 mL/kg of 25% dextrose. ●● Throughout resuscitation, glucose normal saline (GNS) to which potassium has been added should be infused at maintenance rates for age.
Simultaneously Evaluate for Focus of Sepsis ●● Blood and body fluids are collected for culture and a third generation cephalosporin is administered in the initial hours of resuscitation.
Figures 15.21A and B: These two pictures show incision and drainage of an abscess in progress in an infant, who has been intubated and ventilated using the pediatric Jackson-Rees circuit. He is receiving his fluids while inotrope is being infused.
Blood Transfusion Blood transfusion is planned in a semielective manner. If hemoglobin is less than 10 g/dL, transfusion can be considered after correction of shock. Septic shock complicated by other important indicators for transfusion. Fluids, inotropes or intubation should not be delayed, while waiting for blood.
Steroids Hydrocortisone (2 mg/kg) is administered intravenously for children who have been on steroid therapy in the recent
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past. It is also indicated when hypotensive shock is refractory to catecholamine infusion.
IPin: the 196.52.84.10 Drugs to be avoided management of septic cardiogenic shock: ●● Fursemide, mannitol can worsen shock and precipitate cardiac arrest. ●● Nebulized salbutamol to relieve wheeze, due to PE, can worsen hypoxia and precipitate cardiac arrest. The protocol for septic shock provides a broad guideline. Treatment should be individualized for the patient at hand. Refer Protocol 15.1 and 15.2. The physiological response of every critically ill child to resuscitative interventions is variable, unpredictable and occasionally anxiety provoking. In the initial hours of resuscitation in the ED, where radiological, biochemical evaluation and invasive monitoring are unavailable, it is imperative for the treating physician to stand by the bed side and repeatedly perform the cardiopulmonary assess ment to accurately assess trends in patient’s response and intervene appropriately. The rapid clinical assessment and intimate awareness, of the risk of PE, provides the ED physician with a 60 second advantage to change track and save life.
Key Points
ü
1. Recognize septic shock by looking for evidence of decreased mental status and peripheral perfusion in any ill looking child with fever. 2. Altered level of consciousness in a febrile child could be due to septic shock. Correction of the hypoxia and shock often improves mental status in the ED. 3. Resuscitation should be continued till all therapeutic goals of shock and pulmonary edema are resolved.
common errors
û
1. Mistaking the flushed warm peripheries in the presence of abnormal mental status, tachypnea and tachycardia in a febrile child as normal. Recognize warm septic shock. 2. Failing to note diastolic pressure. A diastolic pressure less than 50% of systole will help to recognize vasodilatory (warm) shock. 3. Diagnosing fever with altered mental status as central nervous system infection, atypical febrile fits or febrile encephalopathy. 4. Stopping fluids, if signs of pulmonary edema are identified.
Protocol 15.1: PEMC approach: Early recognition of septic shock in the out patient department
Chapter 15 n Septic Shock
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Protocol 15.2: PEMC approach: Management of septic shock Airway and Breathing
IP : O196.52.84.10 Effortless tachypnea: Provide via non-rebreathing mask 2 Respiratory distress: Provide O2 via Jackson-Rees circuit Apnea: Provide O2 via bag-valve-mask ventilation (plan early intubation using RSI*) Circulation
Establish venous access: If IV access not available → intraosseous access BP (N): Effortless tachypnea: 20 @ 20 minute from reservoir Respiratory distress: 5–10 mL/kg boluses @ 5–10 minute Low BP: Pull push 5–10 mL/kg boluses of NS/RL until BP normalizes Low BP on arrival or any step in protocol: Call for epinephrine infusion and plan early intubation Reassess for response or deterioration following each bolus (5, 10, 20 mL/kg) Broad spectrum antibiotic, collect body fluids for cultures Perform incision and drainage for source control. If focus inaccessible: Shift to OT after resuscitation Correct documented hypoglycemia: 25% dextrose 2–4 mL/kg bolus followed by GNS + KCl agedependent maintenance rates After each 5 mL/kg, 10 mL/kg, 20 mL/kg perform the rapid cardiopulmonary cerebral assessment immediately in 1 minute
Inotrope/CPAP/Intubation triggers Airway: Instability • New cough • Pink froth Breathing: Bradypnea • RR > 80/min • Grunt • New chest retractions • New onset abdominal respiration • New rales/wheeze Circulation: Bradycardia, gallop • Muffling of heart sounds • Fall in BP, low MAP • Liver span↑ Disability: Agitation, GCS < 8 • Fighting mask • SpO2 < 92% • Asking for water • ICP, refractory SE
Caution: Children with septic shock have coexisting acute lung injury and myocardial dysfunction. Fluid administration without initiation of inotrope and/or intubation when “intubation triggers are identified could be dangerous leading to cardiac arrest’’. Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the ED. Pediatr Emerg Care. 2008;24: 647-655.
Chapter 15 n Septic Shock
References 1. Robertson MA, Molyneux EM. Description of serious ill: 196.52.84.10 ness and outcome inIP patients identified using ETAT guidelines in urban, Malawi. Arch Dis Child. 2001;85:214-17. 2. Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the emergency department. Pediatr Emerg Care. 2008;24:647-55. 3. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003;31:1250-256. 4. Micha Maeder, Thomas Fehr Hans Rickli, Peter Ammann Sepsis-Associated Myocardial Dysfunction: Diagnostic and Prognostic Impact of Cardiac Troponins and Natriuret ic Peptides CHEST. 2006;129(5):1349. 1366. doi:10.1378/ chest.129.5.1349. 5. Michael A Matt Hay. Future Research Directions in Acute Lung Injury Summary of a National Heart, Lung and Blood Institute Working Group. Am J Respir Crit Care Med. 2003(167);1027-035. DOI: 10.1164/rccm.200208-966WS. 6. Phillip D. Cardiovascular management of septic shock. Critical Care Medicine. 2003;(31)3:946-55 doi: 10.1097/01. CCM.0000057403.73299.A6.
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7. Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med. 1984;100:483-90. 8. Tranbaugh, et al. Lung water changes after thermal injury the effects of crystalloid resuscitation and sepsis. Ann: Surg; 1980. 9. DG Perina. Non-cardiogenic pulmonary edema. Emerg Med Clin N Am. 2003(21):385-93. 10. Oliviera CF, et al. Time and fluid sensitive resuscitation for hemodynamic support of children with septic shock. Barriers to the implementation of the ACCM/PALS guidelines in a pediatric intensive care unit in the developing world. Pediatr Emerg Care. 2008;24:810-15. 11. Maitland K, et al. Mortality after Fluid Bolus in African Children with Severe Infection. N Engl J Med. 2011;364(26):2483-495. 12. Russel RR, Day T, Faizal MA, et al. Tracheal intubation in meningococcal disease and septic shock. Arch Dis Child. 2007;92:827. 13. Dellinger RP, Mitchell M, Carlet JM, et al. “Surviving Sepsis Guidelines Campaign: International guidelines for management of severe sepsis and septic shock: 2008”. Crit Care Med. 2008;36(1):297-320.
Approach to Recognition and Management of Dengue in the ED IP : 196.52.84.10
16
Figure 16.1: Management of severe dengue involves recognition of appropriate phase of illness, shock correction and meticulous monitoring for successful outcomes (Courtesy: Dr Thangavelu S and Dr Gunda Srinivas).
Learning Objectives 1. Method of implementation of the WHO-Dengue Guidelines: 2012 using the rapid cardiopulmonary cerebral assessment and Pediatric Assessment Triangle (PAT).
Introduction Dengue is an important cause of mortality in children. Epidemic in many parts of India, this disease is typically unpredictable in its course and progression. Key to successful management is the early recognition and early management of severe dengue (Figure 16.1). Dengue is caused by four serotypes of Dengue virus DEN-1, 2, 3, 4. The infection caused by one serotype results in serotype-specific immunity along with transient cross immunity against the other three serotypes. Following the bite of the mosquito infected with Dengue virus, clinical features appear after an incubation period of 7–10 days. Majority of infected children however, do not develop symptoms and severe dengue occurs only in a small proportion. Secondary infection, causes an antibody-dependent enhancement, wherein the pre-existing antibody to the previous serotype paradoxically enhances viral replication. This
2. Highlight use of the Jackson-Rees circuit in children with dengue presenting with respiratory distress. triggers an overwhelming host production of inflammatory mediators, cytokines and chemokines. The resulting vascular endothelial cell dysfunction and derangement of the hemocoagulation system lead to plasma leakage, shock and bleeding. 1. Leakage of plasma from the vascular compartment into interstitial compartment and third space results in hemoconcentration, hypovolemic shock and fluid overload. 2. Bleeding tendencies are secondary to many abnormalities in hemostasis. Hypoxia, acidosis, shock, low platelet count, platelet dysfunction, coagulopathy, vasculopathy and disseminated intravascular coagula tion are some of the many causes.
Clinical Presentation Dengue infection is classified into three clinically recognizable phases (over 4–10 days) namely Febrile phase, Critical phase and Recovery phase (Figure 16.2).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED
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Ù
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Figure 16.2: Time line for the dengue infection
Ù Dengue is classified based on severity (Table 16.1) 2
● Probable dengue. ● Dengue with or without warning signs. ● Severe dengue.
Recognition of Probable Dengue
Hematocrit is a simple bed-side tool to identify severity of capillary leak. Serial evaluation of hematocrit is more informative during resuscitation than serology test that confirm dengue infection. Indian children with DHF have a lower than expected rise in hematocrit during the period of leakage of plasma. This phenomena has been attributed to the high prevalence of iron deficiency anemia in the general population. Normal HCT in healthy Indian children is, 32% ± 3%. It has been proposed that the cutoff for elevated HCT is 36.3%. This value seems to identify > 80% of children with DSS in India.4
Case scenario 1 A 3-year-old girl had fever for 5 days. On the 6th day, she developed erythematous rashes all over body with flushing of palms. Since morning she has been afebrile. She has no abdominal pain or vomiting. There is no evidence of hepatomegaly, splenomegaly, ascites, bleed, edema or puffiness (Figures 16.3 and 16.4).
Clinical clues that distinguish dengue from other fevers in febrile phase are: ●● Fever without a source. ●● Flushed face. ●● History of living in a dengue-endemic area. Two helpful clinical tools which help in the early diagnosis of dengue in the febrile stage: 1. Positive tourniquet test. 2. Leukopenia: Total white blood cell count < 5,000 cell/ mm3.
Figure 16.3: Tourniquet test shows multiple petechiae (Courtesy: Dr Thangavelu S).
Confirmatory Tests NS1 antigen (positive in the first 5–7 days) and dengue IgM identified after 5–7 days are useful to confirm dengue. Viral cultures and PCR are commonly used for research purposes. Whilst their application in clinical practice is limited, the rapid NS1 antigen lab kit is currently being used for early detection in the OPD setting. High titres of NS1 antigen have been noted in the early clinical phase. By day 5, it drops to 56.5%. Possibility of diagnosis is enhanced when IgM antibody is also positive.
Figure 16.4 Physiological status: Her cardiopulmonary cerebral status is normal. She has probable dengue.
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Section V n Circulation Table 16.1: Classification of dengue severity Probable dengue
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Dengue with warning signs*
Live in/travel to dengue-endemic area ●● Abdominal pain or tenderness ●● Fever and two of the following criteria: ●● Persistent vomiting – Nausea/vomiting ●● Clinical fluid accumulation – Rash ●● Mucosal bleed – Aches and pains ●● Lethargy – Tourniquet test positive ●● Restlessness – Leukopenia ●● Liver enlargement > 2 cm – Any warning sign ●● Lab: Increase in HCT Laboratory confirmed dengue ●● Rapid decrease in platelet count (important when no signs of plasma *Requiring strict observation and medical leakage) intervention
Criteria for severe dengue (one or more of the following signs) Severe plasma leakage leading to: ●● Shock (DSS) ●● Fluid accumulation with or without respiratory distress ●● Severe bleeding ●● Severe organ impairment ●● Liver AST or ALT >1,000 ●● CNS-impaired consciousness ●● Heart and other organs
Triage: ER physician should categorize based on severity and treat appropriately.
●● This child can be managed at home. ●● Educate her parents about early warning signs and ask them to report immediately if these signs develop (Table 16.1). ●● Mother can be taught to monitor her urine output at home. ●● Administer ORS as shown in Table 16.2. ●● Avoid NSAIDs. ●● Treat fever with Paracetamol (dose 10 mg/kg). Table 16.25: ORS administration with body weight Body weight in kg
ORS (mL/kg/day)
3–10
100
10–20
75
20–30
50–60
30–60
50–60
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Parents should be instructed to identify early warning signs during defervescence (See Table 16.1). Mothers should also be taught to meticulously monitor urine output.
Management of Dengue with warning signs Case scenario 2 A 10-year-old child has been brought with the history of abdominal pain since morning. He has been having fever for the past 5 days but now the fever had settled. He has been vomiting since the morning. He had voided urine 4 hours ago. His platelet count: 70,000/mm3 and hematocrit 40% (Figure 16.5).
Figure 16.5 Physiological status: Cardiopulmonary cerebral status is normal. Since his HCT is increased and platelets are low he has dengue with warning signs.
●● Repeat the rapid cardiopulmonary cerebral assessment every hour during the critical phase. ●● Monitor urine output 4–6 hourly. ●● Repeat hematocrit after fluid therapy and 6–12 hourly thereafter.
Fluid Therapy ●● 1–2 hours: Initiate isotonic infusion (NS or RL) at the rate of 5–7 mL/kg/h. ●● 2–4 hours: Reduce rate of flow to 3–5 mL/kg/h. ●● Beyond 4 hours: Reduce rate of flow to 2–3 mL/kg/h based on the clinical response and the hematocrit.
Monitoring ●● Monitor urine output every hour. ●● Catheterize to ensure continuous monitoring. ●● Discard the first urine volume after bladder catheterization since the duration within the bladder is unknown.
Chapter 16 n Approach to Recognition and Management of Dengue in the ED
●● Ensure that urine output is about 0.5 mL/kg/hour. ●● Monitor hematocrit before and after every fluid bolus until stable and thenIPevery 4−6 hours. : 196.52.84.10 ●● The interpretation will be meaningful only if the corresponding hemodynamic state and response to fluid therapy is evaluated simultaneously. ●● Random HCT in the absence of information about the hemodynamic status or response to fluids is unlikely to be useful. ●● Check dextrostix for blood glucose (before fluid resuscitation and repeat as indicated).
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Figure 16.6: Respiratory distress with compensated shock. She also has right sided pleural effusion (Courtesy: Dr Thangavelu S).
If hematocrit remains the same or increases minimally and cardiopulmonary assessment is stable: • Continue NS at the rate of 2–3 mL/kg/h for another 2–4 hours. • Change to oral fluids once the patient tolerates oral feeds. If hematocrit increases rapidly and the cardiopul monary assessment suggests deterioration: • Increase fluids to 5–10 mL/kg/h for 1–2 hours. • Further fluid administration is based on the clinical condition and repeat hematocrit values. ●● Titrate fluids to maintain normal perfusion and urine output of 0.5 mL/kg/hour. ●● Fluids should not exceed 1.5 times maintenance.
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Ideal body weight is used for calculation of fluid infusion in obese children. ●● Intravenous fluids are required for 24–48 hours. ●● When the peripheral pulses are felt better and urine output is more than 0.5 mL/kg/h, intravenous fluids should be stopped. Administration of IV fluids for a longer period of time (especially when not needed) can precipitate fluid overload.
Severe Dengue: Compensated shock Case scenario 3 A 10-year-old girl presented with fever for 4 days. Since the morning fever has settled, but she has developed abdominal pain. She is lethargic, does not wish to stand up or walk. She has no bleeding tendency. WBC: 4,000/ mm3, HCT 43%, platelet count: 34,000/mm3.
Figure 16.7: Respiratory distress with compensated shock. She also has right sided pleural effusion. Severe dengue.
Fluid Management in Severe Dengue with Compensated Shock (Figures 16.6 to 16.8) ●● Administer supplemental oxygen through the JacksonRees circuit are non-rebreathing mask. ●● Initiate 0.9 NS 10 mL/kg over 1 hour. ●● Insert urinary catheter to monitor hourly urine output. ●● Repeat cardiopulmonary cerebral assessment. ●● Check hematocrit. Repeat cardiopulmonary cerebral assessment and hematocrit helps guide further fluid therapy. If shock is resolved fluid can be tapered. If not a repeat bolus may be needed if hematocrit is increased. ●● If hematocrit is reduced in a shocked child, consider blood transfusion. ●● If severe overt bleeding occurs, transfuse PRBC or fresh whole blood. ●● If overt bleeding is not noted, infuse colloid. ●● If no improvement after colloid, consider blood or PRBC transfusion.
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No shock and HCT is high: IP : 196.52.84.10 • Isotonic fluids should be gradually reduced to 5–7 mL/kg for 1–2 hours, then to 3–5 mL/kg for 2–4 hours and then to 2–3 mL/kg/h. Further fluid administration is based on clinical response. Fluids should be maintained for a maximum of 24–48 hours. Shock persists: • Check hematocrit after the first bolus. Hematocrit is still increased: • Repeat a second bolus of 10–20 mL/kg/hour • If shock has resolved, reduce the rate of fluids to 7–10 mL/kg/h for 1–2 hours and then reduce further as mentioned above. Hematocrit is reduced (suggests bleeding): • Transfuse 5–10 mL/kg of packed red cells or 10–20 mL/kg of fresh whole blood.
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The patient should be closely monitored. The rapid cardiopulmonary assessment should be performed every 15–30 minutes till shock is corrected and then hourly till the critical phase is over. Fluids may have to be continued for 24–48 hours. Child may go in and out of shock during the critical phase. Judicious administration of fluid is essential to prevent fluid overload. Caution: Restrict fluids such that the urine output is 0.5 mL/kg/hour. If urine output exceeds 1–2 mL/kg/hour, it indicates excessive fluid administration.
Severe Dengue: Hypotensive shock Case scenario 4 A 10-year-old child is rushed into the ER following fever for one week. The fever had settled, but since morning she had been vomiting several times and has become
Figure 16.8: Management of severe dengue with compensated shock (Source: WHO Handbook for clinical management of dengue, 2012).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED
progressively lethargic. She has edema and ascites as shown in Figure 16.9. She has bleeding from intravenous (IV) sites. Hematocrit is 45%.
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Though there is no clear advantage of colloids over crystalloids. Colloids have been shown to restore the cardiac index and reduce the level of HCT faster than crystalloids in patients with intractable shock.6,7,8 ●● Call for inotrope infusion. ●● Dopamine if BP is low normal. Epinephrine if severely hypotensive. ●● Catheterize and monitor urine output. ●● Check hematocrit before and after every fluid bolus. ●● Collect blood for grouping, crossmatching and lab investigations. Repeat rapid cardiopulmonary cerebral assessment
Figure 16.9: Note the facial ecchymoses, fresh bleed in the nasogastric tube and abdominal distension due to ascites (Courtesy: Dr Thangavelu S).
Many severe dengue children especially the older ones with hypotension may deceptively remain alert and may be ambulant. Shock may not be suspected in these children unless they are touched. The cold extremities can then be identified. A rapid cardiopulmonary cerebral assessment is mandatory in these children to detect shock (Figure 16.10).
Shock with normal blood pressure: ●● Repeat a second bolus of crystalloid or colloid 10 mL/ kg over 1 hour. ●● Gradually reduce to 5–7 mL/kg/hour for 1–2 hours, 3–5 mL/kg/h for 2–4 hours and then to 2–3 mL/kg/h or less. ●● Maintain 2–3 mL/kg/h for 24–48 hours. Hypotension not resolved: Check hematocrit. If HCT remains high after the 1st bolus: ●● Repeat another 10 mL/kg of colloid over 30 minutes to 1 hour and reassess. ●● If cardiopulmonary cerebral reassessment reveals that there is improvement, continue colloid at 7–10 mL/kg for 1–2 hours. ●● Reassess: If improvement persists, change to crystalloid infusion and gradually reduce it as mentioned above. If the HCT still remains high after the 2nd bolus and shock persists:
Figure 16.10 Physiological status: Respiratory distress with hypotensive shock and altered mental status.
Fluid Management in Severe Dengue with Hypotensive Shock (Figure 16.11) ●● Provide O2 through the Jackson-Rees circuit. ●● Initiate 0.9% NS or colloid solution 20 mL/kg, IV bolus over 15 minutes. ●● Colloids are preferred, if BP has to be restored urgently.2
●● Repeat 3rd bolus of 10 mL/kg of colloid over 1 hour. ●● Repeat the cardiopulmonary cerebral assessment. ●● If there is improvement, taper as mentioned above. If resuscitation is effective, the hematocrit level will gradually decline by approximately 10% after each dose of colloidal solution with improvement in the cardiopulmonary status. ●● If the hematocrit level declines with no sign of im provement, after the 1st, 2nd or 3rd bolus, it is likely that there may be concealed or internal bleeding.
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Figure 16.11: Management of severe dengue with hypotensive shock (Source: WHO Handbook for Clinical Management of Dengue, 2012)
●● Transfuse fresh packed red cell (5–10 mL/kg/) or whole blood (10–20 mL/kg) without delay. ●● If signs of pulmonary edema or worsening hepatomeg aly is identified during fluid therapy, initiate inotropes. ●● If overt bleed, hypotension persists and HCT is low, start colloid 10–20 mL/kg/h. If HCT remains low, and hypotension persists consider fresh blood transfusion. ●● Continuous monitoring of these patients and careful titration of fluids based on frequent CPA improves survival. ●● Children presenting with severe dengue may have associated metabolic abnormalities such as hypoglycemia, hyponatremia, hypocalcemia and acidosis. These conditions should be identified early and treated appropriately. ●● Monitor blood sugar frequently since glucose free fluids are being infused. ●● If facilities to monitor glucose are unavailable and the child is young, infuse DNS after correction of shock.
It is important to understand that the outcome in severe DSS is very poor despite heroic measures undertaken at a tertiary care center. Hence the goal is to identify the children with dengue early, when they present with warning signs.
Ù
In India DSS often coexists with shock due to sepsis of other etiologies (e.g. UTI, malaria, typhoid, scrub typhus, etc.). Differentiation between DSS and septic shock (see Protocol 16.1). Hence, larger volumes may be needed to correct shock in our setting. ●● Perform sepsis screen and prescribe appropriate antimicrobial therapy. Note: Agitation may be a sign of shock, hepatic failure, metabolic derangement, encephalopathy or cerebral edema. Sedation without correction of the underlying problems may prevent recognition of alteration in mental status (an important sign of critical illness).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED
Complications (Figure 16.12) IP : 196.52.84.10
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●● Children with impaired hepatic function are at increased risk of bleeding. ●● Avoid intramuscular injections. ●● Avoid non-steroidal anti-inflammatory agents. Management when internal bleeding is suspected:
Figure 16.12: The chest X-ray of the child shown in the figure shows right pleural effusion. Note the ET tube positioned at T-4 (Courtesy: Dr Thangavelu S).
The four most common causes of death among DSS patients: ●● ●● ●● ●●
Prolonged shock. Massive bleeding. Fluid overload. Organ disturbance: Acute encephalopathy, hepatic failure.
Ù
As first responders, it is possible that the ED physicians can play a critical role to prevent occurrence of these serious complications. Prevent patient slipping into shock by: 1. Early recognition of dengue in the febrile stage. ●● Leukopenia (WBC < 5,000) ●● Positive tourniquet test.9 2. Early detection of critical stage. ●● Rising hematocrit and decreasing platelet < 100,000. ●● Close monitoring and adjustment of fluid rate. ●● Avoid delay in switching from crystalloid to colloid solution when indicated. Consider occult bleeding in the following situations ●● ●● ●● ●● ●●
Prolonged shock that fails to respond to 40–60 mL/kg. Persistent shock despite reduction of hematocrit level. Unexplained tachycardia. Decline in hematrocrit is greater than expected. Hypotensive shock with low/normal HCT before fluid resuscitation. ●● Persistent or worsening metabolic acidosis in children with severe abdominal tenderness and distension.
●● Send blood for cross matching if epistaxis, hematemesis or melena is noted. ●● Do not wait until the hematocrit drops to 30% (cut-off for transfusion in children with septic shock). Higher hematocrits are expected in children with DSS. ●● Do not hesitate to provide fresh blood transfusion when there is worsening of clinical signs and symptoms and fall in hemotocrit level during the critical stage.
Ù
It is well documented that adequate shock correction is the best way to prevent hemorrhage. ●● Administer vitamin K. ●● Do not call for platelet concentrate infusion. ●● Transfuse 10–20 mL/kg of fresh whole blood. Fresh blood is rich in 2,3 DPG that will correct hypoxia and acidosis.
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Persistent hypoxia and shock are believed to be the cause for bleeding. ●● Avoid platelet concentrates to treat thrombocytopenia. ●● Prophylactic platelet transfusions for severe thrombocy topenia in hemodynamically stable patients are not effective and are not indicated.10 ●● Platelets have a short half-life and are at increased risk of destruction during dengue infection. ●● Avoid routine administration of fresh frozen plasma. These blood products may contribute to fluid overload.
Fluid Overload (Figures 16.13 to 16.15) ED physicians must be aware of common pitfalls during management that may lead to fluid overload: Leading cause of death in children with severe dengue is fluid overload. This may result in pulmonary edema, chest wall edema and abdominal compartment syndrome. All these conditions can lead to respiratory embarrassment and hemodynamic instability. Fluid overload can occur in both the critical and recovery phase leading to therapeutic dilemmas viz respiratory distress and shock. In this scenario, management of one problem can worsen the other.
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Section V n Circulation
IP : 196.52.84.10
●● Large pleural effusions and tense ascites. ●● Chest X-ray and USG abdomen in the ER will supplement the clinical impression.
Figure 16.13: Purpura due to severe dengue (Courtesy: Dr Thangavelu S).
●● Prolonged administration of IV fluid administration (> 48 hour). ●● Higher rate of IV fluid than those recommended in the guidelines. ●● Use of hypotonic solutions. ●● Inappropriate timing of IV fluid administration, e.g. starting IV fluid too early during the febrile stage be fore plasma leakage occurs. ●● Delay in the use of colloids when indicated. ●● Using actual weight when calculating the total fluid rather than ideal body weight for obese children. ●● Not accounting for IV fluid received as prehospital therapy.
Figure 16.14: Chest X-ray taken prior to fluid therapy in a child who presented in shock (Courtesy: Dr Thangavelu S).
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Management of DSS is based on correct replacement of fluid loss occurring due to capillary leak. Too much fluids will lead to fluid overload and too little will not improve shock. Besides, the quantity of leak can change every hour during the critical phase. Repeated assessment of perfusion and urine output with replacement of fluids is key to survival. Paramedics and nurses must be trained to collect data on input/output to guide therapy.
Clinical Clues to Detect Fluid Overload It may be difficult to differentiate ‘fluid overload’ and ‘shock’ in critically ill patients who have been referred from other hospitals after fluid therapy. The following clinical clues may be helpful to the ED physicians to detect fluid overload: ●● > 2 mL/kg/hour urine output in the absence of glycosuria or furosemide. ●● Weight gain, raising respiratory rate, respiratory distress with falling SpO2 requiring oxygen to maintain saturation.
Figure 16.15: Chest X-ray taken the following day shows signs of fluid overload (Courtesy: Dr Thangavelu S).
Management of Fluid Overload The management varies based on the phase of illness and the child’s hemodynamic status. ●● Recovery phase and cardiopulmonary status stable: – Stop intravenous fluids: Most children will void and improve spontaneously. – Provide O2 and CPAP using the Jackson-Rees circuit: CPAP helps to resolve respiratory distress due to pulmonary congestion. – Oral or IV furosemide 0.5–1.0 mg/kg/dose once or twice daily or a continuous infusion of furosemide at 0.1 mg/kg/h: Prior to diuretics ensure that there had been no shock in the preceding 12–24 hours. – Monitor serum potassium.
Chapter 16 n Approach to Recognition and Management of Dengue in the ED
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●● Critical phase but not in shock
Other Complications
●● Hyperglycemia and hypoglycemia. ●● Electrolyte disturbances such as hyponatremia, hypokalemia, hyperkalemia, hypocalcemia and metabolic acidosis. ●● Malaria, leptospirosis, enteric fever or scrub typhus can complicate the clinical presentation and management.
– Provide O2 and CPAP using the Jackson-Rees circuit to resolve pulmonary congestion. IP : 196.52.84.10 – Reduce the IV fluids accordingly. – Monitor closely using the rapid cardiopulmonary cerebral assessment and urine output. – Avoid furosemide in the plasma leakage phase since it may lead to intravascular volume depletion.
●● Critical phase and shock – It is very difficult to balance the IV fluid treatment in DSS patients who are still in shock with fluid overload. If the amount of fluid administered is not adequate, the patient will experience prolonged shock, if the amount of fluid is too much, the patient can develop pulmonary edema. – Provide O2 and CPAP using the Jackson-Rees circuit to resolve pulmonary congestion. – The following IV fluid management techniques may be helpful in the ER. ●● Low or normal HCT with signs of fluid overload and shock – Provide Oxygen via the Jackson-Rees circuit. – Transfuse fresh whole blood for occult hemorrhage. ●● High HCT with signs of fluid overload and shock – Provide oxygen via the Jackson-Rees circuit. – Administer small boluses of colloids.
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Avoid furosemide in children with shock and pulmonary edema.
Severe dengue patients may have severe organ impairment such as acute liver failure, encephalopathy, renal failure. Cardiomyopathy, myocarditis and dengue encephalitis have also been reported. Other atypical manifestations in dengue are acalculous cholecystitis, acute pancreatitis, hemolytic uremic syndrome, ARDS, myositis with raised serum creatine phosphokinase, rhabdomyolysis, infection associated hemophagocytic syndrome and macular hemorrhage.11 Criteria for discharge: All of the following must be present2 Clinical: ●● No fever for 48 hours. Improvement in clinical status: ●● ●● ●● ●● ●●
General well-being. Good appetite. No respiratory distress. Normal hemodynamic status. Normal urine output.
Laboratory: ●● Increasing trend of platelets. ●● Normal hematocrit.
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Section V n Circulation
Key Points
ü
1. Repeated rapid IP cardiopulmonary and cerebral : 196.52.84.10 assessment in conjunction with hematological and urine output monitoring during defervescence helps identify the critical phase. 2. Early diagnosis of dengue with warning signs and appropriate fluid administration at this stage prevents the child from developing shock. 3. Fluid administration is only needed for 24–48 hours in the leak phase. 4. Judicious fluid therapy prevents fluid overload, (dreaded complication). 5. Adequate shock correction is the best method to prevent bleeding 6. Prophylactic platelet transfusion has very little role in the management of hemodynamically stable dengue patients.
common errors
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1. Not reducing the rate of fluid administration after shock correction leads to increase in ascites, pleural effusion and pulmonary edema. 2. Giving furosemide to a child who is hemodynamically unstable can be catastrophic. 3. Not changing the fluid to colloids, when there is no response to initial crystalloid boluses and the hematocrit remains high. 4. Not giving fresh blood to a child, who remains hemo dynamically unstable with a normal hematocrit. 5. Blood transfusion in the convalescent phase for low hematocrit (dilutional). 6. Under estimating shock based on normal conscious level, systolic BP and pulse oximetry (SpO2 95%– 100%).
Protocol 16.1: Differentiation of dengue shock and septic shock
* Usually occurs in defervescence period, hence probe for h/o fever in the recent past . * Shock can recur after correction in the ER, hence warrants close monitoring in wards.
“Men and microbes fight each other for supremacy and survival. Microbes were in existence even before the human race. They may survive even beyond...”
Chapter 16 n Approach to Recognition and Management of Dengue in the ED
References 1. WHO, dengue hemorrhagic fever: Diagnosis, treatment IP :2nd 196.52.84.10 prevention and control. edition. Geneva:World Health Organization;1997. 2. World Health Organizationand the Special Programme for Research and Training in Tropical Diseases.Dengue guideline for diagnosis, treatment, prevention and control. New edition 2009. 3. Kalayanarooj S, et al. Early clinical and laboratory indication of acute dengue illness. Journal of infectious disease. 1997;176:313-21. 4. Gomber S, Ramachandran VG, Satish Kumar, et al. Hematological observations as diagnostic markers in dengue hemorhagic fever-a reappraisal. Indian Pediatrics. 2001;38(5):477-81. 5. 2010 interim guidelines on fluid management of dengue Fever and Dengue Hemorrhagic Fever. 6. Dung NM, Day NP, Tam DT. Fluid replacement in dengue shock syndrome: a randomized double-blind comparison
7.
8.
9. 10.
11. 12.
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of four intravenous fluid regimens. Clinical Infectious Diseases.1999;29:787-94. Nhan NT, Phuong CXT, Kneen R, et al. Acute management of dengue shock syndrome a randomized doubleblind comparison of 4 intravenous fluid regimens in the first hour. Clinical Infectious Diseases.2001;32:204-13. Wills BA, Dung NM, Loan HT, et al. Comparison of three fluid regimens for resuscitation in dengue shock syndrome. N Eng J Med. 2005;353:877-99. Bunnag T. Accuracy in diagnosis of DHF at observation room, dengue corner. Thai pediatric journal. 2001:8(2). Lum L, et al. Preventive transfusion in dengue shock syndrome-is it necessary? Journal of Pediatrics. 2003;143:68284. Gulati S, Maheswari A. Atypical manifestations of dengue. Trop Med Int Health. 2007;12(9):1087-095. Handbook for clinical management of dengue-WHO 2012.
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IP : 196.52.84.10
Anaphylaxis
Figure 17.1: Rapid deterioration can occur in minutes if intervention is not immediate (Courtesy: Dr Radhika, Dr Gunda Srinivas).
Learning Objectives 1. Defining anaphylactic shock. 2. Pathophysiology of anaphylaxis.
Introduction Anaphylaxis is an acute clinical syndrome caused by exposure to a foreign substance to which the patient has been previously sensitized.1 It is defined as a severe, life-threatening, generalized or systemic hypersensitivity reaction.2
PATHOPHYSIOLOGY Anaphylaxis is a type 1 hypersensitivity reaction mediated by immunoglobulin E (IgE) and IgG4 subclass of antibodies. A complement-mediated hypersensitivity reaction occurs in allergic response to blood products. Anaphylaxis occurs sec ondary to release of chemical mediators from the mast cells. The exogenous antigen binds to the immunoglobulin located on the mast cell. This results in degranulation and release of mediators such as histamines, bradykinin, leukotrienes, prostaglandins and thromboxanes. The latter cause various effects on the skin, mucosa, lining of the respiratory tract, blood vessels and the heart. Refer Figure 17.1.
3. Using the pediatric assessment triangle to recognize anaphylactic shock. 4. Evidence-based management of anaphylactic shock. 1. Sudden and severe vasodilation contributes to relative hypovolemia, whereas increased vascular permeability results in absolute hypovolemia. The resultant profound loss of effective circulating volume leads to sudden circulatory failure and hypotension. Cardiovascular collapse is the commonest prearrest manifestation. 2. Edema of the airway results in lethal airway obstruction (stridor) and bronchospasm (respiratory distress with wheeze). 3. Other symptoms include itching, urticaria, sneezing, conjunctivitis, abdominal pain, vomiting and diarrhea. Angioedema manifests as edema of the face, eyes, tongue and larynx. The commonest triggers are, nuts, paralytic agents (suxamethonium, vecuronium and atracurium), antibiotics (commonest being, penicillin, cephalosporin, amphoteri cin, ciprofloxacin and vancomycin), non-steroidal antiinflammatory drugs (NSAIDs) and Aspirin. Other culprits are insect stings, contrast media, blood and blood products,
Chapter 17 n Anaphylaxis
vaccines, food additives and latex. Exercise, especially after ingestion of certain foods has also been known to cause anaphylactic reactions.IP : 196.52.84.10
CASE SCENARIO A 2-year-old child was rushed into the ED, after he developed sudden unresponsiveness. He had been given Brufen syrup by a practitioner in a nearby clinic for fever (Figure 17.2).
171
Ù
Less severe systemic allergic reactions such as urticaria, angioedema or rhinitis should not be described as an anaphylactic reaction, when compromise of the ABCs leading to life-threatening complications are not present.
Time of Onset of Anaphylactic Reactions ●● Fatal food reactions cause respiratory arrest after 30– 35 minutes. ●● Insect stings cause collapse from shock in 10–15 minutes. ●● Death caused by intravenous medication occur within 5 minutes. Note: Death has not been documented beyond 6 hours after contact with the trigger.3
Airway and Breathing
Figure 17.2 Physiological status: Angioedema of the upper airway, respiratory distress with bronchospasm, bradycardia, hypotensive shock.
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Anaphylaxis is likely when all of the following three criteria are met2: • Sudden onset and rapid progression of symptoms. • Life-threatening airway and/or breathing and/or circulation (ABC) problems. • Skin and/or mucosal changes (flushing, urticaria, angioedema). Exposure to a known allergen for the patient supports the diagnosis. Skin or mucosal changes alone do not constitute as sign of an anaphylactic reaction. Sometimes, skin and mucosal changes can be subtle or even absent in up to 20% of reactions, where isolated hypotension may be the sole sign of anaphylaxis. Occasionally, gastrointestinal symptoms such as vomiting, abdominal pain, incontinence have also been noted.2
●● Provide oxygen using a non-rebreathing mask. ●● Intubate if labial, lingual swelling, hoarseness or stridor is noted. Intubation is performed early (rapid, progressive edema can obscure all landmarks, making even bag-valve-mask ventilation difficult).1 Urgent PAI technique is the method of choice for securing the airway.
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Complete airway obstruction with distortion of anatomical landmarks is the worst scenario encountered by the airway manager in the ED. ●● Paralytic agents should be avoided.1 This precaution is taken to permit spontaneous breathing efforts to ensure ventilation, lest intubation is impossible due to inability to intubate. ●● Tracheal tubes smaller than calculated for age should also be available. Fiberoptic intubation, blind digital tracheal intubation, needle cricothyrotomy followed by transtracheal ventilation have been described in securing the airway when conventional methods have failed.
Circulation 1. Secure vascular access and administer isotonic fluid boluses as much as 60–200 mL/kg of isotonic fluids
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Section V n Circulation
may be needed to restore peripheral perfusion and blood pressure. 2. Perform the rapidIP cardiopulmonary cerebral assess: 196.52.84.10 ment following each bolus to determine, whether the child is showing signs of improvement, deterioration or is remaining status quo.
Epinephrine Administer Epinephrine Adrenaline is the drug of choice in anaphylaxis. An α-receptor agonist, it reverses peripheral vasodilation and reduces edema. Its β-receptor activity dilates the bronchial airways, increases the force of myocardial contraction and suppresses histamine and leukotriene release. Adrenaline also acts on the β2-adrenergic receptors on mast cells4 and inhibit activation.5 Hence, early use of adrenaline attenuates the severity of IgE-mediated allergic reactions. Adrenaline seems to work best when given early after the onset of the reaction.6 Administer epinephrine deep IM or IV (if intravenous ac cess is available): Epinephrine is administered at 0.1 mg/ kg per dose (1:1,000) intramuscularly at 5 minute intervals based on patient’s response.
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Dose of epinephrine: 12 years: 500 µg IM (0.5 mL), i.e. same as adult dose. If child is small or prepubertal: 300 µg (0.3 mL). 6–12 years: 300 µg IM (0.3 mL). 6 months–6 years: 150 µg IM (0.15 mL). < 6 months: 150 µg IM (0.15 mL). ●● Subcutaneous or inhaled routes for adrenaline are not recommended for the treatment of an anaphylactic re action because absorption is inadequate.7,8,9 ●● Stridor or airway swelling, respiratory distress and or shock: Administer epinephrine intravenously. The recommended IV dose is 0.5 mL/kg (1:10,000 dilution). ●● The strength of 1:1000, should not be administered intravenously without dilution. ●● If bradycardia or hypotensive shock occurs, initiate epinephrine infusion at 1–4 µg/kg/minute. Though arrhythmias are uncommon in children with anaphylaxis, cardiac rhythm should be monitored.
Antihistamines10 H1-antihistamine helps to counter histamine-mediated vasodilation and bronchoconstriction.
Administer chlorpheniramine maleate intramuscularly or slowly through the intravenous route.
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Dose of Chlorpheniramine maleate: > 12 years and adults: 10 mg IM or IV slowly. 6–12 years: 5 mg IM or IV slowly. 6 months–6 years: 2.5 mg IM or IV slowly. < 6 months: 250 µg/kg IM or IV slowly.
Steroids2 Steroids may reduce the duration of illness. Little evidence is available on the optimal dosing for corticosteroids. The resuscitation council of UK suggest the following dosing schedule:
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Dose of hydrocortisone: > 12 years and adults: 200 mg IM or IV slowly. 6–12 years: 100 mg IM or IV slowly. 6 months–6 years: 50 mg IM or IV slowly. < 6 months: 25 mg IM or IV slowly. There is no data to support the use of H2 receptor blocker in the acute resuscitation of a child with anaphylactic shock.11
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Prolonged CPR is advised in anaphylactic cardiac ar rest since the underlying heart and lungs are normal.
PREHOSPITAL CARE 1. Advice patients with airway obstruction or respiratory distress to adopt a position of airway comfort. 2. If the victim is feeling faint or unable to sit or stand, advise him to lie down. 3. Hypotensive patients could rapidly progress to cardiac arrest, if they are in the upright position.12 4. Place unresponsive children, who are breathing in the recovery position on their side.
ELIMINATION OF TRIGGER 1. Discontinuation of drug suspected of causing an anaphylactic reaction (e.g. stop intravenous infusion of a gelatin solution or antibiotic). 2. Early removal of stinger after a bee sting13 and application of ice at the site of sting may slow antigen absorption.
Chapter 17 n Anaphylaxis
3. After food-induced anaphylaxis, attempts to make the patient vomit are not useful and hence not recommended. IP : 196.52.84.10 4. Observation for 24 hours is recommended, since symptoms could recur within 1–8 hours in 20% of patients.
Key Points
ü
1. Early recognition and anticipation of deterioration in anaphylaxis crucial to survival. 2. IM epinephrine is life saving. 3. Early intubation, aggressive fluid resuscitation and epinephrine in appropriate doses and routes mandatory in hypotensive shock due to anaphylaxis. 4. Aggressive CPR recommended even if cardiac arrest supervenes.
common errors
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1. Delayed administration of epinephrine. 2. Failure to give deep IM epinephrine. 3. Initiating dopamine for anaphylactic shock.
REFERENCES 1. Anaphylaxis, Circulation, Journal of the American Heart Association. 2005;IV 143-IV 145. 2. Johansson SG, Bieber T, Dahl R, et al. Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003. J Allergy Clin Immunol. 2004;113(5):832-36.
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3. Pumphrey RS. Lessons for management of anaphylaxis from a study of fatal reactions. Clin Exp Allergy. 2000;30(8):1144-50. 4. Kay LJ, Peachell PT. Mast cell beta2-adrenoceptors. Chem Immunol Allergy. 005;87:145-53. 5. Chong LK, Morice AH, Yeo WW, et al. Functional desensitization of beta agonist responses in human lung mast cells. Am J Respir Cell Mol Biol. 1995;13(5):540-46. 6. Bautista E, Simons FE, Simons KJ, et al. Epinephrine fails to hasten hemodynamic recovery in fully developed canine anaphylactic shock. Int Arch Allergy Immunol. 2002;128(2):151-64. 7. Simons FE, Gu X, Simons KJ. Epinephrine absorption in adults: intramuscular versus subcutaneous injection. J Allergy Clin Immunol. 2001;108(5):871-73. 8. Song TT, Nelson MR, Chang JH. Adequacy of the epinephrine autoinjector needle length in delivering epinephrine to the intramuscular tissues. Ann Allergy Asthma Immunol. 2005;94(5):539-42. 9. Simons FE, Roberts JR, Gu X, et al. Epinephrine absorption in children with a history of anaphylaxis. J Allergy Clin Immunol. 1998;101(1 1):33-37. 10. Simons FE, Gu X, Johnston LM, et al. Can epinephrine inhalations be substituted for epinephrine injection in children at risk for systemic anaphylaxis? Pediatrics. 2000;106(5):1040-44. 11. Sheikh A, Ten Broek V, Brown SG, et al. H(1)-antihistamines for the treatment of anaphylaxis: Cochrane systematic review. Allergy. 2007;62(8):830-37. 12. Lin RY, Curry A, Pesola GR, et al. Improved outcomes in patients with acute allergic syndromes who are treated with combined H1 and H2 antagonists. Ann Emerg Med. 2000;36(5):462-8. 13. Visscher PK, Vetter RS, Camazine S. Removing bee stings. Lancet. 1996;348(9023):301-02.
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IP : 196.52.84.10
Cyanotic Spell
Figure 18.1: Simple knee-chest position plays an important role in the management of cyanotic spell
Learning Objectives 1. Pathophysiology of cyanotic spell. 2. Using the rapid cardiopulmonary assessment and the pediatric assessment triangle to identify severity of spell.
INTRODUCTION Cyanotic spell is also known as hypercyanotic spell, ‘TET’ spell, hypoxic spell, paroxysmal hyperpnea, anoxic spell and blue spell. Approximately, one fourth of children with cyanotic congenital heart diseases develop this medical emergency (Figure 18.1). Though common in tetralogy of fallot (TOF), it is also encountered in other cyanotic congenital heart diseases with decreased pulmonary blood flow (PBF) such as tricuspid atresia with restrictive VSD and VSD with severe valvular pulmonic stenosis.
3. Management of cyanotic spell in the ED.
out flow obstruction is absent during the spell due to reduced antegrade flow across the muscular obstruction. Children become severely cyanotic, tachypneic and lethargic. With the development of metabolic acidosis, pulmonary vascular resistance increases and systemic vascular resistance falls. Cardiac output becomes compromised due to myocardial ischemia. Impending collapse and death can ensue. Children with iron deficiency anemia have a predisposition to the oc currence of cyanotic spells.
PATHOPHYSIOLOGY The hypercyanotic spell1,2 is characterized by a sudden and striking decrease in the oxygen saturation (Figures 18.2 and 18.3) due to acute and complete or near complete obstruction of the subpulmonary outflow tract. Agitation and decreased hydration can exacerbate dynamic infundibular obstruction. Ejection systolic murmur produced by the right ventricular
Figure 18.2: Pathophysiology of cyanotic spell
Chapter 18 n Cyanotic Spell
175
CASE SCENARIO 1 IP : 196.52.84.10
A 3-month-old infant is brought with history of incessant cry, breathlessness and increasing cyanosis. He is being evaluated for cyanotic congenital heart disease at the cardiology department (Figures 18.4 and 18.5).
Figure 18.3: Note the severe cyanosis in this infant who is receiving 100% oxygen via the flow inflating bag. The knee-chest position is being maintained throughout resuscitation.
Clinical Features Cyanotic spells typically occur in the morning, following crying, feeding and defecation (Box 18.1). Spells are characterized by paroxysm of:
Figure 18.4: Note that one team member is dedicated to holding the knee-chest position during resuscitation of cyanotic spell. Also note that the airway is kept open and oxygen is being administered.
●● Hyperpnea (rapid and deep respiration), irritability, prolonged or inconsolable crying. ●● Diaphoresis. ●● Increasing cyanosis. ●● Decreasing intensity or disappearance of the heart murmur. ●● A severe spell may lead to syncope, limpness, convul sions, cerebrovascular accidents and even death. ●● In the early stages, an older child may spontaneously assume the squatting (or knee-chest) position in order to alleviate symptoms. Box 18.1: Precipitating factors of cyanotic spell Crying Defecation Increased physical activity Dehydration Anemia Anxiety Fever Pain
Age ●● 1 month–12 years (peaking between 2–4 months).
Duration of the Spell ●● This may vary from minutes to several hours.
Figure 18.5 Physiological status: Maintainable airway, effortless tachypnea, normotensive shock with no evidence of cardiac failure, with altered mental status.
Management Treatment is focused on decreasing pulmonary resistance and increasing systemic vascular resistance. This would promote left to right flow across the ventricular septal de fect and subsequently into the subpulmonary outlet.
Prehospital Management3
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Teach parents with a child prone to cyanotic spells to place him in knee-chest position.
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Section V n Circulation
This maneuver increases systemic vascular resis tance and promotes systemic venous return to the right heart. This will theoretically increase intracardiac shunt IP : 196.52.84.10 ing from left-to-right across the interventricular com munication, as well as increase the preload of the right ventricle. ●● Stabilize the airway with the head tilt-chin lift maneu ver. Provide oxygen using the flow inflating ventilation device (reduce risk of pulmonary edema during shock correction). ●● Oxygen decreases peripheral pulmonary vasoconstric tion and improves oxygenation once flow of blood to the lungs is re-established. ●● Intubation may be needed, if the cyanotic spell is re fractory to management. ●● Place the child in a knee-chest position throughout re suscitation in order to trap venous return in the legs thus increasing the SVR (Figure 18.4). ●● Secure intravenous access to administer fluids. ●● Fluids will improve right ventricular preload. ●● If shock is noted, administer 2.5–5 mL/kg NS up to a maximum of 20 mL/kg at the rate of 1 mL/kg/min ute, whilst monitoring for signs of PE as per the PEMC guidelines. ●● Administer Morphine at a dose of 0.1–0.2 mg/kg/dose intravenously or subcutaneously. It decreases release of catecholamines. It also increases the time for right ven tricular filling by decreasing the heart rate and promoting relaxation of infundibular spasm. ●● Administer sodium bicarbonate 1 mEq/kg IV slowly after dilution (1:1) at the rate of 1 mL/kg/minute. Sub sequent doses are infused based on pH.
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Ensure adequate oxygenation and ventilation before administering sodium bicarbonate. Most of the cyanotic spells respond to the above mea sures. If not, the following medications are given:
Beta Blockers Propranolol is infused in a dose of 0.05–0.2 mg/kg/dose IV over 4–5 minutes.
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It is not given in the neonate since it may cause severe cardiac depression.
Its mechanism of action is not clear. It probably acts by reducing spasm of the right ventricular outflow tract and slowing the heart rate. Esmolol, an ultrashort acting beta blocker is an alter native to propranolol. This is administered as a bolus of 0.5–1.0 mg/kg IV, followed by an infusion of 100–300 µg/ kg/min.
Vasoconstrictors Phenylephrine infusion increases SVR, thereby reducing the right-to-left shunt. Dose: 3 mg/kg is diluted in 50 mL NS and infused at 1 mL/kg/h to provide 1 μg/kg/min. The infusion may be increased up to 5 μg/kg/min until oxygen saturations improve. Emergency surgery to repair the defect or to establish systemic to pulmonary artery anastomosis should be con sidered in refractory spells.
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Avoid the use of digoxin and epinephrine as these drugs may exacerbate the obstruction to right ventricular outflow and cause further deterioration.
Prevention ●● Chronic oral therapy with propranolol 1–2 mg/kg/dose q 6 h has been shown to decrease the frequency of the paroxysm. Propranolol stabilizes vascular reactivity of the systemic arteries thereby preventing a sudden decrease in SVR. However, this is discouraged in the newborn, since it may cause severe cardiac depression. ●● Prophylactic iron therapy is useful to prevent recur rence of cyanotic spell. ●● Palliative shunt procedure is performed in children with severe TOF for whom total correction may not be possible. ●● Refer for early corrective surgery. Early identification has become possible due to wide spread availability of pediatric cardiothoracic surgical facilities.
CYANOTIC SPELL WITH CARDIOGENIC SHOCK It is not uncommon for very young infants with com plex cyanotic heart diseases to have increased pulmonary blood flow. These infants present with cyanotic spell with
Chapter 18 n Cyanotic Spell
cardiogenic shock. Recognition of this condition is im portant since the outcomes may not be as favorable as in simple ‘tet spell’. Increased blood flow can pre IP : pulmonary 196.52.84.10 cipitate cardiac failure. The latter manifests as increasing cyanosis, respiratory distress, shock with hepatomegaly. Bedside echocardiography will help in finding out the ex act cardiac malformation.
TREATMENT Management is similar to cyanotic spell. However, smaller aliquots of fluid should be administered due to enhanced risk of pulmonary edema (unlike TOF). Jackson-Rees cir cuit is very helpful in the management of such children with associated pulmonary edema as explained in Chapter 5. Inotropes and early intubation can tide over the crisis, but immediate surgical palliation will be needed for suc cessful outcomes. Refer Protocol 18.1.
Key Points
177
ü
1. Maintenance of knee-chest position throughout resuscitation is key to successful outcome. 2. Baseline pulse oximeter readings will suggest severe hypoxia. 3. Cyanotic spell secondary to uncomplicated TOF usually resolves with emergency resuscitation. 4. Cyanotic spell due to complex cyanotic heart disease coexists with cardiac failure.
common errors
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1. Administration of digoxin. 2. Expecting normalization of saturations. 3. Failure to resuscitate severe cyanotic spell presenting in cardiac arrest aggressively. Many will respond very well to resuscitation.
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Section V n Circulation
References
Protocol 18.1: PEMC approach: Cyanotic congenital heart disease
IP : 196.52.84.10
1. Roekens CN, Zuckerber AL. Emergency management of hypercyanotic crises in tetralogy of Fallot. Annals of Emergency Medicine. 1995;25(2):256-58. 2. Kothari SS. Mechanism of cyanotic spells in tetralogy of Fallot-the missing link? International Journal of Car diology. 1992;37(1):1-5. 3. Bailliard F, Anderson RH. Review Tetralogy of Fallot Orphanet Journal of Rare Diseases 2009, 4:2 doi:10.1186/1750-1172-4-2.
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IP : 196.52.84.10
Hypertensive Emergencies
Figure 19.1: Hypertension in children can present as an emergency with significant morbidity (Courtesy: Dr Radhika R; Dr Devi R)
Learning Objectives 1. Defining hypertensive emergency and urgency. 2. Using the pediatric assessment triangle to identify severity of illness in a child with severe hypertension.
3. Antihypertensive drugs used in the management of hypertensive emergency.
INTRODUCTION High blood pressure is often noted in seriously ill children on arrival into the ED. It occurs as a compensatory re sponse to shock. Occasionally, hypertension is responsible for cardiac failure, seizures and visual loss! Drugs to reduce BP in shocked children can kill. On the contrary, failure to reduce BP in primary hypertension could also be dangerous (Figure 19.1). Recognition and appropriate approach is essential to tide over the crisis of hypertension. Literature suggests that the prevalence of hypertension in the pediatric population is estimated at 1%–2%. Though uncommon in children, the emergency physician may en counter hypertensive emergencies in the ED. The second task force on BP control in children defined hypertension as systolic and or diastolic BP persistently above the 95th percentile (Table 19.1).
Table 19.1: Cut off levels for hypertension by age1 Age
Severe hypertension
Hypertensive crisis
Neonate 1 week
SBP > 106 mm Hg
2–4 week
SBP > 110 mm Hg
Infant < 2 year
> 118/82
145/95
3–5 year
> 124/84
150/95
6–9 year
> 130/86
160/100
10–12 year
> 134/90
165/105
13–15 year
> 144/92
175/110
16–18 year
> 150/98
185/120
(Data from report of the 2nd Task Force on BP Control in Children – 1987Pediatrics 1987;79:1-25 and Burg Fb, Ingelfinger JR, Wald ER. Current Pediatric Therapy. Philadelphia: WB Saunders. 1993;14:158-64)
Severe Hypertension BP above the 99th percentile for age and sex.
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Hypertensive Emergency It describes a situation in which, elevated BP is associated IP : 196.52.84.10 with evidence of secondary organ damage such as hyper tensive encephalopathy or acute left ventricular failure.
Hypertensive Urgency The elevated BP is potentially harmful, but lacks evidence of end-organ damage or dysfunction.
Malignant Hypertension Malignant hypertension is characterized by marked eleva tion in systolic and/or diastolic BP. ●● ≥ 160/ ≥ 105 in children < 10 years. ●● ≥ 170/ ≥ 110 in children > 10 years. It is often associated with spasm and tortuosity of the retinal arteries, papilledema, hemorrhages and exudates. Some patients may have an acute onset and severe el evation of BP. They experience severe headache, altered sensorium, seizures and visual disturbances. MRI and CT shows evidence of vasogenic cerebral edema in the occipi tal and parietal regions. This combination of symptoms is known as ‘Posterior reversible encephalopathic syndrome (PRES)’.
In the ED, an abnormally high BP should be confirmed after reassessment, when the child is quiet. A patient with blood pressure levels greater than the 95th percentile in a physician’s office or clinic who is normotensive outside a clinical setting has ‘white coat hypertension’. Ambulatory blood pressure monitoring (ABPM) is usually required to make the diagnosis.5 A focused history, rapid cardiopulmonary assessment and a thorough physical examination to identify signs sug gestive of causes of hypertension is essential in the evalu ation (Refer Table 12.2).
CASE SCENARIO A 10-year-old child is being evaluated for periorbital puffiness and cola-colored urine. He is rushed into the ED with history of sudden onset of severe headache and loss of bilateral vision. Even as the ophthalmologist is evaluating his fundus, he has a brief generalized tonicclonic convulsion (Figures 19.2 and 19.3).
Such patients are judged to be in imminent hypertensive crisis and are treated as true emergencies.2 For purposes of evaluation and treatment, BP measure ments at or above ‘severe’ levels (above the 99th percentile for age and sex) should be considered as hypertensive ur gency even in the absence of symptoms. The 2004 report on high BP in children and adoles cents reiterates these definitions, but states that children with blood pressures greater than 5 mm Hg above the 99th percentile require prompt treatment.3
Ù Accurate BP measurement requires the use of the ap propriate sized cuff and equipment and the proper tech nique. The width of the inflatable bladder should be at least 40% of the arm circumference at a point midway between the acromion process and the olecranon process. For such a cuff to be optimal for an arm, the cuff bladder length should cover 80%–100% of the circumference of the arm.4
Figure 19.2 Physiological status: Neurogenic stridor, cardiac failure, hypertension, status epilepticus with cortical blindness
History Ask for: ●● Symptoms referable to the renal system. (kidneys are the commonest cause of hypertension in pediatric age group). ●● Flushing, sweating, palpitations, fever and weight loss may indicate presence of pheochromocytoma. ●● Significant family history of hypertension points to es sential hypertension as etiology. Ingestion of certain drugs could increase BP.
Chapter 19 n Hypertensive Emergencies
●● Acute onset breathlessness suggest cardiovascular compromise. ●● Visual changes, seizures, headache and vomiting sug IP : 196.52.84.10 gest disturbance to the central nervous system (Box 19.1). Box 19.1: Hypertensive emergencies that need immediate treatment ●● Hypertensive encephalopathy ●● Hypertension associated with acute heart failure or pulmonary edema ●● Acute renal failure ●● Stroke ●● Adrenergic crisis (pheochromocytoma) ●● Hypertension with intracranial bleed ●● Hypertension-induced blindness ●● Myocardial infarction (rare in children)
181
abdominal bruit or mass, differential pulses and BP record ing in all four limbs help to identify etiology of hyperten sion. Fundoscopy should be performed looking for hemor rhage, papilledema or infarcts. Any increase in blood pressure that is sufficiently acute or elevated to cause symptoms should be considered lifethreatening.
Laboratory Studies Complete blood count (CBC), electrolytes, blood urea ni trogen (BUN), creatinine, uric acid, urinalysis, urine cul ture, chest X-ray (CXR), ultrasonogram (USG) abdomen, electrocordiagram (ECG) and ECHO are needed in all children. Further studies should be individualized and may be done once the BP is controlled.
Physical Examination
Management of Hypertensive Emergency
A rapid cardiopulmonary and cerebral assessment will help to recognize features of cardiac failure with or without fea tures of encephalopathy.
Principles
A more profound fall in mental status or seizures might point towards hypertensive encephalopathy. Evidence of retinopathy, neurocutaneous markers, cushingoid facies,
●● Provide oxygen via the flow inflating ventilation de vice. ●● Secure vascular access. Administer furosemide 1–2 mg/ kg intravenously (slowly), if cardiac failure is noted.
Figure 19.3: Summary of the approach to a child with severe hypertension in the ED
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Section V n Circulation
●● If systolic blood pressure has not responded to furo semide, consider Labetalol. ●● If hypertension does resolve despite Labetalol, IP :not 196.52.84.10 consider drugs mentioned in Figure 19.3. Treatment must be rapid, but cautious. High BP must be reduced gradually. The goal in management is the re duction of 10%–25% of the initial BP in the first 1–2 hours of therapy. A rapid fall in BP could cause hypoperfusion of vital organs resulting in iatrogenic morbidity. Longstanding hypertension is often compensated by altering cerebral vascular autoregulatory mechanisms. When BP is suddenly dropped iatrogenically, these compensatory mechanisms are overwhelmed, the consequences being deleterious to the patient. Hence, in order to reduce BP gradually, intravenous hypertensive drugs need to be ad ministered (Figure 19.1). ●● Standard protocol for status epilepticus. ●● Consider early use of Aspirin, if acute visual loss oc curs in the hypertensive child (after ruling out magnetic resonance imaging (MRI) proven intracranial bleed). ●● CT using contrast may be more easily available. How ever, it should be avoided if child has elevated urea or creatinine. ●● Monitor BP and urine output from the out s et. ●● Insert an arterial line for monitoring intra-arterial pres sure if nitroprusside, diazoxide or nicardipine are being used.
Pharmacotherapy of Hypertensive Emergencies The choice of drug depends on the severity of the patient’s hypertension, current medications, the suspected cause of hypertension and the organs involved (Table 19.3).
Table 19.3: Life-threatening causes of hypertension Infancy
Coarctation of the aorta, valvular insufficiency, congenital adrenal hyperplasia, renal vascular disease, renal parenchymal disease
Childhood
Renal parenchymal disease, renal vascular disease, coarctation of the aorta, pheochromocytoma, increased intracranial pressure, bacterial endocarditis, drug-induced/ toxicologic
Adolescence Renal parenchymal disease, pheochromocytoma, toxemia of pregnancy, druginduced/toxicologic
Nitroprusside Nitroprusside is the drug of choice in hypertensive crisis. It has a rapid onset of action and lasts only as long as the infusion is continued, enabling precise control of BP. A vasodilator of both venous and arterial vasculature, an ar terial line is needed for its monitoring, the drug is prefer ably administered through a central line using an infusion pump. The bottle and intravenous tubing should be cov ered by a black sheet to protect from light. The solution should be changed every 24 hours. Since its use requires intra-arterial monitoring it is not a drug recommended for use in the ED. Dose: 0.3–8 µg/kg/min (Table 19.2). Blood thiocyanate levels should be monitored if the infusion lasts for more than 24 hours. The rate of infusion is maintained at 10 µg/kg/min for a duration longer than 6 hours. It is discontinued, if thiocyanate levels exceed 10 mg/dL. If toxic levels are noted, thiosulfate is the antidote of choice.
Table 19.2: Drugs used for the treatment of hypertensive emergencies Drug
Dose
Onset
Peak
Duration
Sodium nitroprusside IV
0.3–8 µg/kg/min
Within second
1–2 minute
During infusion only
Esmolol IV
100–500 µg/kg bolus over 1–3 min then 50–300 µg/kg/min
Immediate
1–2 minute
10–30 minute
Labetalol IV
0.2–1 mg/kg bolus followed by 0.25–1.5 mg/kg/h
2–5 minute
20–30 minute
2–6 hour
Diazoxide IV
1–5 mg/kg/dose max of 150 mg
1–5 minute
2–4 minute
4–12 hour
Hydralazine IV
0.1–0.5 mg/kg/dose maximum 20 mg
5–30 minute
20–40 minute
4–12 hour
Enalaprilat IV
5–10 µg/kg/dose
Up to 60 minute
3–4 hour
4–6 hour
Nifedipine (Oral)
0.25–0.5 mg/kg/dose
5–15 minute
30–60 minute
3–6 hour
Chapter 19 n Hypertensive Emergencies
183
Labetalol
Hydralazine
Labetalol has α and β blocking effects. The β-adrenergic IP : potent. 196.52.84.10 blockade activity is more Dosing is not affected by poor renal function. It has been reported to be effec tive in the management of severe hypertension that results from pheochromocytoma and coarctation of the aorta. It is also used in the treatment of hypertensive crises in patients with end-stage renal disease. Both intravenous and oral preparations are available.
Hydralazine causes relaxation of smooth muscle of both the arteries and veins. It is less potent than other agents.
Dose: 0.2–1.0 mg/kg/dose intravenously followed by an infusion of 0.25–1.5 mg/kg/h. Side effects are dizziness, gastrointestinal upset, head ache, urinary retention, bradycardia and bronchospasm in asthmatics. It is therefore contraindicated in asthmatic pa tients.
Nicardipine Nicardipine is a calcium channel blocker that can be ad ministered intravenously. It acts by causing vasodilata tion. Dose: Infusion at the rate of 0.5–3 µg/kg/min. Side effects are headache, tachycardia, dizziness, nau sea and vomiting. It is contraindicated in intracranial hem orrhage (ICH) as it increases cerebral blood flow.
Dose: 0.1–0.5 mg/kg/dose.
Esmolol Esmolol is given as a loading dose of 100–500 µg/kg IV over 1–2 minutes, followed by an infusion of 50–300 µg/ kg/minute. It is useful in hypertensive crisis following sur gery for coarctation of aorta.
Diazoxide Diazoxide is given as a bolus of 1–3 mg/kg. It is very ef fective in rapidly lowering the blood pressure. However, it can cause precipitous hypotension and repeated boluses of 1 mg/kg may be preferable to a higher initial dose.
Phentolamine Phentolamine with its rapid onset of action and alpha blocking effect is useful in pheochromocytoma. The high risk of hypotension after the primary lesion (e.g. pheochro mocytoma) is excised, which should not be forgotten. Care should be exercised and the surgeons should be alerted to this possibility. Dose: 0.1 mg/kg/dose IV (max 5 mg).
Nifedipine
Enalaprilat
It is a calcium channel blocker with powerful vasodila tor activity resulting in a decrease in peripheral vascular resistance. Route of administration is oral (bite and swal low). The effectiveness of the drug is due to its absorp tion from the gastrointestinal tract. An exact dose may be difficult to administer especially when given by the sublingual route.
Enalaprilat (intravenous form of enalapril) has been ad ministered as 5–10 µg/kg/dose. It has been used in adult hypertensive emergencies with good results. However, studies of its use in children are limited. Little is known of its side effects in children.
Dose: 0.25–0.5 mg/kg/dose, (max 10 mg).
Fenoldopam is a selective dopamine agonist, causing va sodilation of the renal, cerebral, coronary and splanchnic vasculature. Infusion rates of 0.1–0.2 µg/kg/min have been used in children. Side effects include reflex tachycardia, raised intracranial pressure (ICP) and increased intra-ocu lar pressure. Experience in children is limited.
It is contraindicated when the child has an intracranial bleed.
Ù
Ideally, Sodium Nitroprusside should be used to gradually reduce high blood pressure. This drug mandates intra-arterial monitoring. Hence, Nifedipine is used as an alternate agent in settings without access to intra-arterial monitoring.
Fenoldopam
Hypertensive Urgency6 Administer oral antihypertensive agents to resolve high BP presenting as hypertensive urgency.
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Section V n Circulation
Ensure that one third of the total planned blood pres sure reduction is done during the first 6 hours, another third during the next 24–36 IP hours and the final third during the : 196.52.84.10 next 24–96 hours or even longer. After administration of the antihypertensive agent, ob servation for adverse effects such as orthostasis is essential for at least 4–6 hours. Discharge with the same medications that were used to treat hypertension in the ED. Although, high BP is an emergency, avoid treating it immediately. Often high BP in critically ill children is a compensatory response. ●● Children presenting with septic shock or shock second ary to scorpion sting, etc. often have high systolic blood pressure. As shock is resuscitated, BP normalizes. ●● High BP in children presenting with non-traumatic coma or head injury indicates presence of raised ICP. Treatment should be focused on providing controlled ventilation. ●● High blood pressure may be noted in the initial half hour of status epilepticus. As SE resolves, BP normal izes. Drug therapies to bring down blood pressure in these situations can have lethal consequences. Avoid rushing to administer antihypertensive drug in the ED. High blood pressure is more commonly the result and not the cause of the emergency in the critically ill child.
Key Points
ü
1. Persistence of high BP after correction of hypoxia and shock should be evaluated for hypertension. 2. Hypertensive emergency is characterized by severe hypertension with end-organ injury.
3. Hypertensive urgency is severe hypertension without end-organ damage. 4. Treatment goals are to lower BP gradually in a safe and effective manner. 5. The choice of medication depends on the side effect profile and physician’s familiarity with the drug.
common errors
û
1. Failure to realize that most children with early compensated shock have elevated BP. 2. Rushing to administer furosemide or nifedipine in children with increased BP and shock can precipitate cardiac arrest.
References 1. Julie R Ingelfinger. Evaluation and treatment of hyperten sion in children. In: Thomas W Smith (Ed). Cardiovascular therapeutics a companion to Braunwald’s heart disease. WB Saunders. Company; 1996. pp. 515-26. 2. Hypertensive crises. In Textbook of Paediatric Intensive Care, 4th edition. Rogers MC (Ed): Baltimore, Williams and Wilkins. 2009. 3. Erika Constantine, James Linakis. The assessment and management of hypertensive emergencies and urgencies in children. Pediatic Emergency Care. 2005;21(6):391-96. 4. Gomez-Marin O, Prineas RJ, Rastam L. Cuff bladder width and blood pressure measurement in children and adoles cents. J Hypertens. 1992;10:1235-41. 5. National High Blood Pressure Education Working Group on High Blood Pressure in Children and Adolescents. The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents. Pedi atrics. 2004;114;555-76. 6. Srinivasan Suresh, Prashant Mahajan, Deepak Kamat. Emergency management of pediatric hypertension. Clin Pediatr (Phila): 2005;44;739.
Disability
Section VI
IP : 196.52.84.10
IP : 196.52.84.10
Approach to Decreased Level of Consciousness IP : 196.52.84.10
20
Figure 20.1: Child presenting with cardiogenic shock, coma with raised ICP and uncal herniation being successfully resuscitated
Learning Objectives 1. The risk of failing to recognize early decrease in level of consciousness. 2. Case-based management of non-traumatic coma.
INTRODUCTION
3. Step-wise approach to evaluate decreased level of consciousness in children. 4. Need to correct shock in the presence of raised ICP. 5. Investigations in management of coma.
Ù
Many acutely ill children are not fully conscious. Most make a full neurological recovery as the underlying cause is treated, but considerable skill is required to distinguish the group at high-risk of further deterioration, leading either to death or to severe handicap1 (Figures 20.1 and 20.2).
Based on evidence that even early decrease in the level of consciousness may be catastrophic if not recognized, this group advocated that evaluation and management should be initiated when the GCS dropped to less than 15 or ‘Responsive to voice’ in the AVPU scale.
The Pediatric Accident and Emergency Group in the United Kingdom reported that if the Glasgow Coma Scale (GCS) was less than 12 in children between 1 month and 18 years of age for greater than 6 hours, mortality was as high as 40%.2 This definition was not applicable for children with learning disabilities whose usual GCS was less than 15, critically ill neonates or children with a known diagnosis or with a definite treatment plan.
Recognition of early fall in mental status viz ‘Responsive to voice’ poses a challenge in all ages. In precommunicative children, early fall in mental status is best confirmed by ask ing the mother triage questions (See Chapter 1).
Ù
Children of any age who are restless and talking unintelligibly have a verbal score of 2 and are considered to be deeply unconscious. These children are at high-risk of catastrophic deterioration.3
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Section VI n Disability
IP : 196.52.84.10
Figure 20.2: A typical scene in a PED where most seriously ill children present with decreased level of consciousness. The etiologies for ALOC in this picture are; hypoxia, shock, myocardial dysfunction and non-convulsive status epilepticus. Time sensitive, goal-directed management of these factors could often result in neurologically intact survival.
Ù
At initial presentation, it is preferable to err on the side of recording a lower score, as it is easier to withdraw treatment from a child who is improving than to resuscitate one who deteriorates. If altered mental status is doubtful, it is best to treat than to wait for overt clinical signs to develop. Provide oxygen, administer the first bolus and correct documented hypoglycemia. A clearer picture will emerge, providing clues towards identifying the etiology of decreased level of consciousness.
CASE SCENARIO A 5-year-old boy was brought with history of fever, progressive lethargy and posturing for 3 days. He had been vomiting several times since the morning. His temperature was 40°C (Figures 20.3 and 20.4).
Figure 20.3: Note posturing in this unresponsive boy
Figure 20.4 Physiological status: Neurogenic stridor, respiratory failure, bradycardia, cardiogenic shock, hypertension with nonconvulsive status epilepticus, raised intracranial pressure and uncal herniation.
Ù
Children presenting with altered level of consciousness have several simultaneously occurring problems that need concurrent management! • Hypoxia • Shock • Myocardial dysfunction • Prolonged convulsion, postconvulsive state • Sepsis, intracranial infection • Raised ICP • Metabolic illness (dyselectrolytemia), hypoglycemia, ketosis, etc. • Trauma • Hypertension • Cause unknown—toxins.
Ù
A simple focused history should be obtained simultaneously as assessment and resuscitation are in progress. ●● Convulsions or posturing? ●● Progressive drop in consciousness such as incessant cry, lethargy, more sleepy than usual? ●● Fever? ●● Breathlessness? ●● Vomiting? ●● Headache? ●● Length of symptoms? ●● Previous infant death in the family? ●● Ingestion or availability of drugs at home?
Chapter 20 n Approach to Decreased Level of Consciousness
Box 20.1: Monitor during resuscitation ●● ●● ●● ●● ●● ●● ●● ●● ●● ●● ●●
Airway 196.52.84.10 Respiratory rate, workIP of :breathing (WOB) Heart rate, perfusion, BP, liver span AVPU assessment every 15 minute Eye position, eye movement, pupils Monitor urine output Temperature O2 saturations Electrocardiography (ECG) BP End tidal CO2
Initial management priorities Airway and Breathing In the unresponsive child, loss of tone of the oropharyn geal muscles causes falling back of the tongue resulting in airway obstruction. Furthermore, loss of airway protective reflexes lead to pooling of secretions. An unprotected airway itself could worsen underlying hypoxia, shock, cardiac failure, status epilepticus and raised ICP (Box 20.1). Clinically, airway obstruction manifests as stridor viz neurogenic stridor, which is relieved by the following maneuvers: ●● Open airway by head tilt-chin lift maneuver. ●● Use large bore suction cannula to rapidly clear oropharyngeal secretions. ●● Provide oxygen using the CPAP device. ●● Call for intubation tray using SOAPME protocol. ●● Intubate using ICP precautions.
Ù
Raised ICP may be aggravated by painful or noxious interventions even though the child appears deeply comatose. Since the process of intubation can stimulate the gag reflex and aggravate ICP, drugs are used which blunt the deleterious effects of intubation. Anesthetic drugs used for intubation for children at risk of developing ICP are the following: ●● Lidocaine is the premedication used to bluntgag by acting on the sensory pathway of the glossopharyngeal nerve. ●● Atropine reduces vagal-induced bradycardia. Bradycardia in a shocked child provides clue that raised ICP coexists.
189
●● Thiopental is cerebroprotective and consequently the induction agent of choice. ●● Vecuronium is the paralytic agent of choice, since succinylcholine is known to worsen ICP. ●● Even if a comatose child appears to be breathing, controlled mechanical ventilation should be instituted early to avoid washing out of CO2. While oxygenation is maintained at normal levels, PaCO2 is maintained in the low 30s. Pulse oximeter and end tidal CO2 monitoring enable non-invasive monitoring of gases in the PED.
Indications for intubation in comatose children ●● The Glasgow Coma Scale (GCS) is 12. ●● Deterioration in the GCS. ●● Unstable airway (intubation mandatory, even if the GCS is higher). ●● Respiratory depression (respiratory drive may be compromised in raised ICP). ●● Neurogenic hyperventilation (hyperventilation may be a sign of midbrain involvement). ●● Asymmetric or dilated pupils. ●● Evidence of herniation.
Circulation Correct shock with NS (fluid of choice). If respiratory distress or failure with or without signs of cardiac dysfunction are identified on arrival, the smaller boluses (5–10 mL/kg) are administered. If septic shock is recognized (e.g. meningitis or encephalitis) in the comatose child, larger volumes (60–80 mL/kg) may be warranted to correct shock. Close monitoring for pulmonary edema and hepatomegaly is necessary during fluid resuscitation shock due to sepsis. If coma was due to DKA or isolated head trauma, smaller volumes (10–30 mL/kg) may be warranted to resolve shock. Raised ICP is not a contraindication for shock correction. Indeed, it signals the need for maintenance of high mean arterial pressure (MAP).
Ù
Increased systemic BP is a physiological compensatory response to maintain cerebral perfusion pressure when ICP increases! BP is maintained at the 95th percentile for age/height in order to maintain cerebral perfusion pressure (CPP) in the face of an elevated ICP.
190
Section VI n Disability
●● Antihypertensive drugs can kill, if used to reduce blood pressure in a child with ICP! ●● Infusing hypotonicIP fluids (5% or 10% dextrose) can : 196.52.84.10 lead to cerebral edema in children presenting with ICP. ●● Documented hypoglycemia is corrected with a bolus dose of dextrose. If age is greater than 4 weeks, ad minister 5 mL/kg IV of 10% dextrose as bolus. If age of the child is less than 4 weeks, administer 2 mL/kg IV 10% dextrose bolus. ●● The presence of a very high glucose level may point to a diabetic ketoacidosis (refer to Chapter 34 on DKA).
Disability Clinical Seizures Eye deviation, nystagmus and eyelid twitching, characteristic of non-convulsive status epilepticus, pinpoint a treatable etiology of coma. Unrecognized seizure activity increase ICP and could precipitate cerebral herniation. They may be due to the excitatory toxic and ischemic mechanisms of secondary brain damage.
●● Evaluation for pupillary inequality helps recognize herniation. ●● Examine the fundus for additional clues. ●● If seizures are refractory to anticonvulsants, evaluate electrolytes and correct as shown in Table 20.3. ●● Coma not explained by the presence of seizure activity needs to be evaluated as discussed below.
Recognizing Depth of Coma4 The Glasgow Coma Scale (Table 20.1) was designed to assess the depth of post-traumatic brain injury coma in adults and children beyond the age of 5 years. However, for children between 9 months and 5 years of age, a modified mo tor and eye opening scales has been recommended. Motor response is elicited by applying supraocular pressure (and looked for flexion and extension). It may also be assessed by applying pressure over the nail bed using a pencil. Motor response is M5 if the infant responds by withdrawing. There may be need for flexibil ity due to overlap between the age groups. This method is discussed below:
Table 20.1: Modified Glasgow Coma Score Modified Glasgow Coma Score Score
Infant < 2 year
Child 2–5 year
6 year–adult
4
Open
Open
Open
3
To voice
To voice
To voice
2
To pain
To pain
To pain
1
No response
No response
No response
Eyes
Verbal 5
Coos, babbles
Appropriate words
Oriented and alert
4
Irritable cry, consolable
Inappropriate words
Disoriented
3
Cries persistently to pain
Cries/screams
Inappropriate words
2
Moans
Grunts
Incomprehensible sounds
1
No response
No response
No response
Motor 6
Spontaneous movement
Spontaneous movement
Follows commands
5
Withdraws to touch
Localizes to pain
Localizes to pain
4
Withdraws to pain
Withdraws to pain
Withdraws to pain
3
Decorticate flexion
Decorticate flexion
Decorticate flexion
2
Decerebrate extension
Decerebrate extension
Decerebrate extension
1
No response
No response
No response
Chapter 20 n Approach to Decreased Level of Consciousness
191
Step 1: If eyes are open (E-4) request the mother to talk to her child.
Recognizing Presence of Raised Intracranial Pressure
●● ●● ●● ●● ●● ●●
Raised ICP exists in varying degrees of severity in all encephalopathies of non-traumatic etiologies (infectious and non-infectious causes).
IP : 196.52.84.10 Babbling: < 9 months. Waving bye-bye: 9–10 months. Words: 1 year. Pointing body parts: 15–24 months. Sentences: 2 years. Orientation in place and time from 5 years.
Concurrent and early management of intracranial hypertension in the ED is not only life-saving, but also ensures neurologically intact survival.
Ù
Step 2: If no eye opening or spontaneous speech ●● Ask child to obey simple command such as squeezing finger or eyes (M6).
Step 3: If no response, press firmly on supraorbital notch (beneath medial end of eyebrow) with your thumb and observe whether ●● Eyes open. ●● Moans. ●● Moves arms: 1. Above the clavicle (M5). 2. Below clavicle while flexing elbow (M3). 3. Below clavicle without flexion and with rotation of shoulder (M2).
Step 4: No movement, exert maximal pressure and observe for facial grimace or movement of any body part.
‘Raised intracranial pressure’ must be presumed in all comatose children. Failure to recognize and manage ICP in the ED could lead to death or neurological handicap. How is raised intracranial pressure recognized within the first hour of arrival? Hypoxia, shock and myocardial dysfunction have been corrected, but these clinical features are noted: ●● ●● ●● ●●
Level of consciousness continues to worsen. Abnormal posturing persists. Abnormal breathing pattern persists. Abnormal oculocephalic (Doll’s eye) or oculovestibu lar reflex. ●● Abnormal pupillary response is noted.
Ù
Cushing’s triad (apnea, bradycardia, hypertension) is a late manifestation of raised ICP. It is advisable to identify earlier signs. Careful examination of the fundi is mandatory.
Ù
Step 5: If child flexes, but does not localize, apply nail bed pressure, using a pencil. ●● If finger is withdrawn (M4). ●● If child moves limb across the body to dislodge the painful stimulus (M5).
Step 6: Look for asymmetry of movement in any of the steps (Uncal herniation). Algorithm: Modified from Kirkham FJ et al. Pediatric coma scales. Development Medicine & Child Neurology. 2008;50:267-74.
• Acute elevation of ICP will not cause papilledema
immediately. Hence, its absence must not be taken as a reassuring sign. Neither, is it safe to entirely rely on the computed tomographic images to diagnose raised ICP. ICP is often a clinical diagnosis in the acutely ill child! • If papilledema is noted in association with hypertension (systolic BP greater than 2 SD), reevaluate – BP in all the four limbs. – Send blood for urea and creatinine. – Admit into the ICU. – Refer to the nephrologist.
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Section VI n Disability
Variations in CPP, both decreased CPP (when raised ICP is associated with uncorrected shock) and increased CPP associated with raised ICP is thought to cause brain IP : 196.52.84.10 damage by following two mechanisms:
Figure 20.5: Unequal pupils in a child with raised ICP and uncal herniation (Courtesy: Dr Arun Annamalai).
Decreased Cerebral Perfusion Pressure Cerebral perfusion pressure is the difference between the mean arterial pressure and the intracranial pressure, i.e. (CPP = MAP – ICP). When intracranial pressure is elevated and coexisting shock is not resolved, cerebral perfusion pressure falls causing cerebral ischemia. Ischemia in the border zones between the main arterial territories, cause clinically silent brain damage. It rarely may be associated with seizures or hypertensive encephalopathy.
The pattern of clinical findings to help in recognition of the level of herniation is shown in Table 20.2. Table 20.2: Herniation syndromes Uncal • Hemiparesis • Minimal deviation of eyes on oculocephalic/ oculovesti bular testing • Unilateral ptosis • Unilateral fixed dilated pupil Upper pontine • Extensor response to pain and /or decerebrate posturing • Hyperventilation • Minimal deviation of eyes on oculocephalic/ oculovestibular testing • Midpoint pupils fixed to light Medullary • Slow irregular gasping respiration/respiratory arrest with adequate cardiac output • Pupils dilated and fixed to light
Diencephalic • Flexor response to pain and or decorticate posturing • Hypertonia/hyperreflexia with extensor plantars • Cheyne-Stokes breathing • Full deviation of eyes to oculocephalic/ oculovestibular testing • Small midpoint pupils reactive to light Lower pontine • No response to pain or flexion of legs only • Flaccidity with extensor plantars • Ataxic or shallow respiration • No deviation of eyes on oculocephalic/ oculovestibular testing • Midpoint pupils fixed to light
Herniation Syndromes Untreated, raised ICP leads to herniation syndromes. Differences in pressure between the forebrain compartment and the posterior fossa, may cause uncal (Figure 20.5), diencephalic or midbrain/upper pontine herniation. The temporal lobes herniate through the tentorium. Similarly, a pressure differential between the posterior fossa and the spinal canal can lead to herniation of the brain through the foramen magnum (Figure 20.6). The resulting lower pontine and medullary herniation syndromes can be lethal. Brain herniation causes direct mechanical damage in addition to ischemia and hemorrhage secondary to vascular distortion. Central or uncal herniation through the tentorium is compatible with intact survival; on the contrary, herniation through the foramen magnum is not. Changes from one syndrome to the next signifies progressive worsening.
Figure 20.6: Lesions in various sites in the brain causing herniation syndromes
●● Memorize stages of progressive herniation that are compatible with intact survival. ●● Learn to serially examine the child’s level of consciousness (Table 20.1) and the brainstem reflexes such that progression is recognized immediately and appropriate action is taken swiftly.
Chapter 20 n Approach to Decreased Level of Consciousness
●● Drugs, toxins, metabolic abnormalities and the postictal patient may mimic imminent herniation. Once again, it is best to err the side of treatment than to IP on : 196.52.84.10 await for the whole picture to unfold.
First Tier Treatment of Intracranial Pressure ●● Nurse the child in the 30° head up position. ●● Keep head in neutral position to avoid kinking of the neck. ●● Avoid noxious stimuli. Take efforts to provide pain relief and sedation during painful procedures, since these maneuvers could increase ICP. ●● Maintain euglycemia. ●● Control fever aggressively. ●● Treat seizures. ●● Severe sepsis with or without pyogenic meningitis may also present with varying degrees of coma. Administer an antibiotic (Ceftriaxone) empirically, while awaiting investigation. ●● Hyperosmolar therapy: Infuse hypertonic saline (5 mL/ Kg) followed by continuous infusion between 0.1 and 1.0 mL/kg/h. ●● 3% NS has anti-inflammatory effects, increases intravascular volume and can be used in hypotensive patients who have elevated ICP. A safe intervention, few adverse effects have been noted with sodium levels as high as 160 mmol/L. ●● Ventilate to maintain eucapnia (PaCO2: 35–40 mm Hg). ●● Mannitol role has become limited. Since most children presenting with ICP also have shock or a propensity to develop dehydration in the initial hours of management, it is less often used in the ED setting.
Evaluate for Cause of Coma After the ABCs are stabilized and ICP issues have been addressed to prevent herniation, the patient may be transported for imaging.
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Do not postpone stabilization while waiting for etiology to be identified.
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●● Blood ammonia: Reye’s syndrome, hyperammonemia. ●● Blood lactate: Severe illness, inborn errors of metabolism (IEM). ●● Call for metabolic specialist, if metabolic profile is abnormal. ●● Ketoacids: If finger stick glucose is high. ●● Serum sodium, calcium, magnesium (Table 20.3). ●● Blood urea, creatinine. ●● Peripheral smear: Malaria, hemolytic-uremic syndrome. ●● Erythrocyte sedimentation rate (ESR), complete blood count (CBC). ●● Coagulation profile: If platelets are low or bleeding occurs.
Blood Culture ●● Stool culture: Shigella, Enteroviruses. ●● Mycoplasma IgG, IgM (unless cause known). ●● Viral titers of blood and cerebrospinal fluid (CSF) (stored samples useful). – Elisa for Rickettsia, human immunodeficiency virus (HIV). ●● Mantoux. ●● Resting gastric juice for acid-fast bacilli.
Lumbar Puncture LP may be performed when the child becomes hemodynamically stable with no clinical or radiological evidence of raised ICP. CSF may be sent for polymerase chain reaction (PCR) for viruses, tuberculosis (TB) antibodies, e.g. herpes simplex.
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Avoid LP if abnormal breathing patterns, shock, bradycardia, hypertension, GCS < 8, convulsive or non-convulsive status epilepticus, abnormal dolls eye movement, dilated pupils, abnormal posture and ICP are noted. Delay LP and treat empirically when in doubt.
Electroencephalography EEG helps to confirm the diagnosis of seizure activity,5 even if no clinical seizures (NCSE).
Investigations
Less Common Investigations
●● Dextrostix. ●● Liver function tests even if primary liver cell failure is unlikely.
●● Autoimmune screen for vasculitis. ●● Thyroid function test for encephalopathy associated with Hashimoto thyroiditis (Hashimoto encephalitis).
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Section VI n Disability
While the list appears long, a protocol driven approach may help prevent repeated blood collections. It is good practice to draw extra blood and store for future investigaIP : 196.52.84.10 tions. Investigations are requested in a stepwise manner, especially if the etiology remains unclear.
Imaging If the child is deeply unconscious, afebrile or has focal signs, CT/MRI scan is the initial investigation of choice (even in infants with an open fontanelle). It helps to rule out intracerebral hemorrhage, ischemic stroke, hydrocephalus and space occupying lesion (SOL). However, a normal CT does not rule out the diagnosis of raised ICP. Thus, clinical signs of raised ICT are more important than a normal CT scan. During transfer for investigations, ventilation, sedation and osmotic therapy must be continued. If a surgically correctable cause is identified, call for neurosurgical consultation.
Toxin Screen If etiology of coma has not been identified, consider the possibility of toxins or drugs ingestions. Ideally urine and blood should be collected and stored for evaluation of toxins/drugs early in the management of these children.
Immediate Antimicrobial Coverage ●● A third generation cephalosporin and Acyclovir is empirically administered to cover the possibility of infection. Acyclovir is therapeutic for herpes simplex encephalitis. A positive MRI scan and electroencephalography (EEG) have 95% sensitivity in the diagnosis of herpes encephalitis. If the diagnosis is confirmed, the drug should be continued at a high dose for 2 weeks. ●● Dexamethasone is given prior to the antibiotic, since evidence suggests that it reduces the incidence of deaf-
ness and neurological handicap. Although this data is relevant for Haemophilus influenzae meningitis, the benefit appear less certain for meningitis due to pneumococcus and other organisms. ●● If there is any suspicion of tuberculous meningitis or if hydrocephalus is identified by CT scan, ATT should be considered. ●● Empiric antimalarial treatment is also initiated. ●● Empirical treatment of rickettsia may be wise in epidemic situations. It is best to treat with erythromycin and doxycycline than to wait. When confronted with a child at high-risk of death or disability, it would not be inappropriate to administer several therapies on arrival. As the etiology of coma is confirmed, therapy is withdrawn, e.g. acyclovir acts best when started early. However, if the results of the MRI, EEG and PCR are all negative, therapy may be withdrawn. After the initial period of stabilization, the child must be transported to the PICU. Ideally an afebrile comatose child should be transferred to a pediatric neurosurgical unit. This should be done in the same manner as for imaging. Full sedation, controlled ventilation and minimal handling with the bed/stretcher at a 30° head up angle throughout transport is advised. The prognosis depends on the etiology. Refer Protocol 20.1. Often, lack of laboratory support to establish diagnosis of viral and metabolic disorders results in empirical treatment. However, effective supportive management of the ABCs, maintenance of cerebral perfusion pressure and prevention of further damage often keeps the patient alive till the primary problem resolves.
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Key Points
1. Recognize potential risk of raised ICP and take immediate action to stabilize ABC. 2. Secure airway using ICP precautions. 3. Assess possibility of raised ICP.
Table 20.3: Corrections in electrolyte disturbances Electrolyte
Value
Dose
Rate of infusion
Sodium
115 mmol/L
5 mL/kg 3% NS
5–10 minutes
Calcium
< 0.75 mmol/L
0.3 mL/kg calcium gluconate
5 minutes
Magnesium
0.65 mmol/L
50 mg/kg iv over
1 hour
Chapter 20 n Approach to Decreased Level of Consciousness
4. 5. 6. 7. 8. 9. 10.
Check blood sugar. Check for NCSE and treat. IPif: more 196.52.84.10 Lower temperature, than 38°C. Nurse in 30° head up positions. Insert lines, urinary catheters, etc. under analgesia. Place on continuous monitoring. Administer broad spectrum antibiotic, antimalarial, antiviral, erythrocin and doxycyclin for rickettsial infections and ATT for febrile children with coma. 11. If papilledema is identified in association with hypertension (systolic BP greater than 2 SD), call for nephrology consultation.
common errors
195
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1. Administration of Mannitol without ruling out shock or monitoring hydration status. 2. Dextrose infusions in the absence of hypoglycemia. 3. Failing to recognize non-convulsive status epilepticus. 4. Shifting for imaging without stabilization. 5. Administration of Diazepam for posturing movements in a comatose child. 6. Failure to ensure euglycemia and correct dyselectrolytemia. 7. Failure to protect airway and ventilate the comatose child.
Protocol 20.1: PEMC approach: Altered mental status and abnormal movements in a critically ill child
196 Section VI n Disability
IP : 196.52.84.10
Chapter 20 n Approach to Decreased Level of Consciousness
References 1. Kirkham FJ. Non-traumatic coma in children. Arch Dis IP : 196.52.84.10 Child. 2001;85:303-12. 2. Pediatric Accident and Emergency Group. ‘Evidence based guideline for the management of decreased level of consciousness’. Arch Dis Childhood Edu and Practice. 2006;91.ep115-ep22.
197
3. Santhanam Indumathy, Sangareddi S, Venkataraman, et al. A prospective randomized controlled study of two fluid regimens in the initial management of septic shock in the emergency department. Pediatr Emerg Care. 2008;24:647-55. 4. Kirkham FJ. Newton CR, Whitehouse W. Pediatric coma scales. Development Med Child Neurology. 2008;50:267-74. 5. Bauer, Trinka. Non-convulsive status epilepticus and coma. Epilepsia. 2010;51(2):177-90.
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IP : 196.52.84.10
Status Epilepticus
Figure 21.1: Airway management is as critical as anticonvulsants in the management of status epilepticus (Courtesy: Dr Gunda Srinivas)
Learning Objectives 1. Need for early initiation of bag-valve-mask venti lation in convulsive status epilepticus seizures last ing for more than 5 minutes. 2. Emphasize the need to recognize coexisting pul monary edema that can worsen during phenytoin administration and fluid therapy of shock.
3. Evidence-based drug protocol in the management of status epilepticus. 4. Differentiation between non-convulsive status epi lepticus from postictal states. 5. Emphasize the importance of treating until all parts of the PAT have normalized.
INTRODUCTION
Progression of Status Epilepticus4
Status epilepticus (SE) is defined as seizures persisting for more than 5 minutes in children > 5 years of age or two or more seizures occurring consecutively without an in tervening period of full recovery of consciousness.1 More recently,2 a time sensitive classification has been proposed.
Overt generalized status epilepticus, if left untreated will evolve into non-convulsive status epilepticus.
●● Early or impending SE: 5–30 minutes. ●● Established SE: 30–60 minutes. ●● Refractory SE: Seizures persisting after treatment with adequate doses of 2 or 3 initial antiepileptic medica tions. Seizures that do not cease in 5 minutes are less likely to terminate without intervention.3 Hence, a child who is convulsing on arrival into the ED is more likely to contin ue to convulse and cause respiratory insufficiency unless actively treated (Refer Figure 21.1).
The deleterious cerebral, metabolic and physiological changes that occur as the duration of seizures increase is shown in Box 21.1. Also refer Table 21.1.
PATHoPHYSIOLOGY
Anticonvulsants act by altering the neuropeptide activ ity within the brain. Most seizures terminate spontaneous ly within 2 minutes. Spontaneous resolution, is the result of γ-aminobutyric acid-mediated inhibition that occurs in response to seizures.
Chapter 21 n Status Epilepticus
Box 21.1: Medical complications of status epilepticus
●●
●●
●●
●●
●●
●●
Cerebral – Interictal coma IP : 196.52.84.10 – Cumulative anoxia – Altered autoregulation – Increased cerebral blood flow – Cardiac arrest – Hypertension – Cardiac failure, hypotension – Cardiogenic shock Respiratory system failure – Apnea – Cheyne-Stokes breathing – Tachypnea – Neurogenic pulmonary edema – Aspiration, pneumonia – Respiratory acidosis – Cyanosis Renal failure – Oliguria, uremia – Acute tubular necrosis – Rhabdomyolysis – Lower nephron necrosis Autonomic system disturbance – Hyperpyrexia – Excessive sweating, vomiting – Hypersecretion (salivary, tracheobronchial) – Airway obstruction Metabolic and biochemical abnormalities – Acidosis (metabolic acidosis) – Anoxemia – Hypernatremia, hyponatremia – Hypoglycemia – Hepatic failure – Dehydration Infection – Pulmonary – Bladder – Skin Others – Altered autoregulation – Cerebral metabolic rate for oxygen (CMRO2) – Disseminated intravascular coagulation – Multiple organ dysfunction – Fractures, thrombophlebitis
●● Loss of the GABA5-mediated protective effect leads to ongoing seizure activity. The GABA receptors on the cell membrane are either destroyed or recycled. At the same time, continued seizure activity results in mobili zation of excitatory N-methyl-D-aspartate receptors. ●● The reduced activity of GABA (seizure control neu ropeptides) and increased activity of N-methyl-Daspartate receptors (seizure provoking neuropeptides)
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result in decreased inhibitory control and increased ex citation leading to continuation of status epilepticus. ●● Benzodiazepines bind to GABA-A5 receptors and pro mote neuronal inhibition. ●● Since the number of active GABA-A receptors de creases as an episode of SE progresses,6 the first dose of benzodiazepines should be given as early as possible for seizure termination.
CASE SCENARIO 1 An 8-month-old girl is brought with history of seizures lasting for 20 minutes. She had been having fever for 1 day (Figures 21.2 and 21.3).
Figure 21.2: Active convulsions can make effective bag-valvemask ventilation a challenge. Hence double EC-clamp technique of BVM ventilation is employed.
Figure 21.3 Physiological status: Unmaintainable airway, respiratory failure, tachycardia, shock with high normal blood pressure with convulsive status epilepticus.
Prehospital Therapy ●● Place the convulsing child in the recovery position to enable drainage of secretions.
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Section VI n Disability Table 21.1: Cerebral, metabolic and physiological derangements during prolonged seizures
Parameter
Duration of seizure < 30 min (phase I)
Duration of seizure < 30 min (phase II)
Hours (refractory)
Blood pressure
IP : 196.52.84.10 Increased
Decreased
Hypotension
Arterial oxygen
Decreased
Decreased
Decreased
Arterial carbon dioxide Increased
Variable
Hypercapnia
Lung fluid
Increased
Increased
Pulmonary edema
Autonomic activity
Increased
Increased
Arrhythmias
Temperature
Increased 1ºC
Increased 2ºC
Fever—hyperpyrexia
Serum pH
Decreased
Variable
Acidosis
Lactate
Increased
Increased
Lactic acidosis
Glucose
Increased
Normal or raised
Hypoglycemia
Serum potassium
Increased or normal
Increased
Hyperkalemia
Cerebral blood flow
Increased 900%
Increased 200%
Cerebral edema
Cerebral oxygen consumption
Compensated
Failed
Deficit—ischemia
●● Open airway using the head-tilt chin-lift maneuver (while maintaining the recovery position). ●● Suction oropharyngeal secretions without stimulating the posterior pharyngeal wall. ●● Provide oxygen using a non-rebreathing mask. ●● Administer midazolam (0.2 mg/kg) via the intramuscular or intrabuccal or intranasal route.7 ●● Fever a common cause of seizures in children should be controlled rapidly by tepid sponging and placing a rectal suppository of paracetamol.
Management of SE in the ED (Protocol 21.1) The median duration of convulsions prior to reaching the PED of an academic children’s hospital in Southern India, was 1 hour.8 Most presented with features of pulmonary edema with or without cardiac dysfunction. The modified SE protocol de scribed in this manual is based on this experience.
Airway At least two members (one doctor and one nurse) must be dedicated for airway management. The maneuvers men tioned below should be implemented simultaneously. 1. Open the airway using the head-tilt and chin-lift ma neuver. 2. C-spine precautions are taken if trauma is suspected.
3. Use a large bore rigid suction catheter to suction oropharyngeal secretions. 4. Rapidly decompress stomach with a nasogastric tube to prevent vomiting and pulmonary aspiration. 5. Introduce an appropriate sized oropharyngeal airway, if feasible.
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Avoid forcible opening of clenched jaws during a convulsive episode. ●● Unresponsiveness due to seizure activity results in the falling back of tongue. ●● Loss of airway protective reflexes leads to failure in handling the tracheobronchial secretions. ●● Glottic spasm also contributes to airway obstruction during seizure activity.
Breathing Ineffective respiration is almost always noted during con vulsive status epilepticus. Tonic-clonic activity of the intercostal muscles inhibit the normal inspiratory/expiratory movements of respira tion. ●● Jerky respirations are probably due to contraction of involuntary muscles of diaphragm. ●● Drugs used in the management of status epilepticus can also lead to respiratory failure.
Chapter 21 n Status Epilepticus
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An unstable and obstructed airway in combination with ineffective ventilationIPfor: 196.52.84.10 greater than 5 minutes can cause: • Severe hypoxia. • Shock. • Myocardial dysfunction. • Increased risk of prolonged seizure activity. Emergency medical response systems reach a convuls ing child within 5 minutes after activating the EMS. Pre hospital protocol-based management is rapidly initiated in western countries. Decision to intubate is taken within 20–30 minutes after onset of convulsions9 in the prehospi tal setting.
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Since early and structured prehospital care by EMS is unavailable in many parts of our country, it is recommended that primary care physicians to whom the child is brought, administer early and aggressive airway management to avoid the deleterious effects of hypoxia in convulsing children.
201
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Opening the airway and provision of oxygen without initiating bag-valve-mask ventilation is not enough to correct hypoxia in actively convulsing children in the emergency setting. ●● Whilst, the airway is being cleared by the airway nurse, initiate bag-valve-mask ventilation using the largest sized bag. Almost 50% of children presenting with convulsive SE can be mask ventilated without being intubated.8 ●● If spontaneously breathing, provide O2 using the flowinflating ventilation device. ●● Oxygen saturations are monitored using pulse oximeter. Note: Antiseizure drugs inherently depress respiration and may aggravate the underlying hypoxia in SE. Adminis tration of anticonvulsant without addressing the ABCs (a common error) could result in lethal complications.
Figure 21.5: The tube position being verified before fixing the tube
Indications for Intubation in SE (Figure 21.5) Figure 21.4: A third physician formulates the initial dose of lorazepam and administers it over 1–2 minutes, whilst two responders are managing the airway and breathing on arrival. Pulse oximeter is connected for monitoring during resuscitation.
Failure to provide effective ventilatory support during the emergency management of SE contributes to signifi cant morbidity and mortality in our country. On the con trary, effective respiratory support along with appropriate anticonvulsants can often resolve seizure, whilst simulta neously establishing breathing (Figures 21.4).
●● Failure to maintain optimal saturations despite effec tive bag-valve-mask technique. ●● Features of pulmonary edema or cardiac dysfunction noted at any step in the protocol. ●● Hypotensive shock associated with SE. ●● Prior to starting phenobarbitone or midazolam infusion for SE not responding to benzodiazepines and phenytoin. ●● Severe traumatic brain injury, where there is a need to provide controlled ventilation. ●● Raised intracranial pressure.
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Section VI n Disability
IP : 196.52.84.10
Figure 21.6: This picture shows capillary blood glucose being evaluated during resuscitation
Glucose Hypoglycemia can severely disrupt cerebral blood flow autoregulation leading, to adverse neurological outcomes. Refer Figure 21.6. ●● Dextrostix should be used to measure sugar levels early in the management of SE. ●● Documented hypoglycemia is corrected with an intra venous bolus of 2 mL/kg of 25% dextrose solution. ●● If dextrostix is not immediately available, to avoid the dangerous effects of unrecognized hypoglycemia, 25% dextrose may be administered emperically. ●● Prolonged status epilepticus can cause hypoglycemia. Hypoglycemia can precipitate status epilepticus. Of ten, hypoglycemia can recur after correction. Hence, throughout resuscitation, a maintenance fluid should be infused as per the Holliday-Segar formula. ●● Infuse GNS to which KCl and calcium have been added.
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Glucagon is indicated for treating hypoglycemia and seizure in insulin-dependent diabetes mellitus. Dose: 1–2 years: 500 µg stat
2–18 years: < 25 kg: 500 µg
> 25 kg: 1 mg Route of administration in IDDM: Subcutaneous, intramuscular or intravenous. ●● Monitor serum sodium, calcium and magnesium. ●● Refractory status epilepticus can often be corrected by resolving metabolic abnormalities.
Figure 21.7: This picture shows a convulsing child being mask ventilated on arrival using the two person technique. Bag-valvemask ventilation of the older child is not easy. The respiratory arrest secondary to involvement of the intercostal muscles during active convulsions can make effective bagging very difficult. The airway nurse is suctioning. Two nurses are assigned to secure intravascular access. One more member of the emergency team formulates the initial dose of lorazepam and administers it over 1–2 minutes.
Circulation Shock could occur due to a wide variety of causes in con vulsing children. ●● Neurogenic: Distributive shock. ●● Hypoxia: Distributive shock with or without myocar dial dysfunction. ●● Coexisting sepsis. ●● Coexisting hypovolemia. During SE, cerebrovascular resistance falls due to hypoxia, resulting in severe derangement of cerebral autoregulation. Cerebral perfusion becomes directly dependent on sys temic blood pressure. Within the first ½ hour of SE, blood pressure rises. Later blood pressure either becomes normal or hypotensive. ●● Secure intravenous access on arrival and provide non-glu cose containing isotonic fluids. At least two nurses may be needed to secure intravenous access (Figure 21.7). ●● If IV access is unavailable, intraosseous access must be secured. If shock is identified the first bolus of 20 mL/ kg is administered. ●● If euvolemic restrict fluids to 2–3 mL/kg/h. ●● Shock secondary to idiopathic SE will resolve follow ing administration of 20–30 mL/kg of fluids.
Chapter 21 n Status Epilepticus
●● Shock complicated by diarrhea or sepsis will require large volumes to attain therapeutic goals. ●● Caution: Fluid therapy phenytoin administration can IP :or196.52.84.10 unmask underlying myocardial dysfunction.
203
Metabolic disorders were reported in an average of 6% (range 1%–16%) of children with SE9.
Myocardial Dysfunction and Pulmonary Edema Status epilepticus can precipitate acute lung injury. Severe sepsis can also have the same impact on the alveolar cap illary membrane. Myocardial dysfunction can also occur in children with prolonged SE. Drugs and fluid therapy can unmask PE during management. If signs of PE are not recognized during resuscitation of SE, cardiac arrest can supervene. Repeated cardiopulmonary cerebral assessments are crucial for recognizing these dreaded complications. ●● If signs of pulmonary edema or myocardial dysfunc tion are identified during fluid administration: – Interrupt fluids. – Initiate an inotrope. – Intubate using ICP precautions. ●● After intubation, if features of PE and hepatomegaly resolve, further fluids are administered if shock persists secondary to sepsis or hypovolemia. ●● If child is receiving phenytoin when signs of PE are identified (stop the drug) or avoid phenytoin if not al ready started.
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Aggressive management of shock based on etiology is mandatory for intact neurological survival. Resuscitation of SE requires team effort and coordination in a time sensitive manner (Figure 21.8). ●● One emergency physician and nurse manages the air way and breathing on arrival (the airway nurse assists in suctioning). ●● The second physician performs the rapid cardiorespira tory assessment and documents the clinical findings. ●● Two nurses are needed to secure IV access, administer fluids, dextrose and the first dose of anticonvulsant. ●● The airway manager should also attempt to obtain a focussed history, confirm eye signs, ensure that a thermometer, pulse oximeter and cardiac monitor are placed to monitor the child. ●● Collect blood for Na, K, Ca, Mg, urea and creatinine.
Figure 21.8: This picture shows the management of convulsive SE on arrival: The first responder opens the airway using the headtilt, chin-lift maneuver and initiates bag-valve-mask ventilation. The airway nurse simultaneously suctions the oropharynx inserts an age appropriate nasogastric tube and decompresses stomach contents. Whilst airway management is in progress, the second physician performs the rapid cardiopulmonary cerebral assessment. The pulse oximeter is showing 91% saturation. The third physician or nurse secures vascular access and administers drugs and fluids, etc.
Drug Therapy The goal of drug therapy is the rapid control of convul sions. The longer the duration of convulsion, the greater the risk of complications. Hence, it seems mandatory to follow a clear drug protocol, which is understood by all personnel. Continuous monitoring and skilled care is es sential during administration of drugs due to the grave risk of hypoventilation and hypotension during resuscitation. 1. Benzodiazepines10,11 are the most potent and effective first-line drugs in the management of SE. Presence of apnea is not a contraindication to the administra tion of benzodiazepines. The rapid onset of action of benzodiazepines is often useful in resolving seizureinduced apnea. Due to the risk of respiratory depres sion, ability to support ventilation is a prerequisite during administration of any of the benzodiazepines. ●● Lorazepam controls seizures within 3 minutes in 50% of patients. Despite being comparable in po tency and efficacy to diazepam, lorazepam has a longer duration of antiseizure effect (12–24 hours). Reduced risk of recurrence has made lorazepam the
204
Section VI n Disability
preferred first-line benzodiazepines in the treatment of SE. Besides, lorazepam has less respiratory de pression than diazepam. However, lorazepam needs IP : 196.52.84.10 to be refrigerated and should be diluted and admin istered as a bolus over 1 minute. ●● The anticonvulsant effect of diazepam lasts for 30 minutes resulting in a high risk of recurrence of SE if this drug is used alone. It is therefore recommended that, even if diazepam has stopped a convulsive SE, phenytoin should be given to prevent recurrence of seizures. Even if the fit appears to have been con trolled during administration of benzodiazepines, the full dose should be given in order to avoid con verting a convulsive SE to non-convulsive SE. ●● Midazolam11,12 has no advantage over diazepam or lorazepam. It is advantageous, since it is the only benzodiazepine that can be administered via the in tramuscular route when other routes are not avail able. It has a rapid onset of action and controls sei zures in 90% of patients. Its shorter half-life and resultant increased risk of recurrence makes it a less preferred drug to lorazepam in the initial manage ment of SE in the ED. Midazolam also has an added risk of hypotension, a dreaded complication in SE resuscitation. ●● A second dose of lorazepam or diazepam may be repeated in 5 minutes, if seizures are not controlled with the first dose. 2. Phenytoin13,14,15 is the second-line drug in patients not responding to the initial two doses of benzodiazepines. Since it is poorly soluble in water and precipitates in dextrose containing solutions. It is infused in normal saline (dose of 15–20 mg/kg) at the rate of 1 mg/kg/ min with maximum rate of 50 mg/min. Anti-seizure threshold in the brain is reached within 10–30 minutes after infusion. If convulsions are not controlled, 5 mg/ kg increments can be administered up to a maximum loading dose of 30 mg/kg. ●● Phenytoin decreases automaticity of cardiac tissue by prolonging the effective refractory period. ●● Phenytoin decreases the force of cardiac contrac tion leading to hypotension following rapid IV ad ministration. ●● Severe cardiotoxic reactions and fatalities have been reported with atrial and ventricular conduction depression and ventricular fibrillation. Phenytoin can be safely used in children who come early in the course of seizures. Its use in children presenting
with prolonged uncorrected SE or SE complicating serious sepsis or SE in children with evidence of cardiac dysfunction should be viewed with cau tion.
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Phenytoin is potentially cardiotoxic.16,17 To avoid the worsening of myocardial dysfunction in chil dren presenting with SE in our setting the following pre cautions are taken in planning the drug protocol (Figure 21.9):
Figure 21.9: History that aids in anticipation of pulmonary edema and hence phenytoin is unsafe
1. Check history to find out whether abnormal move ments were truly:
a. Tonic-clonic? or b. Stiffening, upward gaze, squirming movements? etc. c. The caretaker who rushed the child must demon strate whether the movements were indeed convul sions not posturing.
2. Were the movements preceded by precipitating events such as fever, breathlessness or diarrhea.
a. History of altered mental status such as incessant crying, lethargy, increased sleepiness, posturing or stiffening, between precipitating event or not? b. Were the movements not preceded by altered men tal status: Child was playing, performing routine activities?
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If GTCs was preceded by altered mental status, consider the possibility of hypoxia or shock complicating SE. Avoid phenytoin.
Chapter 21 n Status Epilepticus
205
Pyridoxine IP : 196.52.84.10
When seizures are not responsive to phenytoin, pyridox ine (50–100 mg) and the convulsing infant is less than 18 months, pyridoxine should be administered. Watch out for apnea.
Valproic Acid Valproic acid19–23 a broad-spectrum anticonvulsant acts by modulating sodium and calcium channels and inhibiting aminobutyric acid transmission. Figure 21.10: History that rules out of pulmonary edema and hence phenytoin is safe
3. During phenytoin infusion, if the following signs of cardiac dysfunction or pulmonary edema are noted, stop phenytoin infusion.
a. Pink froth. ●● It may be difficult to differentiate froth from oropharyngeal secretions due to GTCs. Onset of froth in a child whose airway was initially clear, may be the first clue that PE is developing in a fitting child. Refer Figure 21.10. b. Retractions, grunting. c. Gallop, muffling of heart sounds, bradycardia, hy potension, widening of pulse pressure with low mean arterial pressures, increasing liver span or drop in oxygen saturations.
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If pulmonary edema or myocardial dysfunction is anticipated or occurs during phenytoin infusion, consider initiating levetiracetam or/and sodium valproate after the initial doses of benzodiazepines. Fosphenytoin, a water-soluble phosphoester of pheny toin has been considered less cardiotoxic effects than phe nytoin and may be safer. However, cardiac dysrrythmias have been reported even with the use of fosphenytoin.18 This drug can be given/administered through the intramus cular route if intravenous (IV) access is not available. The APLS recommends that, the loading dose of phe nytoin should be avoided for children taking chronic phe nytoin therapy.
●● Sodium valproate is given as initially as a bolus: 25 mg/kg bolus (max 40 mg/kg), followed by an infusion of 5 mg/kg/hour. ●● Sodium valproate has less sedation, good cardio vascular profile and lower risk of respiratory failure compared to other anticonvulsants. ●● Sodium valproate should be avoided, if child has evi dence of liver disease or metabolic disease or hemo static abnormalities.
Levetiracetam24-28 Levetiracetam acts through calcium channels, glutamate receptors and g-aminobutyric acid modulation (synap tic vesicle 2A ligand). Intravenous Levetiracetam is not metabolized by the liver, has little affinity to protein, is excreted via renal pathway and has minimal drug-drug in teractions. ●● It is administered as a bolus of 20–30 mg/kg IV at 5 mg/kg/min (max 3 g). ●● When SE is complicated by pulmonary edema, myo cardial dysfunction coagulopathy, liver failure or hy potension, Levetiracetam is an excellent alternative antiseizure agent. ●● In some children it may cause reversible behavioral changes.
Alternative Routes of Drug Administration When intravenous access is not available, midazolam (0.2 mg/kg) can be given intramuscularly, rectally or into the buccal space. ●● All anticonvulsant drugs except phenytoin have achieved therapeutic levels in the blood when ad ministered via the intraosseous route. The doses of these drugs are the same as for the IV route.
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Section VI n Disability
case scenario 2 An 8-years-old girl was rushed into the ER after being : 196.52.84.10 found unresponsive inIPthe bathroom. She has been on treatment for seizures for the past 5 years, but missed her medication for the last 2 days.
Continuation of the aggressive management of the air way, breathing and circulation with the same drug protocol as for CSE until all therapeutic goals are achieved is rec ommended (Figure 21.13).
Figure 21.13: Therapeutic goals of seizure control—Normal cardiorespiratory cerebral assessment Figure 21.11: Conjugate deviation of eyes
The management of NCSE is similar to CSE. Continue therapy until all therapeutic goals of shock and seizure ac tivity has resolved.
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A good indicator of seizure control is return of baseline sensorium. ●● Failure to regain baseline consciousness following a con vulsion often indicates the presence of ongoing NCSE.
Figure 21.12 Physiological status: Airway obstructed, effortless tachypnea, tachycardia, normotensive shock, NCSE.
Non-convulsive Status Epilepticus (NCSE) Conjugate deviation of eyelid twitch, nystagmus or unilat eral clonus in an unresponsive child helps to recognize this condition (Figures 21.11 and 21.12). ●● Anticipate non-convulsive SE in children who pres ent with sudden unresponsiveness or who have been having seizures, but who have not regained baseline consciousness. ●● More commonly, convulsive status epilepticus (CSE) evolves into subtle SE during resuscitation. Active convulsions disappear, but the child remains apneic or tachypneic, shocky and unresponsive. The eye signs indicate persistence of ongoing seizure activity.
Cessation of overt motor movements alone should not be considered as achievement of complete seizure control. Careful monitoring and management should continue until all therapeutic goals (seizure, hypoxia, shock and cardiac dysfunction are achieved).
Ù
Persistence of altered level of consciousness: ‘Responsive to pain or unresponsive’ is often mistaken as ‘postictal state’. A high index of suspicion is needed to identify NCSE or shock in children presenting with seizure activity.
Refractory Status Epilepticus Definitions of refractory status epilepticus (RSE) vary. Since, majority of children have been convulsing for > 1 hour and have not received prehospital respiratory support during the management of seizures, we define this entity as SE not controlled with the initial two adequate doses of benzodiazepines and phenytoin.
Chapter 21 n Status Epilepticus
207
Midazolam
Targeted History
Midazolam a water-soluble benzodiazepine, rapid IP : 196.52.84.10 ly penetrates the blood-brain barrier and exerts its anticonvulsive effect for a short duration. It suppresses neu ronal excitability by modulating the γ-aminobutyric acid receptors. Midazolam is hydroxylated in the liver and the metabolite is excreted by the kidneys. Hence midazolam should be used with caution in children with underlying hepatic or renal dysfunction.
Often panic-stricken parents will be unable to provide a coherent history on reaching the ED with a convulsing child. Nowhere, is a correct history more important than in management of SE. Hence, a short targeted history is essential to ensurse appropriate therapy.
29-35
●● Midazolam a good choice for the initial treatment of RSE, is given as 0.2 mg/kg IV bolus. To avoid hypoten sion, midazolam is given slowly over 1–3 minutes. ●● A continuous infusion of 1 µg/kg/min of midazolam with increments of 1 µg/kg/min every 15 minutes is recommended until the seizures are controlled. The maximum rate of infusion is 50 µg/kg/min. ●● Though higher boluses and more rapid escalation may be associated with more prompt seizure control, hy potension following use of midazolam remains a seri ous concern. ●● Midazolam infusion requires the use of infusion pumps to ensure precise titration.
Phenobarbital36 Indicated in RSE and neonatal SE. It depresses neuronal excitability by enhancing the g-aminobutyric acid recep tor response. Depression of mental status and respiratory failure are common side effects. Intubation is mandatory if Phenobarbital is administered after benzodizepines. Be sides, the drug must be administered slowly to avoid hy potension. ●● The recommended dose is 20 mg/kg up to a maximum of 30 mg/kg and the rate of infusion is 1–2 mg/kg/min. The antiseizure effect occurs within 10–20 minutes. Unlike phenytoin, Phenobarbital can be safely used in patients already maintained on this drug.
Thiopental37 The loading dose of thiopentone sodium is 3–5 mg/kg. It is followed by an infusion. Severe hypotension requiring vasopressor therapy and prolonged postinfusion weakness and delaying weaning make it a less commonly used drug in RSE.
Ù
1. Are the movements tonic-clonic or posturing (stiffening, upward gaze, flexor or extensor posturing, squirming movements, etc.). Since, all abnormal movements should not be treated as CSE, it is worthwhile requesting parents who accompany the child to enact the abnormal movements. 2. Time of onset. 3. Place of onset helps to determine the approximate time taken to reach your hospital (duration of convulsive event). 4. Number of episodes. 5. Did the mental status revert to normal (alert, playing) after the convulsion? 6. History of precipitating event such as fever, diarrhea, vomiting, toxin, trauma? 7. History of altered level of consciousness between fever or diarrhea (precipitating event) and fit (as discussed earlier). – A systematic history helps in determining two important issues, which help in the management: whether the convulsion was a primary event or whether it was precipitated by hypoxia or shock. – The latter suggests a more critically ill child who would need greater aggression in the management of underlying hemodynamic compromise. In these children use of phenytoin should be avoided, since it worsens the underlying myocardial dysfunction. 8. Was the child developmentally normal or abnormal? 9. Did the child have seizures or any other comorbidity in the past? 10. Was he on antiepileptic drugs? How was his drug compliance? 11. What was the nature of prehospital care? Use of benzodiazepines or intravenous phenytoin in prehospital settings could help to titrate the loading dose of these drugs.
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Section VI n Disability
Emergency Investigations Blood is collected for glucose, renal and liver functions, IP : 196.52.84.10 calcium, magnesium, complete blood count (CBC), cul tures, prothrombin time (PT), prothromboplastin time (PTT) and blood gases. As per the recommendations of American Academy of Neurology,38 the following have been suggested: ●● There is insufficient data to support or refute the recommendations for taking blood or CSF for culture on a routine basis (no clinical suspicion of systemic or CNS infection) (Level U). ●● Anticonvulsant levels should be considered when a child with treated epilepsy develops SE (Level B). ●● Toxicology studies and metabolic studies for inborn er rors of metabolism may be considered in children with SE when there are clinical indicators for concern or when the initial evaluation reveals no etiology (Level C). ●● An EEG may be considered in a child with SE as it may be helpful in determining, whether there are fo cal or generalized epileptiform abnormalities that may guide further testing for the etiology of SE, when there is suspicion of pseudostatus epilepticus (non-epileptic SE) or non-convulsive SE (Level C). ●● Neuroimaging may be considered after the child with SE has been stabilized, if there are clinical indications or if the etiology is unknown (Level C). There is insuf ficient evidence to support or refute routine neuroimag ing in a child presenting with SE (Level U).
Treatment of Specific Causes of SE Central nervous system infections, head trauma, cerebral edema, space occupying lesion, hemorrhage, poisons, hy poglycemia, hypoxia, hypertensive encephalopathy, elec trolyte imbalances and drug toxicity can all produce sei zures that are difficult to control. Assessment of patient for possible etiology is performed after controlling the seizures. Refer Table 21.2 for drugs used.
The presence of strict treatment protocols for SE made readily available for the treating staff could potentially im prove the outcome of patients.
Key Points
ü
1. Differentiation of convulsion from hypoxic postur ing. 2. Differentiation of postictal state from persistence of altered level of consciousness secondary to ongoing NCSE or hemodynamic compromise. 3. Failure to initiate bag-valve-mask and correction of shock during management of status epilepticus could be lethal. 4. Administration of IM diazepam will worsen seda tion and respiratory failure without resolving seizure activity. 5. Phenytoin administration could be dangerous in children who develop signs of pulmonary edema and myocardial dysfunction during management of status epilepticus. 6. Rapid IV administration of midazolam could result in hypotension.
common errors
û
1. Oxygen via non-rebreathing mask is sufficient to correct hypoxia in a child convulsing for more than 5 minutes. 2. All abnormal movements are convulsions. 3. Unaware that use of anticonvulsants in hypoxic pos turing could precipitate cardiac respiratory arrest. 4. Failure to remember that the longer duration of ac tion of lorazepam helps to prevent recurrence. 5. Failure to realize that rapid administration of mi dazolam or phenobarbital can precipitate hypoten sion. 6. Failure to continue treatment after active convulsion has stopped in a child who remains hemodynami cally compromised with NCSE.
Chapter 21 n Status Epilepticus
209
Table 21.2: Drugs used in emergency room for management of status epilepticus Drug
Initial dose
Route
IV administration
IP : 196.52.84.10
Onset of action
Half-life
Adverse effects
Lorazepam
0.05 mg 0.1 mg/kg Max: 4 mg
IV
IV 0.5 mg/kg Infusion: 0.01-0.1 mg/kg/h
1–3 minute
Neonates: 40 hour Children: 10 hour
Sedation, hypotension, bradycardia, respiratory depression, hyperactivity.
Diazepam
0.05–0.3 mg/kg Max: < 5 y–5 mg > 5 y–10 mg PR dose–0.5 mg/kg
IV PR
0.1 mg/kg/min
1–3 minute
Neonates: 50.95 h. Infants: 40–50 hour Children: 15–20 hour
Sedation, hypotension, bradycardia, respiratory depression, hyperactivity thrombophlebitis.
Midazolam
0.1–0.15 mg/kg Max: 0.15 mg/ kg
IV PR
Infusion: 1 mg/kg/ min - to max of 24 mg/kg/min
1–5 minute
Neonates: 4–12 hour Children: 3–4 h
Sedation, hypotension, bradycardia,(if hypotensive or bradycardic avoid midazolam) respiratory depression, apnea, laryngospasm, hyperactivity.
Phenytoin
15–20 mg/kg Max: 1 g
IV
Slow IV over a period of 20 minute @ 1 mg/kg/min to max of 50 mg/kg/ min. Monitor heart rate and BP during administration. Infusion may be titrated to maintain base line heart rate.
10 minute after the infusion is over
7–24 hour (first order kinetics do not apply)
Tachyarrhythmia commonly seen during administration. Decreased infusion rate. Bradyarrhythmia, gallop, pulmonary edema, hypotension noted during infusion is suggestive of underlying myocardial depression due to RSE, severe sepsis, etc. Stop PHT and consider alternative. Dysarthria, ataxia, sedation, thrombophlebitis, purple glove syndrome.
Fosphenytoin
15–20 mg PE/ kg
IV IM
3 mg PE/kg/min to max 150 mg PE/ min
7 minute 5/12 to convert to phenytoin
12–29 h (first order kinetics do not apply)
Dysarthria, ataxia, sedation, hypotension, arrhythmia.
Valproic acid
15–20 mg/kg Max: 25 mg/kg
IV
5 mg/kg/min Infusion: 1–4 mg/ kg/h
> 2 month 7–13 hour 2–14 year 40–20 hour
Hypotension, arrhythmia, hepatitis, pancreatitis.
Paraldehyde
200–400 mg/kg Max: 10 g PR
PR
n/a
4–10 hour
Rectal irritation, lung toxicity.
Levetiracetam
Bolus of 20–30 mg/kg
IV
5 mg/kg/min (max 3 g)
1 hour
6-8 hour
Behavioral changes
Phenobarbitone
15–20 mg/kg up to max 1 g/ dose
IV
1 mg/kg/min up to max of 60 mg/min
5 minute
Neonates: 45–200 hour Infants: 20–133 hour Children: 33–73 hour
Respiratory depression, prolonged sedation, hypotension immunosuppression. Intubate, if used following benzodiazepines. Contd...
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Section VI n Disability
Contd... Drug
Initial dose
Route
IV administration
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Onset of action
Half-life
Adverse effects
Thiopentone
2–4 mg/kg
IV
1–6 mg/kg/h
30–60 second
14–34 hour
Sedation, hypotension, respiratory depression, accumulation due to lipid solubility, extravasation can cause skin necrosis due to pH of 10.6.
Lidocaine
2–3 mg/kg (Max: 200–300 mg)
IV
3–10 mg/kg/h
50 mg/min
1.5–2 hour in adults
Sedation
Chapter 21 n Status Epilepticus
211
Protocol 21.1: PEMC approach: Recognition and management of convulsive and non-convulsive status epilepticus in ED
IP : 196.52.84.10
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Section VI n Disability
REFERENCES 1. Lowenstein DH, Bleck T, Macdonald RL. It’s time to IP :of196.52.84.10 revise the definition status epilepticus. Epilepsia 1999;40:120-22. 2. Nicholas S, Abend, MD, et al. Medical treatment of pediatric status epilepticus. Semin Pediatr Neurol. 2000;17:169-75. 3. Shinnar S, Berg AT, Moshe SL, et al. How long do new-on set seizures in children last? Ann Neurol. 2001;49:659-64. 4. Wasterlain CG, Chen JW. Definition and classification of status epilepticus. In: Wasterlain CG, Treiman DM (Eds). Status Epilepticus. Cambridge MA: MIT Press;2006.11-16. 5. Sperk G. Changes in GABA-A receptors in status epilepti cus. Epilepsia. 2007;48(Suppl 8):11-13. 6. Loscher W. Mechanisms of drug resistance in status epilep ticus. Epilepsia. 2007;48(Suppl. 8):74-77. 7. McIntyre J, Robertson S, Norris E, et al. Safety and ef ficacy of buccal midazolam versus rectal diazepam for emergency treatment of seizures in children: A randomized controlled trial. Lancet. 2005;366:205-10. 8. M Ballaaji, I Santhanam, P Venkatesh, et al. Clinical profile and risk factors for intubation in children presenting with status epilepticus to the pediatric emergency department. Proceedings of National Assembly on Pediatric Emergency Medicine. 2011. p. 189. 9. KD Statler, CB Van Orman. Status Epilepticus Roger’s Handbook of Pediatric Intensive Care, 4th edition. 2009. 10. Riviello JJ Jr, Ashwal S, Hirtz D, et al. Practice parameter: diagnostic assessment of the child with status epilepticus (an evidence-based review): report of the Quality Stan dards Subcommittee of the American Academy of Neurol ogy and the Practice Committee of the Child Neurology Society. Neurol. 2006;67(9):1542-550. 11. Appleton R, Macleod S, Martland T. Cochrane review 2009: Drug management for acute tonic-clonic convul sions including convulsive status epilepticus in children. 12. McMullan, et al. Midazolam versus Diazepam for the treatment of status epilepticus in children and young adults: A Meta-analysis. Academic Emergency Medicine. 2010;17:575-82. 13. Rivera R, Segnini M, Baltodano A, et al. Midazolam in the treatment of status epilepticus in children. Crit Care Med. 1993;21:991-94. 14. Brevoord JC, Joosten KF, Arts WF, et al. Status epilepticus: Clinical analysis of a treatment protocol based on midazo lam and phenytoin. J Child Neurol. 2005;20:476-81. 15. Lewena S, Young S. When benzodiazepines fail: How ef fective is second line therapy for status epilepticus in chil dren? Emerg Med Australas. 2006;18:45-50. 16. York RC, Coleridge ST. Cardiopulmonary arrest following intravenous phenytoin loading. Acta Neurologica Scandi navica. 1992;3(85):174-76.
17. JG Boggs, et al. Analysis of electrocardiographic changes in status epilepticus. Epilepsy Research. 1993;(14):187-94. 18. BD Adams. Fos-phenytoin may cause hemodynamically unstable bradydysrhythmias. Presented at the Southern Medical Association Annual Scientific Assembly. Wash ington, DC: November 2002;13-16. 19. Limdi NA, Knowlton RK, Cofield SS, et al. Safety of rapid in tra-venous loading of valproate. Epilepsia. 2007;48:478-83. 20. Yu KT, Mills S, Thompson N, et al. Safety and efficacy of intravenous valproate in pediatric status epilepticus and acute repetitive seizures. Epilepsia. 2003;44:724-26. 21. Uberall MA, Trollmann R, Wunsiedler U, et al. Intrave nous valproate in pediatric epilepsy patients with refrac tory status epilepticus. Neurology. 2000;54:2188-189. 22. White JR, Santos CS. Intravenous valproate associated with significant hypotension in the treatment of status epi lepticus. J Child Neurol. 1999;14:822-23. 23. Mehta V, Singhi P, Singhi S. Intravenous sodium valproate ver-sus diazepam infusion for the control of refractory sta tus epilep-ticus in children: a randomized controlled trial. J Child Neurol. 2007;22:1191-197. 24. Szaflarski JP, Meckler JM, Szaflarski M, et al. Leve tiracetam use in critically ill patients. Neurocrit Care. 2007;7:140-47. 25. Ramael S, Daoust A, Otou C, et al. Levetiracetam intra venous infusion: A randomized, placebo-controlled safety and pharmacokinetic study. Epilepsia. 2006;47:1128-135. 26. Patel NC, Landan IR, Levin J, et al. The use of levetiracetam in refractory status epilepticus. Seizure. 2006;15:137-41. 27. Nicholas S, Abend MD, et al. Intravenous levetiracetam in critically ill children with status epilepticus or acute repeti tive seizures. Pediatr Crit Care Med. 2009;10(4):505-10. 28. Levetiracetam in children with refractory status epilepti cus. Epilepsy Behav. 2009;14(1):215-18. 29. Koul RL, Raj Aithala G, Chacko A, et al. Continuous mida zolam infusion as treatment of status epilepticus. Arch Dis Child. 1997;76:445-48. 30. Igartua J, Silver P, Maytal J, et al. Midazolam coma for refractory status epilepticus in children. Crit Care Med. 1999;27:1982-985. 31. Ozdemir D, Gulez P, Uran N, et al. Efficacy of continu ous midazolam infusion and mortality in childhood refrac tory generalized convulsive status epilepticus. Seizure. 2005;14:129-32. 32. Gilbert DL, Gartside PS, Glauser TA. Efficacy and mortal ity in treatment of refractory generalized convulsive status epilepticus in children: A meta-analysis. J Child Neurol. 1999;14:602-09.
Chapter 21 n Status Epilepticus
33. Morrison G, Gibbons E, Whitehouse WP. High-dose mida zolam therapy for refractory status epilepticus in children. Intensive Care Med. 2006;32:2070-076. IP : 196.52.84.10 34. Koul R, Chacko A, Javed H, et al. Eight-year study of childhood status epilepticus: Midazolam infusion in man agement and outcome. J Child Neurol. 2002;17:908-10. 35. Hayashi K, Osawa M, Aihara M, et al. Efficacy of intrave nous midazolam for status epilepticus in childhood. Pediatr Neurol 2007;36:366-72.
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36. Lee WK, Liu KT, Young BW. Very-high-dose phenobarbi tal for childhood refractory status epilepticus. Pediatr Neu rol. 2006;34:63-65. 37. Andrea O Rossetti. Which anesthetic should be used in the treatment of refractory status epilepticus? Epilepsia. 2007;48(Suppl. 8):52-55. 38. Riviello JJ, Ashwal S, Hirtz D, et al. Practice parameter: Di agnostic assessment of the child with status epilepticus (an evidence based review). Neurology. 2006;67:1542-550.
Section VII
IP : 196.52.84.10
Envenomation
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22
IP : 196.52.84.10
Scorpion Sting
Figure 22.1: Appropriate knowledge of the pathophysiology is essential to manage children with scorpion bite successfully (Courtesy: Dr Thangavelu S).
Learning Objectives 1. Newer concepts on how the venom affects the autonomic system, heart and lungs. 2. To assess the severity of scorpion envenomation using the rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle.
Introduction Scorpion stings are common in rural areas. Although 99 species of scorpion have been identified in India, only two, Mesobuthus tamulus (the common red scorpion) (Figure 22.1) and Palamnaeus swammerdami are poisonous.1 Cardiac manifestations, are common in Indian red scorpion envenomation. If not treated, death can occur in up to 25% of children below the age of 5 years.
Pathophysiology Pulmonary edema (PE) is the most common cause of death in scorpion envenomation.2 Cardiac dysfunction is the commonest cause of this dreaded complication.3,4 In addition, acute lung injury due to increased alveolar capillary membrane permeability (non-cardiogenic pulmonary ede ma) has also has been noted.3,5,6 Pathogenesis of myocardial dysfunction and increased blood pressure has been at-
3. Evidence-based drug protocol. 4. Case scenarios illustrating how the PAT can be used to decide management.
tributed to excessive catecholamine release.7,8,9 The venom induces excessive catecholamine release or an autonomic storm which activates the α-receptors, leading to the effects mentioned above viz. pulmonary edema, myocardial dysfunction, tachycardia, shock, hypertension and excessive sweating.
Clinical Features Clinical manifestations may be local or systemic. The symptoms may progress to maximal severity in 3–5 hours and subside within 1–2 days. ●● The local manifestations include intense pain at the site of sting, swelling and ecchymosis. It has also been observed that if the pain is severe, there is less propensity for progression to the more severe manifestations. ●● The initial cholinergic stimulation causes vomiting, salivation, sweating, cold extremities, priapism and
218
●●
●●
●● ●●
●●
Section VII n Envenomation
bradycardia. Sweating and salivation may persist for 6–13 hours. Occurrence of priapism, a poor prognostic sign seems to be associated with myocardial dysfuncIP : 196.52.84.10 tion. Stimulation of the sympathetic system leads to tachypnea, pulmonary edema, tachycardia, arrhythmias, hypertension, peripheral vasoconstriction, shock and myocardial dysfunction. Hypertension usually lasts for 4–8 hours. Hypotension which occurs in the early cholinergic phase (1–2 hours) secondary to bradycardia indicates a poor prognosis. It has also been noted at 4–48 hours when it has been attributed to severe left ventricular dysfunction. Hypotension can also manifest 48–72 hours secondary to depletion of stored catecholamine. Pulmonary edema, either cardiogenic or non-cardiogenic can occur as early as 30 minutes after the scorpion sting. Neurotoxicity secondary to scorpion envenomation though uncommon is reported in India.10 The signs include uncoordinated neuromotor hyperactivity, oculomotor and visual abnormalities, restlessness, agitation, abnormal behavior, altered sensorium, convulsions, hemiplegia and cerebral thrombosis.11,12 Other rare, but fatal complications include DIC, hemolysis, and pancreatitis.
Figure 22.3 Physiological status: Impending respiratory failure with hypotensive cardiogenic shock.
Interventions ●● ●● ●● ●●
Position airway and suction. Provide O2 via the JR circuit. 5–10 mL/kg NS bolus (pull push technique). Watch for signs of improvement or deterioration (evidence of PE). ●● Withhold Prazosin till BP normalizes. ●● After 10 mL/kg, the assessment was repeated.
Case scenario 1 A 10-year-old child is rushed into the ED with a history of having been stung by a scorpion 3 hours ago. He has increased salivation and has vomited twice. He also has severe diaphoresis (Figures 22.2 to 22.4).
Figure 22.4 Physiological status: Worsening of pulmonary edema, but his heart rate and BP have improved.
●● Initiate Dobutamine infusion at 10 µg/kg/min. ●● Intubate using PAI. Figure 22.2: Sweating and salivation may persist for 6–13 hours (Courtesy: Dr Bawaskar HS).
CASE SCENARIO 2 A 3-year-old girl had been rushed to the ED as soon as she was bitten by a scorpion an hour ago at her home.
Chapter 22 n Scorpion Sting
She was crying due to severe pain over right foot. She was also having increased salivation and was profusely sweating (Figure 22.5). IP : 196.52.84.10
219
Prazosin is available as 1 mg (scored) tablet. Sustained release tablets are not advised in this condition. The recommended dose is 30 µg/ kg/dose. Administration of Prazosin in the prehospital setting is one of the most useful strategies to reduce mortality in scorpion envenomation.
Ù
Indeed, Prazosin must be stocked in every primary health center and administered when signs of ‘autonomic storm’ are identified.
Figure 22.5 Physiological status: Her cardiopulmonary and cerebral assessment was normal. However, she is showing signs of autonomic storm and has higher than normal blood pressure with peripheral vasoconstriction.
Management of Local and Systemic Effects ●● Local pain is managed with ice compression, oral paracetamol and regional nerve block using low concentration of lidocaine (without epinephrine). ●● Antiemetics may be needed if vomiting is severe. ●● Seizures are managed with benzodiazepines. ●● Tetanus toxoid should be given intramuscularly. ●● Routine antimicrobials are not needed.13 ●● Profuse diaphoresis and vomiting can cause fluid loss. If the cardiopulmonary assessment suggests that the child is stable but dehydrated, the hydration status is corrected by fluid replacement. ●● Prazosin is administered orally in the prescribed dose.
Prazosin
Prazosin is administered only when features of autonomic storm are identified. In hemodynamically unstable patients, the priority remains in stabilization of the airway, breathing and circulation. If shocked and hypotensive, it seems intuitive to correct shock and BP prior to administration of Prazosin. This drug should not be given prophylactically in the absence of the ‘autonomic storm’. If the child is unable to swallow, it may be administered through a nasogastric tube. The mother should be instructed to keep the child in the supine position to avoid ‘first dose hypotension’ due to Prazosin. The rapid cardiopulmonary assessment should be performed every 30 minutes for 3 hours, every hour for next 6 hours and later every 4 hours till improvement. Prazosin is repeated in the same dose at the end of 3 hours and later every 6 hours till extremities are warm and dry. Not more than 4 doses are usually required in children.
CASE SCENARIO 3 A 2-year-old boy was rushed into the ED with history of unknown insect bite over his right elbow. He had vomited twice and had profuse sweating. He had been taken to the nearest PHC prior to referral and had reached the ED 6 hours after the bite (Figures 22.6 and 22.7).
Mechanism of action Prazosin suppresses the sympathetic outflow and activates venom inhibited potassium channels. It blocks the postsynaptic α-1 receptors and also prevents prostaglandin production. It reduces cardiac preload, afterload, BP and CNS sympathetic stimulation without increasing the heart rate or cardiac output (cardioprotective effect). Thus, it prevents the hypertensive stress on the myocardium. Its mechanism of action seems to counter the activity of the scorpion venom. Oral Prazosin is fast acting, easily available, relatively cheap, free from any anaphylaxis and highly effective.
Figure 22.6: Priapism, a poor prognostic sign seems to be associated with myocardial dysfunction (Courtesy: Dr Thangavelu S).
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Section VII n Envenomation
IP : 196.52.84.10
Figure 22.7 Physiological status: Respiratory distress probably due to cardiogenic or non-cardiogenic pulmonary edema with normotensive shock.
Figure 22.8: This picture shows pink froth which should be differentiated from salivation (Courtesy: Dr Thangavelu S).
Ù
Autonomic storm or pulmonary edema or priapism confirm the diagnosis of scorpion sting. ●● Provide O2 using a JR circuit. ●● Secure vascular access. ●● Administer 10 mL/kg of NS or RL; Prescribe oral Prazosin (via NGT if he is unable to tolerate orally or is vomiting). ●● Advice mother to keep her child supine to avoid druginduced hypotension. ●● Repeat cardiopulmonary cerebral assessment. ●● If therapeutic goals of shock have not resolved and no signs of pulmonary edema are noted, administer 5–10 mL/kg of fluids (maximum of 20 mL/kg) until shock resolves. ●● Administer Prazosin 4th hourly as needed. ●● If shock has not resolved at 20 mL/kg or signs of pulmonary edema are noted at 5 or 10 or 15 or 20 mL/kg, initiate Dobutamine if BP is high3,8,9,10 and plan intubation.
CASE SCENARIO 4 A 6-year-old girl was rushed into the ED for having been stung by a scorpion the previous night. The nurse in the PHC where she had been taken, had injected her with Decadron, Avil and Paracetamol and adviced to return home. Next day she was found to be drowsy, breathless with profuse sweating, vomiting. She was coughing pink, frothy sputum (Figures 22.8 to 22.10).
Figure 22.9 Physiological status: Respiratory failure, bradycardia, hypotensive cardiogenic shock with altered mental status.
Management of Complications Airway and Breathing (Refer Protocol 22.1) Since the risk of pulmonary edema is great in scorpion envenomation, oxygen is administered using the JR circuit. This device, helps to provide CPAP in addition to oxygen during resuscitation in the ED.
Circulation Likewise, since the risk of myocardial dysfunction and pulmonary edema exists in children presenting with shock, it would be wise to administer smaller boluses of 5 mL/kg up to a maximum of 20 mL/kg. ●● If shock improves, further fluids may be stopped.
Chapter 22 n Scorpion Sting
●● If shock does not improve after the initial 20 mL/kg, check for history of hypovolemia such as vomiting or diaphoresis. If yes, IP smaller boluses may be considered. : 196.52.84.10 If not, consider initiating an inotrope infusion. ●● If during fluid therapy, signs of pulmonary edema or hepatomegaly are noted, stop fluids, initiate inotrope and plan intubation. ●● Dobutamine may be used if BP is high or normal. ●● Severe myocardial dysfunction manifested by hypotension may be treated with epinephrine infusion. ●● Arrhythmias should be managed as per PALS guidelines.
221
Ù
Children who received steroid and antihistaminics either with or without Prazosin had a significantly higher mortality than those who did not receive any treatment.3
Recovery
Ù
Vomiting, salivation, sweating contribute to dehydration. Correction of hypovolemia is a priority.
Investigations ●● Monitor sugar, urea, creatinine and liver enzymes. ●● ECG is useful in identifying ST depression, inverted T waves, deep Q-waves in lead I and AVL, various degrees of heart block and arrhythmias. ●● Echocardiogram may reveal systolic LV dysfunction.
Scorpion Antivenom Though considered as the specific treatment for scorpion envenomation, it must be administered within 30 minutes of sting.18 Scorpion antivenom has not been found to be more effective in reversing the cardiovascular toxic effects of the venom. Indeed, Prazosin has been found to prevent and relieve the cardiovascular manifestations in severe scorpion envenomation. Avoid following drugs in the emergency management of cardiogenic shock due to scorpion sting. ●● ●● ●● ●● ●● ●●
Lytic cocktail. Morphine. Steroids. Antihistamines Digoxin. Diuretics.
Figure 22.10 Physiological status: Alertness, normalization of respiratory rates, work of breathing, heart rates with warm dry normal peripheries, normal BP and liver span are suggestive of recovery.
Prognosis
Ù
Pain and age greater than 6 years are good prognostic signs. Delay in initiation of Prazosin therapy, pulmonary edema, arrhythmias, encephalopathy and age less than 6 years, indicate a poor prognosis. Children presenting with scorpion sting envenomation should be observed for at least 24 hours even if asymptomatic. Outcomes have improved with early identification and management of pulmonary edema and shock in the ED. The early use of Prazosin also seems to have improved the speed of recovery.
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Section VII n Envenomation
Key Points
ü
1. Prehospital Prazosin improves outcome and IP therapy : 196.52.84.10 prevents complications. 2. Keep the patient in lying posture for about 3 hours (even while examining the case) in order to prevent ‘first dose phenomenon’ (hypotension). 3. Recognize pulmonary edema and shock since cardiac manifestations are common in Indian red scorpion envenomation. 4. Use JR circuit to provide oxygen if child has respiratory distress. 5. Administer small aliquots of fluids to resolve shock. 6. Initiate inotrope and perform early intubation if signs of pulmonary edema are noted during shock management.
common errors
û
1. Restriction of fluid due to fear of pulmonary edema. 2. Failure to administer Prazosin to a stable child with features of autonomic storm. 3. Administration of Prazosin in a shocked child without attempting to resolve shock. 4. Administration of large volume of fluids (40–60 mL/kg) in the absence of history suggestive of hypovolemia. 5. Failure to recognize development of pulmonary edema during fluid therapy. 6. Failure to use JR circuit to provide oxygen in respiratory distress. 7. Use of morphine, digoxin, atropine, antihistamine or furosemide for pulmonary edema.
IP : 196.52.84.10
Caution: ●● Risk of cardiogenic or non-cardiogenic pulmonary edema complicates shock management due to scorpion envenomation. ●● During fluid therapy, monitor for airway instability, pink froth, increase or decrease in respiratory rates, grunt, retractions, abdominal respiration, fresh rales, gallop, increasing liver span, agitation, fighting the mask and drop in oxygen saturations (i.e. signs of pulmonary edema). If any one or a cluster of signs develop, stop further fluid, initiate inotropes and prepare to intubate.
Protocol 22.1: PEMC approach: Management of scorpion sting in the ED
Chapter 22 n Scorpion Sting
223
224
Section VII n Envenomation
References 1. Utpal Kant Singh, Layland FC, Sanjay, et al. Animal poiIP :in196.52.84.10 soning. In: Poisoning children, 2nd edition. Jaypee Brothers Medical Publishers (P) Ltd. 68-74. 2. Mahadevan S. Scorpion sting. Indian Pediatrics. 2000;37:504-14. 3. Biswal N, Bashir RA, Murmu UC, et al. Outcome of scorpion sting envenomation after a protocol guided therapy. Indian J Pediatr. 2006 Jul;73(7):577-82. 4. Boyer LV, Theodorou AA, Berg RA, et al. Arizona Envenomation Investigators, Chávez-Méndez A, García-Ubbelohde W, Hardiman S, Alagón A. Antivenom for critically ill children with neurotoxicity from scorpion sting. N ENGL J MED. 2009 May 14;360(20):2090-098. 5. Bahloul M, Rekik N, Chabchoub I, et al. Neurological complications secondary to severe scorpion envenomation. Med Sci Monit. 2005 Apr;11(4):CR196-202. Epub 2005 Mar 24. 6. Handbook on treatment guidelines for snake bite and scorpion sting. Tamil Nadu Health Systems Project, Health and Family Welfare Department, Government of Tamil Nadu, Chennai. 2008.
7. Peker E, Oktar S, Dogan M, et al. Prazosin treatment in the management of scorpion envenomation. Hum Exp Toxicol. 2010 Jan 12 [Epub ahead of print]. 8. Gupta BD, Parakh M, Purohit A. Management of Scorpion Sting: Prazosin or Dobutamine. J Trop Pediatr. 2009 Aug 26 [Epub ahead of print]. 9. Patil SN. A retrospective analysis of a rural set up experience with special reference to dobutamine in prazosin-resistant scorpion sting cases. J Assoc Physicians India. 2009 Apr;57:301-04. 10. Bawaskar HS, Bawaskar PH. Clinical profile of severe scorpion envenomation in children at rural setting. Indian Pediatr. 2003 Nov;40(11):1072-075. 11. Bawaskar HS, Bawaskar PH. Efficacy and safety of scorpion antivenom plus prazosin compared with prazosin alone for venomous scorpion sting(mesbuthus tamulus): Randomised open label clinical trial. BMJ. 2010:341 C7136 12. Deshpande SB. Antiscorpion venom scores over other strategies in the treatment of scorpion envenomation. J Postgrad Med. 2010;56:253-54. 13. Boyer LV, Theodorou AA, Berg RA, et al. Arizona Envenomation Investigators. Chαvez-Mιndez A, et al. Antivenom for critically ill children with neurotoxicity from scorpion stings. N Engl J Med. 2009;360:2090-098.
23
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Snake Bite Envenomation
Figure 23.1: Evidence-based resuscitation of snake envenomation leads to successful outcomes (Courtesy: Dr Balaji J and Dr Gunda Srinivas)
Learning Objectives 1. Evidence-based prehospital care. 2. Recognition of symptoms and signs of envenomation. 3. Management of snake envenomation using the modified rapid cardiopulmonary cerebral assess-
ment and incorporating it into the pediatric assessment triangle. 4. Evidence-based management of snake envenomation.
INTRODUCTION
First Aid
Three hundred and thirty species of snakes are found in India, of which 70 species are poisonous. 70% of snake bites are ‘dry’ bites and do not result in envenomation. The majority of bites occur in rural areas between April and October. Most significant envenomations in India are caused by the common krait (Bungarus caeruleus) and Indian cobra (Naja naja), which are neurotoxic and the saw-scaled viper (Echis carinatus) and Russell’s viper (Daboia russelii) both of which are hemotoxic1,2,3 (Figure 23.1).
Prehospital care should focus on stabilization and rapid transport to a health care facility where antivenom is available.6
PATHOPHYSIOLOGY OF SNAKE VENOM Snake venom is a complex mixture of enzymatic compounds (Table 23.1) (Phospholipases A2, D hydrolases, proteases, hyaluronidase, nucleotidase and ATPases) and non-enzymatic compounds such as neuro and hemotoxins.4,5
Do it ‘RIGHT’ ●● R: Reassure the patient. 70% of all snake bites are by non-poisonous species. ●● I: Immobilize the bitten limb in a manner similar to a fractured limb. Use bandages or cloth to hold the splints. Do not block blood supply or apply pressure. Do not tie tight ligatures.6,7,8,9,10
Ù
Tight ligatures are dangerous.
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Section VII n Envenomation
Table 23.1: Pathophysiology of snake venom Snake
Type of venom General site of action Type of venom component IP :action 196.52.84.10
Clinical effects
Viper, cobra
Local toxins
Bite site and bitten limb
Neurotoxins, cytotoxin
Local—pain, swelling, blistering, bruising, necrosis
Cobra, krait, coral snake
Neurotoxins
Neuromuscular junction
Neurotoxins (presynaptic, postsynaptic), dendrotoxins, fasciculins
Progressive flaccid paralysis of skeletal muscle and diaphragm
Sea snakes
Myolytic toxins
Skeletal muscle
Myotoxins
Destruction of skeletal muscle
Viper
Hematologic toxins
Effect hemostasis— damage vessel walls, promote bleeding
Procoagulants, fibrinolytics, Consumptive coagulopathy, anticoagulants, hemorrhagin complete defibrination, hemorrhage, thrombosis, infarction, embolism
Viper
Nephrotoxic toxins
Kidneys
Nephrotoxins
Renal damage, failure, necrosis
Viper
Cardiotoxic toxins
Heart
Cardiotoxins
Cardiac arrhythmias, failure, arrest
●● G, H: Get to the Hospital immediately.11
Ù Do not waste time in traditional remedies which have NO PROVEN benefit.
●● T: Tell the doctor of any systemic symptoms such as ptosis that manifest on the way to hospital.
Indian National Snakebite Protocol 20077 The following traditional methods are not recommended: ●● Do not wash the wound.
Ù
Washing the wound increases the flow of venom into the system by stimulating the lymphatic system. ●● Do not apply tourniquets.
Ù
Tourniquet made of rope, string, belt and cloth increase the risk of ischemia, necrosis and limb loss. When tourniquet is removed, there is risk of massive neurotoxin release or occurrence of embolism. ●● Do not incise the wound.
Ù
Incision of the wound due to hemotoxic bite increases the risk of severe bleeding. ●● Do not apply suction to the wound.12,13
Ù
Suction does not reduce the amount of circulating venom. It may in fact increase envenomation and also increase the risk of necrosis at the site of bite. ●● Do not apply electric shock or cryotherapy to the wound.
Ù
Both measures have no benefit, but enhance the necrotic effect of the venom. ●● Avoid pressure immobilization.14
Ù
Pressure immobilization widely recommended in other countries is not applicable in the Indian setting. Bandages increase the risk of local necrosis.
Approach to an Individual Allegedly Bitten by a Snake ●● Determine whether the patient has been bitten by a poi sonous snake.
Look for Fang Marks ●● The depth of the bite varies anywhere from 1 to 8 mm. ●● In some cases, there may be no external evidence of snake bite. ●● Absence of fang marks do not rule out snake bite in agricultural areas.
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Chapter 23 n Snake Bite Envenomation
Table 23.2: Summary of manifestations of bites from various species of snakes Feature
Cobras
IP : 196.52.84.10 Local pain/tissue damage Yes
Kraits
Russell’s viper
Saw-scaled viper
Hump-nosed viper
No
Yes
Yes
Yes
Ptosis/neurological signs
Yes
Yes
Yes
No
No
Hemostatic abnormalities
No
No
Yes
Yes
Yes
Renal complications
No
No
Yes
No
Yes
Response to neostigmine
Yes
No?
No?
NA
NA
Response to ASV
Yes
Yes
Yes
Yes
No
Note Time of Bite ●● Time of onset of poisoning may be as early as 5 minutes or as late as 10 hours as in cobra bites. In viper bites, the mean duration of onset of symptoms may be 20 minutes, while in sea snake bites, myotoxic features may occur within 2 hours.
Ù
In regions where snake bites are common, a high index of suspicion based on symptoms and signs is needed to initiate therapy.
Ù
Ptosis is an early sign of kraits and cobra bites. ●● Bleeding occurs at the site of bite, skin, gastrointestinal tract, urinary tract and within the brain. Prolongation of clotting time can occur in asymptomatic victims.
Ù
Hemostatic abnormalities are the hallmark of viper bites.
●● Severe vomiting, headache, myalgia, vertigo and hy persalivation are common.
●● Cardiotoxicity manifests as tachycardia, hypotension, myocardial infarction and cardiac arrest. ●● Hypotension and shock occur due to hemorrhage, vasodilation, increased capillary permeability, acute pituitary, adrenal insufficiency (Russell’s viper bites) and anaphylaxis due to ASV. ●● Acute renal failure (oliguria) is a complication of viper bite-induced muscle necrosis and myoglobinuria.16 ●● Ongoing absorption of the venom from blood (half-life of venom is between 26 and 96 hours) can lead to recurrence of symptoms. ●● Frequent evaluation of the patients is essential for 3–4 days. ●● Delayed manifestations in the initially stabilized patients may occur even after 3 weeks. Venom released from local blebs (venom depots, not accessible to antivenom) may be the cause of this phenomenon.
Neurological Symptoms
Late-onset Envenomation
●● Ptosis, external ophthalmoplegia, hyperacusis and weakness of muscles of palate, jaw, tongue, larynx, neck and muscles of deglutition have been noted. Cranial nerve involvement, drowsiness, coma and respiratory muscle paralysis are other signs of severe envenomation. The diaphragm is the last to be affected.15,16
●● Closely observe patients for at least 24 hours. ●● Krait and the hump-nosed pit viper poisoning can manifest as late as 6–12 hours after the bite. At the start of the rainy season, juvenile snakes tend to bite the victim in the hard tissue of the foot resulting in late signs of envenomation.
Local Manifestations ●● Local pain, tenderness, edema, erythema or discoloration occur within 6–30 minutes (Table 23.2). ●● Tingling and numbness over the tongue, mouth and scalp are common in viper bites. ●● Local bleeding including petechial and purpuric rash are common in viper bites. ●● Wet gangrenous lesions and compartment syndrome are common in cobra bites. ●● Regional lymphadenopathy has been reported as an early and reliable sign of systemic poisoning.15
Systemic Manifestation
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Section VII n Envenomation
CASE SCENARIO 1 A 10-year-old boy was brought to the ED with history of IPthumb. : 196.52.84.10 snake bite over the right He had severe pain over bite site with progressive swelling (Figures 23.2 and 23.3).
Figure 23.4: Progression of edema (after 19 hours).
Figure 23.2: This child was rushed within an hour after snake bite. His mother had immediately tied a tight tourniquet above the forearm. On arrival he received 8 vials of ASV. Subsequently, he received up to 30 vials based on rapidly progressing cellulitis. This picture showing fang marks with bleb was taken 19 hours after the bite.
Figure 23.5: Note the rapidity of progression in 24 hours. Wound was exposed for re-examination (note the date on photograph).
APPROACH TO ENVENOMATION IN THE ED Investigations (Figures 23.6A and B) 20 minute whole blood clotting test (20 WBCT). Figure 23.3 Physiological status: Cardiopulmonary cerebral assessment is normal with signs of severe envenomation
At 19 hours after the bite, the swelling had extended almost to the axilla (Figure 23.4). Note the mark made by the physician on the forearm, showing the extent of the edema. This child was referred to the surgeon for rapid progressive formation of gangrene on the same day. Within the next 12 hours, unfortunately, the surgeon who had taken up the child for debridement had to disarticulate the thumb due to gangrene of the joint (Figure 23.5).
Figure 23.6A: Sample for whole blood clotting time collected at 11:00 AM. C, Control; T, Test.
Chapter 23 n Snake Bite Envenomation
●● Take a 1–2 mL of fresh venous blood in a new, clean, dry test tube and leave it undisturbed for 20 minutes. ●● Gently tilt the tube without shaking. If the blood is still IP : 196.52.84.10 liquid, then the patient has incoagulable blood.
229
●● Urine analysis: Hematuria, proteinuria, hemoglobinuria or myoglobinuria. ●● Blood group type and crossmatch. ●● ECG: Changes are usually non-specific and include bradycardia, AV block with ST segment elevation or depression. The ECG may also show features of hyperkalemia with peaked T waves.
Local Wound Management
Figure 23.6B: WBCT sample at 11:20 AM. C, Control; T, Test.
●● If the 20 WBCT is normal, repeat the test every 30 minutes for 3 hours and then hourly thereafter for at least 24 hours to avoid missing late-onset envenomation. ●● If 20 WBCT is abnormal, repeat 6th hourly (the liver takes 6 hours to replace the clotting factors). ●● Although coagulation parameters such as prothrombin time, partial thromboplastin time and thrombin time may be prolonged, these tests are not immediately needed during resuscitation in the emergency service.
Ù
20 minutes WBCT is a reliable test of coagulation, can be carried out at the bedside without specialist training in the most basic settings.6,7 Other laboratory tests which are useful for monitoring, prognosticating and determining the stages of intervention include: ●● CBC: Anemia, leukocytosis and thrombocytopenia. ●● Peripheral smear may provide evidence of hemolysis and DIC especially in viperine bites. ●● Coagulation profile: PT, PTT, fibrinogen, FDP, clotting time and clot lysis time provide objective information regarding DIC. The quality of clot formed may be a better indicator of coagulation capability than the actual time required for formation. Clot lysis has been observed in several patients who have a normal clotting time. ●● BUN, creatinine, electrolytes, azotemia and hyperkalemia.
●● Cleanse the wound and leave it open. ●● Mark with ink the proximal edge of the swelling or where tenderness is noted. Note the time, such that progression may be easily monitored. ●● If swelling is noted, elevate the affected limb using a pillow. ●● Measure the circumference of the injured extremity every hour to monitor the level of edema. ●● Elevate limb in the initial stages to reduce edema. However, there is no evidence to support its effectiveness.6,7
Indication for Surgical Call Over ●● ●● ●● ●● ●●
Ulcer at the site of fang marks. Necrosis of the skin and underlying tissues. Gangrene of the toes and fingers. Debridement of necrotic tissue. Compartment syndrome.
Ù
Consider compartment syndrome if any of the following 6 Ps are noted: Pain on passive stretching Pain (out of proportion) Pulselessness Pallor Paresthesia Paralysis.
Care of the Wound ●● Minimize unnecessary blood loss. ●● Remove debris and necrotic tissue by gently irrigating with normal saline. ●● Expose viable tissues and excise eschar after controlling the hemotoxic complications. ●● Apply topical agents and non-adherent dressing. This will ensure epithelialization and prevent contamination of the wound.
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Section VII n Envenomation
●● Perform surgical debridement, if needed. ●● Prepare for skin grafting if required.6
Fasciotomy
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●● Prophylactic fasciotomy does not remove or reduce envenomation. ●● Visual impression is an unrealistic guide of intracompartmental pressure. ●● Tissue injury after compartment syndrome may be dis proportionate to the clinical status.
Ù
Fasciotomy is not required for every case (there is little evidence that intracompartmental pressure) increases to such an extent that fasciotomy is warranted.6,7 ●● If fasciotomy is required for compartmental syndrome the wound needs to be taken care to prevent secondary bacterial infection.
Criteria for fasciotomy 1. Hemostatic abnormalities should have been corrected. 2. Clinical evidence of compartmental syndrome. 3. Intracompartmental pressure exceeds 30–40 mm of Hg (normal < 20 mm Hg, measured using Stryker pressure monitor or saline monitor).6,7,10
Ù
Early treatment with adequate antivenom remains the best way of preventing irreversible muscle damage.10
Medications ●● Administer tetanus toxoid. ●● Administer antibiotic. ●● Mix 8–10 vials of ASV in NS or GNS and administer over 1 hour. ●● Re-evaluate WBCT every 6 hours.
Figure 23.7 Physiological status: Respiratory distress, hypotensive shock with altered mental status and nonconvulsive status epilepticus.
Resuscitation ●● Provide oxygen through the Jackson-Rees circuit. Plan intubation. ●● NS boluses of 5–10 mL/kg up to 20 mL/kg. If shock persists after 20 mL/kg and significant bleed is noted more fluids may be warranted. Call for epinephrine infusion. ●● Specific management: ASV: 8–10 vials. ●● Repeat WBCT every 6 hours. ●● If WBCT is abnormal, repeat 5–10 vials of ASV up to a maximum of 30 vials. ●● If bleeding persists consider FFP, cryoprecipitate, fibrinogen, factor VIII, fresh whole blood and platelets.
CASE SCENARIO 3 A 10-year-old boy was rushed into the ED with history of snakebite on his right forearm, whilst playing in the gar den. He complained of pain at the site of bite. Fang marks were noted. His 20 WBCT was normal (Figure 23.8).
CASE SCENARIO 2 A 10-year-old girl was rushed into the ED following snake bite over her right foot during the night, while she was sleeping in the open field. She was lethargic and breathless with swelling of the right foot. Bleeding was noted from the bite site. She was also passing red colored urine. Refer Figure 23.7. She did not have ptosis, but had conjugate gaze to the right. Whole blood clotting time prior to transfer to the hospital was more than 20 minutes.
Figure 23.8: Hemodynamically stable child with snake bite.
Chapter 23 n Snake Bite Envenomation
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3. Swelling extending: a. 15 cm or more within 1 hour. b. Swelling reaching the knee or elbow < 4 hours after bite involving the limbs. c. Swelling involving the whole limb within 8 hours. d. Extension to the trunk. e. Swelling causing airway compromise or shortness of breath. f. Compartment syndrome or major vessel entrapment.
Ù
Figure 23.9 Physiological status: Cardiopulmonary cerebral assessment normal
Ù
Swelling confined to the site of bite or fang mark from an apparently venomous snake are not grounds for ad ministration of ASV. Refer Figure 23.9.
Specific Therapy: AntiSnake Venom Antisnake venom (ASV) a polyvalent venom, is effective against all four common species such as Russell’s viper, common cobra, common krait and saw-scaled viper. It is available in both liquid and lyophilized forms. Liquid ASV has a 2-year shelf life, requires refrigeration and a reliable cold chain during transportation. Lyophilized ASV in powder form does not need refrigeration for storage. This is particularly useful in remote areas where power supply is inconsistent.6,7 ASV is a scarce and costly commodity. Every snake bite, even if poisonous, does not warrant snake antivenom. The prophylactic use of antivenom should be avoided due to the inherent risk of hypersensitivity reactions. Antivenom is indicated only if there are signs of systemic envenomation or severe local swelling. Refer Protocol 23.1.
Indications for Administration of ASV 1. Evidence of coagulopathy: Whole blood clotting time exceeds 20 minutes or signs of spontaneous bleeding are noted. 2. Evidence of neurotoxicity: Ptosis, inability to lift the head, diplopia, stridor, respiratory distress, neuroparalysis or coma.
Painful swelling that is both progressive and severe is a definitive indication for ASV. 4. Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmias, abnormal ECG patterns. 5. Persistent and severe vomiting or abdominal pain.6
ASV Dose ●● 8–10 vials of ASV should be administered over 1 hour (Figures 23.10A and B). It is given to neutralize the venom. There is no benefit in administering it over longer periods and prolonging the time to neutralize. Snakes inject the same amount of venom into adults as in children. Hence it is intuitive that children receive the same ASV dosage as adults. The recommended dosage level has been based on published research that Russell’s viper injects around 63 mg of venom (range 5–147 mg).17 One vial of ASV neutralises 6 mg of Russell’s viper venom. Hence the requirement ranges from 8–25 vials. The approximate requirement ranges from 8–25 vials. The dose of antisnake venom is determined by the amount of venom that is injected. In fact, the amount of venom per square body surface may be more for children and young infants than adults.
Ù
Avoid using smaller doses for young infants and children. Administer 8–25 vials for all ages if signs of envenvomation are noted. The patient must be closely monitored for reactions to ASV for a minimum of 2 hours. The lyophilized form is diluted in 10 mL of water and rolled between the palms. Shaking is not advisable since, it could cause denaturation of the protein.
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Section VII n Envenomation
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Figure 23.10A and B: Method of administration of ASV.
●● IV infusion: Reconstituted ASV is diluted in 5–10 mL/ kg body weight of NS or GNS and infused in 1 hour at a constant speed and closely monitored for 2 hours.
Ù
Avoid administering ASV into the bite site. It is ineffective, painful and raises the intracompartmental pressure, particularly in the digits.
●● Interrupt ASV infusion. ●● Administer 0.1 mL/kg of 1:10,000 adrenaline IV (since IV access is already available during ASV administration). ●● Administer 2–6 mg/kg hydrocortisone IV. ●● Administer Antihistamine. ●● If any one sign is noted along with abnormal cardiorespiratory status: – Respiratory arrest: Initiate bag-valve-mask ventilation and plan early intubation. – Respiratory distress with shock: Provide oxygen through non-rebreathing mask and nebulize. – Nebulize with Salbutamol and Adrenaline for bronchospasm and laryngeal edema respectively. – Initiate epinephrine infusion at the rate of 0.1–0.4 µg/kg/minute if hypotensive or bradycardic. – Administer 20 mL/kg of NS boluses until shock resolves (60–200 mL/kg may be needed to resolve shock). ●● Antihistamine is controversial and is contraindicated in the setting of hypotensive shock. ●● Continue ASV infusion at slower rates for 10–15 min utes keeping the patient under close observation. The normal drip rate may be resumed. Monitor cardiopulmonary status and provide supportive measures.6
CASE SCENARIO 4 A 1-year-old boy was rushed into the ED with history of snakebite on his right leg whilst playing in the garden. He complained of pain and swelling at the site of bite. Fang marks and swelling of the right leg were noted. He also had ptosis (Figures 23.11 and 23.12).
Precautions Taken During ASV Administration ●● Do not administer test dose. A test dose does not predict occurrence of anaphylactoid or late serum reactions. These reactions may sensitize thereby creating a greater risk of anaphylaxis. ●● Monitor for anaphylaxis.
Anaphylaxis During ASV Administration (Refer Figure 17.1, right extreme photograph)
If any one sign is noted, but rapid cardiopulmonary status is normal:
Figure 23.11: Note the ptosis in this child brought with history of envenomation (Courtesy: Dr Balaji J).
Chapter 23 n Snake Bite Envenomation
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IP : 196.52.84.10
Figure 23.12 Physiological status: Cardiorespiratory cerebral assessment is normal with ptosis.
Specific Management of Neurotoxic Envenomation Neostigmine An anticholinesterase, Neostigmine prolongs the effect of acetylcholine thereby reversing respiratory failure and other neurotoxic symptoms. It is particularly helpful in resolving postsynaptic neurotoxins (Cobra). There is some doubt over its usefulness against the presynaptic neurotoxins secreted by Krait and Russell’s viper. However it is worth trying in these cases.7
Neostigmine test ●● Administer 0.04 mg/kg of neostigmine IM along with 0.05mg/kg of atropine. ●● If the victim responds to the neostigmine test, then continue with 0.04 mg of neostigmine IM half hourly plus 0.05 mg of atropine IV half hourly until neurological recovery. Continuous infusion over 8 hours has been advised in adults. If there has been no improvement in symptoms after one hour, neostigmine should be stopped.7
CASE SCENARIO 5 A 7-year-old boy was rushed into the ED. He was found to be gasping for breath and unconscious since morning. He had been normal when he had gone to sleep the previous night . There was no history of trauma or poisoning. A swelling was noted over the right elbow (Figure 23.13). Suspect snake envenomation in rural areas when sudden deterioration of hemodynamic status occurs in a previously normal child. Unprovoked bites usually occur due to Krait.
Figure 23.13 Physiological status: Imminent cardiorespiratory arrest.
Resuscitation ●● Initiate bag-valve-mask ventilation followed by intubation and ventilation. ●● Chest compression, if bradycardic. ●● Epinephrine: 0.1 mL/kg (1:10,000) up to a maximum of 3 doses until heart rate improves to > 100/minute. ●● Administer NS bolus: 20 mL/kg (maximum 30 mL/kg unless anaphylaxis occurs or hypovolemia is noted in history). ●● Initiate epinephrine, if hypotensive or dopamine if normotensive.
Specific Management ●● 8–10 vials of ASV mixed with 100 mL of GNS and administered over 1 hour. ●● Atropine: 0.02–0.05 mg/kg intravenously every 30 minutes. ●● Neostigmine: 0.04–0.1 mg/kg every 30 minutes.
Repeated ASV Doses Hemostatic bites: ●● After the initial dose has been administered, no further ASV is given for six hours. ●● Repeat whole blood clotting time. If it exceeds 20 minutes (performed every 6 hours) it will help determine whether additional ASV is required (max 30 vials).6 Neurotoxic bites: ●● If 2 hours after the first dose of ASV and neostigmine, the victim has not improved or has worsened or has developed respiratory failure a second and final dose should be given.
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Section VII n Envenomation
●● Administer the second dose of 10 vials over 1 hour. Maximum dose of ASV is 20 vials.6
Recovery Phase
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If an adequate dose of appropriate antivenom has been administered, the following responses may be seen: ●● Spontaneous systemic bleeding such as gum bleeding usually stops within 15–30 minutes. ●● Blood coagulability is usually restored in 6 hours. ●● Postsynaptic neurotoxic envenoming (Cobra) may begin to improve as early as 30 minutes after antivenom, but can take several hours. ●● Presynaptic neurotoxic envenoming (Krait), usually takes a considerable time to improve reflecting the need for the body to generate new acetylcholine emitters. ●● Active hemolysis and rhabdomyolysis may cease within a few hours and the urine returns to its normal color. ●● In hypotensive patients, blood pressure may increase after 30 minutes. What ASV cannot do? 1. Prevent or reverse necrotic action of the venom on tissue. 2. Prevent or reverse local swelling. 3. Reverse coagulopathy (Liver regenerates clotting factors). 4. Reverse presynaptic envenomation. Nerve damage is structural and large quantities of ASV are ineffective. Body must regenerate synaptic vesicles. 5. Reverse acute kidney injury.
Renal Failure Acute kidney injury (AKI) a potentially lethal complication, can occur even if WBCT has normalized. Overt clinical features of AKI are seen 5–12 days after the bite. ●● Recognize and refer for hemodialysis.
conclusion The ability to identify poisonous from non-poisonous snakes may help mitigate fear, facilitate effective treatment strategies and reduce mortality. Most snakebites are due to non-venomous snakes. A large number of snakebites by poisonous snakes are also asymptomatic. Reassurance, allaying of anxiety, rapid shift to the hospital and hospitalization for 24–48 hours are all that is required for the majority of cases. If signs of envenomation develop,
stabilize airway breathing and circulatory problems and consider early antivenom administration.
Key Points
ü
1. Relieve anxiety and reassure victims that fatality is minimal. Most will recover. 2. Cellulitis and hemostatic abnormalities are the hall mark of Viperine envenomation. 3. Ptosis is an early sign of krait and cobra (elapid envenomation). 4. 20 minutes WBCT test is the most useful bedside test to detect hemostatic abnormalities. 5. Children should receive the same ASV dosage as adults, since snakes inject the same amount of venom into adults and children. 6. ASV neutralizes the unbound venom and must be given as early as possible. 7. ASV is required only to those who show definite signs and symptoms of envenomation. 8. Anaphylaxis or late serum sickness cannot be determined or prevented by test dose. 9. Even if the patient develops reaction(s), the total dose required should be administered slowly after the patient recovers from the reaction(s).
common errors
û
1. Resorting to traditional treatment rather than rushing to the hospital immediately. 2. Incision (cutting) of the site of bite and suctioning the incoagulable blood. 3. Applying tight tourniquets over the bite site. 4. Local administration of ASV is ineffective, painful and raises intracompartmental pressure. 5. Using wet (not properly dried) test tube for the 20 minutes WBCT test. 6. Washing the test tube with detergent (inhibit the contact element of the clotting mechanism). 7. Administration of ASV without adequate agents for managing anaphylaxis. 8. Administration of ASV as IV bolus or IM directly. 9. Discontinuation of ASV after mild reactions. 10. Failure to treat shock and failure to provide early ventilatory support in neuropoisonous snakebite. 11. Proceed to surgical management before coagulation resolves.
Chapter 23 n Snake Bite Envenomation
Protocol 23.1: PEMC approach to the management of snake bite in the ED
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Section VII n Envenomation
References 1. Chippaux JP. Snake bites: Appraisal of the global situation. IP : 196.52.84.10 Bull World Health Organ. 1998;76(5):515-24. 2. Gaitonde BB, Bhattacharya S. An epidemiological survey of snake-bite cases in India. Snake. 1980;12:129-33. 3. Whitaker R. Common Indian Snakes-A Field Guide. Delhi: MacMillan India Ltd; 1978. pp. 1-154. 4. Philip E. Snake bite and scorpion sting. In: Srivatava RN (Ed). Paediatric and Neonatal Emergency Care. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd. 1994. pp. 227-34. 5. Pillay VV. Comprehensive Medical Toxicology, 1st edition, Hyderabad: Paras Medical Publishers; 2003. 6. Handbook on Treatment Guidelines for Snake Bite and Scorpion Sting. Tamil Nadu Health Systems Project, Health and Family Welfare Department, Chennai: Government of Tamil Nadu, 2008. 7. Indian National Snakebite protocols 2007, Indian National snakebite protocol consultation meeting 2nd August 2007, Delhi. 8. Simpson ID. The paediatric management of snake bite: The National Protocol. Indian Pediatrics. 2007;44:173-76. 9. Simpson ID. Snakebite: Recent Advances 2006 in Medicine Update 2006 Ed Sahay BK The Association of Physicians of India. 639-643.
10. Warrell DA. WHO/SEARO Guidelines for the clinical management of snake bites in the Southeast Asian region. Southeast Asian J Trop Med Public Health. 1999;30 (Suppl 1):1-85. 11. McKinney PE. Out-of-Hospital and interhospital management of crotaline snake bite. Ann Emerg Med. 2001;37(2):168-74. 12. Alberts MB, Shalit M, Logalbo F. Suction for venomous snakebite: a study of “mock venom in a human model”. Ann Emerg Med. 2004 Feb;43(2):181-86. 13. Bush SP. Snakebite suction devices don’t remove venom: they just suck. Ann Emerg Med. 2004;43(2):187-88. 14. Gray S. Pressure Immobilization of Snakebite. Wilderness and Environmental Medicine. 2003;14(1):73. 15. Wallace JF. Disorders caused by venoms, bites and stings. In: Wilson JD, Braunwald E, Isselbacher KJ, Petersdorf RG, Martin JB, Fauci AS, Root RK (Eds). Harrison’s Principle of Internal Medicine. Volume 2. 12th Edition. New York: McGraw-Hill. 1991:2187-194. 16. Theakston RDG, Phillips RE, Warrell DA, et al. Envenoming by the Common Krait (Bungarus caeruleus) and Sri Lankan Cobra (Naja naja) efficacy and complications of therapy with Halfkein antivenom. Transactions of the Royal Society of Tropical Medicine and Hygiene 1990;84:301-08. 17. Tun P, Khin AC. Amount of venom injected by Russell’s Viper (Vipera russelli): Toxicon. 1986;24:730-33.
Poisoning
Section VIII
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Poisoning: General Approach
24
Figure 24.1: Children with poisoning need to be managed appropriately as fast as possible
Learning Objectives 1. Principles of management specific for the poisoned child. 2. Toxidromes which help recognize seriously ill poisoned children.
3. Evidence-based approach for prevention of absorption of toxins. 4. Methods available for enhancement of excretion.
Ingestion of a harmful substance is among the most common causes of injury to children less than 6 years of age. Fortunately, in most cases the ingested agent has minimal or no clinically important toxic effects. Rarely, the ingested amount is life-threatening resulting in death. Some of the commonest toxin-induced injuries encountered in our country are following ingestion of kerosene, herbal medicines such as vasambu (Acorus calamus or commonly called Sweet Flag), camphor, neem oil, insecticides and corrosives. Commonest drugs ingested by children are dapsone, iron preparations, oral hypoglycemics and antihypertensives (Figure 24.1).
evidence such as an empty bottle, presence of tablets or spillage of house hold chemicals near a child. ●● Evaluate constituents of the ingested substance and calculate its per kilogram body weight. ●● In young infants, presume that maximum amount has been ingested by comparing the volume of liquid or number of the tablets remaining in the container. Take spillage into account.1
Identification of Poison A high index of suspicion is needed to recognize poisoning if history is unavailable. ●● Suspect poisoning if an apparently normal child devel ops symptoms of organ dysfunction with circumstantial
Management
1. Cardiopulmonary cerebral assessment and resuscitation. 2. Prevention or reduction of absorption. 3. Enhancement of excretion. 4. Administration of antidotes.
Ù
Early aggressive efforts to eliminate the toxin is the best guarantor for successful outcomes.
240
Section VIII n Poisoning
Cardiopulmonary Cerebral Assessment and Resuscitation1 IP : 196.52.84.10
Ù
“Treat the patient not the poison.” ●● Plan early intubation, if victim presents with an unmain tainable airway or/and respiratory failure. ●● Profound depression of mental status can result in airway compromise and respiratory failure. ●● Correct shock with 10–20 mL/kg isotonic fluids. Shock may occur due to vomiting and diarrhea. ●● If cardiogenic shock is noted initiate appropriate iono trope infusion based on blood pressure (BP) (Establish euvolemia prior to starting intrope).
●● Perform dextrostix and correct documented hypogly cemia with boluses of 5 mL/kg of 10% dextrose. Initiate intravenous fluids at maintenance rates if the victim presents with nausea and vomiting in the absence of shock. ●● Avoid treating mild metabolic acidosis, since it is often encountered, but does not require specific therapy. ●● Treat convulsions using the standard protocol for status epilepticus. ●● Monitor hepatic and renal function.
Management of Arrhythmias ●● Treat hypoxia and hypercarbia. ●● Correct dyselectrolytemia and acid-base abnormalities.
Table 24.1: Toxidromes Toxidromes Anticholinergic activity
Associated signs
Possible toxin
1. Hot as a hare: Hyperthermia 2. Dry as a bone: Dry mucosa and skin 3. Red as a beet: Flushing 4. Mad as a hatter: Delirum 5. Blind as a bat: Mydriasis 6. Tachycardia 7. Urinary retention
Atropine Antihistamine Antispasmodics Phenothiazines Tricyclic antidepressants Mushroom poisoning Antiparkinsonian drugs
1. Salivation 2. Lacrimation 3. Urination 4. Defecation 5. Gastrointestinal cramping 6. Emesis 7. Miosis
Organophosphorus toxins (insecticides)
Stimulation followed by paralysis of preganglionic and somatic nerve fibers, excessive cholinergic stimulation of the motor end plate
Fasciculations, weakness, paralysis
Organophosphorus poisons
Sympathetic nervous system activity
Fever, flushing, tachycardia, hypertension, miosis, sweating
Cough and decongestants, theophylline
Methemoglobinemia
Cyanosis resistant to oxygen
Alamine dyes, nitrates, benzocaine, phenacetin, nitrobenzene, chlorates
Cholinergic activity Muscarinic effect
Nicotinic effect
Acute ataxia and nystagmus
Antihistamines, alcohol, anticonvulsants, bromides, organic solvents
Metabolic acidosis
Effortless tachypnea
Ethanol, carbon monoxide, iron, diabetic medications, salicylates, tricyclic antidepressants
Renal failure
Oliguria, anuria, hematuria, myoglobinuria Carbon tetrachloride, ethylene glycol, methanol, mushrooms, oxalates
Chapter 24 n Poisoning: General Approach
Ù
Arrhythmias are usually rare, but if present, treatment of IP : 196.52.84.10 hypoxia, hypercarbia, dyselectrolytemia and acid-base abnormalities are usually sufficient to correct them.
241
Ù
Gastric lavage, can be considered, when a potentially life-threatening amount of a poison has been ingested.
●● Consider specific therapy, if supportive measures are not adequate to correct arrhythmias.
Poison Syndromes2 (Toxidromes) Toxins can result in a cluster of signs, which help to recognize the specific agent (Table 24.1). Perform a complete neurological assessment, while resuscitation is in progress. It could reveal clues, which point towards the specific toxin especially when history is unavailable.
Laboratory Investigations Laboratory analysis of serum or urine should be guided by the substance ingested, its anticipated degree of toxicity and the value of measuring these concentrations. The need for toxicologic screening tests in children is rare, since the ingested substance is usually known.
Prevention or Reduction of Absorption The term ‘gastrointestinal decontamination’ includes interventions that are used to prevent the absorption of an ingested toxin (Figure 24.2).
Ù
Routine induction of emesis is not recommended in the management of toxin ingestion.
Syrup Ipecac3 Ipecac has no role in the routine management of acutely poisoned patients.
Gastric Lavage4,5,6
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Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients. American Academy of Clinical Toxicology; European Association of Poisons Centers and Clinical Toxicologists recommend the following:
Figure 24.2: Activated charcoal is being administered as a slurry through the nasogastric tube
●● Unless intubated, gastric lavage is contraindicated, if children whose airway protective reflexes are lost. ●● Gastric lavage is contraindicated, if a hydrocarbon with high aspiration potential has been ingested. ●● Gastric lavage is also contraindicated, if a corrosive substance has been ingested.
Ù
Patients, who are more likely to benefit from aggressive gastrointestinal decontamination.7 • Obtunded patients presenting very soon after ingestion. • Ingestion of a life-threatening or massive amount. • Drugs that could delay gastric emptying. • Ingestion of sustained release tablets.
Method 1. Competence of the gag reflex should first be con firmed. 2. Once properly restrained, the child should be placed in a left lateral decubitus (Trendelenburg position) in order to limit the movement of the gastric contents into the duodenum and minimize the risk of aspiration. 3. A large bore, single lumen tube should be placed by an orogastric route. 4. The proper placement of the tube is confirmed by the spontaneous or aspirated return of gastric contents or by auscultation of insufflated air when a stethoscope is placed over the stomach after placement of the tube.
242
Section VIII n Poisoning
5. NS in aliquots of 10–15 mL/kg of body weight are instilled through the tube and then aspirated. This process is continued until aspirated contents are clear. IP :the 196.52.84.10 Volumes as large as several liters may be necessary to produce a clear aspirate. When performed 1 hour after the ingestion of a toxic substance, lavage retrieves less than 30% of the toxin. Hence, its use beyond the 1st hour is questionable. If not properly performed, gastric lavage has the potential com plication of propelling toxins into the duodenum, thereby increasing the likelihood of absorption.8
Ù
The greatest risks associated with gastric lavage are: • Inadvertent placement of the tube into the trachea or a main stem bronchus. • Esophageal injury. • Hypothermia. • Hyponatremia. • Water intoxication. Avoid gastric lavage if: • Mental status is depressed and airway protective reflexes are lost. • Kerosene ingestion (low-viscosity hydrocarbon). • Corrosive agent ingestion. Nasogastric aspiration is performed by placing a nasogastric tube (smaller than a orogastric tube) and aspirating gastric contents without instilling water. Nasogastric aspiration may be effective in cases of liquid poison ingestion,9 but it is not adequate for ingestion of pills.
Activated Charcoal
Ù
Activated charcoal should be administered within 1 hour of ingestion of toxin.10 Activated charcoal ‘adsorbs’ poisons dissolved in the intestine such that the poison remains in the gut rather than being absorbed into circulation. It limits the systemic absorption of many drugs in a time-dependent manner and may decrease the need for antidotal therapy for patients who present within 2 hours of acetaminophen ingestion.11 However, activated charcoal has not been shown to improve the outcomes of non-selected poisoning patients. Currently superactivated charcoal products with in creased surface area are available. These products de
creased systemic absorption of the ingested toxins when compared with standard activated charcoal.12,13 They are also more palatable than standard charcoal products. When administered within 1 hour after ingestion, activated charcoal can reduce the absorption of toxins by up to 75%. Optimal adsorption occurs when the ratio of charcoal to toxin is 10:1 or higher.14 ●● Recommended dose is 1 g/kg body weight.
Method of Administration Normal mental status: ●● Mix activated charcoal in fruit juice or bottled drinks as a slurry for children. ●● Additives, such as bottled drinks or fruit juices, make charcoal more palatable without reducing its efficacy.13 ●● Young children will not voluntarily drink activated charcoal quickly enough for it to work optimally. ●● Introduce a nasogastric tube in young children to ensure prompt administration. Depressed mental status or respiratory failure: ●● Intubate (for airway protection) and use nasogastric tube for administration. ●● Elevate head end by 45°.
Complications The main hazards associated with the administration of activated charcoal are vomiting and aspiration.15,16,17,18 Although activated charcoal is often described as inert, data from experimental studies indicate that aspirated charcoal can produce pulmonary parenchymal injury or bronchioli tis obliterans. The installation of charcoal into the lungs through the inadvertent placement of an orogastric or na sogastric tube into the trachea has had disastrous results including, death. Bowel sounds should be monitored, since constipation and rarely intestinal obstruction have been reported.
Indications for Activated Charcoal Medications that are well bound by charcoal are drugs that undergo enterohepatic or enteroenteric circulation such as: ●● Salicylates. ●● Phenobarbital.
Chapter 24 n Poisoning: General Approach
●● Carbamazepine. ●● Digoxin. ●● Theophylline.
IP : 196.52.84.10
Substances which are not adsorbed by activated charcoal are remembered by the mnemonic PHAILS: ●● ●● ●● ●● ●● ●●
P: Pesticides. H: Hydrocarbons. A: Acids, alkalis, alcohols. I: Iron. L: Lithium. S: Solvents.
Catharsis Cathartic agents have been advocated in poisoned victims to increase gastrointestinal motility and hasten expulsion of the toxin or the toxin-adsorbent complex.19 Commonly used osmotic agents are magnesium citrate and sorbitol. These agents promote retention of colonic fluid and stimulate gastrointestinal motility.
Ù
Currently, cathartic agents are contraindicated. The risk of hypernatremic dehydration and cardiovascular collapse is high with sorbitol, while hypermagnesemia is a hazard in children with renal disease.
Whole Bowel Irrigation (WBI)20,21,22 In this procedure, large volumes of solution are administered enterally until the rectal effluent is clear. Polyethylene glycol-electrolyte (PEGLEC) lavage solution has been formulated to prevent extensive absorption or secretion of fluid across the gastrointestinal mucosa (Table 24.2). ●● Elevate head end of bed to at least 45° to prevent aspiration. ●● Discontinue the infusion for 30 minutes, if emesis occurs and restart at half the previous rate. ●● Increase the rate as tolerated.
243
●● Administer Metoclopramide (antiemetic), since it in creases GI motility. ●● Provide a bedside commode for patients who are awake. Whole bowel irrigation is safe in children, volumes as large as 44 L have been administered without ill effects. Typical rates of administration are 500–1,000 mL/h, orally or by nasogastric tube. The adverse effects associated with this procedure consist of vomiting, abdominal cramps and bloating. Patients with trivial ingestion do well without treatment and their greatest risk is an iatrogenic complication. Even patients with more serious ingestions usually have good outcomes with supportive care alone. It is no longer sufficient to justify gastric lavage or forced administration of activated charcoal with the supposition that “the patient could have taken something bad”. However, there are some overdoses, where limiting the systemic absorption of the poison may limit the toxic effects and prevent serious toxicity. After careful consideration of the risks, GI decontamination should be targeted at patients who, in the opinion of the treating physician, have a potentially lifethreatening exposure.3
Enhancement of Excretion: Ion Trapping Urine Alkalinization Urine alkalinization23 is a treatment regimen that increases elimination of poison by the administration of intravenous sodium bicarbonate to produce urine with a pH of 7.5. The term urine alkalinization emphasizes that urine pH manipulation rather than a diuresis as the prime objective of treatment. ●● Consider urine alkalinization as first line treatment for patients who have moderately severe salicylate poisoning and who do not meet the criteria for hemodialysis. ●● Urine alkalinization cannot be recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose activated charcoal is superior.
Table 24.2: Whole bowel irrigation Route
Nasogastric tube
Indication
Iron tablets, slow release drugs, lithium21,22
Dose
30 mL/kg /h
End point
Clear effluent after several hours
Contraindication
GI bleed, bowel obstruction
244
Section VIII n Poisoning
Table 24.3: Commonly available specific antidotes Poison Anticholinergics
IP : 196.52.84.10
Antidote and dose Physostigmine [0.5 mg, slow IV over 5 (atropine group) minute; repeated every l0 minute till a maximum of 2 mg].
Arsenic, mercury
Dimercaprol
β-blockers
Glucagon
Benzodiazepines
Flumazenil
Calcium channel blockers, hydrogen fluoride
Calcium
Carbon monoxide
Pure oxygen
Copper
Penicillamine
Cyanide
Sodium nitrite 3% solution, 0.2 mL/kg, IV over 2 minute followed by sodium thiosulphate (25% solution, 1 mL/kg, IV, over l0–20 minute)
Digoxin
Digoxin-specific FAB fragments
Ethylene glycol and Methanol (used in antifreeze, heating fuel, wind screen wiper and deicing products)
Fomepizole
Heparin
Protamine
Iron
Desferrioxamine l5 mg/kg/h IV in 100–200 mL 5% glucose solution (maximum of 6 g)
Isoniazid, ethylene glycol
Pyridoxine
Lead
Sodium calcium edetate
Methemoglobinemia
Methylene blue
Narcotics (opium)
Naloxone—0.l mg/kg, IV or intratracheal, morphine from birth up to 5 year or 20 kg of weight, at which time a minimum of 2 mg is used
Nitrate and nitrites
If methemoglobinemia, treat with methylene blue
Opioids
Naloxone, Nalmefene
Organophosphates
Atropine—0.05 mg/kg IV, every 10 minute until signs of atropinization. PAM 25–50 mg/kg IV, in older children and 250 mg IV in infants over 5–10 minute, 8 hourly up to 36 hour
Paracetamol
N-acetylcysteine; Oral—intially 140 mg/kg, then 4 hourly, up to 72 hour. IV—150 mg/kg by infusion Over 15 minute followed by 50 mg/kg 4 hourly for 72 hour
Phenothiazine
Benadryl (diphenhydramine) 1–2 mg/kg (promethazine)
Sulfonylurea class of oral hypoglycemic drugs
Octreotide
Warfarin
Vitamin K
Chapter 24 n Poisoning: General Approach
●● Urine alkalinization and high urine flow (approxi mately 600 mL/h) increases urine elimination of 2,4dichlorophenoxyacetic and mecoprop poisoning. IP :acid 196.52.84.10
Ù Hypokalemia is the most common complication, but can
be corrected by giving potassium supplements. Alkalotic tetany occurs occasionally, but hypocalcemia is rare. There is no evidence to suggest that relatively short-duration alkalemia (more than a few hours) poses a risk to life in normal individuals.
Forced Neutral Diuresis This is a method of flushing the toxin out of the system by increasing the administration of fluids. Increase urinary flow by infusion of large volume of intravenous crystalloid. 1. Indications: Lithium, bromide ingestion. 2. Contraindications: Pulmonary edema, cerebral edema and renal failure.
Ù
Forced neutral diuresis has limited clinical value.
Hemodialysis An invasive procedure, hemodialysis is reserved for specific life-threatening toxins in the intensive care setting.
Indications Methanol, ethylene glycol, salicylate, phenobarbital, theophylline, lithium.
Antidotes (Table 24.3)
Rarely, emergency management involves the administration of an antidote such as Naloxone after an over dose of an opioid drug. Despite the vast number of toxins and drugs that are ingested, only a few antidotes are available.
Ù
Medicolegal entries should be made by physicians not involved in resuscitation. In summary, poisoned children derive more benefit from early and aggressive resuscitation of the ABCs and
245
removal of toxins than from advanced intensive care after entry of toxins into the human circulation.
Key Points
ü
1. Energetic emergency care and elimination of toxin is key to survival in the poisoned victim. 2. Emesis has been replaced by activated charcoal and whole bowel irrigation. 3. Gastric lavage should not be performed routinely in all children with toxin ingestion.
common errors
û
1. Failing to consider poisoning in an apparently normal child with profound fall in mental status. 2. Performing gastric lavage for minimal ingestion. 3. Not using activated charcoal or whole bowel irrigation for the appropriate toxins.
REFERENCES 1. M Riordan, G Rylance, K Berry, et al. Poisoning in children 3: Common medicines. Arch Dis Childhood. 2002 87:400-402 doi:10.1136/adc.87.5.400. 2. Diane P Callelo, et al. New and novel antidotes in pediatrics. Pediatr Emerg Care. 2006;22(7). 3. K. Heard, Gastric Decontamination. Med Clin N Am 89. 2005:1067-078. 4. Vale JA. Position statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35:711–19. 5. Vale JA, Kulig K; American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. Position paper: Gastric lavage 2004;42(7):933-43. 6. Tucker, Jeffrey R. Indications for techniques of complications of and efficacy of gastric lavage in the treatment of the poisoned child. Current Opinion in Pediatrics. 2000; (12). pp. 163-65. 7. Bond GR. The role of activated charcoal and gastric emptying in gastrointestinal decontamination: a state-of-the-art review. Ann Emerg Med. 2002;39:273-86. 8. Grierson R, Green R, Sitar DS, et al. Gastric lavage for liquid poisons. Ann Emerg Med. 2000;35:435-39. 9. Saetta JP, March S, Gaunt ME, et al. Gastric emptying procedures in the self-poisoned patient: are we forcing contents beyond the pylorus? J R Soc Med. 1991;84:274-76. 10. Chyka PA, Seger D. Position statement: single-dose activated charcoal. American Academy of Clinical Toxicol-
246
11.
12.
13. 14. 15. 16.
Section VIII n Poisoning
ogy; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35:721-41. Buckley NA, Whyte IM, O’Connell DL, et al. Activated IP : 196.52.84.10 charcoal reduces the need for N-acetylcysteine treatment after acetaminophen (Paracetamol) overdose. J Toxicol Clin Toxicol. 1999;37:753-57. Roberts JR, Gracely EJ, Schoffstall JM. Advantage of highsurface-area charcoal for gastrointestinal decontamination in a human acetaminophen ingestion model. Acad Emerg Med. 1997;4:167-74. Krenzelok EP, Heller MB. Effectiveness of commercially available aqueous activated charcoal products. Ann Emerg Med. 1987;16:1340-43. Osterhoudt, Kevin C, Alpern, et al. Activated Charcoal Administration in a Pediatric Emergency. Department Pediatric Emergency Care; 2004(20)8. pp. 493-98. Arnold TC, Willis BH, Xiao F, et al. Aspiration of activated charcoal elicits an increase in lung microvascular permeability. J Toxicol Clin Toxicol. 1999;37:9-16. Moll J, Kerns W II, Tomaszewski C, et al. Incidence of aspiration pneumonia in intubated patients receiving activated charcoal. J Emerg Med. 1999;17:279-83.
17. Liisanantti J, Kaukoranta P, Martikainen M, et al. Aspiration pneumonia following severe self-poisoning. Resuscitation. 2003;56:49-53. 18. Pollack MM, Dunbar BS, Holbrook PR, et al. Aspiration of activated charcoal and gastric contents. Ann Emerg Med. 1981;10:528-29. 19. Barceloux D, McGuigan M, Hartigan-Go K. Position statement: cathartics. American Academy of Clinical Toxicology; European Association of Poisons Centers and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35:743-52. 20. Anonymous. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42:844-54. 21. Tenenbein M. Whole bowel irrigation as a gastrointestinal decontamination procedure after acute poisoning. Med Toxicol. 1988;3:77-84. 22. Buckley N, Dawson AH, Howarth D, et al. Slow-release verapimil poisoning. Use of polyethylene glycol whole-bowel lavage and high-dose calcium. Med J Aust. 1993;158:202-04. 23. Proudfoot AT, Krenzelok EP, Vale JA, et al. Position Paper on Urine Alkalinization. 2004;(42):1-26.
25
IP : 196.52.84.10
Specific Poisons
Figure 25.1: Common household products that carry potential risk of poisoning in young children
Learning Objectives 1. Approach to management of poisoning in children using the rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle.
Specific poisons The common household products, which are easily accessible to children is shown in the Figure 25.1. These have potential to cause poisoning when consumed in large quantities. Kero sene, organophosphorus compounds (OPC) and carbamates are the other most commonly consumed poisons. Used as fuel and pesticides in agricultural households, accidental poison ing can occur from inhalation of spray, ingestion and absorp tion through the skin and mucosa. Fatal poisoning from OPC can result from contamination of clothing and food articles. The worst affected are farm workers and their children.1 Ado lescents consume OPC with suicidal intent.
ORGANOPHOSPHATE INSECTICIDES Common Agents Malathion, Parathion (fatal dose 0.l mg/kg), Octamethyl pyrophosphoramide (OMPA), Hexaethyltetraphosphate
2. Management of organophosphorus poisoning based on the Cochrane 2012 guidelines. 3. Approach to kerosene, opioids, barbiturates, iron, paracetamol and button battery ingestion. (HETP), Diazinon, Tik-20, Methyl Parathion, Metacide and TEPP: ● ● HETP is the least toxic. ● ● TEPP is the most toxic and fastest acting OP com pound. ●● The noxious odor and taste of OP ensures that accidental ingestion is minimal and therefore non-lethal. On the con trary, homicidal administration is usually lethal.
Pathophysiology OPC binds irreversibly to enzyme acetylcholinesterase, preventing the breakdown of acetylcholine. Acetylcho line accumulates resulting in muscarinic, nicotinic and parasympathetic stimulation of the central nervous system (Figure 25.2). Respiratory route of absorption leads to the fastest onset of action. Clinical features appear when cholinesterase ac tivity falls to 25%–30% of normal.
248
Section VIII n Poisons
IP : 196.52.84.10
Figure 25.2: The sites of nicotinic and muscarinic acetylcholine receptors. (ACh, acetylcholine; N, nicotinic; NE, norepinephrine; NT, neurotransmitter).
Ù
Muscarinic effects of acetylcholine is represented by the two mnemonics: (seen more commonly in adults) SLUDGE—Salivation, Lacrimation, Urination, Defecation, Gastrointestinal cramping and Emesis. DUMBBELS—Diarrhea, Urinary incontinence, Miosis, Muscle fasciculation, Bronchorrhea, Bronchospasm, Bradycardia, Emesis, Lacrimation, Salivation. ●● Nicotinic effect initially results in stimulation followed by paralysis of the preganglionic and somatic nerve fi bers leading to twitching of eyelids, tongue and facial muscles. This is followed by neuromuscular blockade and paralysis. ●● Preganglionic sympathetic stimulation may lead to tach yarrhythmias, hypertension and cardiorespiratory arrest. ●● Acetylcholine also causes initial stimulation followed by depression of the CNS. ●● One of the commonest effects of OPP is respiratory failure (Table 25.1). The latter is aggravated by secre tions that flood the airway and the lungs. ●● The usual cause of death is respiratory failure.
Clinical Picture Table 25.1: Clinical manifestations of organophosphates poisoning (OPP) RS
Rhinorrhea, bronchorrhea, bronchoconstriction, wheezing, dyspnea, pulmonary edema, respiratory arrest within 72 hours
CVS
Bradycardia, heart block, cardiac arrest
CNS
giddiness, coma, convulsions (most ÙHeadache, common)
GIT
Nausea, vomiting, diarrhea, abdominal cramps
Eye
Miosis, blurred vision, lacrimation (red tears due to porphyrin accumulation in lacrimal glands), papilledema
Skin
Sweating, dermatitis
Others Fasciculation, flaccidity, salivation, delirium, psychosis likely to produce tachycardia.
The clinical manifestations appear within 30 minutes to 1 hour and reach the peak in 2–8 hours.
Ù
Secretions, altered mental status and miosis are the commonest presentations in children.2,3
Chapter 25 n Specific Poisons
Clinical scenario 1 (Figure 25.3) 2-year-old boy rushed to the ED when he was found unIP : 196.52.84.10 responsive after accidently consuming an insecticide.
249
●● 2 mg in children > 12 years and adults This dose will relieve symptoms in a child with OPP, but cause the side effects of atropinization in a normal child.
Airway and Breathing Profuse secretions and respiratory failure could occur due to overwhelming bronchorrhea. Mechanical ventilation may be required in up to 25% of patients.
Ù
Correction of hypoxia is mandatory prior to atropinization to avoid the risk of ventricular fibrillation.
Figure 25.3 Physiological status: Airway is obstructed with secretions, respiratory distress, bradycardia with hypotensive shock, coma with miosis.
Prehospital Therapy ●● Remove patient from source of exposure. ●● Remove clothing rapidly. ●● Decontaminate skin by washing with copious amounts of water and soap. ●● If a large quantity of poison has been ingested and the child has been brought within 1 hour of ingestion gas tric lavage may be helpful.
Ù
The Cochrane group suggests that gastric lavage is an easily performed and cheap intervention. It could be used as an adjunct in the treatment of OP poisoning.4 ●● Irrigate eyes with normal saline, if contamination is suspected.
Clinical Diagnosis in the ED 1. A high index of suspicion is needed to consider OP poisoning, when a child is brought in profound altered mental status and history of exposure is not forthcom ing. The clinical features described in (Table 25.1) will help in the diagnosis. 2. In case of doubt, a therapeutic challenge of atropine may be attempted: ●● Administer 0.01 mg/kg Atropine in children < 12 year (minimum dose of 0.1 mg).
●● Oropharyngeal suctioning. ●● Provide oxygen using a JR circuit.. ●● Intubate using the pharmacologically assisted intuba tion (PAI) technique.
Ù
Avoid Succinylcholine since it increases secretions and can prolong muscle paralysis in OPP.
Circulation ●● Administer NS 10 mL/kg (max 20–30 mL/kg may be needed to correct shock). ●● Inotrope may be needed if hypotensive or hypoxia has caused cardiogenic shock.
Disability Manage convulsions using the standard protocol for status epilepticus.
Specific Treatment4 Atropine neutralizes the muscarinic effects of acetyl choline by competitive antagonism at postsynaptic mus carinic receptors. Dose: Children < 12 years with signs of moderate to severe toxicity: ●● Administer 0.05 to 0.1 mg/kg of atropine. ●● In children > 12 years and adults with signs of moder ate to severe toxicity: Administer 2 to 4 mg. ●● Double the previous dose after every 5 minutes in terval, until secretions resolve (dry mouth), crepita
250
Section VIII n Poisons
tions disappear, oxygenation improves and tachycardia > 140/minute occurs. ●● Repeat doses, based recurrence of symptoms for IPon : 196.52.84.10 2–12 hours.
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Atropine should be used for at least 24 hours to reverse the cholinergic signs, while the organophosphate is metabolized. ●● Dosing can be decreased when symptoms do not recur for 6 hours.
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The Cochrane group recommends incremental dose administration of atropine as the standard of care. The role of glycopyrrolate alone or in combination with atropine is not clear.4 ●● Pralidoxime (2-PAM) is a cholinesterase reactivator and counteracts the nicotinic effects. It is useful when the victim has respiratory muscle weakness (Figure 25.4). ●● Administer 2-PAM, as an IV infusion after the loading dose, until signs of weakness improve. ●● Dose: 30 mg/kg (5% solution) in isotonic saline over 5–10 minutes as early as possible followed by a con tinuous infusion of 8 mg/kg/hour. ●● The drug is probably not useful 36 hours after expo sure.
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The Cochrane group (2012) reports that the current evidence is insufficient to indicate whether oximes are harmful or beneficial.4
Figure 25.4: Pralidoxime and atropine used in organophosphorous poisoning.
CARBAMATES Carbofuran (Furadan), propoxur (Baygon), Bufencarb (Bux) are carbamate insecticides. Non-toxic compounds such as Sevin (of carbaryl group) are also included in the group. Their mode of action is similar to OP, though they are less toxic. The latter is due to the fact that they do not penetrate into the CNS and reversibly carbamylate the es ter site of the cholinesterase (ChE) enzyme. Their dura tion of action is also short. Hemolytic anemia has been reported, but no intermediate or chronic effects has been described. ●● Management of carbamate toxicity is similar to that of OP poisoning. ●● Oximes are not recommended.
Kerosene Acute accidental ingestion of kerosene is common in lower socioeconomic groups. Due to its low surface tension, kerosene tends to get aspirated into the lungs during ingestion, vomiting and in halation of vapors. Kerosene toxicity has also been noted following application of kerosene on the skin of neonates, indicating that transdermal absorption can also result in toxic effects.
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Ingestion of 30 mL is lethal.
Pathophysiology Aspiration of kerosene causes chemical pneumonitis, which may progress to atelectasis, pneumatoceles or pneu mothorax. Hyperemia, edema, small airway obstruction, inflammation, diffuse hemorrhages and cellular infiltra tion of the lungs are the various conditions which interfere with gas exchange resulting in hypoxia. The latter leads to alteration in mental status. Liver damage, cardiomyo pathy, renal toxicity and gastrointestinal (GI) involvement have been reported. Temperature regulation may also be impaired due to its direct effect on the CNS. ●● Cough and breathlessness due to aspiration pneumonia, may appear as early as l5 minutes or as late as 24 hours after kerosene ingestion. Hemoptysis, has been reported in very severe toxicity. ●● Fever occurs later and may persist for as long as 10 days after kerosene ingestion.
Chapter 25 n Specific Poisons
●● Primary CNS toxicity can present with lethargy, dizzi ness, headache, visual disturbances, seizures and hyper pyrexia. Coma and respiratory paralysis lead to death. IP : 196.52.84.10 ●● Leukocytosis is often noted, though bacteria are not the cause of aspiration pneumonia. ●● Hyperexpansion of the chest is occasionally seen. ●● Most children, however recover and symptoms resolve between the 2nd and 5th day.
Case Scenario 2 A 2-year-old child is rushed into the ED, after he was found vomiting and drowsy near an overturned bottle of kerosene. He is smelling of kerosene (Figure 25.5).
251
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If the child is asymptomatic it is unlikely that significant problems will occur. ●● Observe asymptomatic children for at least 24 hours, since symptoms may appear late.
Radiographic Findings ●● Chest X-ray helps to identify pulmonary involvement (60% are not appreciable by auscultation). ●● Chest X-ray may be normal for as long as 6–8 hours after ingestion. ●● Chest X-ray may reveal perihilar mottling, consolida tion, areas of collapse or pulmonary edema. Pneumoni tis commonly involves both lower lobes. There may be evidence of pleural effusion, cysts and pneumothorax. Pneumatoceles, may appear 2–3 weeks after clinical resolution.
Prevention
Figure 25.5 Physiological status: Unmaintainable airway, respiratory failure, normotensive shock with altered mental status.
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Do not induce emesis. Do not perform gastric lavage. Both procedures can enhance risk of aspiration.
Resuscitation ●● Administer oxygen via the JR circuit, since this child has presented with impending respiratory failure. ●● Initiate bag-valve-mask ventilation and proceed to in tubate using PAI technique, if he had presented with respiratory arrest. ●● Treat shock with 10 mL/kg boluses of NS (up to a maximum of 20 mL/kg). Consider more, only if hypo volemic due to persistant vomiting. If shock persists, initiate appropriate inotrope. ●● Prophylactic antibiotics are not indicated. ●● Avoid corticosteroids (may be harmful).
●● Counsel parents about the hazards of storing kerosene in familiar beverage or household containers. ●● Teach them to avoid placing these containers on the floor (within easy reach of infants and toddlers). ●● Avoid using palm oil as a household remedy.
Barbiturates Barbiturate poisoning in children is usually due to acci dental ingestion. Mental confusion resulting in repeated dosages have been reported in adults and is also known as ‘involuntary suicide’ or ‘barbiturate automatism’. Toxic ingestion of barbiturate can cause global de pression or neuronal excitability. Large doses depress both the respiratory and vasomotor centers. Renal function may be compromised secondary to drug-induced hypotension. Box 25.1: Common household things of low toxicity No treatment required Bar soap, lipstick, dry cells, newspaper, candles, pencil, chalk, shampoo, clay (modeling), shaving cream and lotions, crayons, shoe polish, dehumidifying packets, striking surface of matches, detergents, sweetening agents, hand lotion and creams, thermometer, ink, toothpaste. Removal necessary only, if large amounts ingested After shave lotion, body conditioners, colognes, deodorants, fabric softners, hair dyes, hair tonic, marker ink, match stick > 20, oral contraceptive, perfumes, toilet cleaner.
252
Section VIII n Poisons
●● Correct shock. Not more than 20 mL/kg may be need ed. Epinephrine is indicated, if hypotension persists after fluid bolus. If blood pressure stabilizes, dopamine is indicated.
Case Scenario 3 A 5-year-old child could not be woken up. An open botIP for : 196.52.84.10 tle of tablets prescribed his brother’s seizure disorder was found half empty near him. His temperature: 96.5°F (Figure 25.6).
Decontamination Severe Poisoning ●● Perform gastric lavage, if a large quantity has been in gested and the child has been brought within 1 hour of ingestion. ●● Insert nasogastric tube and administer 1 g/kg of acti vated charcoal prepared with aerated drink as a slurry (refer Chapter 24 on Poisoning: General Approach).
Mild to Moderate Poisoning Admit for observation. They require no vigorous treatment. If gag is intact, make the child drink a 1 g/kg of slurry of activated charcoal mixed with aerated drinks. Urine alka linization is no more recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose acti vated charcoal is superior.5
Figure 25.6 Physiological status: Airway is unmaintainable, respiratory failure, hypotensive shock with altered mental status.
Diagnosis is based on the history, clinical features and circumstantial evidence. Serum levels of barbiturate > l0 mg/dL reflect the severity of intoxication. An EEG pro vides useful evidence of poisoning. Differential diagnosis includes other causes of non-traumatic coma.
OPIUM AND ITS DERIVATIVES
Resuscitation
Morphine, Codeine, Pethidine, Heroin, Propoxyphene, etc (Box 25.1 and Table 25.2).
●● Initiate bag-valve-mask ventilation and plan early intu bation for respiratory failure and coma.
●● These toxins are easily absorbed from the GIT, muscle and lungs. Opioid overdose can occur in adolescents.
Table 25.2: Clinical findings of sedative-hypnotic overdose Clinical signs
Sedative-hypnotics
Hypothermia
Barbiturates, bromides, ethchlorvynol
Unique odors
Chloral hydrate (pear), ethchlorvynol (new vinyl shower curtain)
Cardiotoxicity •
Myocardial depression
•
Meprobamate
•
Dysrhythmias
•
Chloral hydrate
Muscular twitching
GHB, methaqualone, propofol, etomidate
Acneiform rash
Bromides
Fluctuating coma
Glutethimide, meprobamate
GI hemorrhage
Chloral hydrate, methaqualone
Discolored urine
Propofol (green/pink)
Anticholinergic signs
Glutethimide
Chapter 25 n Specific Poisons
Accidental overdose have been documented in infants following its use for diarrhea and sedation. ●● Fatal dose: oral > 0.3 > 0.l g. IPg: parenteral 196.52.84.10
CASE SCENARIO 4 4-month-old infant was treated with 2 teaspoons of codeine syrup for coughing and crying in the night. He was not arousable in the morning (Figure 25.7).
253
Belladonna Alkaloids, Datura (Atropine Group) The toxic effects are due to parasympathetic blockade (an ticholinergic effect) at the muscarinic receptors. The nico tinic receptors at neuromuscular junctions are unaffected in datura poisoning.
CASE SCENARIO 5 2-year-old toddler was found chewing a green fleshy pod. On arrival he was agitated. His cardiopulmonary cerebral assessment was stable except for widely dialated pupils. His temperature was 38.5°C. He was also looking flushed and his mucosa was dry.
Figure 25.7 Physiological status: Airway unmaintainable, respiratory failure, bradycardia, shock, BP: Normal, coma with miotic pupils.
He had bladder distension and his temperature was 35.4°. Diagnosis: It is evident by the history of ingestion and typical clinical picture.
Resuscitation ●● Stabilize airway, breathing and circulation. ●● Administer naloxone (specific antidote) immediately in the dose of 0.01 mg/kg IV or IM. ●● Repeat the dose of naloxone in 3–10 minutes if no re sponse is noted.
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Response is evident when the depth and rate of respiration improve. Pupils do not dilate and are not the end point of therapy. ●● Gastric lavage is useful only if a large life-threaten ing amount has been ingested and the child has been brought within 1 hour of ingestion. ●● Use activated charcoal. ●● Administer via nasogastric tube as a slurry (1 g/kg). ●● Intubate to protect the airway, if the child’s mental sta tus has dropped significantly.
●● Mild poisoning results in dryness of the mouth, hyper pyrexia and widely dilated pupils. ●● Higher doses cause tachycardia, flushing of face (red, hot, dry face), hyperpyrexia, mental disturbances (‘muttering’ delirium, hallucinations and excitation) and cardiac rhythm disturbances. ●● If left untreated, seizures, coma and death can occur. Diagnosis: Datura poisoning. Differential diagnosis: Encephalitis, cerebral malaria, acute meningitis, intracranial bleed, over dose of antihista mines and tricyclic antidepressants.
Resuscitation ●● Stabilize the airway, breathing, circulation.
Decontamination ●● Administer activated charcoal 1 g/kg . ●● Gastric lavage, if large life-threatening amount has been ingested and the child reaches within the first hour of ingestion.
Antidote Specific antidotes are used in the presence of seizures, hal lucinations and arrhythmias. ●● Neostigmine methyl sulfate (dose: 0.5–2.5 mg IM at frequent intervals). ●● Physostigmine: Dose: 0.5 mg slowly IV/IM (repeat ev ery 5 minutes up to a maximum of 2 mg). Note: This drug crosses the blood brain barrier.
254
Section VIII n Poisons
●● If the patient is excited and restless, phenobarbitone l00 mg or diazepam 0.2–0.3 mg/kg/24 hours is admin istered once in 6 hours. IP : 196.52.84.10 ●● Correction of fluid and electrolyte imbalance.
Paracetamol (Acetaminophen)6 Inadvertent ingestion of pain killers and antipyretics are some of the commonest reasons, why parents rush to the ED. Parents must be educated about the hazards of par acetamol and taught that the maximum permissible dose of paracetamol is 60 mg/kg per day (15 mg/kg/dose q 6th hourly). Fortunately, paracetamol-induced liver damage in children is less common than in adults.
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Paracetamol dose less than 150 mg/kg does not warrant further action. The drug is rapidly absorbed and metabolized in the liver to metabolically inert excretory products. Up to 2%–4% is metabolized by the cytochrome P450 mixed function oxidase system with glutathione to form a nontoxic product (mercapturic acid). With paracetamol over dose, hepatic stores of glutathione are depleted to less than 70% of normal, resulting in the formation of highly reac tive intermediate metabolites that bind to hepatic macro molecules resulting in damage to the hepatocytes. Besides hepatocellular damage, they also cause renal tubular dam age and hypoglycemic coma. Enzyme inducers (e.g. an ticonvulsants, antitubercular drugs) worsen hepatocellular damage by promoting cytochrome P450 metabolism. The clinical course comprises of four stages (Table 25.3).
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Stage 1: Symptoms appear within an average of 6 hours after ingestion • Diaphoresis, though children less than 6 years of age do not have this symptom. • Vomiting is more common. Stage 2: Symptoms become less • Biochemical evidence of liver damage becomes apparent. Stage 3: (48–96 hour after ingestion) • Less than 1% of patients develop fulminant hepatic failure on the 3rd to 6th days. • Serum glutamic-oxaloacetic transaminase (SGOT) levels may be as high as 20,000 or 30,000 IU/L. • Death may occur. Histopathology reveals centri loblar necrosis with periportal sparing. Stage 4: High liver enzyme levels persist in a few patients.
Diagnosis i. History of ingestion. ii. Clinical features. iii. Plasma acetaminophen levels. ●● Once the plasma level has been determined, plot it on the Matthews-Rumack nomogram. This will help to de termine whether the level in relation to time is toxic. Alternatively, draw a line on semilogarithmic graph joining 200 µg/mL at 4 hours and 50 µg/mL at l2 hours after ingestion. With values above this line there is a 60% chance of severe liver damage (Figure 25.8).
Table 25.3: Time course and clinical stages of acetaminophen toxicity Stage
Time course
Name
Symptoms
Signs
1
0–12 (up to 24–36) hour
Preinjury
Nausea, vomiting, anorexia, malaise, diaphoresis
Elevated serum acetaminophen concentration, PT normal
2
8–36 hour
Liver injury
Nausea, vomiting, right upper quadrant abdominal tenderness, mild hepatomegaly
Transaminitis (AST begins to rise 8–36 h after ingestion), mild jaundice
3
2–4 day
Maximum liver injury
Liver failure (encephalopathy, coagulopathy, hemorrhage, acidosis)
Hemorrhage, ARDS, sepsis/SIRS, multiorgan failure, cerebral edema
4
> 4 day–2 week
Recovery
None
Complete hepatic histologic recovery
Chapter 25 n Specific Poisons
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Activated charcoal or alkalinization of urine is of no : 196.52.84.10 value in paracetamol IP toxicity.
Antidote ●● N-acetylcysteine, the drug of choice is more effective when given orally, preferably within 10 hours (even if the drug level cannot be determined in time). Dose: The oral loading dose is 140 mg/kg followed by 70 mg/kg every 4 hours for 3 days up to a total of 17 doses. Since it has an unpleasant smell of sulfur that makes it un palatable, the concentrate is diluted by mixing one part with three parts of any carbonated beverage or (orange) juice.
255
●● Monitor liver function tests frequently. ●● Most patients (99%) will recover within a week.
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NSAID group of drugs8 cause little toxicity and ingestion is considered life-threatening only, if the amount consumed is: 1. > 100 mg/kg of brufen. 2. > 25 mg/kg mefenamic acid. Treat vomiting-induced dehydration.
IRON9 Iron ingestion is common in children under 5 years of age. It can be fatal, if not managed appropriately (Table 25.4).
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The lethal oral dose is between 200 and 500 mg/kg el emental iron. ●● GI symptoms can be seen at doses of l5–30 mg/kg.
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Significant toxicity is uncommon at amounts less than 50 mg/kg. The toxic dose is not absolute and fatal reactions have been reported even with small amounts. All ingestions should therefore be considered potentially dangerous. Figure 25.8: Time course of rise, peak and fall of laboratory values in patients with paracetamol poisoning who survive. Peaks are not proportional. Significant individual variations may occur.
Table 25.4: Common iron preparations Compound
N-acetylcysteine ●● ●● ●● ●●
150 mg/kg in 5% D over 1 hour. 10 mg/kg/hour for 20 hours (delay < 10 hours). 32 hours (delay 10–16 hour). 72 hours (delay > 16 hour) and longer, if encephalo pathic. ●● Monitor potassium levels. Oral Methionine is an alternative drug. Dose: 2.5 g stat followed by 2.5 g 4 hourly up to a total of l0 g over 12 hours (it is not as reliable as NAC).
Supportive Treatment ●● Maintain electrolyte balance. ●● Treat coagulopathy.
Elemental iron %
Ferrous sulfate
20
Ferrous fumarate
33
Ferrous gluconate
12
Ferric pyrophosphate
30
Ferrocholinate
14
Ferroglycine sulfate
16
Ferrous sulfate, dried
33
Ferrous carbonate, anhydrous
38
Carbonyl iron
99
The antenatal mother is the commonest source of iron tablets. Prescribed for a period of a month and attractively packaged, hence these tablets are easily accessible by curi ous young children.
256
Section VIII n Poisons
Table 25.5: Toxicity of iron by amount ingested and peak serum levels Elemental iron (mg/kg)
IP : serum 196.52.84.10 Peak iron Toxicity (μg/DL)
< 20
50–150
None
20–40
150–300
Mild
40–60
300–500
Moderate
> 60
> 500
Severe
Pathophysiology ●● Iron directly damages the GI mucosa resulting in mas sive fluid loss and hemorrhage (Table 25.5). ●● Vasodilation, occurs secondary to ferritin and other iron metabolites in the liver. ●● Both factors predispose to the development of shock due to absolute or relative hypovolemia. ●● Acidosis occurs due to the action of iron on oxidative metabolism. ●● Coagulopathy and the resultant bleeding predispose to circulatory failure. ●● The absorbed iron causes direct damage to the liver parenchymal cells leading to massive hepatic necrosis and liver failure.
●● Iron levels, less than 350 µg/dL, when drawn 2–6 hours after ingestion, predict an asymptom atic course. ●● Iron levels greater than 500 µg/dL suggest signifi cant risk for phase III manifestations. In absence of serum iron levels, early clinical assess ment and several simple laboratory tests may be used to predict approximate iron levels.
Ù
Vomiting, diarrhea, S. glucose > l50 mg/dL, WBC > l5,000/mm3 and radiopaque material on abdominal radiograph correlate with an elevated serum iron level greater than 300 µg/dL.
Case scenario 6 4-year-old child was brought to the ED after he was found to have eaten up most of his mother’s monthly prescription of iron tablets for pregnancy (Figure 25.9).
Clinical Course l. Gastrointestinal stage: The early symptoms include vomiting, rapid onset of diarrhea, colicky abdominal pain and GI hemorrhage. 2. Relatively stable stage: Reports have suggested that there is a period of relative stability, which begins 3–4 hours after ingestion and lasts for as long as 48 hours. Subtle signs, such as mild GI bleeding, hyper ventilation and poor capillary refill may exist during this stage and may go unrecognized. 3. Shock stage: The third stage is characterized by circula tory failure and profound shock, which may be fatal. 4. Hepatotoxicity stage: Hepatotoxicity occurs within the first 48 hours. This is the second most common cause of death. 5. Gastric scarring is a late manifestation occurring 2–6 weeks after ingestion and is manifested by obstruction of the gastric outlet and portions of the small intestine. The amount of iron ingested often is hard to quantify clinically. Serum iron levels, if obtained promptly, have been shown to correlate with the symptoms:
Figure 25.9 Physiological status: Normal
Resuscitation 1. Care of the airway, breathing is the priority in manage ment, if the patient has altered level of consciousness. 2. Correct shock if identified. Since this 4-year-old child is stable, plan to decontami nate.
Decontamination ●● Perform gastric lavage for large life-threatening inges tion, if the child presented within the first few hours of ingestion.
Chapter 25 n Specific Poisons
●● Whole bowel irrigation is considered as the technique of choice. ●● Mix PEGLEG in a IP carbonated drink and administer it : 196.52.84.10 in the dose of: – 6–12 years: 1,000 mL/hour. – 9 months to 12 years: 500 mL/hour. – > 12 years 1,500–2,000 mL/hour.
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Avoid PEGLEG, if airway is unprotected, shock, intractable vomiting, GI bleed, perforation, ileus or obstruction.10 ● ● Gastrostomy should be considered in massive overdoses.
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Activated charcoal is not effective in binding iron salts. Ipecac-induced emesis is not found to be beneficial.
257
●● Chelation is continued until the urine color and serum iron level return to normal or the maximum daily dose has been reached. ●● Patients with mild symptoms or those who are asymp tomatic, but have high serum iron or a positive chal lenge test, should receive: – 20–40 mg/kg of desferrioxamine infused over 4 hours or 20 mg/kg IM, 4–8 hourly.
Supportive Treatment ●● Blood transfusion should be considered in severe hemorrhage. ●● Persistent metabolic acidosis may require treatment with sodium bicarbonate. ●● Dyselectrolytemia and hyperglycemia should be man aged appropriately. ●● Liver and renal failure are treated symptomatically.
CORROSIVES The most frequently ingested alkalis are button batteries, dishwashing powder, disinfectants and caustic soda used for cleaning ovens and degreasers. These may produce ir reversible damage at the site of contact. Absence of antidotes or definitive treatment modalities makes this toxin particularly dangerous. In addition, it can cause permanent damage to the gut resulting in strictures.
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Figure 25.10: Desferrioxamine administration in iron toxicity results in excretion of vin rose color urine (Courtesy: Dr S Thangavelu).
Prevention is better than cure. Parents must be taught to store house hold disinfectants and cleaning agents away from children.
●● Blood should be drawn for complete blood cell count, blood glucose, electrolytes, BUN, liver function tests, serum iron, total iron binding capacity, typing and cross matching.
Pathophysiology
Antidote
Presence of two or more symptoms namely vomiting, drooling or stridor correlates well with esophageal and la ryngeal injury. This may be accompanied by clinical signs of lip swelling, tongue erythema, leukoplakia or oral ulcer ation. Substernal chest pain, abdominal pain and rigidity suggest profound injury and perforation of the esophagus or stomach.11
●● Initiate desferrioxamine infusion at a dose of l5 mg/ kg/h (max 6 g/day). Higher infusion rates associated with risk of hypotension. ●● The appearance of a pinkish (Vin rose) urine indicates the presence of iron desferrioxamine complexes. Refer Figure 25.10.
Patients with significant ingestion may have vomiting, drooling, stridor, dyspnea, hematemesis, fever and oral burns (Figure 25.11).
258
Section VIII n Poisons
Specific Management IP : 196.52.84.10
●● Immediate dilution and irrigation with clean water for 30 minutes.
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Neutralization agents, such as vinegar is contraindicated as it is thought that an exothermic reaction will occur, further injuring the tissue .12 Emesis, lavage, charcoal and cathartics are contraindicated in corrosive poisoning.
Figure 25.11: The infant presented with stridor and respiratory distress with impending failure. He was intubated in the ED. Examination of the oral cavity shows leukoplakia and ulceration (Courtesy: Dr P Ramachandran).
CASE SCENARIO 7 2-month-old infant was fed floor cleaner by his grandmother by mistake (Figure 25.12).
Figure 25.12 Physiological status: Obstructed airway, respiratory distress, tachycardia, normotensive shock with altered mental status.
Resuscitation ●● Plan intubation. Call for ENT/anesthetist to help secure the airway. Plan for cricothyrotomy or tracheostomy depending upon the severity of damage. ●● Anticipate a difficult airway and call for help. ●● Positive pressure ventilation may be required in pa tients who develop pulmonary edema. ●● Correct shock with 20 mL/kg of NS.
●● Order lateral neck and chest X-rays as part of the initial assessment to corroborate any underlying suspicion of perforation. ●● Do not order barium swallow. This of little use in the acute phase, since it delays endoscopy and will not re veal first or second degree mucosal injuries.13 ●● Plan to perform esophagoscopy within 48 hours after the inciting event. ●● During this time period, the effects of the injury would have demarcated itself, enabling grading of severity. Prior to this time period, one may underestimate the severity of injury, since erythema may be seen in the early phases of even grade 2 and 3 injuries. ●● Endoscopy after 72 hours, increases the chance of iat rogenic perforation.13 ●● Avoid steroids. Multiple trials and reviews have shown little or no measurable benefit from varying doses of steroids in their ability to reduce the rate of stricture formation. 14,15,16 ●● Prescribe Omeprazole, Pantoprazole, for 6 weeks.17,18,19 Antireflux therapy prevents reflux associated esopha geal injury, which could further aggravate the already damaged area. ●● Prescribe third generation cephalosporin and if oral in take is tolerated change over to clindamycin for 1 week to ensure a broad spectrum cover.14 ●● Introduce nasogastric tube only during endoscopy. It can be used for enteral feeding during the period when the patient is kept without oral feeding. It also keeps the esophageal lumen patent, so that adherence and obliteration of the lumen does not occur. The nasogas tric tube may be removed at 1 week and normal oral feeding commenced as tolerated by the child.14
Button Battery Ingestion20 ●● NPO instructions should be followed until the posi tion of the esophageal battery is confirmed by CXR.
Chapter 25 n Specific Poisons
●● Anesthesia may be required for removal. Do not in duce vomiting. ●● If the patient is asymptomatic, determine the diameter IP : 196.52.84.10 based on the size of a comparable battery. ●● If the patient is ≤ 12 years, immediately obtain an X-ray to locate the battery. Batteries lodged in the esophagus may cause serious burns in as little as 2 hours. Do not wait for symptoms to develop. Patients with a battery in the esophagus may be asymptomatic initially. ●● If the patient is > 12 years and the battery diameter is > 12 mm or unknown, immediately obtain an X-ray to locate the battery.
Ù
If the patient is > 12 years and the ingested battery is ≤ 12 mm, no X-ray to locate the battery is required, if all of the following conditions are met: • The patient is entirely asymptomatic and has been asymptomatic, since the battery was ingested. • Only one battery was ingested. • A magnet was ingested. • The battery has been reliably identified and size confirmed as less than < 12 mm. • There is no history of pre-existing esophageal dis ease. ●● Order X-rays of entire esophagus, neck and abdomen. Obtain both AP and lateral X-rays for batteries in the esophagus to determine orientation of the positive and negative poles. On the lateral film, if the step-off is on the negative side of the battery (the negative pole has a slightly smaller diameter). Anticipate complications based on battery posi tion and orientation. Damage will be more severe in tissue adjacent to the negative pole. Immediately remove batteries lodged in the esophagus. Serious burns can occur in 2 hours. Do not delay removal, even if the child has eaten recently. The esophageal bat tery should not be pushed into the stomach as the risk of esophageal perforation may increase. After removing a battery from the esophagus, the child should be observed for delayed complications, such as tracheoesophageal fistula, esophageal perforation, medi astinitis, vocal cord paralysis, tracheal stenosis or trache omalacia, aspiration pneumonia, empyema, lung abscess, pneumothorax, spondylodiscitis or exsanguination from perforation into a large vessel. Esophageal perforations and fistulas involving the trachea or major vessels may be de
259
layed for up to 27 days postremoval. Esophageal strictures may not manifest for weeks to months postingestion.
Ù
Retrieve batteries, endoscopically if possible from the stomach or beyond if: • A magnet is ingested and the patient develops signs or symptoms that are likely related to the battery ingestion. • A large battery (≥ 15 mm diameter), ingested by a child younger than 6 years, remains in the stomach for 4 days or longer. • If battery diameter is unknown, estimate it from the X-ray, factoring out magnification (which tends to overestimate battery diameter). ●● Allow batteries to pass spontaneously, if they have passed beyond the esophagus and no clinical indication of GI injury is evident. Avoid unnecessary endoscopic or surgical removal in asymptomatic patients. ●● Promptly re-evaluate all patients who develop signs or symptoms possibly related to the battery. Endoscopic removal of batteries still in the stomach should be pur sued for even minor symptoms. For batteries beyond the reach of the endoscope, surgical battery removal may be required in the unusual patients with evidence of occult or visible bleeding, abdominal pain, pro foundly decreased appetite, vomiting, signs of an acute abdomen and/or fever, unless these clinical manifesta tions are clearly unrelated to the battery. ●● Confirm battery passage by inspecting stools. Con sider repeat radiographs to confirm passage if passage not observed in 10–14 days. Confirming passage may avoid urgent diagnostic intervention for minor symp toms developing later. ●● Manage ingestion of a hearing aid containing a battery as an ingestion of a small battery (≤ 12 mm).
Ù
Avoid these ineffective, unnecessary or unproven thera peutic interventions: • Ipecac administration (ineffective). • Laxatives (ineffective). • PEGLEC solution (unproven effectiveness and not known, if solution enhances electrolysis).
NEEM OIL INGESTION This is the commonest cause of refractory seizures. Symp toms may start as early as 10 minutes. The active ingredient,
260
Section VIII n Poisons
which causes the toxicity is not known. Treatment is simi lar to the management of status epilepticus.
IP : 196.52.84.10 CAMPHOR POISONING21 ●● Camphor poisoning is a common ingredient in many camphorated oils, ointments and inhalants for the home treatment of colds. It is also used for pooja. Children are attracted by the smell, texture and feel. ●● Camphor is rapidly absorbed when taken orally, but a considerable amount can also be absorbed via inhala tion or through intact skin. Typically, symptoms begin 5–90 minutes after ingestion of a toxic dose. ●● Seizures may occur as soon as 4 minutes after inges tion of 28 g of camphorated oil. Death may result from respiratory depression or complications of status epi lepticus.
●● Other neurologic symptoms include confusion, verti go, restlessness, delirium and hallucinations. Increased muscular activity, tremors and jerky movements, which can often progress to epileptiform convulsions.●● GI symptoms consist of oral and intestinal burning, nausea and vomiting. ●● Tachycardia, mydriasis, visual disturbances, urinary retention can also occur. ●● Albuminuria, mild transient elevations of the aspartate dehydrogenase and lactic dehydrogenase concentra tions and rarely, hepatic failure have been noted. Although a variety of other conditions or intoxica tions can exhibit similar symptoms, a strong odor of camphor on the breath or a history of recent treatments with camphor-containing agents will strongly suggest camphor intoxication.
Table 25.6: Common herbal medications and adverse/toxic effects Herbal name Betel nut
Botanical name Areca catechu
Cantharidin (blister beetle) Cantharis
Uses
Adverse effects
Stimulant
Bronchospasm
Aphrodisiac
Priapism, dermatitis, renal
Ephedra (ma huang, chinese)
Ephedra sinica
Stimulant, asthma
Hypertension, tachycardia, CNS, MI
Fenugreek (methi)
Trigonella foenum-graecum
Expectorant, anti-inflammatory
None reported
Feverfew (parthenium)
Chrysanthemum parthenium
Migraines, antipyretic
Postfeverfew syndrome, rebound migraine
Garlic (lasoon)
Allium sativum
Infection, CAD, hypertension
Dermatitis, GI
Ginger (adrak)
Zingiber officinale
Motion sickness, GI illness
None reported
Henbane (stinking nightshade)
Hyoscyamus niger
Sedative, GI discomfort
Anticholinergic toxicity
Jimson weed
Datura stramonium
Asthma
Anticholinergic toxicity
Kava kava
Piper methysticum
Sedative, aphrodisiac
Euphoria, CNS
Licorice
Glycyrrhiza glabra
Cough, GI illnesses
Hypokalemia, drug interactions
Mistletoe
Viscum album
GI illness, cancer, HIV
GI, bradycardia, CNS
Nutmeg
Myristica fragrans
Aphrodisiac, hallucinogen
CNS, GI
St John’s wort
Hypericum perforatum
Depression, anxiety
Drug interactions
Sassafras
Sassafras albidum
GI stimulant (root beer), anticoagulant, syphilis
Hepatotoxicity, carcinogen
Soy
Glycine max
Menopause, CAD
Carcinogen
GI illness, cancer
Dizziness, bradycardia
Sexual disorders, aphrodisiac
Hypertension, agitation, CNS effects
Himalayan Yew (paclitaxel) Taxus baccata Yohimbine
Pausinystalia yohimbe
Chapter 25 n Specific Poisons
Supportive Treatment ●● Decontamination of gut or skin by gastric lavage. IP epilepticus. : 196.52.84.10 ●● Management of status
Table 25.7: Drug interactions with herbal products Herbal product
Methemoglobinemia Blood sample from a child who had accidentally ingested dapsone has turned chocolate brown (Figure 25.13). The control sample on the right is normal.
Interacting drugs
Ginkgo biloba
Aspirin, warfarin (Coumadin), ticlopidine (Ticlid), clopidogrel (Plavix), dipyridamole (Persantine)
Ephedra
Caffeine, decongestants, stimulants
Ginestra
Warfarin
Kava Betel nut Ephedra, Fenugreek Ginseng Licorice Soy Yohimbine
Sedatives, sleeping pills, antipsychotics, alcohol Prednisone, salbutamol, MAO inhibitors Warfarin Ethanol,Warfarin Prednisolone, Antihypertensives Warfarin Tricyclic antidepressants
St John’s wort
SSRI
Pyrethroids Pyrethroids (mosquito repellents) are non-toxic to humans. Pyrethrins from chrysanthemum flowers are neurotoxic to insects. In sensitive individuals it may cause skin manifes tations and rarely neurological manifestations.
261
Theophylline Digoxin Cyclosporine Indinavir Irinotecan Nevirapine Simvastatin
(serotonin syndrome)
Decreased drug concentration
Box 25.2: Sedative hypnotic poisonings Figure 25.13: Methemoglobin formation due to Dapsone ingestion (sample on left) (Courtesy: Dr Shankar Srinivasan).
MISCELLANEOUS22, 23 A growing number of people, especially in our coun try, still use herbal products for preventive and thera peutic purposes. The manufacturers of these products, both indigenous practitioners and commercial ventures, are not required to submit proof of safety and efficacy to regulatory agencies before marketing. For this rea son, the adverse effects (Table 25.6) and drug interac tions (Table 25.7) associated with herbal remedies are largely unknown. For example, Ginkgo biloba extract, advertised as improving cognitive functioning, has been reported to cause spontaneous bleeding and it may in teract with anticoagulants and antiplatelet agents. Seeds of stone fruits like cherry, plum, peach, apricot, bitter almond, roots of cassava contain amygdalin, which on ingestion release cyanide. Laboratory personnel, children inhabiting colonies around factories/chemical plants and those caught in the
Barbiturates
Ultrashort acting—Methohexital
Short and intermediate acting—Pentobarbital
Long acting—Phenobarbital
Non-barbiturates
Benzodiazepines
Carbamates—Meprobamate
Chloral derivatives—Chloral hydrate
Ethchlorvynol
Piperidines—Glutethimide
Quinazolinone—Methaqualone
Imidazopyridine—Zolpidem
Antihistamines—Diphenhydramine and doxylamine
GHB—Gamma-hydroxybutyrate
crossfire of biological warfare and military repression may be exposed to inhaled pollutants/toxins with adverse ef fects on growth and development.
262
Section VIII n Poisons
Many household things kept within reach of the chil dren are often ingested by them due to their curiosity to explore nature. A list ofIPthings which are innocuous or of : 196.52.84.10 low toxicity are given in Box 25.1. Reassurance of the par ents is all that is needed.
Key Points
ü
1. Organophosphorus compounds are the commonest toxin ingested in the rural agricultural areas. 2. Atropine usage is based on the recommendations of the Cochrane data base 2012. 3. Ingestion of corrosives and button batteries are hazardous and should be handled using a protocol based approach. 4. Usually common house hold products are safe unless large quantities are ingested. 5. Always resuscitate ABCs in addition to poison elimination or treatment.
common errors
û
1. Performing gastric lavage for kerosene and caustic ingestion. 2. Failing to ventilate for severe OP poisoning. 3. Not considering the potential for oesophageal damage following battery ingestion. 4. Failure to seek assistance from regional poison center.
References 1. Srivastava A, Peshin SS, Kaleekal T, et al. An epidemio logical study of poisoning cases reported to the National Poisons Information Centre. All India Institute of Medi cal Sciences, New Delhi. Human Experimental Toxicol. 2005;24:279-85. 2. van Heel W, Hachimi-Idrissi S. Accidental organophos phate insecticide intoxication in children: a reminder. Int J Emerg Med. Jun 15 2011;4(1):32. 3. Kozer E, Mordel A, Haim SB, et al. Pediatric poisoning from trimedoxime (TMB4) and atropine automatic injec tors. J Pediatr. Jan 2005;146(1):41-44. 4. Interventions for acute Organophophate poison South Asian Cochrane Network and Centre (SASIANCC) 2012. 5. Proudfoot AT, Krenzelok EP, Vale JA. Position Paper on Urine alkalinization Journal of Toxicology Clinical Toxi cology. 2004;42(1):1-26. 6. Hanhan UA. The poisoned child in the pediatric intensive care unit. Pediatr Clin N Am. 2008; 55: 669-86.
7. Frank Shann Drug Doses Intensive Care Unit, Royal Chil dren’s hospital Austrailia, 15th Edn 2010. 8. Riordan M, Rylance G, Berry K. Poisoning in children1: General management. Arch Dis Child. 2002 ;87:392-396. 9. Salgia AD, Kosnik SD. When acetaminophen use becomes toxic. Treating acute accidental and intentional overdose. Postgrad Med. 1999;105:81-4, 87, 90. 10. Singhi SC, Baranwal AK, M J. Acute iron poisoning:clinical picture, intensive care needs and Outcome. Indian Pediatr. 2003; 40:1177-182. 11. GP Cantwell, RS Weisman. Poisoning Roger’s Handbook of Pediatric Intensive Care 2009; 4th edition, N. Delhi Wil liams and Wilkins. 12. F Riffat, A Cheng. Pediatric caustic ingestion: 50 consecu tive cases and a review of the literature Diseases of the Esophagus. 2009(22), 89-94DOI: 10.1111/j.1442-2050. 2008.00867. 13. Millar A, Numanoglu A, Rode H. Caustic strictures of the esophagus. In: Grosfeld J, O’Neill J, Coran A, Fonkalsrud E (eds). Grosfeld: Pediatric Surgery, Chapter 68. St. Louis, MO: Mosby. 2006; 969-79. 14. Friedman EM. Caustic ingestions and foreign bodies in the aero digestive tract of children. Pediatr Clin North Am. 1989; 6: 1403-410. 15. Ulman I, Mutaf O. A critique of systemic steroids in the management of esophageal burns in children. Eur J Pediatr Surg. 1998;8:71. 16. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990;323:637. 17. Poley J, Steyerberg E, Kuipers E, et al. Ingestion of acid and alkaline agents: outcome and prognostic value of early endoscopy. Gastrointest Endosc 2004;60(3):372-7. 18. Rothstein FC. Caustic injuries to the esophagus in chil dren. Pediatr Toxicol Pediatr. Clin North Am. 1986;33(3): 665-74. 19. Pintus C et al. Caustic ingestion in childhood: current treat ment possibilities and their complications. Pediatr Surg Int 1993; 8: 109. 20. Litovitz T, Whitaker N, Clark L, et al. Emerging bat tery ingestion hazard: Clinical implications. Pediatrics 2010;125(6): 1168-1177. epub 24 May 2010. Guideline from the National Battery Ingestion Hotline at the National Capital Poison Center ©National Capital Poison Center, 2009. 21. Theis JGW, Koren G.Camphorated oil: Still endanger ing the lives of Canadian children.Can Med Assoc J. 1995;152:1821-824. 22. Cupp MJ. Herbal Remedies: Adverse Effects and Drug In teractions.1999; Accessed from www.aafp.org (59)-5. 23. Fugh-Berman A, Ernst E. Herb±drug interactions: Review and assessment of report reliability Br J Clin Pharmacol. 52:587-95.
Trauma
Section IX
IP : 196.52.84.10
IP : 196.52.84.10
26
Approach to Traumatic Brain Injury (TBI) IP : 196.52.84.10
Figure 26.1: Head injuries are very scary and can prove fatal if not managed appropriately (Courtesy: Dr Gunda Srinivas)
Learning Objectives 1. Pathophysiology of severe traumatic brain injury. 2. Spectrum of head injuries.
3. Case scenario-based management. 4. Pearls and pitfalls in management.
Introduction Over 1.5 million pediatric head injuries are reported each year1. Motor Vehicle Accidents (MVA) associated head trauma have the highest morbidity and mortality in all age groups (Figure 26.1). Mild traumatic brain injury (TBI) appears to be the most common injury but generally has good outcomes. In India, severe traumatic brain injury oc curs most commonly following falls from upper stories of buildings with unbarred windows and verandahs refer Fig ure 27.1 Chapter of Polytrauma. Child abuse should also be considered when children present with unexplained head trauma or when there has been delay in seeking care.
Closed Head Trauma Pathophysiology Closed head trauma implies that an injury has not pen etrated the covering of the brain. Concussion results in dysautoregulation of cerebral blood flow (CBF). ●● Brain injury can be primary and secondary (Figure 26.2).
Figure 26.2: Primary injury leads to secondary injury. CBF, cerebral blood flow; BBB, blood-brain barrier.
●● Primary injury results from the direct force of impact. ●● Unlike adults, increased head to torso ratio and in creased brain water content are some of the factors responsible for the diffused injury noted in children.
266
Section IX n Trauma
●● Secondary brain injury may develop acutely or subacutely following primary brain injury. Neurochemi cally mediated vasospasm and astrocytic swelling com IP : 196.52.84.10 presses the microcirculation within the first 24 hours of injury. This reduces cerebral blood flow. Disruption of the blood-brain barrier (BBB) and alteration in cere bral autoregulation also play a significant role. Release of excitotoxic neurotransmitters, elevated intracellular calcium and potassium concentrations, formation of free radicals and apoptosis additionally contribute to secondary injury. The brain maintains a constant blood flow by a mecha nism known as autoregulation (Figure 26.3). Autoregula tion of cerebral blood flow occurs over a wide range of blood pressures by a process of changing cerebral resis tance in response to fluctuations in mean arterial pressure. Under normal circumstances, CBF is maintained at a con stant between a MAP of 60–150 mm Hg. At 60 mm Hg, ce rebral vasculature is maximally dilated and at 150 mm Hg, it is maximally constricted. Fluctuations of MAP beyond either end of this range lead to alterations in CBF, which can either cause ischemia or disruption of the blood-brain barrier. CBF can also be altered by changes in partial pres sure of oxygen or carbon dioxide. Hypoxia causes vasodilatation with significant in crease in CBF. On the contrary, increases in oxygen pres sure causes vasoconstriction. Hypercarbia increases CBF, up to 350% of normal whereas, hypocapnia produces a decrease in CBF. This mechanism is preserved even when autoregulation is lost.
Intracranial Pressure Normal intracranial pressure is maintained by its contents; brain, CSF and blood. The Monroe-Kellie doctrine states that in order to main tain intracranial pressure in the normal range, an increase in intracranial volume of one compartment is counter bal anced by reduction in volume in the other compartment. Critical increase in volume of any one compartment results in increased ICP (Figures 26.4–26.5).
Ù
Anticipate raised ICP in every child with TBI. Initiate measures to prevent and treat raised ICP in every step of resuscitation. Maintenance of normal cerebral perfusion pressure and cerebral blood flow are crucial for intact survival. Resolution of shock takes precedence over raised ICP, since, Cerebral perfusion pressure = Mean arterial pres sure – Intracranial pressure. CPP is a critical determinant of cerebral blood flow. Unresolved shock with raised ICP could compromise cerebral perfusion pressure resulting in cerebral ischemia.
Ù Raised ICP is not a contraindication to correct shock. Correction of shock and maintenance of BP can help maintain normal cerebral pressure.
Figure 26.3: Mean arterial pressure – intracranial pressure = cerebral perfusion pressure
Ù
CBF remains constant over a wide range of cerebral perfusion pressures.
Figure 26.4: Relation between intracranial pressure and intracranial volume
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
267
IP : 196.52.84.10
Figure 26.5: Monroe-Kellie doctrine
Simultaneously, steps must be taken to lower ICP to a level that is adequate to increase cerebral perfusion pres sure (CPP). This important step is key to improving cere bral oxygenation and preventing cerebral ischemia. In this context, Mannitol, a drug that acts by causing diuresis is not preferred. It reduces ICP, but worsens shock thereby reducing CPP. Efforts must also be focussed on early de tection of cerebral herniation.
MINOR HEAD TRAUMA Head trauma associated with a GCS > 13. ●● ●● ●● ●● ●● ●● ●●
Loss of consciousness (< 1 minute). Seizure, vomiting, confusion, headache or lethargy. Normal mental status at time of exam. Normal physical exam (including fundus). No evidence of skull fracture (hemotympanum, Bat tle’s sign or palpable bone depression). CT brain is recommended. Skull radiographs are recommended only if, CT scan is unavailable, or for children less than 2 years. If child abuse is suspected. Infants younger than 2 years.
●● Alert the parents/caretakers for the possibility of a postconcussive syndrome.
Ù Children under 2 years of age with normal mental status, no scalp hematoma (except frontal), no loss of consciousness (LOC) or brief loss of consciousness < 5 sec, non-severe mechanism, no palpable skull fracture and behaving normally as reported by the parents are less likely to have a severe traumatic brain injury.2
Ù Children over 2 years of age were at low-risk if mental status was normal, there had been no loss of con sciousness, no vomiting, non-severe injury mechanism, no signs of basilar skull fracture and absence of a headache.2
Scalp Lacerations
Management
The scalp is a very vascular structure made up of five lay ers that include: skin, subcutaneous tissue, galea aponeu rosis, loose areolar tissue and the pericranium (SCALP). The large vessels that supply the scalp run just above the galea aponeurosis and injury to this layer may result in sig nificant blood loss (Figure 26.6).
●● Reassure. ●● Advice rest and follow-up.
Debris from the accident site, as well as hair or clothing, may become entangled in the wound.
●● ●●
268
Section IX n Trauma
IP : 196.52.84.10
Figure 26.6: Bleeding from scalp lacerations can result in hemorrhagic shock
Figure 26.7: Skull radiograph of a simple linear skull fracture
Ù
Clean wound meticulously prior to wound closure. Explore all scalp lacerations to rule out a skull fracture prior to closure. In rare instances, an injury to the scalp may lead to bleed ing into the subgaleal space. The degree of trauma may be very minor or completely unrecognized by the patient. The area of swelling associated with the subgaleal hematoma may be variable and is frequently associated with headache. Subgaleal hematomas cross the suture lines and can lead to significant blood accumulation and hypovolemia. In general, these hematomas will resolve spontaneously.
Ù
Do not attempt to tap the fluid since they frequently reaccumulate.
SEVERE TRAUMATIC brain INJURY Skull Fracture Children often present with linear, depressed or basilar skull fractures. About 75% of skull fractures are linear, with the parietal bone being the most common site. The significance of a skull fracture is that it indicates the amount of energy that was applied to the patient’s head. A large amount of concentrated force is necessary to crack both tables of the skull. The amount of energy that is transmitted to the un derlying structures is therefore of concern. Hence, presence of a fracture denotes that a more severe injury to the brain exists. Approximately, 48% of patients have associated in tracranial lesions (Figures 26.7 to 26.8 and Table 26.1).
Figure 26.8: Compound depressed skull fracture caused by a hammer blow
In almost all cases, a simple fracture of the skull will heal with time. The edges of the fracture are fixed into rig id approximation of the skull itself enabling spontaneous healing. In skull fractures, the dura, which is closely approxi mated to the inner table of the skull, may be lacerated. In children under the age of two, a dural laceration may re sult in herniation of the leptomeninges into the bony cleft. At this age, as the brain is growing at a very rapid rate, the bony edges may not have time to heal completely. The growth and pulsation of the brain may lead to a growing skull fracture or leptomeningeal cyst. Repair of these cysts can be very difficult if they are left untreated.
Ù
Children who sustain skull fractures under the age of two should have neurosurgical follow-up to ensure that the fracture closes and does not grow into a large cyst.
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
Depressed Skull Fracture Depressed skull fractures (Figure 26. 8) result from forces IP : 196.52.84.10 applied to a small cross-sectional area and often require surgical repair. The skin over the injury site may be open, closed, con tused or absent. Brain may be present in the wound or on rare occasions, severe cortical bleeding from a lacerated artery or vein may also be present. ●● Complicated injuries require vigorous debridement and closure. ●● If brain matter is exposed, the wound should be cov ered with saline-soaked gauze to prevent drying of the brain prior to surgical repair. ●● Children with depressed skull fractures are at higher risk for developing seizures and need prophylactic an ticonvulsants.
Ù All depressed skull fractures should be evaluated by a neurosurgical specialist to determine the appropriateness of surgical decompression and repair.
Basilar Skull Fracture Fractures of base of skull are not seen well on plain Xray films, but should always be considered in patients with head trauma. In these patients, the fracture almost always heals without surgical intervention except in the most se vere cases. The factor that differentiates the basilar skull fracture from a fracture over the convexity of the brain is the associated structures that run through the base of the skull. Injury to the cranial nerves, vascular structures or basilar dura may be disabling or in some cases fatal. The carotid artery enters the base of the skull deep to the temporomandibular joint. ●● Injury to the carotid vessels in basilar skull fracture causes either a vascular thrombosis or bleeding into the middle ear with a resultant hemotympanum or blood in the external auditory canal.
Ù
All cranial nerves passing through the base of skull are at risk for injury from basilar skull fractures. The anatomy of injured region determines the frequency of cranial nerve deficits.
269
●● A fracture through the anterior cranial fossa with injury to the olfactory apparatus will result in loss of the sense of smell. ●● Anterior fossa fractures can also lead to injury of the optic or oculomotor nerves passing through the supe rior orbital fissure. ●● The most commonly injured cranial nerves are the VII and VIII, leading to a facial paralysis and sensorineural hearing loss. Sometimes, the VII nerve damage may manifest later. Therefore, it is crucial to examine and document severity of loss of facial movements. Injury to the lower cranial nerves passing through the jugular or hypoglossal foramen is relatively uncommon. ●● Basilar skull fractures are often associated with venous bleeding in soft tissues behind the ear.
Ù Bleed behind the ear is called the ‘battle sign’ and an accumulation of blood in the periorbital region is known as the ‘raccoon sign’. Either of these signs should alert the clinician to the possibility of a basilar fracture and a computerized tomog raphy (CT) scan should be ordered.
Cerebrospinal Fluid Leak At the base of the skull, the dura is tightly adherent to the bony structure in a number of places. Should a fracture oc cur, the meninges is at risk of tearing leading to CSF leak through the fracture. ●● The CSF may leak into the air-filled sinuses and na sopharynx, resulting in CSF rhinorrhea. ●● CSF can also leak through the mastoid or floor of the middle fossa into the middle ear, where it may pass through a ruptured tympanic membrane, producing otorrhea or through the eustachian tube into the na sopharynx. In most cases, a CSF leak will stop within two weeks. The use of prophylactic antibiotics for this type of injury is controversial. Some suggest that bacterial flora is reduced by the use of antibiotics and therefore the risk of infection is reduced. Others suggest that antibiotic usage encourages resistance without protection and if meningitis were to re sult from a CSF leak, the organism would be more difficult to treat.
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Section IX n Trauma
Table 26.1: Localization of head injury Site examined
Findings
Interpretation
Small pupil
IP : 196.52.84.10 Unilateral or Horner’s syndrome
Sympathetic chain disruption, common carotid injury, arterial dissection in neck or skull base (may progress to stroke)
Ocular movements
Conjugate tonic eye movement
Ipsilateral frontal lobe injury or contralateral seizure activity
Ipsilateral conjugate lateral gaze palsy
Dysfunction of parapontine reticular formation
V CN
Corneal reflex absent
Pontine dysfunction
VII CN
Unilateral LMN
Nerve injury from basilar skull fracture
VIII CN Vestibular calorics
Absent [normally cold-opposite, warm-same side (COWS)]
Brain stem dysfuntion between pontine vestibular nuclei and oculomotor nucleus in midbrain
IX and X
Gag and cough reflexes
Test integrity of medullary centers
Breathing
Periodic or Cheyne-Stokes
Bilateral hemispheric or upper pontine injury
Apneustic
Mid-caudal pontine injury
Ataxic
Medullary respiratory centers site examined
Scalp, skull
Contusions, lacerations, depression of skull
Underlying brain injury
Face
Periorbital, retroauricular bruising (blue discoloration will occur the following day)
Basilar skull fracture
Ear and nose
Hemotympanum, rhinorrhea, otorrhea
Basilar skull fracture
Fundus
Petechial hemorrhages
Shaken baby syndrome
Papilledema (Not to be expected in acute phase)
Raised ICP
Neurological examination (secondary survey)
In addition to the GCS, which must be done at regular intervals
Transient LOC
Concussion
Dilated pupils
Unilateral fixed dilated +/- contralateral hemiparesis
Transtentorial herniation
Enlarged non-reactive (mydriasis)
Midbrain, third nerve or direct orbital trauma
Bilateral or fluctuating mydriasis
Ictal or postictal phenomena
Bilateral
Drugs used in CPR
Ù The child with CSF leakage should be evaluated by a neurosurgeon, who may either drain the CSF with a lumbar catheter or surgically repair the site of leakage.
Intracranial Lesions The cranium is a closed space within which only a limited amount of volume can accumulate. The layers of the skull above the brain are the arachnoid, which contains the CSF, the dura and the skull. Blood may accumulate in any of these areas, producing distinctive radiological and clinical syndromes.
An epidural hematoma (Figure 26.9) results from blood accumulating between the dura and the skull. The clinical presentation, characterized by a period of lucency followed by rapid deterioration of consciousness, is rare in children. Epidural hematomas in this population occur from bleeding of the diploic veins. The more characteristic source of blood causing the epidural hematoma is arterial. The middle meningeal ar tery runs within the structure of the temporal bone and in the first part of its course may be completely surrounded by bony investiture. Fracture of the bone across this bony canal will commonly lacerate the artery and cause a hema toma under pressure. This rapid accumulation of blood is the reason for the classical lucent period following head
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
trauma prior to the onset of unconsciousness. In general, the relatively focal nature of the epidural hematoma and mechanism of injury leading to less diffuse brain trauma IP : 196.52.84.10 herald a better outcome than would be expected with other sites of hematoma accumulation.
Figure 26.9: Hematoma causes mass effect. This radiograph shows an epidural (extradural) hematoma viz collection of blood between duramater and skull (It can also occur in the spinal cord). Build up of epidural hematoma can rapidly result in compression of the underlying brain and spinal cord leading to severe neurological dysfunction. Most epidural hematomas are due to injury to the artery. An epidural hematoma is potentially fatal but complete recovery is possible if detected early.
If the small bridging vessels of the subdural space are torn, a subdural hematoma results. The plane of dissection for blood is along a path of much less resistance than that for the epidural hematoma and leads to the characteristic crescent shape seen on the CT scan. In general, the out come from a subdural hematoma is worse, perhaps because of associated brain trauma. The bleeding source, like in the epidural hematoma, may be either venous or arterial and the clinical course will vary depending on the rapidity of accumulation and mass effect. Bleeding may also occur within the parenchyma of the brain as seen in Figures 26.10A and B. The common areas for intraparenchymal bleeds are the frontal and temporal lobes. It is not uncommon in the traumatized brain to identify injury in
271
one area ‘coup injury’ of the brain with a similar injury direct ly across the head called a ‘contra coup’ injury. Parenchymal bleeding may extend into the subarachnoid space or into the ventricles and may occasionally lead to acute hydrocephalus.
Figures 26.10A and B: This child presented with profuse bleeding from a scalp injury following MVA. On arrival he was unresponsive and apneic. His HR was 60/minute and his blood pressure was 160/120 mm Hg. The airway physician initiated bag-valve-mask ventilation. One member was dedicated to manually stabilize the C-spine and perform the jaw thrust maneuver. As the airway tray was being prepared, his blood pressure dropped to 60/?. 40 mL/kg NS was rushed using pull -push technique. Epinephrine infusion was initiated, blood was transfused and the bleed ligated. He was intubated using ICP precautions and loaded with phenytoin prior to shifting for CT (26.9A). The CT scan shows evidence of ICH. This case illustrates the importance of correcting shock in the background of ICP.
Ù
Fluid resuscitation of shock in severe traumatic brain injury: Isolated head trauma with no external evidence of injury: Plan 20–30 mL/kg NS Severe TBI with fractures, intra-abdominal trauma, cervical transection scalp laceration: > 30–50 mL/kg.
272
Section IX n Trauma
Case scenario 1 7-year-old boy was rushed into the ED after fall from IP : to 196.52.84.10 first floor (Figures 26.11 26.14).
Figure 26.13: This CT with contrast taken just after resuscitation shows a large lesion in the right parietal cortex with a hypodense center with surrounding darker zone suggestive of fluid collection. There is a midline shift to the left. This picture is suggestive of intraparenchymal hemorrhage and edema.
Figure 26.11 Physiological status: Airway unmaintainable and obstructed, bradypnea, bradycardia, shock, hypertension, no features of myocardial dysfunction with evidence of ICP, herniation and non-convulsive status epilepticus.
Figure 26.14: A happy mother with her son after successful resuscitation. He was attending the rehabilitation department for hemiparesis and dysphasia. First-tier management of shock, hypoxia and raised ICP in the ED appears to have been crucial for survival in this child with severe traumatic brain injury.
Figure 26.12: The airway was stabilized using the jaw thrust maneuver, cervical collar was applied and he was immobilized on a spinal board. Orogastric tube was used to decompress the stomach. Orotracheal intubation was performed using ICP precautions. During intubation, care was taken to avoid flexing or extending the neck using in-line manual cervical stabilization. Shock was corrected with one bolus of NS. He was catheterized, given pain and sedation drugs to avoid further increase in ICP during transfer for CT scan and neurosurgeon’s opinion. His head end was elevated and 3% NS was initiated at the rate of 1 mL/kg.
Secondary survey revealed no obvious evidence of ex ternal injuries or bleeds. His fundus was normal.
Therapeutic Goals of Traumatic Brain Injury in the ED
Ù
Maximize oxygen delivery to the brain C-spine precautions Correct shock Maximize cerebral perfusion pressure Lower intracranial pressures Maintain eucapnia. Primary survey is performed even as a focused history is being obtained in the ED.
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
Airway: Is the airway unstable or obstructed?
Ù
IPfacial, : 196.52.84.10 Look for bleeding from mandibular injury, laryngeal and tracheal injury, broken teeth, bone fragments, any other foreign bodies. Breathing: Bradypnea or respiratory distress
Ù
Look for tension pneumothorax, flail chest, hemothorax or pneumothorax. Circulation: Bradycardia, shock, hypertension.
Ù Look for bleeding injuries. Disability: Raised intracranial pressure, non-convulsive status epilepticus. Following resuscitation of the ABCs the secondary survey is performed to include a formal assessment of the level of consciousness using the Glasgow Coma Scale (GCS). ●● Patients are described as having: Severe head injury if the GCS is 8 or less. ●● Moderate head injury is considered when the GCS is 9–12. ● ● Minor head injury correlates with a GCS of 13– 15. These classifications guide therapy as well as progno sis. Severity of intracranial injury may also be classified as mild, moderate and severe based on clinical examination (Box 26.1).
MANAGEMENT 5,6,7,8 Airway ●● Open airway using the jaw thrust maneuver. ●● Head tilt-chin lift maneuvers should be avoided. ●● Manually hold the C-spine in-line until an age appro priate collar can be placed along with the spinal im mobilization.
Ù
Manual in-line cervical immobilization throughout intubation, which helps to prevent neck movement and the dreaded risk of quadriplegia.
273
C-spine injury is presumed in all children with TBI since it is difficult to rule out spinal cord injury on arrival. Furthermore, children are prone to have spinal cord injury without radiological abnormality (SCIWORA). It is therefore advisable to plan on removal of cervical collar and spinal immobilization device only after ruling out spinal cord injury by CT scan, X-ray spine and neurologist’s opinion. Box 26.1: Classification of severity of intracranial injury based on signs and symptoms as per the CHALICE guidelines3 ●● Mild Asymptomatic Mild headache Three or fewer episodes of vomiting Glasgow Coma Scale score of 14–15 Loss of consciousness for less than 5 minute ●● Moderate Loss of consciousness for 5 min or more Progressive lethargy Progressive headache Protracted vomiting (more than three times) or associated with other symptoms Post-traumatic amnesia Post-traumatic seizure Multiple trauma Serious facial injury Signs of basal skull fracture Possible penetrating injury or depressed skull fracture Suspected child abuse Glasgow Coma Scale score of 11–13 ●● Severe Glasgow Coma Scale score of 10 or less, or decrease of 2 points or more not clearly caused by seizures, drugs, decreased cerebral perfusion or metabolic factors Focal neurologic signs Penetrating skull injury Palpable depressed skull fracture Compound skull fracture
Other Airway Precautions ●● Prepare to suction large volume particulate material.
Ù
Both central and electrical suction with Yankauer suction tip should be available. ●● Introduce orogastric tube. ●● Intubate using orotracheal route (Figure 26.15).
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Section IX n Trauma
Ù Nasogastric/orotracheal tube may enter the base of skull IP : 196.52.84.10 in unsuspected basilar fracture.
Box 26.2: Drugs used to reduce the risk of increasing ICP during intubation in TBI ●● ●● ●● ●●
Atropine: Prevents bradycardia Lidocaine: Anesthetizes glossopharyngeal nerve Thiopental: Cerebroprotective, anticonvulsant Rocuronium, vecuronium: Does not worsen ICP unlike succinylcholine
Prevention of hypoxia and hypercapnia are vital in improving outcomes in severe traumatic brain injury. One of the most important therapeutic interventions therefore is provision of assisted ventilation for which early and elective intubation is necessary in the PED. The other indications for intubation in severe traumatic brain injury are given in Box 26.3. Figure 26.15: Orogastric tube inserted and orotracheal intubation performed in child presenting with TBI to the ED (Courtesy: Dr Gunda Srinivas).
Breathing ●● Provide oxygen via a non-rebreathing mask. ●● If the child is bradypneic initiate bag-valve-mask ven tilation whilst one more team member keeps the airway manually open using the jaw thrust maneuver until in tubation is accomplished.
Ù
Intubate using pharmcologically assisted intubation (PAI) technique with ICP precautions (see Chapter PAI). ●● Lidocaine (1–2 mg/kg) should be administered 2–5 minutes before laryngoscopy. ●● Sodium thiopental, etomidate or propofol can be used as sedative agents for their cerebroprotective effect. ●● Midazolam, may be used but is contraindicated if hy potension complicates head trauma. ●● Ketamine was thought to be contraindicated in head injury, but recent studies have shown that not only is ketamine safe in this setting, it may be neuroprotective. In the setting of hypotension, ketamine is the induction agent of choice.4 ●● Use non-depolarizing agents such as rocuronium (0.6– 1.2 mg/kg) for paralysis (Box 26.2).
Box 26.3: Indications for intubation in traumatic brain injury ●● ●● ●● ●● ●● ●● ●● ●●
Unstable airway Facial, neck trauma Respiratory compromise, hypoxia Decompensated shock Decreased level of consciousness ‘P’, ‘U’ Seizures Raised ICP Other major injuries
Securing the airway in child presenting with TBI is fraught with risk due to the following reasons: 1. Difficulty in visualizing airway. a. Secondary to a distorted airway. b. Airway bleed. c. Cervical immobilization during ET. 2. Risk of precipitating quadriplegia if associated spinal trauma. 3. Aggravation of ICP.
Ù Manual in-line cervical immobilization throughout intubation process IS NECESSARY to avoid aggravating SPINAL CORD INJURY due to neck movements with its risk of quadriplegia
Ù
Many team members are needed during the process of intubation in severe traumatic brain injury.
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
1. Airway physician: Responsible for intubation (Team leader: The only voice to be heard). 2. Nurse or physician to the neck manually in-line dur IPhold : 196.52.84.10 ing intubation (to prevent excessive extension). Should be prepared to perform BURP/Sellick if needed). 3. Physician who assesses following intubation and keeps track of the the monitors and saturations. 4. Nurse for suctioning the airway (positioned on the left of the airway manager). 5. Airway nurse for handing the laryngoscope, tube, fixing tube, etc. (positioned on the right of the airway manager).
Circulation Secure IV/IO access and correct shock with 20 mL/kg of NS. Hypovolemia is a common problem noted in pediatric trauma victims. Signs of hypoperfusion include increased heart rate, loss of peripheral pulses, peripheral coolness and prolonged capillary refill.
Ù Bradycardia and high blood pressure secondary to ICP may mask features of shock in TBI. In addition, children often maintain systolic blood pressure despite significant blood loss until they develop acute hypotension. Pulse pressure is usually narrow in hemorrhagic shock. However if the diastolic pressure is less than 50% systolic, then the possibility of vasodilatory neurogenic shock should be considered secondary to severe CNS injury. Blood loss inside cranium (closed head injury with out multisystem trauma) is not sufficient to cause hy povolemic shock. Hence, not more than 20–30 mL/kg of fluids may be needed to resolve shock in isolated head injury. If shock persists after administering 20 mL/kg in TBI, consider the following possibilities. ●● Scalp injuries can cause significant blood loss in young children. ●● Fracture of long bones with or without intra-abdominal injury. ●● Vasodilatory shock due to spinal cord transection. ●● More volume will be needed to resolve shock for the first three conditions. Isotonic normal saline is pre ferred to lactated Ringer solution, since the former is isonatremic compared to RL. ●● Persistent hypotension refractory to volume resuscita tion should be treated with dopamine or epinephrine to ensure adequate cerebral perfusion.
275
Ù
Optimization of mean arterial pressure (MAP) with fluid therapy and vasoactive drugs is crucial for maintaining CPP. ●● If the hemoglobin is less than 10 mg/dL consider blood transfusion using warmed blood.
Ù
Dextrose containing fluids are contraindicated during the initial resuscitation of TBI. It can aggravate cerebral edema. ●● If shock is not due to the three causes mentioned above, perform needle thoracocentesis to rule out obstructive shock due to pneumothorax. ●● A minimal cerebral perfusion pressure of 40 mm Hg for infants and 50 mm Hg for adolescents is consid ered optimal.
Disability ●● Head injury patients are prone to develop raised ICP which can potentiate secondary injury. Careful neuro logical monitoring helps in early detection of cerebral herniation. ●● The goal of treatment is to lower the ICP to a level that is adequate to increase cerebral perfusion pressure (CPP) as this is key to improve cerebral oxygenation and prevent cerebral ischemia. Note: Risk of raised ICP exists even in infants despite open AF or sutures.
Management of Raised Intracranial Pressure (Box 26.4) Box 26.4: Management of raised intracranial pressure Measures to improve jugular venous flow from brain ●● Place head and neck in midline ●● Elevate head end of the bed not more than 30° ( if elevated less than 30° CPP could fall) ●● Avoid tight ties for the ET tube ●● Minimize stimulation (suctioning and movement) Other measures ●● Provide Morphine 0.1 mg/kg and lorazepam 0.1 mg/kg ●● Adequate sedation and analgesia should be maintained with opioids and benzodiazepines to avoid anxiety and pain, which may cause spikes in intracranial pressure ●● Propofol as a sedative, is avoided owing to the risk of metabolic acidosis Contd...
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Section IX n Trauma
Contd... ●● Prescribe Paracetamol suppository: 10 mg/kg ●● Maintain normothermia IP normocarbia : 196.52.84.10 (PaCO2 = 35 mm Hg) ●● Maintain normoxia and ●● Administer hypertonic saline (3% saline 0.1 mL/kg – 1 mL/ kg) on a sliding scale11 ●● Avoid prophylactic hyperventilation11 ●● Administer prophylactic phenytoin for seizure control
Osmotic therapy9,10: There is increasing evidence for the use of hypertonic saline (HS) in children. It has been shown that an increase in serum sodium concentration sig nificantly decreases ICP and increases CPP in severe TBI. Sustained hypernatremia and hyperosmolarity is safely tolerated in these patients. Avoid prophylactic hyperventilation11 Mechanical ventilation should provide adequate oxygen ation (oxygen saturation > 90%) and avoid hypercarbia (PaCO2 > 38 mm Hg). In children, hypocarbia (paCO2< 35 mm Hg) decreases cerebral blood flow and can induce ce rebral ischemia hence hyperventilation should be avoided. Administer prophylactic phenytoin for seizure control if CT scan shows parenchymal damage Continuous EEG (if possible) is helpful to detect subclini cal/subtle seizures especially in sedated patients so that adequate anticonvulsants can be given. CSF drainage: CSF drainage provides immediate but transient effect and is especially indicated in situations where the raised ICP is secondary to hydrocephalus. How ever, diffuse brain swelling as in TBI may cause chinked ventricles making CSF drainage difficult.
Surgery: Surgery is not a first-line treatment except to evacuate compressive subdural or epidural hematomas. Refractory intracranial hypertension can be treated with decompressive craniectomy. Children likely to benefit from surgery are those with diffuse cerebral swelling, within 48 h of injury, no episodes of sustained ICP > 40 mm Hg, secondary clinical deterioration, evolving cere bral herniation syndrome (Table 26.2). Routine antibiotics are not warranted. However, they may be indicated if the child has sustained a penetrating injury. Steroids have no role in the management of TBI. While resuscitation is in progress, one physician who is not part of the resuscitation team should elicit history. History should focus on the following: ●● ●● ●● ●● ●●
Mechanism of injury. Severity of altered mental status. Posturing. Seizures. Vomiting at the scene of injury or during transport.
If the patient was confused at the scene and is now normal, there is less reason for concern. However, the contrary scenario is more worrisome. Besides, a detailed medical history is frequently unavailable during the ini tial assessment of the patient and associated medical conditions such as insulin-dependent diabetes may not be known.
Table 26.2: Surgical interventions in STBI Injury
Features
Treatment
Subgaleal hematomas
Collection of blood above periosteum
No needling; Watch hematocrit
Cephalhematoma
Subperiosteal; limited by suture line
No treatment required
Skull fractures
Linear, diastatic or depressed
Depressed fractures may require urgent elevation
Basilar skull fractures
CSF otorrhea or rhinorrhea β2 transferrin distinguishes CSF or not
Expectant management; no packing of ear, no prophylactic antibiotics; 85% spontaneously seal; 4% meningitis; if leak persists ENT repair
Epidural hematoma
Lucid interval
Urgent evacuation if mass effect
Subdural hematoma
Underlying brain injury common, cortical bridging veins tear; if chronic, think of child abuse
Evacuate if large and causing mass effect
Intraparenchymal injury
Fatal contusions, diffuse axonal injury, hematomas
Neurosurgical intervention is usually not helpful, decompressive craniotomy with or without lesionectomy
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
Ù Resuscitation of TBI in the ED is perhaps the most IP : 196.52.84.10 complex of all resuscitations requiring a larger team performing many tasks simultaneously. A separate physician (Casualty Medical Officer) not involved in the resuscitation should be responsible for obtaining history and documenting medicolegal entries.
277
LABORATORY AND RADIOLOGY Blood counts and chemistries, arterial blood gases and se rum alcohol levels, routine clotting studies [PT (prothrom bin time) and PTT (partial thromboplastin time)] should be performed. When severe injury to the brain occurs, fac tors released into the blood can lead to a fulminant dis seminated intravascular coagulopathy. This complication is a hallmark of a bad outcome and indicates the degree of brain injury that may be present.
Case scenario 2 A 6-year-old girl falls from a construction site of the 2nd floor (Figure 26.17 and 26.18).
Computerized Axial Tomography (CAT or CT) (CHALICE Guidelines)12 CT of the brain will help determine the presence of a surgically removable mass lesion or identify a pa tient with an injury more severe than clinical exami nation indicated and will require expectant observa tion (Box 26.5). Box 26.5: A head CT is required if any of the following are present12
Figure 26.16: She is intubated with ICP precautions and Cspine precautions. One bolus of 20 mL/kg of NS is administered. Following intubation her HR: 160/minute, but her BP is unrecordable. A quick secondary survey reveals no injury to the long bones or scalp. Her abdomen is scaphoid and soft. A needle thoracocentesis in the right midclavicular line releases a gush of air due to a pneumothorax.
Figure 26.17: In this picture taken 24 hours later, her cardiopulmonary assessment is apparently normal. Obstructive shock (due to tension pneumothorax in this child) had complicated severe traumatic brain injury.
History ●● Witnessed LOC > 5 min ●● Abnormal drowsiness ●● Vomiting ≥ 3 episodes ●● Suspicion of non-accidental trauma ●● Seizure in a patient who has no history of seizures Examination ●● GCS < 14 or GCS < 15 if less than 1-year-old ●● Suspicion of penetrating or depressed skull injury or tense fontanelle ●● Signs of basal skull fracture ●● Focal neurological deficit (motor, sensory, coordination or reflexes) ●● Bruise, swelling or laceration > 5 cm if less than 1-year-old Mechanism ●● High speed traffic accident (> 64 km/h) ●● Fall > 3 m in height ●● High speed injury from a projectile or an object High-risk factors ●● GCS < 15 at 2 hour after injury ●● Suspected open or depressed skull fracture ●● History of worsening headache ●● Irritability on examination This would require 30% of patients to get a head CT. Medium-risk factors ●● Any sign of basal skull fracture ●● Large boggy hematoma of the scalp ●● Dangerous mechanism of injury (MVA, fall from height > 0.9 m or 5 stairs, fall from a bicycle with no helmet
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Section IX n Trauma
There is no role for contrast enhanced head CT in the acutely injured child, unless an angiogram is being per formed to evaluate for IP concomitant vessel injury. CT scan : 196.52.84.10 is a safe and accurate investigation for older children who are able to lie still for the procedure. In younger children, particularly those under 5 years, general anesthesia or pro cedural sedation may be required to achieve CT scanning. In addition, the risks of cranial irradiation need to be con sidered. Therefore, particularly in younger children, the risk of CT should be balanced against the risk of delayed diagnosis (Refer Protocol 26.1).
X-rays in Severe Traumatic Brain Injury There is some controversy over the usefulness of plain skull X-rays. For almost all types of head trauma, the CT scan provides more information than plain skull films. In limited instances (associated mandible or facial fractures) skull X-rays, are indicated in addition to CT scan. Many studies have illustrated that the presence of a skull fracture significantly increases the risk of intracranial injury. The patient with serious head trauma should also have rou tine cervical spine X-rays to rule out an associated injury. Cervi cal injury must be anticipated in young infants, where the head mass is disproportionately large compared to the cervical spine.
Indications for Skull Radiography ●● ●● ●● ●● ●●
Possible penetration. Possible depressed fracture. Compound fracture. Previous craniotomy with indwelling shunt. Child less than 2 years of age with ‘boggy’ scalp he matoma. ●● Suspected non-accidental trauma.
Conclusion The long-term neurocognitive and behavioral consequenc es of head trauma can vary widely, based on the extent of injury. Overall, children have a better prognosis and improvement in function may continue for years after in jury. Those patients with a GCS score less than three have a high mortality and morbidity. Children with coma that lasts less than 2 weeks, have considerable better neurocog
nitive outcome and fewer developmental and behavioral sequelae.13 Head injury education and prevention, i.e. car seats, seat belts and helmets help reduce the incidence and se verity of head injury. Children who have suffered mildmoderate concussions should not return to contact sports until they are completely symptom free, both at rest and with exertion. Any child with symptoms persisting greater than a week after a head trauma should be referred for neu rocognitive evaluation.
Key Points
ü
1. C-spine immobilization should be performed along with airway opening maneuvers. Protect C-spine until it is cleared. 2. Resuscitation should not be delayed while awaiting neurosurgical opinion or CT scan. 3. Once ABCDEs are stabilized management focused on cerebroprotective measures. 4. Refractory shock in apparently isolated TBI, con sider cord transection, internal bleed, pneumothorax and cardiac tamponade. 5. Mannitol could aggravate shock in the ED. 6. Hypertonic saline more useful in ICP and shock due to TBI. 7. Avoid hypoxia. 8. Avoid hypotension. 9. Avoid hyperventilation. 10. Avoid hypoglycemia. 11. Avoid hyperglycemia. 12. Avoid hypothermia.
common errors
û
1. Shifting the child for CT scan without stabilization. 2. Waiting for neurosurgeon opinion without correct ing hypoxia and shock. 3. Failure to maintain C-spine precautions and spinal immobilization until clearance of spine. 4. Focusing on the medicolegal entries prior to stabili zation 5. Steroid therapy.
Chapter 26 n Approach to Traumatic Brain Injury (TBI)
Protocol 26.1: Indications for CT brain
IP : 196.52.84.10
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Section IX n Trauma
REFERENCES 1. Canadian Paediatric Society (CPS) Management of chil IP :CMAJ. 196.52.84.10 dren with head trauma. 1990;142(9):949-52. 2. Filanovsky Y, Miller P, Kao J Myth. Ketamine should not be used as an induction agent for intubation in patients with head injury. CJEM. 2010;12(2):154-57. 3. Greenes DS, Schutzman SA. Clinical indicators of head in jury in head injured children. Pediatrics. 1999;104:861-67. 4. Kupperman N, Holmes JF, et al. Identification of children at very low risk of clinically important brain injuries after head trauma: a prospective cohort study. PECARN. Lancet 2009;374:1160-170. 5. Mazzoa CA, Adelson PD. Critical care management of head trauma in children. Crit Care Med. 2002;30(11 Suppl):S393-401. 6. Meyer PG, Ducrocq S, Carli P. Pediatric neurologic emer gencies. Curr Opin Crit Care. 2001;7(2):81-87. 7. Nationl Collaborating Centre for Acute Care. Head injury. Triage, assessment, investigation and early management of head injury in infants, children and adults. London (UK): National Institute for Health and Clinical Excellence (NICE);2007 Sep. 54 p. (Clinical guideline; no.56).
8. Orliaget GA, Meyer PG, Baugnon T. Management of criti cally ill children with traumatic brain injury. Pediatric An esthesia. 2008;18:455-46. 9. Wakai A, Roberts IG, Schierhout G. Mannitol for acute traumatic brain injury Cochrane Database of System atic Reviews 2007, Issue 1. Art. No: CD001049. DOI: 10.1002/14651858.CD001049. 10. Upadhyay P, Tripathi VN, et al. Role of hypertonic saline and mannitol in the management of raised intracranial pressure in children: A randomized comparative study. J Pediatr Neurosci. 2010;5:18-21. 11. Kohanek P, et al. Guidelines for acute medical manage ment of severe traumatic brain injury in infants, children and adolescents. Pediatr Crit Care Med. 2012;(13)1S 1-16. 12. Osmod MH, Klassen TP, et al. CATCH: a clinical de cision rule for the use of computed tomography in children with minor head injury. PERC. CMAJ. 2010;182(4):341-48. 13. Dunning J, Daly JP, et al. Derivation of the children’s head. injury algorithm for the prediction of important clinical events decision rule for head injury in children. CHALICE. Arch Dis Child. 2006;91:885-91.
27
IP : 196.52.84.10
Approach to Polytrauma
Figure 27.1: Common hazards: Lack of balcony railings, walkers, unsupported TVs and lack of supervision in construction sites (Courtesy: Dr Gunda Srinivas)
Learning Objectives 1. Principles of primary and secondary survey. 2. Management of orthopedic trauma.
INTRODUCTION Major trauma is not as common as medical emergencies. Children are exposed to potential environmental hazards as shown in Figure 27.1. In addition, at the time this manual has been written, the initial assessment of trauma victims is being performed on arrival into the ED and not at the site of accident. The rapid cardiopulmonary cerebral assessment must be performed, while evaluating for life-threatening injuries. Simultaneously, aggressive resuscitative measures must also be undertaken. Assessment of injuries involves primary survey and secondary survey.
PRIMARY SURVEY Airway with Cervical Spine Protection ●● Open the airway using the jaw thrust maneuver. ●● Suction if secretions are seen.
3. Recognition of abdominal trauma. 4. Recognition of trauma to nerves and vessels. ●● Introduce orogastric tube if altered mental status is noted or abdominal trauma is suspected. ●● Stabilize the C-spine, using age-appropriate cervical collars for children beyond infancy, towels and tape for infants. ●● Intubate early using PAI technique (refer Chapter 3) if the victim is: – Responsive to pain or unresponsive. – Craniofacial injuries. – Inhalational injuries due to burns. ●● Talking or crying suggests that the airway is patent and breathing is spontaneous. For spinal immobilization refer to Chapter 41.
Breathing ●● Provide oxygen using the non-rebreathing mask if spontaneously breathing. ●● Check respiratory rate, work of breathing, air-entry and pulse oximetry.
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Section IX n Trauma
●● If not breathing adequately, initiate bag-valve-mask ventilation and plan early intubation. ●● In the absence of obvious external injury or cervical IP : 196.52.84.10 cord transection, if the child has unexplained hypotensive shock despite initial fluid bolus, suspect tension pneumothorax. Perform needle thoracocentesis to rule out this life-threatening emergency.
Ù
Do not delay needle thoracocentesis in order to take a chest X-ray if tension pneumothorax is suspected.
Circulation ●● If shock is noted, 20 mL/kg of normal saline is admin istered up to a maximum of 50 mL/kg, if shock persists, plan blood transfusion. ●● Blood is collected for grouping and crossmatching. Fresh whole blood preferable ●● If hypotensive and intra-abdominal injury is suspect ed, the bolus must be administered cautiously to avoid dislodging clots (permissive hypotension). ●● Apply direct pressure if obvious bleeding is noted. ●● Splint bones if obviously fractured. ●● Wrap and splint pelvis to reduce bleeding into pelvic or retroperitoneal space due to pelvic fractures.
Ù
Rapid shift to OR is planned if hypotension is noted.
Disability ●● Mental status is evaluated in the AVPU scale. ●● Check pupils for reaction and size along with eye po sition and movements for non-convulsive status epilepticus in unresponsive children. ●● Evaluate for spontaneous movement. Note presence of posturing or seizure activity. ●● Assess for pain and sensation. ●● Look for obvious limb deformities.
Exposure ●● Remove clothing and diaper for complete secondary survey. ●● Burns are calculated using the patient’s palmar surface as 1% (refer Chapter 28). ●● If burns are noted, the affected surface is covered by moist saline dressings.
Secondary Survey Secondary survey is a more detailed evaluation for injuries prior to transfer for definitive care. 1. Head and skull ●● Scalp lacerations are major cause of loss of blood resulting in shock in young children. Saline irrigation, debridement and suturing should be performed at the earliest. ●● Bulging anterior fontanels suggest intracranial injury. ●● Depressed fontanels suggest hypovolemia. 2. Maxillofacial and intraoral trauma ●● Check nasal and oral patency. Edema could develop during fluid resuscitation in children with craniofacial trauma. ●● Intubate early for significant maxillofacial trauma. ●● Blood in oral cavity should be checked for basal skull fracture, nasal or oral trauma, tongue laceration or/and injury or avulsion of teeth. ●● Thorough irrigation with saline and antibiotics may be warranted. ●● Loose tooth should be preserved for reimplantation. ●● Call for urgent ophthalmologic and plastic surgeon for their assessment of injuries. 3. Neck ●● Since the short neck of infants are difficult to assess, we can safely presume that an active child moving all four limbs is unlikely to have cervical cord injury. ●● Maintain C-spine precaution in the unresponsive child or infant. 4. Chest ●● Fracture of ribs and therefore, flail chest is not common in young children. ●● Initial chest X-ray may not show evidence of lung contusion. 5. Abdomen ●● Spleen and liver—Refer to section on Abdominal and Pelvic trauma. 6. Perineum/rectum/vagina ●● Inspection of the perineum and the orifices give information on pelvic trauma (more common in children than in adults). ●● Blood in the vagina or rectum warrants examination under anesthesia. ●● Unless blood is seen in the orifices, speculum examination need not be routinely performed in the prepubertal girl. 7. Musculoskeletal (refer to section on Orthopedic trauma).
Chapter 27 n Approach to Polytrauma
8. Neurological evaluation ●● Altered mental status due to hypoxia and shock may prevent accurate IP evaluation of the neurological status. : 196.52.84.10 ●● Emesis may suggest presence of raised intracranial pressure. ●● Loss of tone, flaccidity and loss of sensation warrant neurosurgical consultation. ●● However, lower spinal injuries are uncommon in children.
Interventions During Secondary Survey ●● Antibiotics are administered for fractures, craniofacial injuries and abdominal trauma. ●● Tetanus prophylaxis. ●● Analgesia: – Morphine (0.1 mg/kg/dose). – Fentanyl (1 μg/kg/dose). – Paracetamol (15 mg/kg/dose PO/PR/NG). ●● Steroids: Steroids not warranted for suspected spinal cord injury.
Ù
If a child fails to stabilize with aggressive resuscitation or has blood detected within the chest or abdomen, urgent operative intervention must be undertaken.
ORTHOPEDIC TRAUMA Pathophysiology Fractures can occur in the diaphysis (shaft), metaphysis (flare), physis ( growth plate) or epiphysis (secondary centers of ossification). Cartilaginous growth plates, which persist at the end of growing bones, are responsible for the longitudinal growth of bones. These growth plates are weaker than the nearby bone making them prone for fractures. Fortunately, most growth plate injuries heal readily with simple or no treatment. Indeed, growth plate and metaphyseal fractures heal in half the time taken for diaphyseal fractures. Trauma occurring as a result of traveling in motor vehicles, cyclist or pedestrian being hit by a moving motor vehicle, fall from twice the height of the child result in high-energy fractures. Play-ground injuries and falls from lesser heights usually result in low-energy fractures. Highenergy mechanism is associated with injuries to nerves, vessels, open fractures, swelling or compartment syndromes, growth plate damage and systemic injuries.
283
Primary Survey and Initial Management Cervical spine stabilization in the neutral position should be maintained not only throughout resuscitation but also during transport for imaging. These precautions are taken until bony or ligamentous injuries have been excluded. This is done by employing the following methods: ●● Use appropriate sized collar. ●● If immobilization device is not available use rolled towels (thick) or sand bags secured against the side of the neck.
Ù
The larger head in infants and children less than 4 years, results in flexion of the neck when placed supine on flat surfaces. ●● Use a spinal board with hollow beneath the head. ●● Place folded towel under the shoulders.
Ù
Children presenting with head trauma, neck pain following trauma or any neurological deficit are considered at greater risk of cervical cord injury.
Circulation ●● Apply direct pressure over open wounds. ●● Simultaneously, realign the injured limb or limbs in the near anatomic position. ●● Splint injured limbs.
Ù
Realignment and splinting can significantly improve circulation. Femoral fractures can result in loss of 20% of blood resulting in shock.
Disability ●● Assess gross motor function and circulation of each limb during the primary survey.
Secondary Survey Comfort If airway, breathing and circulation are stable, ensure that the child is as comfortable as possible:
284 ●● ●● ●● ●●
Section IX n Trauma
Move the deformed limb as little as possible. Early splinting is the best analgesic. Avoid eliciting fracture IP : crepitus. 196.52.84.10 Remove the spinal board after spinal injuries have been ruled out by thorough neurological, radiological and magnetic resonance imaging (MRI) assessment.
Look, Feel, Move Use your fingers to look, feel and move: ●● From sternum and scapula to finger tips. ●● From anterior superior iliac spine to toes. ●● Examine pelvis for shape, tenderness, horizontal and vertical stability. ●● Horizontal stability assessed by medial followed by lateral pressure on both anterior superior iliac spines. ●● Vertical stability assessed by traction on one leg at a time, while stabilizing the pelvis.
Ù
Pelvic fractures can cause exsanguinating bleed. ●● Bind the pelvis circumferentially with a sheet to decrease its internal volume. ●● Refer early for orthopedic intervention. ●● Pelvic injury often associated with abdominal trauma. Laparotomy may be needed and may be performed along with pelvic stabilization (Figure 27.2).
Ù Examine an unstable pelvis only once. Repeated assess-
ments could disrupt a clot and lead to blood loss. Bind the pelvis with a cloth/sheet to reduce volume and motion.
Spinal Injury Palpate cervical spine for tenderness. ●● A fully conscious child, who is cooperative can be requested to turn his head in all directions after removing the collar. ●● Log roll the child and inspect and palpate the thoracic and lumbar spine up to the sacrum. Signs of injury include: – – – –
Tenderness. Bruising. Swelling. Deformity.
Ù
Boggy swelling over the lumbar spinous process or seat belt bruise denotes seat belt injury to spine. However, multiple injuries may be difficult to diagnose when the child is not alert or in pain. On the contrary, after a careful initial examination, a repeat physical examination at 24 hours or when the child becomes alert minimizes chances of missing injuries. Commonly missed injuries in motor vehicle accidents are fractures of metatarsal, tarsal, metacarpal and carpal bones.
Vascular Examination
Ù
Integrity of circulation should be evaluated early in the management of a critically injured child. ●● Examine and document presence or absence of radial, ulnar, dorsalis pedis and posterior tibial pulses in all four limbs whether the limb appears injured or not. ●● Document color, temperature and motor function of all four limbs.
Neurological Examination Evaluation of the power of each muscle according to the Medical Research Council (MRC) classification establishes, whether the nerve is intact along its course. Younger children may be examined by observation using toys. 0 = No movement Figure 27.2: Child with polytrauma (Courtesy: Dr Gunda Srinivas).
1 = Flicker 2 = Moves without gravity (gravity eliminated)
Chapter 27 n Approach to Polytrauma
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3 = Moves with gravity (against gravity)
Imaging
4 = Weaker than full strength
Plain X-rays ordered for initial trauma survey are:
5 = Full strength
●● ●● ●● ●●
IP : 196.52.84.10
Sensory examination along with motor examination is shown in the Table 27.1. Table 27.1: Neurological examination Nerve
Sensory
Motor
Radial nerve
First dorsal web space
Thumb extension, extension across MCP joints
Median nerve
Ulnar border of the index finger
Thumb opposition
Ulnar nerve
Tip of small finger
Abduction of index finger
Anterior interosseous nerve
N/A
Flexion of DIP joint of index finger and thumb
Peroneal nerve
Deep branch—first dorsal web space
Tibial nerve Sole of foot at metatarsal heads
Great toe dorsiflexion Ankle and toe plantar flexion
Open Wounds with or without Open Fractures ●● Surface irrigation with saline. ●● Apply sterile dressing. ●● Administer antibiotics (Table 27.2) and tetanus toxoid where needed. ●● Tetanus prophylaxis. Tetanus toxoid is administered, if the child has not be immunized as per the national immunization schedule or if he is older than 5 years (booster dose would have been given).
Risk Factors for Infection Based on whether: ●● ●● ●● ●●
Injury is due to high-energy trauma. Extensive soft tissue damage. Contamination. Circulatory impairment.
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Transfer for imaging ONLY after stabilization.
Lateral C-spine. Chest. Pelvis. Two views at 90° for injured limb segments and spine. ●● Include the joint above and below the injured segment. Table 27.2: The Gustilo classification of open fractures to decide on antibiotic prophylaxis Gustilo grade Soft tissue injury I Small laceration < 1 cm II Laceration 1–10 cm, graft or flaps needed to cover III a Large laceration > 10 cm, extensive degloving injury, but bone can be covered III b
Large laceration, bone cannot be covered, often extensive contamination III c Open fracture with arterial injury in same limb pen, pencillin; cef, cefazolin.
Antibiotic prophylaxis Cefazolin 40 mg/kg If pencillin/ cef allergy: clindamycin 10 mg/kg Cefazolin 40 mg/kg IV with gentamicin 2.5 mg/ kg IV with metronidazole 10 mg/kg if grossly contaminated (fecal, soil) or devitalized tissue 10 mg/kg clindamycin if pen/cef allergy
10 mg/kg clindamycin if pen/cef allergy
CT Scan ●● Useful if complex flat bone trauma such as pelvis, spinal injuries are suspected.
MRI ●● Does not play a major role in management of orthopedic injuries. ●● Indicated if clinical signs of spinal cord injury are noted.
ABDOMINAL AND PELVIC TRAUMA Pathophysiology Since children are small, they are more susceptible to the transmission of kinetic energy over a smaller area. The ribs
286
Section IX n Trauma
are soft and more compliant resulting in more force being transmitted to thoracic and upper abdominal organs. Thinner abdominal wall offers less protecIP musculature : 196.52.84.10 tion to intra-abdominal organs. Close proximity of all the intra-abdominal organs also predisposes to a greater risk of trauma to the solid organs within the abdomen.
●● Blood. ●● Palpable bony fragments. ●● Linear ecchymosis ‘seat belt injury’ is often associated with intra-abdominal injury.
In India, common causes of abdominal trauma are motor vehicle accidents, fall from heights and bull gore injuries.
Whilst abdominal X-ray is not useful in evaluation of intra-abdominal injury, radiographic evidence of gas in soft tissue (taken after stabilization) may provide some clues suggestive of bowel injury.
Suspect abdominal injury if secondary survey reveals the following (Refer Figure 27.3 for hemothorax):
Splenic Injury
●● ●● ●● ●●
Abdominal distension. Abdominal tenderness. Abrasions. Ecchymosis.
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• Suspect serious abdominal trauma if infants are having predominantly chest breathing or the older child is lying still and whimpering or has referred pain to the shoulder. Trauma to the lower six ribs or abdominal distension in a hemodynamically unstable child is also associated with serious intra-abdominal injury. • Gastric distension due to aerophagia in young infants may be misinterpreted as abdominal distension. An orogastric tube should be placed early in the evaluation to avoid misdiagnosis.
●● ●● ●● ●●
Left shoulder pain (Kehr’s sign). Abrasions and tenderness in left upper quadrant. Abdominal distension. Associated with shock.
Hepatic Injury ●● ●● ●● ●● ●●
Abdominal distension. Right shoulder pain. Abrasions and tenderness in right side of abdomen. Hypotensive shock. Injuries to the ribs are common.
Urological Injury ●● Blood at penile meatus. ●● Perineal bruising or swelling. ●● High riding prostate.
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If any of these signs are present, DO NOT insert a Foley catheter. Diagnosis is confirmed by performing a retrograde urethrogram.
Imaging
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Figure 27.3: This child was nearly run over by a vehicle. Note the tyre markings on the lateral chest. He developed a hemothorax that was relieved by a thoracostomy.
Bowel Injury Suspect injury to the gut if digital rectal examination reveals evidence of:
Whilst routine X-rays for lateral spine, pelvis and chest are obtained, plain abdominal films are not useful in evaluation of acutely injured children. 1. Focused abdominal sonogram for trauma (FAST). ●● FAST is a focused goal-directed sonographic examination of the abdomen used to rapidly assess for free fluid (bleed in peritoneal space, abdomen, pleural space and pericardial sac).
Chapter 27 n Approach to Polytrauma
●● FAST has replaced diagnostic peritoneal lavage (DPL) to identify intra-abdominal bleed. ●● Helps in triaging for the need to perform abdomen IP : 196.52.84.10 computerized tomography (CT) scan. ●● Recently eFAST (extended focused assessment with sonography for trauma) has been used, which allows an emergency physician to detect whether a patient has pneumothorax, hemothorax, pleural effusion, mass/tumor or a large foreign body. This examination allows for visualization of the echogenic tissue, ribs and lung tissue using few radiographic signs. 2. Intravenous contrast enhanced CT abdomen is the diagnostic modality of choice to identify intra-abdominal injuries. 3. Magnetic resonance imaging not needed for evaluation of abdominal or pelvic trauma. Acute coagulopathy, hypothermia and acidosis also known as the ‘lethal triad’ can occur following severe exsanguinating trauma. To avoid these dangerous complications, resuscitation is focused towards damage control. 1. Permissive hypotension ●● Replacement of large volume normal saline in major exsanguinating trauma can result in clot dislodgement, rebleeding, hyperchloremic acidosis and dilutional coagulopathy. ●● Give just enough fluids to maintain 70–80 systolic blood pressure.
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This strategy works only when time between inciting trauma and shifting to the OT is less than 30–40 minutes. Permissive hypotension SHOULD BE AVOIDED when head injury coexists. Cerebral perfusion pressure must not be compromised. 2. Hemostatic resuscitation ●● Infuse whole blood as initial resuscitation fluid. – This strategy helps to treat intrinsic acute traumatic coagulopathy and prevent dilutional coagulopathy.
287
●● Use small volumes of 3% saline for resuscitation to treat life-threatening hypotension. ●● Consider vasopressin infusion to maintain blood pressure at minimally acceptable ranges.
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Major exsanguinating trauma: Urgently shift to OT for damage control surgery and resuscitation. 3. Damage control surgery. ●● Traditional surgery is not performed until the victim has been stabilized. ●● Surgical strategies are focused to control bleeding and reduce wound contamination.
Key Points
ü
1. Avoid rushing to evaluate obvious injuries and fail to stabilize the ABCs. 2. Stabilization and immobilization of the spine is a priority in trauma victims. 3. Rule out hemo/pneumothorax and control bleeding in addition to stabilization of the ABCs. 4. Ensure comfort for children who do not have lifethreatening injuries. 5. MRI is not a useful modality in orthopedic trauma. 6. FAST mandatory in ruling out intra-abdominal bleed.
common errors
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1. Failure to manually immobilize C-spine until the cervical collar and spinal board have been applied. 2. Failure to shift to OT when shock is refractory to fluid therapy. 3. Transferring trauma victim for imaging without stabilization. 4. Not infusing whole blood early in the management of exsanguinating bleed due to trauma.
Section X
Environmental Injury IP : 196.52.84.10
IP : 196.52.84.10
28
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Burns
Figure 28.1: Adequate supervision is needed to prevent burns in children
Learning Objectives 1. Pathophysiology of burns. 2. Calculation of percentage of burns.
3. Management of the ABCs specific for burns. 4. Care of the burned area.
INTRODUCTION
BURN CLASSIFICATION
Scalds are perhaps the commonest type of burn injury that are encountered in our setting (accidental spillage of hot rasam, sambar, water in the kitchen). Severe burns involves rapid assessment of degree of burns, aggressive resusci tation and early referral to a burn center (Figure 28.1).1
Burn classification is based on depth, extent and involvement of hands or face or perineum.
PATHoPHYSIOLOGY
2. Second degree/partial thickness
Loss of cutaneous barrier results in insensible fluid loss. Increased capillary permeability also causes loss of flu ids. Locally, fluid shift into the burn wound leads to burn wound edema. Systemic capillary leak in burns greater than 25% of body surface area (BSA) could result in hy povolemia. Hypoproteinemia, systemic inflammatory re sponse sysdrome (SIRS) and hormone derangements are other contributing factors to loss of fluids in severe burns. Circumferential burns can lead to formation of eschars which can cause vascular insufficiency by pressure effect. Hence, these need to be removed to prevent the same dur ing healing.
1. First degree/superficial ●● Red, dry painful. ●● Will heal after a few days with no scar. ●● Wet, red, very painful. ●● Superficial or deep partial thickness. ●● Will heal by scar (may require skin graft). ●● Needs wound care and possible debridement, but will heal after weeks. 3. Third degree/full thickness ●● Leathery, dry, loss of sensation, waxy. ●● Will heal with excision and grafting. 4. Fourth degree ●● Involves subcutaneous tissue, tendon and bone.
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Section X n Environmental Injury
Total Burn Surface Area ●● Calculate using rule of nine (Figure 28.2). : 196.52.84.10 ●● Exclude first degreeIPburns when calculating total burn surface area (TBSA) (Table 28.1).
MAJOR BURNS ●● ●● ●● ●● ●● ●● ●●
Burns involving the hands, face, feet or perineum. Burns that cross major joints. Circumferential burns to any extremity. Burns associated with inhalational injury. Electrical burns. Burns associated with fractures or other trauma. Burns in infants.
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Consider early intubation, if the following signs are noted: • Singed nasal hairs and eyebrows. • Carbonaceous deposits in oropharynx and face. • Oropharyngeal edema. • Hoarseness, persistent coughing, stridor. • Face, neck, upper torso burns. • Aspiration of hot liquids can also cause airway compromise. • Anticipate a difficult airway and call for ENT or anesthesiologist help and use a smaller size ET tube.
Prehospital Care 1. Do not remove burned clothing. Make sure the victim is no longer in contact with hot or burning material or exposed to smoke or heat. 2. Cool the area within 30 minutes of the burn with cool water. This intervention reduces the depth of burnt area and pain.
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Do not put ice on the burn. 3. Do not immerse large severe burns in ice cold water. Doing so could cause a drop in body temperature (hy pothermia) and deterioration of blood pressure and circulation (shock). 4. Cover the area of the burn. Use a cool, moist, sterile bandage; clean, moist cloth; or moist cloth towels.
Management ●● Elevate the burned body part or parts above heart level, when possible.
Airway and Breathing ●● If there is no breathing or other sign of circulation, be gin CPR. ●● Airway is most commonly affected by smoke or steam and could be compromised even in the absence of skin burns. ●● Respiratory failure could result from loss of airway patency, pulmonary edema, bronchospasm, diminished lung compliance and small airway occlusion. ●● Consider the potential for carbon monoxide poisoning.
Figure 28.2: Calculation of burns percentage based on parts of body involved
Circulation ●● Two large peripheral intravenous lines should be obtained. ●● Correct shock with normal saline (NS) boluses. ●● If the child has suffered inhalation injuries along with skin burns, 40%–50% more fluid may be warranted.
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Burns GREATER THAN 15% BSA are associated with significant fluid loss, which should be aggressively corrected. Burns LESS THAN 15% BSA are not associated with significant capillary leak.
Chapter 28 n Burns
●● In burns < 15% encourage oral intake of fluids. ●● Monitor urine output and maintain 1–2 mL/kg/h output.
IP : 196.52.84.10 SPECIFIC INJURIES Scalds ●● Scald burns do not require surgery, if daily wound cleansing and dressing changes are done (Figure 28.3). ●● Provide adequate analgesia.
293
Facial Burns ●● Rule out corneal injury. ●● Lubricate, if eyelids are swollen. ●● Secure endotracheal (ET) tube with wire, if the face is extensively involved. ●● Avoid using adhesive tapes. Scalp Burns ●● Shave hair to assess extent of burns. ●● Keep wound clean. Hand Burns ●● Meticulous wound cleaning and dressing. ●● Plastic surgery follow-up to avoid contractures. Commissure Burns (Burns Around Mouth)
Figure 28.3: This picture shows a child, who is being ventilated for cardiorespiratory failure due to scalds secondary to spillage of hot sambar while being cooked (Courtesy: Dr Thangavelu S).
●● Warn parents about the risk for late bleeding (The la bial artery can get exposed when the eschar separates after 5–10 days).
Table 28.1: Calculation of burns percentage 5–9 year
10–14 year
Head
Birth–1 year 19
1–4 year 17
13
11
15 year 9
Adult 7
Neck
2
2
2
2
2
2
Anterior trunk
13
13
13
13
13
13
Posterior trunk
13
13
13
13
13
13
Right buttock
2.5
2.5
2.5
2.5
2.5
2.5
Left buttock
2.5
2.5
2.5
2.5
2.5
2.5
Genitalia
1
1
1
1
1
1
Right upper arm
4
4
4
4
4
4
Left upper arm
4
4
4
4
4
4
Right lower arm
3
3
3
3
3
3
Left lower arm
3
3
3
3
3
3
Right hand
2.5
2.5
2.5
2.5
2.5
2.5
Left hand
2.5
2.5
2.25
2.5
2.5
2.5
Right thigh
5.5
6.5
8
8.5
9
9.5
Left thigh
5.5
6.5
8
8.5
9
9.5
Right leg
5
5
5.5
6
6.5
7
Left leg
5
5
5.5
6
6.5
7
Right foot
3.5
3.5
3.5
3.5
3.5
3.5
Left foot
3.5
3.5
3.5
3.5
3.5
3.5 Total TBSA
Burn size estimate
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Section X n Environmental Injury
Parkland Resuscitation Formula2
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IP : 196.52.84.10
4 mL/kg of fluids/% total burn surface area. ● ● Time zero for fluid resuscitation = Time of burn injury. ●● Total fluids to be given for first 24 hours = Normal main tenance for age + 4 mL/kg/% total body surface area. ●● Give half of calculated fluids over first 8 hours from time of injury. ●● Give remaining half of calculated volume over the fol lowing 16 hours. ●● Do not forget on-going losses such as vomiting. ●● Adjust fluids to maintain output of 1–2 mL/kg/hour. ●● Loss of albumin in open wounds could result in hy poalbuminemia. However, during resuscitation, albu min is not advised. Refer Figure 28.4 showing recovered child.
Do not Forget ●● ●● ●● ●●
Tetanus prophylaxis. Avoid prophylactic antibiotics. Provide pain relief. Intravenous antibiotics are recommended only in those with large and severe burns.3
Minor burns For minor burns, including first-degree burns and seconddegree burns limited to an area no larger than 7.5 centime ters in diameter, take the following action.
Prehospital Care 1. Cool the burn: Hold the burned area under cool (not cold) running water for 10–15 minutes or until the pain subsides. If this is impractical, immerse the burn in cool water or cool it with cold compress. Cooling the burn reduces swelling by conducting heat away from the skin. 2. Cover the burned area with a sterile gauze bandage. Avoid fluffy cotton, or materials that may get into the
wound. Wrap the gauze loosely to avoid applying pressure on burned skin. Bandaging keeps air off the burn, reduces pain and protects blistered skin. 3. Prescribe paracetamol: 10 mg/kg/dose.
Management ●● Call the surgeon for debridement cleaning and dressing. ●● Silver sulfadiazine is not recommended, since it pro longs healing time.4 ●● Apply biosynthetic dressing.5 Evidence supports the fact that this may speed healing.
HISTORY ●● ●● ●● ●● ●● ●● ●●
Where, when and how did the burn injury occur? Petroleum, kerosene, or steam, hot water? Pain related to burns. Breathlessness. Cough. Loss of consciousness. Past history.
BURN-SPECIFIC SECONDARY SURVEY ●● ●● ●● ●● ●● ●● ●● ●●
Rule out intracranial trauma. Corneal fluorescein exam for corneal injury. Assess for burns and exposed cartilage. Circumferential burns around chest may warrant es charotomy. If the limb has been exposed to circumferential burns, elevate it above the level of the heart to reduce edema. Abdominal compartment syndrome could occur. Check foreskin for genitourinary injury. Pain during passive/voluntary movements (consider escharotomy, if circumferential burns).
INVESTIGATIONS ●● ●● ●● ●● ●●
Complete blood count (CBC) Serum electrolytes. Serum albumin. Renal function. Chest X-ray.
Chapter 28 n Burns
common errors
IP : 196.52.84.10
1. 2. 3. 4.
295
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Failure to provide pain relief. Application of native medications. Covering the child with warm clothes during transport. Breaking blebs.
REFERENCES
Figure 28.4: Child seen in Figure 28.3 recovered after ventilatory and wound care. Note his tracheostomy. The airway had been compromised due to edema following inhalational burns (Courtesy: Dr Thangavelu S).
Key Points
ü
1. Wash burned areas with tap water in the prehospital setting. 2. Anticipating need for early intubation, if airway is involved. 3. Estimation of burned surface and calculating the appropriate fluids. 4. Removal of eschars in circumferential burns to prevent vascular insufficiency.
1. Bhattacharya S. Principles and practice of burn Care. In dian J Plast Surg.2009;42:282-83. 2. Tintinalli, Judith E. Emergency Medicine: A Compre hensive Study Guide [Emergency Medicine (Tintinalli)]. New York: McGraw-Hill Companies 2010. ISBN 0-07148480-9. 3. Avni T, Levcovich A, Ad-El DD, et al. “Prophylactic an tibiotics for burns patients: systematic review and metaanalysis”. BMJ 2010;340:c241. doi:10.1136/bmj.c241. PMC 2822136. PMID 20156911. 4. Storm-Versloot MN, Vos CG, Ubbink DT, et al. In: StormVersloot Marja N. (Ed)2010 Mar 17. “Topical silver for pre venting wound infection”. Cochrane database of systematic reviews (Online) (3): CD006478. doi:10.1002/14651858. CD006478.pub2. PMID 20238345. 5. Hubley P. “Review: evidence on dressings for superficial burns is of poor quality”. Evid Based Nurs” 2009 (3): 78. doi:10.1136/ebn.12.3.78. PMID 19553415.
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Electrical Injury
Figure 29.1: Few seconds of negligence can cause severe and occasionally fatal electrical burn injuries (Courtesy: Dr Gunda Srinivas)
Learning Objectives 1. Pathophysiology of electrical injury. 2. Assessment of severity of injury based on cardiopulmonary cerebral assessment and the pediatric assessment triangle.
3. Resuscitation and investigations following electric injury.
INTRODUCTION
PATHOPHYSIOLOGY
Young children are usually referred to the ED with low voltage injuries. Electrical burns can occur due to exposure to electrical appliances and electrical wall outlets (Figure 29.1).
Electricity passes between two points through the path of least resistance. The most dangerous pathway for the current is along the vertical axis of the body as it passes through all vital organs. Hand to hand flow will involve the heart, respiratory muscles and spinal cord.
Ù
High voltage injuries could lead to death.
CLASSIFICATION Of the two types of current viz alternating current (AC) and direct current (DC), the former is more dangerous. Tetanic muscle contractions occur as a result of prolonged contact. AC is used for domestic purposes and DC is used in batteries, defibrillators and pacemakers. ●● Low voltage: < 600 V. ●● High voltage: > 1,000 V. ●● Lightning: > 30 × 106 V.
Low voltage current can cause tetanic contraction of the respiratory muscles and ventricular fibrillation. High voltage current can throw the victim and cause trauma in addition to the effects mentioned above.
CASE SCENARIO 1 A 10-year-old boy is rushed into the ED after being found unconscious near a high tension wire. Thinking the wire as a rope, boy had tried swinging while holding
Chapter 29 nSequence ElectricalIntubation Injury Chapter 3 n Modified Rapid
the wire. Skin wound was not bleeding. Edges showed signs of coagulation (Figures 29.2 to 29.5).
IP : 196.52.84.10
297297
●● Circulation: Low voltage causes ventricular fibrillation, heart block, bundle branch block, supraventricular tachycardia, ST changes, atrial fibrillations. Cardiogenic shock can supervene. High voltage can cause asystole. ●● Disability: Evaluate for altered mental status, seizures, visual and auditory disturbances, quadriplegia (vertebral fractures) and cranial nerve deficits (rupture of tympanic membrane). ●● Obtain targeted history:
Figure 29.2: Charred wound at the site of contact with wire
a. High voltage or low voltage. b. Loss of consciousness. c. Duration of contact. d. Thrown from site or not.
●● Assess for entry and exit wounds. ●● Even if wound looks small, there may be severe underlying injury. Cutaneous injuries may extend from erythema to full thickness burns. Coagulation and necrosis of deep muscles can occur, while sparing the skin. Delayed bleeding is possible after the eschar falls off. ●● Electrocardiography (ECG), computed tomography (CT) of head for altered mental status, X-rays for musculoskeletal injuries. ●● Complete blood count (CBC), electrolytes, renal function, cardiac enzymes, blood group and crossmatch. Figure 29.3 Physiological status: Airway not maintainable, cardiogenic shock, altered level of consciousness with nonconvulsive status epilepticus.
PREHOSPITAL CARE At site ●● Turn off current source, prior to accessing the victim. ●● Assess whether pulseless and initiate cardiopulmonary resuscitation (CPR) as per pediatric advanced life support (PALS) guidelines. ●● Airway and breathing: Direct injury to the respiratory control center can cause apnea. Tetanic contractions of the respiratory muscles (especially diaphragm) can also cause respiratory arrest.
Figure 29.4: This boy was referred to the ED with loss of consciousness following swinging on a high tension wire. The skin wound was not bleeding with the edges showing signs of coagulation. He was intubated, after administration of 5 mL/kg of fluids and Dobutamine for cardiogenic shock.
298298
Section X nIIEnvironmental Injury Section n Airway
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Figure 29.5: This picture shows the child following recovery with his relieved parents after successful resuscitation. Fortunately no major vessels or nerves had been injured.
CASE SCENARIO 2 (Figures 29.6A and B, 29.7) A 12-year-old boy was accidentally holding an high tension wire and standing on iron rod in a terrace.
Figure 29.7 Physiological status: Cardiopulmonary cerebral status normal. Extensive skin burns with exit wounds on his soles.
INTERVENTIONS ●● Since his ABCs were stable monitor for cardiac arrhythmias. ●● Skin care for burns. Refer Chapter 28. ●● Look for compartment syndrome. ●● Complete blood count (CBC), electrolytes, renal function, cardiac enzymes, blood group and crossmatch.
Key Points
ü
1. Arrhythmias are common, leading to cardiac arrest or cardiogenic shock. Obtain ECG to evaluate for myocardial damage. 2. CT head to evaluate central nervous system (CNS) in high voltage injuries. 3. Orofacial injuries could bleed later and should be advised follow-up.
common errors
Figures 29.6A and B: Entry wound in the forearm, and exit wound on the soles, where the tissues have become charred. This boy was accidentally holding a high tension wire while standing on iron rod (Courtesy: Dr Gunda Srinivas).
û
1. Assuming that tissue and vessels are viable immediately after injury following high voltage exposure. 2. Assuming that the small size of the external wound determines extent of internal damage.
30
IP : 196.52.84.10
Submersion Injury
Figure 30.1: Children’s natural attraction to water enhances their risk of drowning in water bodies (Courtesy: Dr Gunda Srinivas)
Learning Objectives 1. Pathphysiology following submersion injury. 2. Principles of prehospital care.
3. Using the PAT to assess a drowning victim. 4. Steps in management of a drowning victim.
INTRODUCTION
PATHOPHYSIOLOGY
Drowning is the leading cause of accidental death of children in industrialized countries.1 In these countries, it has been noted that the site of drowning was bathtubs for infants, swimming pools for children between 1 and 4 years of age, and natural collection of water in older children (Figure 30.1).2
Submersion results in loss of normal breathing patterns, panic and laryngospasm. Apnea and pulmonary aspiration, which follow, lead to hypoxemia.6 The resultant hypercar bia, hypoxia and acidosis lead to circulatory arrest and multiorgan failure.
Drowning is the result of respiratory impairment from submersion or immersion in a liquid.3,4 The presence of liquid/air interface at the entrance of the airway prevents the victim from breathing air. The victim may live or die after this event. Despite the outcome, he is defined as being involved in a drowning incident. The Utstein statement recommended that the term near-drowning should not be used.4 It has also de-emphasized the classification based on the nature of submersion fluid viz salt water versus fresh water.4 Although there are differences that have been reported in laboratory conditions, they have not been found clinically significant.
Loss of surfactant, atelectasis, acute lung injury, pulmonary edema, intrapulmonary shunting and ventilation perfusion mismatch are some of the causes of respiratory failure. Prolonged hypoxia, severe peripheral vasoconstriction, intravascular fluid loss, extravascular fluid shifts, bradycardia and ventricular fibrillation are perhaps the commonest causes of cardiac arrest.7,8
Prehospital Management Though there are no modifications to the standard basic life support maneuvers, some precautions have been
300
Section X n Environmental Section II n Airway Injury
considered appropriate for cardiopulmonary resuscitation (CPR) in drowning victims.9
IP : 196.52.84.10 Recovery from Water ●● Remove from water immediately. When rescuing the victim, the rescuer should reach the victim at the earliest, while being fully aware of personal safety. ●● Routine spinal stabilization is not recommended, unless spinal injury is suspected.10 History of diving, use of water slide, signs of injury or alcohol intoxication suggest the need for spinal immobilization.
Provide Cardiopulmonary Resuscitation Treatment should be based on the guidelines provided by the pediatric advanced life support (PALS) and the advanced cardiac life support (ACLS) algorithms.9
Ù
Attempts to remove water from the air passages by abdominal thrusts or Heimlich maneuver are potentially dangerous and are contraindicated.11,12
CASE SCENARIO 1 1-year-old infant, was found unresponsive after accidentally falling into a bucket of water (Figure 30.2).
●● If airway is maintainable and the child has respiratory distress, provide supplemental oxygen using the Bain circuit. ●● Early use of continuous positive airway pressure (CPAP) is helpful in reversing hypoxia secondary to the capillary leak in the alveoli. ●● If the airway is not maintainable and breathing is inad equate, initiate bag-valve-mask ventilation. Plan early intubation using ICP precautions, if airway is unprotected, respiratory failure, cardiogenic shock or hypotension is identified.
Circulation
Ù
Plan smaller aliquots of NS (5–10 mL/kg). ●● Due to the risk of pulmonary edema secondary to acute lung injury or myocardial dysfunction, avoid administering more than 20 mL/kg. ●● At any point during bolus therapy, if signs of pulmo nary edema develop or worsen, initiate an appropriate inotropic agent and plan intubation.
Ù
If shock persists after intubation, AVOID further fluids unless history is suggestive of hypovolemia. Occasionally, torrential bleeding from a scalp injury can lead to hypovolemic shock.
Disability ●● Treat GTC seizures, if identified. ●● Eye signs of non-convulsive status epilepticus if noted, suggest severe shock or hypoxia. Treatment should be targeted towards early intubation and shock correction. If eye signs persist, the SE protocol may be implemented cautiously. ●● Take ICP precautions when intubating a drowning victim. Drowning victims have features of hypoxic ischemic encephalopathy.13 A secondary survey, is performed for other injuries such as head trauma, abrasions, lacerations or contusions.
Figure 30.2 Physiological status: Stridor with respiratory distress, pulmonary edema and shock.
Submersion in a bathtub should raise a suspicion of child abuse. Teenage drowning is frequently associated with illicit drug or alcohol abuse14 and appropriate toxicol ogy tests may be warranted.
ChapterRapid 30 n Submersion Injury Chapter 3 n Modified Sequence Intubation
●● All victims of submersion should be observed for at least 4–6 hours even if they do appear hemodynamically stable on arrival. IP : 196.52.84.10 ●● Electrocardiography (ECG) and blood gas determina tion should be performed as soon as possible. ●● Victims with respiratory and other organ dysfunction symptoms, decreased oxygen saturation and altered sensorium, require monitoring in the intensive care unit (ICU). Severe bradycardia and intense vasoconstriction as sociated with marked hypothermia may make victims appear dead, but resuscitative attempts should not be abandoned.13,15,16
Key Points
ü
1. Prevention can reduce the incidence of drowning.17 2. Immediate and appropriate bystander CPR and early basic life support (BLS) care can improve survival.19,20 3. Improved outcomes, if rescue breathing is provided even before the victim is pulled out of water. 4. Routine cervical spine stabilization is not necessary.
common errors
û
1. Attempts to remove water from the air passages by abdominal thrusts or Heimlich maneuver are potentially dangerous and are contraindicated. 2. Failure to provide oxygen with a flow inflating ventilation device. 3. Failure to recognize that respiratory distress could be due to cardiogenic or non-cardiogenic pulmonary edema.
REFERENCES 1. Rowe MI, Arango A, Allington G. Profile of pediatric drowning victims in a water-oriented society. J Trauma. 1977;17:587.
301 301
2. Karch SB. Pathology of lung in near-drowning. Am J Emerg Med. 1986;4:4. 3. Karpovich PV. Water in the lungs of drowned animals. Arch Pathol Lab Med. 1933;15:828. 4. Idris AH, Berg RA, Bierens J, et al. Recommended guidelines for uniform reporting of data from drowning: the “Utstein style” Resuscitation. 2003;59:45-57. 5. Hoff BH. Multisystem failure: a review with special reference to drowning. Crit Care Med. 1979;7:310. 6. Karch SB. Pathology of heart in near-drowning. Am J Emerg Med. 1985;109:76. 7. Lunt DW, Rose AG. Pathology of human heart in drowning. Arch Pathol Lab Med. 1987;111:939. 8. American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. IV-133-135. Part 10.3: Drowning. Circulation. 2005;112:24. 9. Watson RS, Cummings P, Quan L, et al. Cervical spine injuries among submersion injury. Pediatrics.1994;94:137-42. 10. Rosen P, Stoto M, Harley J. The use of the Heimlich maneuver in near drowning. Institute of Medicine Report. J Emerg Med. 1995;13:397-405. 11. Sarnaik AP, Preston G, Lieh-Lai M, et al. Intracranial pressure and cerebral perfusion pressure in near-drowning. Crit Care Med. 1985;13:224. 12. Howland J, Hingson R. Alcohol as a risk factor for drowning A review of literature (1950-1985). Accid Anal Prev. 1988;20:19. 13. Kyriacou DN, Arcinue EL, Peek C, et al. Effect of immediate resuscitation on children with submersion injury. Pediatrics. 1994;94:137-42. 14. Siebke H, Rod T, Breivik H, et al. Survival after 40 minutes; submersion without cerebral sequeae. Lancet. 1975;1(7919)1275-77. 15. Southwick FS, Dalglish PH Jr. Recovery after prolonged asystolic cardiac arrest in profound hypothermia. A case report and literature review. JAMA. 1980;243:1250-53. 16. Thompson DC, Rivara FP. Pool fencing for preventing drowning in children. Cochrane Database Syst Rev 2000;(2):CD001047. 17. Quan L, Wentz KR, Gore EJ, et al. Outcome and predictors of pediatric submersion victims receiving prehospital care in King County, Washington. Pediatrics. 1990;86:586-93.
Section XI
IP : 196.52.84.10
Special Topics
IP : 196.52.84.10
31
IP : 196.52.84.10
Gastrointestinal Bleeding
Figure 31.1: Spectrum of gastrointestinal bleeding (Courtesy: Dr Thangavelu S, Dr Gunda Srinivas)
Learning Objectives 1. Approach to gastrointestinal bleed. 2. Cases illustrating common presentations of gastrointestinal bleeds.
Introduction Approach to gastrointestinal (GI) bleeding in children varies based on etiology, age and site of bleeding1-5 (Figure 31.1).
3. Evidence-based approach to therapeutic interventions.
acute rheumatic fever for which he had been prescribed aspirin (Figure 31.2).
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Identify whether bleeding is localized or systemic. History of retching and vomiting suggest Mallory-Weiss syndrome. NSAIDS intake point towards drug-induced gastritis. Stigmata of liver disease are clues to diagnose portal hypertension. Fever, sepsis or capillary leak suggest severe sepsis or Dengue. Presence of hepato splenomega ly, lymphadenopathy and mucosal bleeds are indicative of malignancies.
Case Scenario 1 A 7-year-old male child with hematemesis is rushed into the ED. He had been recently diagnosed ashaving
Figure 31.2 Physiological status: Airway stable/Tachypnea/ Tachycardia with shock (no features of myocardial dysfunction or pulmonary edema). GI bleed due to drug-induced gastritis.
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Section XI n Special Topics
APPROACH TO GI BLEEDING IN THE ED Airway and Breathing IP : 196.52.84.10
●● Provide supplemental oxygen using non-rebreathing mask. ●● Insert nasogastric tube. ●● Plan to intubate if airway is compromised.
Circulation Simultaneously secure 2 vascular lines, collect blood for grouping and cross matching, Hb, CBC, coagulation profile and LFT. ●● Perform the rapid cardiopulmonary cerebral assessment. ●● Connect pulse oximeter and cardiac monitors. ●● Infuse first bolus of RL/NS (20 mL/kg). Continue fluid bolus until therapeutic goals of shock are resolved. ●● Establish etiology by careful history, physical examination (in this child, look carefully for signs of cardiac failure, infective endocarditis). Monitor carefully for signs of pulmonary edema and myocardial dysfunction secondary to fluid therapy since this child has RHD. ●● Catheterize and monitor urine output. ●● Monitor hematocrit every 2–3 hour, until bleeding stops and later 4–6 hourly (maintain hematocrit at 30%). ●● Arrange for blood transfusion if hemoglobin (Hb) < 7–8 g/dL. ●● If 1 unit of blood is needed every 2 hours, massive transfusion protocol is implemented to avoid coagulopathies.
●● Ranitidine: IV—1 mg/kg/dose (max 50 mg) 6–8 hourly Oral 2–4 mg/kg/dose (max 150 mg) 8–12 hourly. ●● Omeprazole: IV— 2 mg/kg/dose (max 80 mg) stat forward by 1 mg/kg (max 40 mg) 8–12 hourly. Oral: < 3 year: 10 mg 12 hourly, > 3 years: 20 mg 12 hourly. Sucralfate: 500 mg 6 hourly. Sucralfate: ●● ●● ●● ●●
1 month–2 years: 250 mg Q 4–6 hourly. 2–12 years: 500 mg Q 4–6 hourly. 12–15 years: 1 g Q 4–6 hourly. Somatostatin and octreotide are not routinely recommended for patients with acute ulcer bleeding7. ●● Order chest X-ray (CXR), ultrasonogram. ●● Request for an emergency endoscopy after stabilization.
Case Scenario 2 A 4-year-old girl with fever for 5 days has been afebrile since morning. She has vomited several times and the last 2 episodes were coffee ground in color. She has been complaining of severe abdominal pain. While she was being transferred she had become lethargic.
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Massive transfusion protocol • For every 3 units of RBC, 2 units of FFP are trans fused. • For every 5 units of RBC, 1 unit of platelets is transfused. • Goal of blood transfusion: HCT of 21–24 or Hb of 7–8 g/dL. • Transfuse whole blood based on the presence of continued bleed. Once bleeding stops, transfuse packed cells.
Pharmacologic Management of Drug-Induced Gastritis6 ●● Omit offending drug. ●● Antacids: 0.5 mL/kg (Not to exceed 30 mL/dose) every 1–2 hours.
Figure 31.3 Physiological status: Airway maintainable, effortless tachypnea/shock/altered mental status (probable etiology: severe dengue).
Resuscitation and specific management (See Chapter on Dengue) (Figure 31.3).
Case Scenario 3 A 10-year-old boy was rushed to the ED with complaints of two episodes of hematemesis and one episode of black tarry stools. His mother denied history of fever or drug intake. He had been apparently normal
Chapter 31 n Gastrointestinal Bleeding
till date, except for admission in the newborn period for jaundice. He had received an exchange transfusion during his stay in the IP NICU (Figure 31.4). : 196.52.84.10
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Gastric Lavage Use normal saline (room temperature) if needed. Chilled or ‘iced’ saline does not stop bleeding and may cause central hypothermia, particularly in young infants.
Pharmacologic Management of Portal Hypertension Pharmacologic therapy10 to decrease portal pressure may be considered in patients with continued bleeding. Vasopressin and its analogues act by increasing splanchnic vascular tone thereby decreasing portal blood flow.
Figure 31.4 Physiological status: Airway stable/Tachypnea/ Tachycardia with hypotensive shock. (probable etiology: extra hepatic portal hypertension with variceal bleed8).
●● Take care of the ABCs. ●● CBC, Hb, grouping, cross matching, Dengue serology, electrolytes, sugar, urea and creatinine. ●● Coagulation profile: – Elevated PT indicates coagulopathy (i.e. disseminated intravascular coagulation) or profound impairment of liver synthetic function. – Prolonged aPTT indicates hemophilia or coagulopathy. ●● Order LFT. – Increased aspartate aminotransferase and alanine aminotransferase enzyme levels are suggestive of portal hypertension with liver disease.
Fluid Therapy In most children with extrahepatic portal hypertension and normal hepatic synthetic function, bleeding stops spontaneously.9 Caution: Aggressive fluid resuscitation can increase risk of rebleed due to high venous pressure.
Introduce a Nasogastric Tube Placement of a nasogastric tube (NGT) helps to remove blood from the stomach. It prevents development of encephalopathy in cirrhosis and also helps to monitor recurrence of bleed.
1. Terlipressin:11 Dose: Administer 0.04 mg/kg IV (bolus) followed by 0.02-0.04 mg/kg, every 4–6 hours till a bleeding free interval of 24–72 hours is achieved. It is less cardiotoxic than vasopressin and is the drug of choice in variceal bleed. It is more effective than endoscopic injection sclerotherapy (EIS), safer than vasopressin in combination with nitroglycerin and EIS. It also improves survival. However, continuous infusion can cause necrosis. 2. Octreotide11,12 (Synthetic analogue of somatostatin) Dose: Loading dose of 1 μg/kg IV over 30 minutes, followed by 0.5 μg/kg/h. Its high cost, propensity to cause nausea, flatulence, malabsorption and bowel ischemia should be taken to consideration. 3. Vasopressin11 Dose: 6 U/kg in 50 mL at 1-5 mL/h. The drug has a half-life of approximately 30 minutes (Vasopressin 1 mL = 20U). Its use is limited by side effects such as vasoconstric tion, impairment of cardiac function and perfusion to the heart, bowel and kidneys. It also exacerbates fluid retention.
Endoscopy ●● The site of upper GI bleeding can be identified in 90% of cases, when endoscopy is performed within 24 hours. Emergency sclerotherapy can also be performed if needed. However, it should be undertaken after correction of coagulation disorders and hemodynamic instability.
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●● Endoscopic variceal ligation is currently considered a superior option to endoscopic sclerosis since, complications are rarer with the former modality. IP : 196.52.84.10 ●● In patients who continue to bleed despite pharmacologic and endoscopic methods to control hemorrhage, a Sengstaken-Blake more tube may be placed to stop hemorrhage by mechanically compressing esophageal and gastric varices (mechanical tamponade). It poses a particularly high risk for pulmonary aspiration and the tube is not well tolerated in children without significant sedation.
Surgical Procedures that Divert Portal Blood Flow and Decrease Portal Pressure ●● A transjugular intrahepatic portosystemic shunt (TIPS) is a method by which a stent is placed by an interventional radiologist between the right hepatic vein and the right or left branch of the portal vein. It aids providing temporary relief in children with portal hypertension. It is particularly useful in children needing liver transplantation. However, the TIPS procedure may precipitate hepatic encephalopathy and is prone to thrombosis. ●● Recent studies indicate that a combination of endoscopic sclerotherapy with β-blockers is far superior than any other form of treatment for the prevention of recurrence of UGI bleeding.
Coagulopathy IV Vitamin K, cryoprecipitate, FFP, recombinant factor VIIa and platelet transfusions are some of the interventions, which are useful in controlling bleeds due to coagulopathy secondary to hepatic dysfunction and thrombocytopenia.13,14 ●● Prolonged PT–INR is diagnostic of vitamin K deficiency. ●● Administer vitamin K: 0.3 mg/kg IV over 1 hour (max 10 mg). ●● Infuse 10 mL/kg of FFP. ●● Administer Ranitidine (2 mg/kg/dose) intravenously to reduce risk of bleeding from gastric erosions.
Disseminated Intravascular Coagulation The British Committee for Standards in Haematology, Blood Transfusion Task Force Guidelines for the use of fresh frozen plasma, cryoprecipitate and cryosupernatant2004 suggest that fresh frozen plasma and platelets are indicated when there are demonstrable multifactor deficiencies associated with severe bleeding and/or DIC.
●● Order cryoprecipitate if plasma fibrinogen is less than 1 g/L, although there is no clear threshold for clinically significant hypofibrinogenemia. ●● Uncontrolled massive bleeding, unresponsive to conventional blood component therapy: Consider rFVIIa, (dose: 100 μg/kg). A repeat dose may be given after an interval of 30 minutes to 1 hour. The same dose may be repeated at an interval of 1–4 hours until cessation of bleeding has been achieved.14 ●● Simultaneously treat underlying cause. The etiological factors associated with upper gastroin testinal bleeding vary with age.15,16
Infancy–1 Year 1. Esophagitis, gastritis. 2. Severe dengue (see Chapter on Dengue). 3. Stress ulcer: GI bleeds in infants admitted for burns, sepsis, raised ICP, head injury, encephalitis and gastroesophageal reflux disease (GERD). 4. Mallory-Weiss tear: Fresh bleed following repeated retching is suggestive of esophageal tear (MalloryWeiss syndrome). 5. Vascular malformation. 6. GIT duplication. 7. Malrotation.
1–12 Year 1. Severe dengue (see Chapter on dengue). 2. Esophageal varices due to extrahepatic portal hypertension or cirrhosis with portal hypertension.7 a. Liver disease (hepatic cause for portal hypertension like cirrhosis). b. Neonatal umbilical sepsis or umbilical vein catheterization (extrahepatic portal hypertension). 3. Esophagitis, gastritis, peptic ulcer disease.17 Recurrent abdominal pain is suggestive of peptic ulcer. 4. Stress ulcer: Stress related GI bleed in critically ill children being managed in the ED. 5. Mallory-Weiss tear (see above). 6. Drug intake: non-steroidal anti-inflammatory drugs (NSAIDS) and steroids are the commonest drugs causing gastritis. 7. Bleeding tendency: DIC manifests as GI bleed, bleeds from IV site, skin, hemarthrosis, etc. in seriously ill children. 8. Family history of bleeding disorder: Von Willebrand’s disease, hemophilia.
Chapter 31 n Gastrointestinal Bleeding
9. Odynophagia with oral candidiasis is suggestive of candidal esophagitis ( HIV).
IP : 196.52.84.10 Case Scenario 4 A 6 month infant is rushed to the ED with incessant cry accompanied by episodes of straining. He has vomited his feeds and is passing blood and mucus along with stools (Figure 31.5).
Figure 31.5 Physiological status: Airway stable/Tachypnea/ Tachycardia and shock (possible etiology: intussusception).
Management ●● Provide O2 using a non-rebreathing mask. ●● Introduce NGT. ●● Secure two lines and administer RL (20 mL/kg) bolus. Repeat cardiopulmonary cerebral assessment and continue boluses until therapeutic goals of shock are resolved. ●● Since, the etiology of shock is hypovolemia due to GI loss up to 120 mL/kg may be needed in the initial hours of resuscitation. ●● Collect blood for grouping crossmatching, RFT, LFT, coagulation profile, CBC and sepsis screen. ●● Arrange for blood. ●● X-ray abdomen can help identify intestinal obstruction ●● Request for color Doppler ultrasonography. It helps to diagnose intussusception. ●● Involve pediatric surgeon and radiologist urgently ●● Order enema studies.18 Barium enema reduction have traditionally been used with success rates of 50% –90%. Rate of detection of intussusception is more when symptoms are present
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for less than 24 hour. Barium study is contraindicated if perforation is suspected. Air contrast enemas have also been used with similar success rates, with air enemas requiring less radiographic exposure, but having slightly higher perforation rates. Enemas with saline contrast require experienced sonographers. Evaluate for other etiologies of lower GI bleed 1. Infants ●● Anal fissure—presents with constipation and painful defecation. ●● Intussusception. ●● Infective colitis—passing small quantities of blood and mucus in the stool, crampy lower abdominal pain and tenesmus. ●● Midgut volvulus. ●● Meckel’s diverticulum. ●● Vascular malformations. ●● Coagulation disorders. 2. Older children ●● Anal fissure: Pain during defecation with bloodstreaked stools. ●● Rectal prolapse: Associated with mass seen per rectum. ●● Bacterial enteritis: Dysentry, fever and crampy lower abdominal pain. ●● Polyps—painless rectal bleeding with a large amount of bleed per rectum. ●● Gangrenous bowel due to volvulus is characterized by bilious vomiting, abdominal distension and bleeding per rectum. ●● Meckel’s diverticulum: Intermittent, painless hematochezia. ●● Vascular malformations: Painless, massive bleed. ●● Bleeding disorder: GI bleed will be associated with bleeds from other sites. ●● Inflammatory bowel disease: Associated with chronic diarrhea and failure to thrive. Physical examination in acute GI bleed, which can suggest the etiology ●● Examine ears, eyes, nose and throat: Look for epistaxis, nasal polyps and oropharyngeal erosions from caustics and other ingestions. ●● Look for abdominal surgical scars and elicit the indication for surgery. ●● Abdominal tenderness with or without a mass, raises the suspicion of intussusception or ischemia.
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●● Hepatomegaly, splenomegaly, jaundice or caput medusae suggests liver disease and subsequent portal hypertension. IP : 196.52.84.10 ●● Splenomegaly is suggestive of portal hypertension; but following a massive bleed, the spleen may contract and hence may be impalpable. (Smith-Howard syndrome). ●● Inspect perianal area: Look for fissures, fistulas, skin breakdown or evidence of trauma. ●● Look for evidence of child abuse, such as perianal tearing, tags or irregularities in anal tone and contor. ●● Specifically include bowel sound frequency in the abdominal examination. Hyperactive bowel sounds are more common in upper GI bleeding. ●● Examine skin for evidence of systemic disorders, such as inflammatory bowel disease: intermittent maculopapular rash. ●● Henoch-Schönlein purpura: palpable purpura in both lower limbs and Peutz-Jeghers polyposis. ●● Digital rectal exam should be performed in the OT under sedation. It may reveal polyps, masses or occult blood.
Workup Laboratory Studies ●● Confirm presence of blood by requesting for peroxide based tests such as the hemoccult or hematest to identify lower GI bleeding and gastroccult for upper GI bleeding. ●● Red meat, iron and peroxidase containing vegetables (e.g. turnips, horseradish, broccoli, cauliflower and cantaloupe) can give false-positive results.
Imaging Studies ●● Meckel scan, using technetium-99m pertechnetate helps to identify ectopic gastric mucosa. ●● Push enteroscopy is a long endoscope that is placed through the mouth into the jejunum. It can reach about 160 cm beyond the ligament of Treitz. One study has shown that push enteroscopy identified a large number of mucosal lesions that could not be identified by a standard endoscope. ●● Colonoscopy should be performed only when the patient is stable and when blood and feces will not conceal proper visualization. ●● Sigmoidoscopy19 is indicated in children who have symptoms of chronic lower GI bleeding for 1 year or
longer; the most common etiologies are juvenile colorectal polyps and non-specific proctitis.
Key Points
ü
1. Find out whether GI bleed is localized or systemic. 2. Identify whether the bleed is secondary to varices or clotting defects. 3. Control bleed based on etiology. 4. Transfuse appropriately. 5. Treat coagulation defects.
common errors
û
1. Children with epistaxis or oropharyngeal bleeding or hemoptysis often vomit bright red blood. 2. Failure to recognize intussusception leading to late referral to the surgeon. 3. Delay in resuscitation in an effort to search for the etiology.
References 1. Arain Z, Rossi TM. Gastrointestinal bleeding in children: An overview of conditions requiring non-operative management. Semin Pediatr Surg. 1999; 8 (4):172-80. 2. Erlich F. Gastrointestinal bleeding. In:Fleisher GR, Ludwig S, (Eds). Synopsis of Pediatric Emergency Medicine. Baltimore: MD Lippincott Williams and Wikins; 1996. pp. 100-05. 3. Arora NK, Ganguly, S Mathur P, et al. A Upper gastrointestional bleeding: Etiology and Management. Ind JI Pediatrics. 2002;69 (2):155-68 4. Berkowitz C. Gastrointestinal bleeding. In: Pedaitrics: A Primary Care Approach. Philadelphia, PA: WB Saunders; 1996. 5. Peters JM. Management of Gastrointestinal Bleeding in Children. Curr Treat Options Gastroenterol. 2002;5(5):399-413. 6. Thapa BR, Bansal D.Management of upper Gastrointestinal bleeding in children.Ind JI Practical Pediatrics. 200; 4:398-416. 7. Alan N Barkun, Marc Bardou, Ernst J, Kuipers, et al. International Consensus Upper Gastrointestinal Bleeding Conference Group. International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding. Ann Intern Med. 2010;152 (2):101-13. 8. Molleston JP. Variceal bleeding in children. J Pediatr Gastroenterol Nutr. 2003;37(5):538-45.
Chapter 31 n Gastrointestinal Bleeding
9. Comar Kevin M,Sanyal AJ. Portal hypertensive bleeding Gastroentrol Clin North Am. 2003;32(4):1079-105. 10. Tatro DS, Borgsdorf Lopez JR, et al. A to Z Drug IPLR, : 196.52.84.10 facts. 5th edition. St Louis,MO: Facts and Comparisons; 2005. 11. Frank Shann. Drug Doses; 15th edition, Victoria Austrailia. 2010. 12. Ioannou GN, Doust J, Rockey DC. Systematic review: Terlipressin in acute oesophageal variceal haemorrhage. Aliment Pharmacol Ther. 2003;17(1):53–64. 13. E Mileti, P Rosenthal. Management of Portal Hypertension in Children. Curr Gastroenterol Rep (2011); 13(1):10– 16 DOI 10.1007/s11894-010-0151-y.” 14. Ampaiwan C, et al. Recombinant-activated factor VII for control and prevention of hemorrhage in non-hemophilic
15. 16. 17. 18. 19.
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pediatric patients. Blood coagulation and Fibrinolysis. 2010;21:354-362. Huang CS. Lichtenstein DR. Non-variceal upper gastrointestinal bleeding. Gastroentrol Clin North Am. 2003;32 (4):1053-78. Fox VL. Gastrointestinal bleeding in infancy and childhood. Gastroentrol Clin North Am. 2000;29(1):37-66. Johnson D, L’Heureux P, Thompson T. Peptic ulcer disease in early infancy: Clinical presentation and roentgenographic features. Acta Paediatr Scand. 1980;69(6):753-60. Henikson S, Blane CE, Koujok K, et al. The effect of screening sonography on the positive rate of Enemas for intussusception. Pediatr Radiol. 2003;33(3):190-93. Mandhan P. Sigmoidoscopy in children with chronic lower gastrointestinal bleeding. J Paediatr Child Health. 2004;40(7):365-68.
Interpretation of Chest X-rays in Critically Ill Children IP : 196.52.84.10
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Figure 32.1: Interpretation of X-rays in critically ill children is a skill adjunct to clinical acumen and guide therapeutic decisions (Courtesy: Dr Thangavelu S, Dr Gunda Srinivas)
Learning Objectives 1. Systematic approach to reading an chest X-ray (CXR) in the ED. 2. Case scenarios illustrating various respiratory emergencies. On most occasions, the first responder in the ED who is confronted with the need to take life saving decisions based on a chest X-ray is also the least experienced. This chapter teaches a structured approach to the interpretation of a chest radiograph in emergency settings (Figure 32.1). ●● The physician who ordered the chest X-ray must see the film within 5–10 minutes. ●● Occasionally, even a delay of 5 minutes would be lethal in scenarios such as pneumothorax, or a displaced endotracheal tube. In these situations, rapid clinical assessment and intervention is life saving rather than waiting for chest film interpretation.
Stepwise assessment General Data: Check 1. Name. 2. Age. 3. Gender.
3. Pearls and pitfalls in interpretation of chest radio graphs.
4. Date and time of taking the X-ray. 5. Whether right and left side have been documented correctly. 6. Whether, the X-ray was taken in the anteroposterior or posteroanterior view.
Ù
Anteroposterior view: a. A notch in the middle of the clavicle. b. Lung tissue not seen above the clavicle. Posteroanterior view: a. Clavicle will appear straight. b. Lung tissue will be seen above the clavicle. 7. Whether the film has been centered or rotated.
Ù
Symmetry of both medial ends of clavicle indicate that the CXR is not rotated. 8. Phase of respiration in which the X-ray is taken.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
313
Ù The middle of the diaphragm should correspond to the IP : 196.52.84.10 anterior end of 5th to the 7th ribs. Anterior end stops short and the posterior end joins the vertebral column.
Figure 32.3: Normal CXR of an infant showing normal thymus (sail-shaped).
Figure 32.2A: Normal AP view
9. In a well-penetrated chest film, the vertebral bodies and intervertebral discs will be noticeable (but not very clear) behind the heart. In an under-penetrated film, the lungs will be diffusely white and the vertebral bodies will not be visible. 10. In the over-penetrated film, the lungs are diffusely dark with poorly differentiated lung markings and the vertebral bodies will be seen very clearly.
Specific Data
Figure 32.2B: Normal PA view
Normal X-ray: In the AP view, there will be a notch in the middle of the clavicle (Figure 32.2A). No lung tissue will be seen above clavicle. When the X-ray is taken in the inspiratory phase, the anterior end of the 5th rib corresponds to middle of the dome of diaphragm (marked by horizontal arrow in Figure 32. 2B) (the posterior end of rib is marked by the vertical arrow). The two vertical yellow lines indicate the medial end of clavicle and lateral margin of vertebrae. If the lines are equidistant on both sides of the vertebra, it implies that the film has been centered without rotation.
1. Tubes: endotracheal tube, tracheostomy tube, chest tube or rarely pig tail catheter left in pericardial cavity. 2. Lines: external jugular (EJV), internal jugular (IJV), subclavian lines, PORT-A-CATH (subcutaneously implantable venous access system) or tunneled lines. 3. Above the diaphragm. Scan from periphery to center. – Soft tissue. – Chest wall. – Costophrenic angle. – Mediastinum and normal thymus (Figure 32.3). – Cardiophrenic angle. – Lung tissue. – Heart. 4. Below the diaphragm. – Look for air under the diaphragm – Air fluid levels suggestive of intestinal obstruction. – Bowel shadows crowded in the center is indicative of ascites.
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Lung Parenchyma
Air Bronchogram
Compare both hemithoraces.
IP : 196.52.84.10
●● Size of the hemithorax. ●● Color or lucency. – Black shadows and air bronchogram. ●● Costophrenic angle: intact or obliterated. ●● Mediastinal shift.
These are luminal, linear branching gas shadows in the background of parenchymal opacities such as pneumonia, collapse and ARDS. Air bronchograms are not seen in the presence of pleural fluid or pulmonary edema.
Costophrenic Angle
Size of Hemithorax
Obliteration of costophrenic angle suggests presence of pleural fluid.
a. Increase in size of hemithorax compared with the opposite side may be due to pneumothorax or emphysema. b. Decrease in size, may be due to collapse or fibrosis.
Mediastinal Shift
Compare the Color and Lucency a. Darker hemithorax indicates presence of abnormal air (pneumothorax or emphysema). b. Opacity indicates any one of the causes mentioned in Table 32.1.
a. Shift to the same side occurs in collapse or fibrosis. b. Shift to the opposite side occurs in pleural effusion or pneumothorax.
Ù
Note: Usually one finger breadth or 1/4th of the heart shadow will be seen on the right side.
Table 32.1: Types of opacity and its diagnosis Type of opacity
Diagnosis
Heart Cardiomegaly
Linear and branching
Normal bronchovascular markings
Patchy
Bronchopneumonia or subsegmental collapse
Homogeneous
Consolidation
Presence of air bronchogram
Consolidation
Absence of air bronchogram
Pleural fluid or tumor
Pericardial Effusion
Bilateral
ARDS, pulmonary edema, extensive bronchopneumonia
Lung volume decreased
Collapse or fibrosis
Uniform density, costophrenic angle lost
Pleural fluid
a. Loss of normal shape of the heart. b. Obtuse cardiophrenic angle. c. Absence of pulmonary plethora.
Varying density, air bronchogram
Pneumonia
Uniform density, decreased volume, mediastinal shift, rapid change
Collapse
Triangular, uniform density
Segmental collapse
a. Cardiothoracic ratio > 0.6. b. Normal shaped heart. c. Acute cardiophrenic angle. d. Pulmonary plethora.
Tubes and Lines
Black Shadows
Tubes and lines are important artificial structures to be identified in addition to the natural structures in a critically ill child. Tubes introduced for various purposes can be the cause of many life-threatening complications in critically ill children. Check for position of the endotracheal tube, tracheostomy tube, chest tube or rarely pig tail catheter within the pericardial cavity.
Normal appearance of the lung is gray color interspersed with bronchovascular markings. Presence of air will make it darker than normal.
Lines may have been inserted into the external jugular, internal jugular or subclavian veins. Check for placement and position.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
Interpretation of CXR with case scenarios IP : 196.52.84.10 Case scenario 1 (Figure 32.4)
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Case scenario 2 (Figure 32.5) This child with DSS, was referred after fluid therapy.
A 3-week-old infant brought for cough and fever.
Figure 32.5
Figure 32.4
Your Observations
Your Observations
Diagnosis: Normal lung fields. Fracture clavicle with callus formation. Though, this CXR shows no evidence to support the history of a respiratory infection, verification of the chest wall for soft tissue and bones reveals fracture clavicle with callus formation . The 3 bones that can be evaluated in a CXR are clavicle, ribs and humerus. Finding: Fracture clavicle with callus formation. The clavicle, ribs and humerus also help in recognizing important bone disorders. ●● Absent clavicle is characteristic of cleidocranial dysostosis. ●● Widening of the anterior ends of ribs, cupping and fraying of the upper end of humerus are features of vitamin D deficiency. This is particularly useful when a child presents with seizures.
Finding: Chest wall edema probably due to capillary leak due to volume overload in dengue shock syndrome.
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Case scenario 3 (Figure 32.6)
Case scenario 4 (Figures 32.7A and B)
History of fever and respiratory distress for 3 days.
A 7-year-old girl, presents with fever, respiratory distress and oral thrush.
IP : 196.52.84.10
Figure 32.6
Figure 32.7A: Oral thrush
Your Observations
Figure 32.7B
CXR: Bilateral extensive opacities. Diagnosis: This picture can occur in three conditions.
Both hemithoraces are of the same size. The opacity is homogeneous with no mediastinal shift. Diagnosis: Consolidation.
●● Extensive bronchopneumonia. ●● ARDS. ●● Pulmonary edema. Diagnosis is made based on clinical findings. Picture shows oral thrush, hence the diagnosis is extensive bronchopneumonia with probable immune deficiency. Radiographs, such as the one above, can reveal opacities in the lung. However, it cannot pin-point etiology. As in this case, the diagnosis becomes apparent only from clinical history.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
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Case scenario 5 (Figure 32.8)
Case scenario 6 (Figure 32.9)
A 2-year-old boy presented with fever and respiratory 196.52.84.10 distress for 3 days. He IP had: been grunting since morning.
A 3-year-old child presented to emergency 1 hour after consumption of kerosene. She was in respiratory failure and hypotensive. She needed urgent intubation and ventilation in the ED.
Figure 32.8
Your Observations
Figure 32.9
Your Observations
Homogeneous density on the whole of left side with no air bronchogram. Costophrenic angle is obliterated. Mediastinal shift is absent. In acute collection of fluid, mediastinal shift may be absent.
CXR: Completely whitened lung.
Diagnosis: Left-sided pleural fluid.
Diagnosis: ARDS.
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Case scenario 7 (Figures 32.10A and B)
Case scenario 8 (Figures 32.11A to C)
A 6-year-old girl presented with severe respiratory disIP : 196.52.84.10 tress, 8 hours after scorpion sting. She developed ventricular tachycardia followed by fibrillation and could not be revived. The ET tube was flooded with pink, frothy secretions due to pulmonary edema.
A 2-year-old child presents with brief history of fever and breathlessness.
Figure 32.10A: Froth oozing out from ET tube due to pulmonary edema
Figure 32.11A
Your Observations Patchy opacity on the right side with pneumatocele. Note the air bronchogram.
Figure 32.10B: The bilateral butterfly-shaped opacities is suggestive of pulmonary edema
Your Observations Figure 32.11B
Your Observations Presence of bilateral hilar opacities, in the background of scorpion sting confirm the diagnosis as pulmonary edema. But this classical picture may not be seen in all situations.
Since the child developed respiratory failure, she was ventilated. The pneumatocele increased in size.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
319
Case scenario 9 (Figure 32.12) IP : 196.52.84.10
A 5-year-old child admitted for breathlessness.
Figure 32.11C
Your Observations Figure 32.12
Your Observations
The right hemithorax is larger than the left. It is more lucent without vascular markings and the mediastinum has shifted to the left suggesting the presence of a right-sided pneumothorax.
Note the homogeneous opacity on the right, obliteration of the costophrenic angle and mediastinal shift to the opposite side. A chest tube was introduced after suspecting empyema. Since there was no relief, the possibility of tumor was considered. CT revealed a mediastinal tumor.
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Section XI n Special Topics
Case scenario 10 (Figure 32.13)
Case scenario 11 (Figures 32.14A and B)
Following measles, a 7-year-old boy developed highIP : 196.52.84.10 grade fever and breathlessness.
A toddler was rushed into the ED for sudden onset of breathlessness. His elder brother, who was playing near by was eating peanuts. Breath sounds were diminished on the left side.
Figure 32.13
Homogeneous opacity in the right base with obliteration of the costophrenic and cardiophrenic angles. Presence of air fluid level on the right side suggests the diagnosis of pyopneumothorax. Mediastinal shift is not apparent, probably due to the thoracostomy. Note the presence of the chest tube. In the background of measles and respiratory distress, one may anticipate pneumonia or empyema. Training one’s eyes to see what is expected in the clinical backdrop can often clinch the diagnosis (Table 32.2).
Figure 32.14A
The left hemithorax appears bigger and has greater radiolucency (appears more black) compared to the right. Presence of bronchovascular markings and absence of collapsed lung margins favor the diagnosis of obstructive emphysema on the left side.
Table 32.2: X-ray clues to diagnosis Description
Diagnosis
Circular air collection in the Pneumatocele background of white opacities Bigger and darker hemithorax with bronchovascular markings
Obstructive/compensatory emphysema (here opposite lung will be abnormal)
Confined to one lobe with herniation to opposite side and collapse of the adjacent lobe
Congenital lobar emphysema
Bigger and darker hemithorax, Pneumothorax no bronchovascular markings, collapsed lung margins are seen Continuous diaphragm sign, lifting of the thymic shadow
Pneumomediastinum
Figure 32.14B
This chest X-rays of a different child with similar history shows similar findings though very subtle.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
Case scenario 12 (Figures 32.15A and B)
Case scenario 13 (Figures 32.16A to D)
A young infant presented with breathlessness of 1 IP : 196.52.84.10 month duration.
History of aspiration of a nail.
321
Figure 32.16A Figure 32.15A
Figure 32.16B Figure 32.15 B
Your Observations
Your Observations The volume of the left lung is more than the right (emphysematous). The left lower lobe is collapsed with a sharp margin with herniation of the upper lobe to the right side. Note the mediastinal shift to the right. The bronchovascular markings in the emphysematous left lung differentiates it from a pneumothorax. Diagnosis: Congenital lobar emphysema of the left upper lobe.
Nail in the right lower lobe with segmental collapse of the lower lobe. Bronchoscopic removal failed and child developed pneumothorax.
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Case scenario 14 (Figure 32.17) IP : 196.52.84.10
A 3-day-old neonate was referred to the ED with breathlessness, cyanosis, dextrocardia and a scaphoid abdomen.
Figure 32.16C
Chest tube was inserted and pneumothorax drained.
Figure 32.17
Your Observations
Figure 32.16D
Your Observations
Compare the size, lucency, color, CP angles of both the hemithoraces. Then look at the mediastinum. Size: The left sided hemithorax appears larger than the right side. Color or lucency: Left hemithorax is filled with cyst like structures (bowel shadows). Costophrenic (CP) angle: The CP angle on the right is free, but obliterated on the left. Mediastinal shift: The mediastinum is shifted to the right. Other findings: Absence of abdominal gas shadows. The diaphragm is not visible. Note presence of umbilical artery and umbilical vein catheters.
Nail removed and pneumothorax resolved. Normal X-ray.
Diagnosis: Diaphragmatic hernia.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
323
Case scenario 15 (Figure 32.18)
Case scenario 16 (Figure 32.19)
A 6-month-old presented with cough, fever and respiIP duration. : 196.52.84.10 ratory distress of 4 days
Another 8 month infant presented with the history of cough, fever and acute onset breathlessness.
Figure 32.18
Your Observations
Figure 32.19
Your Observations
There is less lung volume on the right than the left. A homogeneous opacity is also seen on the right upper lobe. It has a sharp margin suggesting the presence of right upper lobe segmental collapse.
Reminder When evaluating lung fields, four aspects need to be compared. ●● ●● ●● ●●
Volume of hemithorax. Color or lucency. Costophrenic angles. Mediastinal shift.
Both hemithoracis have similar volume. There is no significant mediastinal shift. A homogeneous triangular opacity is seen on both sides with sharp margins suggesting the diagnosis of bilateral lower lobe segmental collapse.
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Section XI n Special Topics
Case scenario 17 (Figure 32.20)
Case scenario 18 (Figures 32.21A and B)
A 5-year-old child with history of recurrent wheezing, IP : 196.52.84.10 presented with distressing cough and breathlessness.
A 3-year-old child had been intubated in a peripheral hospital for respiratory failure. On arrival, his air-entry was reduced on the left and his SpO2 was 88%.
Figure 32.20
Your Observations
1. Usually the cardiac silhouette and the thymic silhouette are merged and seen as single cardiothymic shadow. In this CXR the thymic shadow is separated from cardiac shadow (see the upward arrows). 2. The shadow of diaphragmatic domes also merge with the cardiac shadow. Here, in this picture, a dark line of air separates the diaphragm from the lower border of the heart. ‘Continuous diaphragm sign’ (double headed horizontal arrow): Also has subcutaneous emphysema on the right side. Both signs are diagnostic of pneumomediastinum.
Figure 32.21A
Your Observations
The endotracheal tube has slipped into the right main bronchus resulting in the collapse of the left lung. The tip of the ET is almost at the level of T5 vertebra. Normally, it should be positioned at the level of T2-T3. 1. The volume of the left lung is less than the right lung. The ribs on the left side appear to be crowded in comparison to the right. There is a homogeneous opacity of the left side with mediastinal shift. 2. The left costophrenic angle appears to be obliterated. The tube was repositioned and fixed. Air-entry improved on both sides and SpO2 normalized. Repeat CXR after repositioning of ETT.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
325
Case scenario 19 (Figure 32.22) IP : 196.52.84.10
A 5-year-old boy was intubated following submersion injury and referred to the PED. He suddenly desaturated, developed hypotension and bradycardia. Consider ‘DOPE’ Air-entry on both sides were equal confirming the tube position. No air was heard over the epigastric region. Suctioning the tube yielded nothing ruling out obstruction. Equipment failure was ruled out. The last possibility was pneumothorax. A bed X-ray taken just prior to needle thoracocentesis showed the following.
Figure 32.21B
Your Observations
Figure 32.22
Reminder
Repeat CXR after repositioning of ETT. ●● The left lung has expanded. The volume of both lung fields are normal. The mediastinum is in the midline. ●● There is minimal pleural fluid on the left side. ●● The ET is now at T4. Still needs to be pulled out.
●● Displacement: Clinical finding that is diagnostic is the absence of breath sounds on the left side. ●● The radiograph will show collapse of the left lung. ●● Obstruction: Is characterized by resistance, while ventilating with bag. The radiograph will not show any change. ●● Pneumothorax is characterized by absent breath sounds with resonance on percussion on the side of the pathology viz pneumothorax. ●● The right hemithorax is bigger and darker than the left. ● ● No bronchovascular markings are seen on the right side. ●● Also note the collapsed lung on the right side. Diagnosis: Right-sided pneumothorax.
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Case scenario 20 (Figures 32.23A and B)
Case scenario 21 (Figures 32.24A and B)
A 12-year-girl presented with history of fever, hemopt196.52.84.10 ysis and expectorationIPof:foul smelling yellow sputum.
A 4-year-old boy presented with failure to thrive, breathlessness and oxygen dependency since infancy. Two siblings had died earlier with similar history. This child developed respiratory failure requiring ventilation.
Figure 32.23A Figure 32.24A
Figure 32.23B
Your Observations Figure 32.24B
The 2nd chest radiograph shows the development of a small pocket of air in the right upper and lower zone. Compare the contour of the diaphragm on both sides. On the side of the pneumothorax the usual contour is lost. 1. Homogeneous opacity with air fluid level in the right lower lobe. 2. Also has scoliosis. CT chest confirms lung abscess with air fluid level.
a. The reticulogranular pattern of opacity on both side suggests the diagnosis of interstitial pneumonia. b. This CXR shows pneumothorax that occurred during mechanical ventilation.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
327
Case scenario 22 (Figure 32.25)
Case scenario 23 (Figure 32.26)
This child presented with respiratory distress. He had IP : 196.52.84.10 diminished breath sounds on the left side.
A 2-year-old girl presented with respiratory distress since birth. She had tachycardia, gallop and hepatomegaly.
Figure 32.25
Your Observations
Figure 32.26
Your Observations
1. The left hemithorax is smaller since the left dome of diaphragm is at a higher level than the right. 2. The mediastinum is shifted to the right. 3. The fundus of the stomach lies just below the left dome of diaphragm (gastric bubble is always below the diaphragm).
1. Cardiothoracic ratio is > 0.6 (increased). 2. Cardiophrenic angle is acute. 3. Pulmonary congestion suggestive of pulmonary edema.
Diagnosis: Eventration of diaphragm.
Diagnosis: Cardiomegaly.
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Case scenario 24 (Figures 32.27A and B) A 14-month-old infant presented with fever, breathlessIP : 196.52.84.10 ness, tachycardia, hepatomegaly and seizures.
Figure 32.27B
Your Observations Figure 32.27A
Your Observations
Wrist X-ray shows classical features of rickets. 1. The cardiothoracic ratio is greater than 0.6 is suggestive of cardiomegaly. 2. The associated pulmonary plethora is diagnostic of congestive cardiac failure. 3. The upper end of humerus, shows cupping, fraying of metaphyseal ends and widening of physis suggestive of rickets. Note: When a child presents with seizures, X-ray chest can give clues to the etiology of seizures such as rickets or lead poisoning.
In lead poisoning, a dense band will be noted in the metaphyseal end (lead deposits). The ECHO of this child revealed a low ejection frac tion without evidence of anatomical abnormalities. Serum ionized calcium was 0.7 (low). Serum 25-hydroxyvitamin D level was low. Diagnosis: Vitamin D deficiency rickets, cardiomegaly and cardiac failure. Treatment with vitamin D and calcium was curative.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
329
Case scenario 25 (Figures 32.28A to C) IP : 196.52.84.10
Figure 32.28C Figure 32.28A
Figure A: The normal shape of the heart is preserved, the cardiophrenic angle is acute with increased pulmonary congestion.
Your Observations
Whenever CXR shows cardiomegaly, always look again to see the signs of pericardial effusion as it can be relieved only by pericardiocentesis. Diagnosis: Cardiomegaly with CCF.
Figure 32.28B
The normal shape of the heart is not seen, the cardiophrenic angle is obtuse and pulmonary plethora is not seen. Diagnosis: Pericardial effusion.
CXR after pericardial tap. Note the presence of pig tail catheter, which was kept in situ. Also note the change in the shape of the heart and the cardiophrenic angle. Diagnosis: After pericardiocentesis.
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Case scenario 26 (Figures 32.29A to C) A 5-year-old playing boy was referred with history of IP : 196.52.84.10 breathlessness while playing with a top.
Figure 32.29B
Your Observations Figure 32.29A
Your Observations Lateral view shows the top’s metallic axis penetrating the posterior wall of trachea causing air leak.
Figure 32.29C: The FB after it was retrieved
Order a lateral view to visualize the nature of the foreign body. Coin shadow seen in the neck. If the FB is seen in the sagittal plane, it is caught up in the trachea. If it is placed in the coronal plane, the object is in the cricopharynx.
The shadow, which appeared as a circular shadow characteristic of a coin in the AP view, was a top. This was apparent in the lateral view.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
331
Case scenario 27 (Figures 32.30A to D) 2-year-old child with Down syndrome was brought IP : 196.52.84.10 with stridor. X-ray showed a coin shadow in the neck. Despite removal of FB, he deteriorated and developed respiratory distress. Child developed bilateral pneumothorax and was treated with chest tube insertion and ventilatory support.
Figure 32.30C
Figure 32.30A: Child ventilated with bilateral ICD
Figure 32.30B: Coin shadow in the neck with heart and lungs being normal.
Right hemithorax is wide, more black with collapsed lung margin suggestive of right pneumothorax. Subcutaneous emphysema is also seen in the neck as vertical translucencies in the neck. Continuous diaphragm sign: pneumomediastinum.
Figure 32.30D
Your Observations
Your Observations
The foreign body was cleaned and re-examined. It was a button battery and not a coin. The deterioration was due to corrosive necrosis, which can occur as early as 4 hours after ingestion.
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Section XI n Special Topics
Case scenario 28 (Figure 32.31)
Case scenario 29 (Figures 32.32A and B)
A 8-year-old boy presented with fever, biphasic stridor IP : 196.52.84.10 and hepatosplenomegaly.
A girl with T-cell lymphoma, developed fever, abdominal pain and shock.
Figure 32.31
Figure 32.32A
Your Observations
Your Observations
Figure 32.32B
Your Observations
Mediastainal node is seen (arrow). It is probably causing intrathoracic airway obstruction.
Haziness suggestive of peritonitis, multiple fluid levels with air under diaphragm.
Diagnosis: Lymphoma.
Diagnosis: Pneumoperitoneum secondary to perforation.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children
333
Case scenario 30 (Figure 32.33)
Case scenario 31 (Figures 32.34A to D)
A 2-year-old boy presented with fever, acute diarrhea IP He : 196.52.84.10 and vomiting for 3 days. developed tense abdominal distension.
A 10-year-old girl fell down from a cycle and appeared bloated. Cycle tube nozzle injury caused injury to the heel causing extensive air leakage and subcutaneous emphysema over the face, submandibular region and chest wall.
Figure 32.34A: Site of nozzle injury Figure 32.33
Your Observations
Figure 32.34B
This intubated infant has chest wall and abdominal wall edema. She also has air under the diaphragm. Bowel loops are dilated with air fluid levels. Diagnosis: Pneumoperitoneum.
Figure 32.34C: Subcutaneous emphysema of face and chest wall
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Section XI n Special Topics
Key Points IP : 196.52.84.10
Figure 32.34D
Your Observations
1. Subcutaneous emphysema in chest wall. 2. Pneumomediastinum. 3. Air under diaphragm. 4. Perinephric air.
ü
1. Clinical background should be taken into consideration, before interpreting X-rays. 2. Stepwise evaluation is mandatory to avoid missing subtle findings. 3. Scan the X-ray from periphery to center and from less obvious to obvious radiological finding. 4. Familiarity with normal X-ray films will aid in recognizing abnormalities. 5. If clinical background and X-ray findings grossly disagree, repeat the film to avoid simple errors leading to serious consequences.
common errors
û
1. Pneumothorax is one of the most serious conditions that could be missed in a X-ray film in a rapidly deteriorating child. In a rapidly deteriorating child if a CXR has been taken recently, it is wise to give a closer look for pneumothorax. Change in the contour of diaphragm may be a clue. Avoid mistaking a skin fold or emphysematous change in the lung as pneumothorax. 2. Missing findings such as pneumoperitoneum in a child with suspected air leak. 3. Whenever endotracheal tube depth is assessed, consider the neck position also. A flexed neck will push the tube deeper and extended neck will pull out higher. 4. Failing to identify features of pericardial effusion in a child presenting with cardiomegaly. Remember pericardiocentesis is life saving. 5. Missing basic data such as name, date, time and side mark may lead to disastrous outcome, if wrongly judged.
IP : 196.52.84.10 Procedural Sedation and Management of Pain in Children
33
Figure 33.1: Pain management in children helps in smooth performance of procedures
Learning Objectives 1. Defining procedural sedation. 2. Steps taken to administer sedation for procedures in the ED.
3. Pearls and pitfalls in the use of sedative and analgesic drugs. 4. Discharge criteria.
Introduction
Procedural sedation
Sedation reduces anxiety and minimizes pain and discomfort.1,2 The availability of safer drugs with precise, short duration of action, a clear knowledge of adverse events and improved non-invasive monitoring have made procedural sedation a safe and valuable tool in the management of painful and anxiety provoking procedures.3
Procedural sedation (conscious sedation) is the technique of administering sedatives or dissociative agents with or without analgesics, to induce a state or a level of consciousness that allows the child to tolerate procedures, while being able to maintain cardiorespiratory function and airway without assistance.2 Procedural sedation is also essential for the comfort of children and improves their overall experience during the procedure.4 A list of procedures requiring sedation is provided in Table 33.1. Also refer Figures 33.1 and 33.2.
Steps of Procedural Sedation Step 1: Presedation Assessment History Figure 33.2: Wong-Baker faces pain scale (WPFPS) and faces pain scale-revised (FPSR).
1. Obtain history on the present health status, associated comorbid conditions, weight, allergies, prior medical
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Section XI n Special Topics
Table 33.1: Procedures requiring sedation Painful procedures Laceration repair
Imaging
IP : 196.52.84.10 Magnetic resonance imaging (MRI)
Miscellaneous Electroencephalography (EEG)
Vascular access (central line placements)
Nuclear scans (e.g. bone scans)
Audiology (brainstem evoked response studies)
Fracture reduction
Computerized tomography (CT) scans with contrast
Biopsy
Chest tube placement
Fluoroscopy (e.g. nasogastric tube placement)
Foreign body removal
Lumbar puncture (chemotherapy) Bone marrow aspiration
history, pertinent past anesthesia/sedation experience, current medications and last meal/drink. 2. Categorize risk based on the guidelines of the American Society of Anesthesiologists (ASA) 5,6 (Table 33.2). 3. Call for help from anesthetists for class III/IV. Procedural sedation by non-anesthesiologists may be risky in class III/IV.
Ù
The Mallampati classification can be performed only in the older child who can cooperate and open his/her mouth when requested.
Table 33.2: American Association of Anesthesiologists (ASA) classification Class
Description
I
No underlying problems
II
Mild systemic illness
III
Severe systemic illness
IV
Severe illness that is a constant threat to life
V
Patient unlikely to survive beyond 24 hour
(Courtesy: American Society of Anesthesiologists)
Physical examination Airway assessment includes:
1. Neck mobility and length. 2. Ability to open mouth widely. 3. Size of oral cavity. 4. Anatomical jaw abnormalities (e.g. Pierre-Robin syndrome, macroglossia). 5. Ability to protrude the jaw. 6. Keep mouth wide open and evaluate the airway for ease of assisted ventilation.
Mallampati classification is useful in predicting difficult airways (class III/IV). It is based on whether the posterior pharynx can be visualized well or not (Figure 33.3).
Figure 33.3: Mallampati classification Table 33.3: Fasting guidelines Age
Clear liquids
Solids/breast milk
Non-clear fluids
Infants
2 hour
4 hour
6 hour
Children
2–3 hour
6 hour
6 hour
Chapter 33 n Procedural Sedation and Management of Pain in Children
337
Both assisted ventilation and oxygenation can be difficult in children who have difficult airways.
Step 3: Measures Which Ensures Safety During Sedation in the Emergency Room
: 196.52.84.10 Sedation should be IP performed by anesthesiologists and not by other caregivers for the following categories:
Personnel and Equipment
●● Children assigned a category three or above by ASA classification. ●● Very young infants (less than 6 month). ●● Children with airway abnormalities.
Step 2: Presedation Preparation Fasting The nil per oral (NPO) guidelines have been recommended by the ASA to prevent aspiration in the event of loss of protective airway reflexes (Table 33.3). Table 33.4: University of Michigan Sedation Scale (UMSS) Score
Level of sedation
0
Awake and alert
I
Minimally sedated: Tired/sleepy, appropriate response to verbal conversation and/or sound
II
Moderately sedated: Somnolent/sleeping, easily aroused with light touch or a simple verbal command
III
Deeply sedated: Deep sleep, arousable only with significant physical stimulation
IV
Unarousable
1. Avoid solids for 6 hours and clear fluids for 2 hours in healthy patients undergoing elective surgery. 2. Carbohydrate containing fluids may safely be given, up to 2 hours prior to sedation for malnourished children with poor glycogen reserves.8 Studies have noted that more than a third of children who underwent sedation, fasted less than 4 hour, for solids, but still had no higher incidence of adverse effects or aspiration.9 The incidence of adverse events had not significantly increased when fasting guidelines were not observed.10 Prolonged fasting (6 hour, instead of 2 hours for liquids) offered no additional benefit and did not reduce risk.11,12 An urgent procedure may override NPO guidelines for sedation provided, the airway is protected. Factors such as gastroesophageal reflux, young infants (< 6 month), severe systemic illness and developmental delay may increase risk of aspiration.
1. The physician who is administering procedural sedation should be trained in the use of anesthetic drugs. He/she should be aware of the nature of drugs, adverse events, timing, etc. of the sedative agents. 2. The physician must have expertise in recognition (e.g. chest wall rigidity) and management of adverse events during sedation. He/she should also have skills in managing the airway. 3. A nurse or physician (not performing the procedure) should be present throughout sedation to observe the child for adverse events until return to baseline status. 4. Lighting, oxygen source, suction apparatus and airway equipment (nasal cannulas, nasal/oral airways, bag/mask devices, laryngoscope blades, endotracheal tubes) must be available. 5. The heart rate, blood pressure, pulse oximeter and preferably capnography to monitor nasal end tidal carbon dioxide should be connected to patient throughout the procedure. 6. Emergency resuscitation drugs (e.g. epinephrine), isotonic intravenous fluids (normal saline) and reversal agents (naloxone, flumazenil) should also be readily available. Monitoring 1. All children undergoing procedural sedation should be closely monitored till they return to baseline alertness and level of functioning according to established guidelines.13 2. Monitoring should include frequent blood pressure, heart rate and respiratory rate measurements along with continuous pulse oximetry. 3. The monitoring personnel should have complete access and non-obstructed views of the child undergoing sedation. 4. Pulse oximetry is useful in detecting hypoxia, but its accuracy may be impeded by movement, decreased circulation, temperature changes, etc. Since pulse oximeters do not detect very low saturations (less than 75%), it may not be useful in children with cyanotic heart disease. During respiratory depression, pulse oximetry may initially be normal, especially in healthy adolescents as the respiratory reserve may be adequate to meet the oxygen demands. Hypoventila-
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Section XI n Special Topics
tion often precedes hypoxia in children undergoing procedural sedation. 5. Respiratory depression may be recognized by capnogIP : 196.52.84.10 raphy earlier than pulse oximetry.14,15 Capnography has also been noted to be superior to clinical observation in the detection of hypoventilation.16 6. Supplemental oxygen in the absence of oxygen requirement can be deleterious as it may prevent the early detection of respiratory depression.17,18 Therefore, routine supplemental oxygen is not recommended. 7. The depth of sedation could be assessed using several sedation scales (Ramsay sedation scale, University of Michigan sedation scale) and the severity of pain from pain scales depending on age (Table 33.4).19 8. Repeated assessment of sedation scores have been found to be beneficial in reducing risks associated with sedation.11
Step 4: Choice of Drugs Description of sedatives/analgesics A host of factors influence the decision making in drug selection during procedural sedation. The choice of drugs is dependent upon: 1. Age. 2. Type of procedure (painful vs painless, short vs long).
Table 33.5: Specific indications for sedatives/analgesics Indication
Sedative/analgesic
Non-invasive painless procedures (imaging, EEG)
Chloral hydrate, midazolam, pentobarbital, thiopental, propofol
Ultra short painful procedures (lumbar puncture, chest tube insertion)
Morphine*, fentanyl
Brief procedures (laceration repair, fracture reduction, central venous line placement)
Ketamine*, fentanyl
Dental procedures
Nitrous oxide
*Drugs often administered in combination with sedatives (e.g. midazolam)
3. Prior sedative experience of the child. 4. Required depth of sedation (Is there a need to be absolutely still?). 5. Specific risk factors (ketamine contraindicated in head trauma). 6. Experience and familiarity of the sedation provider with the various drug options. Considerable differences may exist between individual responses to various sedatives and the drug doses should be titrated to effect. 1. Painless procedures that do not require intravenous access, oral or intranasal routes may be utilized for anxiolysis. 2. The specific indications for the various sedatives and the doses and in which these drugs are recommend-
Table 33.6: Sedatives and analgesics—pharmacodynamics Drug
Dose
Route
Onset
1–2 mg/kg IV* 4–6 mg/kg IM‡ 10 mg/kg PO
PO† IV IM
1 minute
15–30 minute ( IV)
Midazolam
0.05–0.1 mg/kg IV 0.5 mg/kg PO ( max 20 mg) 0.2 mg/kg IN( max 5 mg)
IV PO IN§
1 minute
30–60 minute
Pentobarbital
2 mg/kg ( total 6 mg/kg)
IV
3-5 minute
30–60 minute
Propofol
1.5–3 mg/kg
IV
< 1 minute
5–10 minute
Etomidate
0.3 mg/kg
IV
Fentanyl
1–2 µg/kg (max 100 µg)
IV
rapid
30 minute
Morphine
0.1 mg/kg
Chloral hydrate
30–100 mg/kg
PO
25 minute
8–12 hour, up to 24 hour
Naloxone
0.1 mg/kg
IV
1 minute
1 hour
IV, SC
2–3 hour half-life
||
IV, Intravenous route; PO, Oral route; IM, Intramuscular route; §IN, intranasal route; SC, subcutaneous route.
*
Duration
Ketamine
†
‡
||
Chapter 33 n Procedural Sedation and Management of Pain in Children
ed have been highlighted (Tables 33.4 to 33.6). The doses have been adopted the consensus guidelines on sedation and analgesia critically ill children.20 IP : in 196.52.84.10
Chloral Hydrate: 30–100 mg/kg/dose (max dose 2 g).
Midazolam Even though all benzodiazepines are useful, diazepam and lorazepam are longer acting than midazolam (preferred benzodiazepine for procedural sedation).
Sedatives Chloral Hydrate Chloral hydrate (active ingredient trichloroethanol) can be given both orally and rectally. It is rapidly absorbed from gastrointestinal tract (almost 100%). Its sedative effect which occurs within 25 minutes, lasts for 8–12 hours. Chloral hydrate can cause myocardial depression and arrhythmias (Table 33.7). Table 33.7: Adverse events of sedatives Sedative
339
Adverse event
Chloral hydrate
Myocardial/respiratory depression (can be delayed)
Ketamine
Apnea, delirium, increased secretions, laryngospasm, increased IOP/ICP
Midazolam
Paradoxical excitement, hypotension, bradycardia, respiratory depression
Pentobarbital
Respiratory depression, apnea and hypotension with rapid administration
Morphine
Respiratory depression, vomiting
Fentanyl
Hypotension, bradycardia, respiratory depression, rarely chest wall rigidity
Etomidate
Local pain on injection, thrombophlebitis, myoclonus
Propofol
Bradycardia, hypotension, dosedependent respiratory depression and apnea
Avoid chloral hydrate in children who are on tri cyclic antidepressants and phenothiazines (The combination has been noted to have a greater predisposition to ventricular dysrhythmias). Higher doses may result in respiratory depression or airway obstruction, which could be fatal.21
Midazolam acts through GABA and produces hypnosis and anxiolysis. The advantages of midazolam include its short duration and the convenience of administration by additional routes. It can be repeated IV every 3 minutes. It has a rapid onset of action, with duration of action up to 30–60 minutes. Intranasal or sublingual midazolam is usually given at a higher dose (0.2–0.4 mg/kg). Midazolam produces anxiolysis in 15–20 minutes orally and 5–10 minutes intranasally. Midazolam is unpleasant orally and causes burning sensation when given via nose (preservative—benzyl alcohol). The side effects include paradoxical excitement, hypotension or bradycardia, respiratory depression or apnea. Even though midazolam alone produces sufficient anxiolysis, other sedatives such as pentobarbital (imaging studies) or ketamine (fracture reduction, laceration repair) are usually given in addition. Intravenous midazolam in conjunction with ketamine is the most common combination regimen utilized in the United States for procedural sedation. Midazolam provides no analgesia. Even though combination regimens are used frequently and have been found to be safe, additional sedatives (e.g. narcotics) may increase the likelihood of respiratory depression/apnea. Midazolam: 0.01–0.1 mg/kg IV (max dose 3 mg/dose).
Barbiturates Thiopental Thiopental has a short duration of action (5–10 minutes).
It is still widely used and could be dangerous owing to its long half-life and side effects occurring beyond the period of observation.
Thiopental should not be given in volume depleted children. It can cause hypotension due to vasodilata tion and negative inotropic effects on the heart.
When children are discharged after chloral hydrate, parents should be advised to watch for possible delayed side effects, including respiratory depression.
Rectal administration is effective, but the prolonged duration of action (up to 90 minutes) limits its use. Thiopental: 25–50 mg/kg IV.
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Pentobarbital Pentobarbital is a rapidly acting barbiturate with an onset IP : 196.52.84.10 of action within 3–5 minutes and duration of action of 30– 60 minutes. It is widely used for imaging studies (e.g. MRI) since it provides prolonged sedation with sufficient depth to allow the child to remain still for an extended period of time.
Ù
Major side effects include respiratory depression and hypotension. Pentobarbital: 2 mg/kg IV, (max 6 mg/kg).
Ketamine The rapid onset (1 minute), short duration of action, (15–30 minutes), the predictable excellent analgesia and sedation and the ability to be administered through multiple routes have made ketamine the most popular drug for painful procedures. Ketamine produces ‘dissociative sedation,’ a cataleptic state characterized by significant analgesia and amnesia. It is postulated to act on the thalamic/limbic systems in mechanisms not clearly understood. Ketamine offers an ‘all or none phenomena’ in terms of sedation and does not have a dose related escalating effect. As an effective bronchodilator, it is safe and indicated in asthmatic children. Side effects include apnea if used in infants less than 3 months, increased secretions, laryngospasm, transient nystagmus, hallucinations during recovery and seizures in children at risk. Unlike other sedatives, ketamine may increase heart rate and blood pressure due to its effect on the sympathetic nervous system. Avoid ketamine when raised intracranial or intraocu lar pressure is suspected. Ketamine: 1–2 mg/kg IV.
Propofol Propofol, a GABA agonist, is a sedative and hypnotic. It is rapidly effective and has an ultrashort duration of action (5–10 minutes). It has antiemetic and antiepileptic properties. Since propofol can decrease intracranial pressure (ICP) and cerebral metabolic rate, it is used in head trauma and in children with seizures.
Ù
Side effects include bradycardia, hypotension, dosedependent respiratory depression and apnea. Pro longed use of propofol for more than 48 hours has been associated with metabolic acidosis. It is useful in ultra short painless procedures (e.g. spinal tap). Propofol is usually given with a narcotic for painful procedures. Even though it is gaining popularity, its use is restricted to anesthesiologists in many medical facilities due to its cardiovascular side effects. Propofol: 1.5–3 mg/kg IV bolus followed by 50–100 μg/kg maintenance.
Etomidate Etomidate acts by altering chloride conductance on the GABA receptors. It can be administered intravenously and is available as a mixture with propyl glycol. It is rapid in onset and produces excellent sedation and amnesia. Etomidate is very safe with an excellent cardiovascular profile.
Ù
Side effects include pain at site, thrombophlebitis and myoclonus. Suppression of endogenous steroid production has been noted with its use. Etomidate: 0.3 mg/kg IV.
Management of Pain Pain in children is often overlooked and frequently undertreated. Adequate management of pain will improve compliance of children, enhance the quality of outcome of the procedure performed and improve parental satisfaction. Opioids are the mainstay in the management of severe pain in the emergency room. When dosed correctly with the understanding of duration, side effects and interactions with other sedatives, they can be safe and effective in the treatment of pain.
Morphine Morphine is the most commonly used narcotic due to its quick onset, predictable duration and adequate safety profile. Its half-life is 2–3 hours. In children < 3 months, morphine may not be cleared quickly as the neonatal liver
Chapter 33 n Procedural Sedation and Management of Pain in Children
341
is immature to permit effective glucuronidation, the main pathway of morphine metabolism. Hence, repeat doses of morphine have to be administered with caution in infants IP : 196.52.84.10 and in those with liver disease.
as they can cause severe withdrawal syndrome or increased seizure threshold.
Morphine: 0.1 mg/kg IV.
Naloxone is an opioid antagonist neutralizing all the analgesic, sedative and side effects of narcotics by binding to the μ receptor. The onset is within 1 minute and it has a half-life of 1 hour though the duration may be prolonged in infants. Due to its low affinity, repeat doses may be required to reverse the side effects of long acting narcotics (e.g. meperidine) and in overdose situations. In young infants born to narcotic addicted mothers and in chronic overdose situations, naloxone can precipitate withdrawal symptoms.
Fentanyl Fentanyl, a morphine analogue, is a pure analgesic and offers no sedation. It is rapid in onset and short in duration (30 minutes). Fentanyl is very effective (potency—100 × morphine) and is indicated in painful orthopedic procedures. Side effects of fentanyl include hypotension, bradycardia and respiratory depression. Watch for chest wall rigidity, a unique life-threatening side effect of fentanyl associated with rapid administration. Chest wall rigidity will require immediate reversal with the antidote, naloxone and if required, paralysis with succinyl choline. Caution should be exercised in calculating the amount of fentanyl to be given due to the high concentration in solution (available as a 50 μg/mL solution). Newer preparations such as remifentanyl are ultra short with recovery within 5–20 minutes. Fentanyl: 1–2 μg/kg IV.
Mepiridine (Demerol) Even though it is an effective narcotic and offers pain control lasting up to 4 hour, it is falling out of favor due to the increased incidence of CNS side effects (tremors, seizures) due to its metabolite, normeperidine, which can accumulate after repeated doses. Anticonvulsants can also increase the production of normeperidine resulting in increased seizure activity.
Sucrose Oral sucrose is easy to administer and effective in pain control in neonates during painful short procedures (vaccinations, lumbar punctures). Sucrose mediates release of endogeneous opiates resulting in alleviation of pain.22
Reversal Agents Reversal agents should always be available in the event of serious cardiovascular or respiratory adverse event which does not improve immediately with simple supportive measures (supplemental oxygen, assisted ventilations). However, administering reversal agents is not without risk
Naloxone
Naloxone: 0.1 mg/kg.
Flumazenil Flumazenil is a benzodiazepine antagonist and is used when cardiovascular and respiratory depression occurs with toxic dose of benzodiazepines. Even though it fully reverses benzodiazepine-induced sedation, its effect on respiratory depression is not as pronounced. Hence, assisted respirations and supplemental oxygen are necessary for successful recovery from sedation-induced respiratory depression. It is contraindicated in children on long term benzodiazepines as it may increase the likelihood of seizures. Adverse events include agitation, headache and dizziness. Flumazenil: 5 µg/kg every 1 minute to max of 40 µg/kg (adult 2 mg), then 2–10 µg/kg/h IV.
Management of Adverse Events The incidence of serious adverse events is low if procedural sedation is performed by well trained personnel.23,24 Lack of knowledge of the onset and duration of action, inadequate monitoring and discharging children when criteria for discharge are not met can contribute to an increased frequency of adverse events in sedation.25 ●● Sedation drugs, should be used only by physicians trained in its use. Combinations of sedatives and narcotics can increase the incidence of respiratory depression. Studies have noted that adverse events were higher when more than three drugs were utilized for sedation.26
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●● Use only one appropriate drug. ●● Respiratory depression is the most common adverse event apart from failed inadequate sedation.27 IP :or196.52.84.10 ●● Respiratory depression during sedation is often a result of hypercarbia, hypoventilation or obstruction of the airway. ●● Open the airway with head tilt-chin lift maneuver and provide supplemental oxygen. ●● Assisted ventilation may be needed. ●● If respiratory depression is protracted, not responding to simple measures or cardiac irregularities are noted, naloxone is warranted for a child receiving narcotics. ●● Bradycardia during sedation occurs secondary to respiratory depression. It improves with assisted ventilation and oxygenation. ●● More adverse events were noted, when benzodiazepines were used for sedation in children at high risk (ASA classification III, IV).28 Sedation was associated with more adverse events when benzodiazepines alone were used for sedation and in those considered high risk by ASA classification.28 The incidence of respiratory depression/apnea has been reported to be up to 20%–29% of patients receiving procedural sedation even though large studies in children’s hospitals have lower rates of 3%– 4%.23,28 The specific common adverse events of the sedatives and analgesics are listed in Table 33.7.
Discharge Criteria Once the procedure is complete, monitor the child until the child becomes awake and returns to baseline mental status. Most complications have been noted in the initial 5 minutes (induction phase) after administration of intravenous sedatives. All serious complications were noted in the first 30 minutes of sedation.29 It is important to note that painful procedures such as fracture reduction may obscure the potential depth of sedation due to the pain associated with the procedure. Hence, respiratory depression may manifest after a painful procedure, well beyond the induction phase. If the child has symptoms such as vomiting or emergence reactions, the child should be observed for a longer period of time. The criteria for discharge as recommended by the American Academy of Pediatrics (AAP) are provided in Box 33.1.
The parents should be informed about delayed adverse effects, such as chloral hydrate. They should be provided contact telephone numbers, if the need arise. Box 33.1: Discharge criteria Stable cardiorespiratory function Patient is easily arousable and protective reflexes are intact Patient can talk or verbalize (age-appropriate verbal response) Child can sit up unaided (if appropriate for age and development) Level of responsiveness is close to baseline Child is adequately hydrated
Key Points
ü
1. Children should not be exposed to pain during elective procedures in the ED. 2. The health care provider must be well versed in recognizing and managing respiratory depression during administration of sedative drugs. 3. Two trained health care providers must be available. One to perform the procedure and the second to monitor and resuscitate.
common errors
û
1. Failure to provide adequate pain relief during procedures such as lumbar puncture, bone marrow aspiration, thoracostomy, etc. 2. Administration of sedation without adequate analgesia. 3. Lack of awareness of potential side effects. 4. Premature discharge without ruling out whether the child has recovered.
REFERENCES 1. Dresser S. The effectiveness of conscious sedation on anxiety, pain and procedural complications in young children. Pediatric Nursing. 2003;29:320-23. 2. Krauss B, Green SM. Procedural sedation and analgesia in children. In: Lancet: Lancet; 2006. pp. 766-80. 3. Green SM. Research advances in procedural sedation and analgesia. Ann Emerg Med. 2007;49:31-36. 4. Claar RL, Simons LE, Logan DE. Parental response to children’s pain: The moderating impact of children’s emotional distress on symptoms and disability. In: Pain (03043959); 2008. pp. 172-79.
Chapter 33 n Procedural Sedation and Management of Pain in Children
5. Burgoyne LL, Smeltzer MP, Pereiras LA, et al. How well do pediatric anesthesiologists agree when assigning ASA physical status classifications to their patients? In: Pediatric AnesIP : 196.52.84.10 thesia Blackwell Publishing Limited; 2007. pp. 956-62. 6. Ragheb J, Malviya S, Burke C, et al. An assessment of interrater reliability of the ASA physical status classification in pediatric surgical patients. In: Pediatric Anesthesia: Blackwell Publishing Limited; 2006. pp. 928-31. 7. Rosenstock C, Gillesberg I, Gatke MR, et al. Inter-observer agreement of tests used for prediction of difficult laryngoscopy/tracheal intubation. In: Acta Anaesthesiologica Scandinavica: Blackwell Publishing Limited; 2005. pp. 1057-062. 8. Sareide E, Eriksson LI, Hirlekar G, et al. Pre-operative fasting guidelines: an update. In: Acta Anaesthesiologica Scandinavica: Blackwell Publishing Limited; 2005. pp. 1041-047. 9. Roback MG, Bajaj L, Wathen JE, et al. Preprocedural fasting and adverse events in procedural sedation and analgesia in a pediatric emergency department: are they related? Ann Emerg Med. 2004;44:454-59. 10. Bell A, Treston G, McNabb C, et al. Profiling adverse respiratory events and vomiting when using propofol for emergency department procedural sedation. Emergency Medicine Australasia. 2007;19:405-10. 11. Hoffman GM, Nowakowski R, Troshynski TJ, et al. Risk reduction in pediatric procedural sedation by application of an American Academy of Pediatrics/American Society of Anesthesiologists Process Model. Pediatrics;109 2002:236-43. 12. Treston G. Prolonged pre-procedure fasting time is unnecessary when using titrated intravenous ketamine for paediatric procedural sedation. In: Emergency Medicine Australasia: Blackwell Publishing Limited; 2004 pp.145-50. 13. Cote CJ, Wilson S, Work Group on S. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: an update. Pediatrics. 2006;118:2587-602. 14. Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med. 2002;9:275-80. 15. Lightdale JR, Goldmann DA, Feldman HA, et al. Microstream capnography improves patient monitoring during moderate sedation: a randomized, controlled trial. Pediatrics. 2006;117:1170-178. 16. Burton JH, Harrah JD, Germann CA, et al. Does end-tidal carbon dioxide monitoring detect respiratory events prior
17.
18. 19. 20. 21. 22. 23.
24.
25. 26. 27.
28. 29.
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to current sedation monitoring practices? Acad Emerg Med. 2006;13:500-04. Keidan I, Gravenstein D, Berkenstadt H, et al. Supplemental oxygen compromises the use of pulse oximetry for detection of apnea and hypoventilation during sedation in simulated pediatric patients. Pediatrics 2008;122:293-98. Fu ES, Downs JB, Schweiger JW, et al. Supplemental oxygen impairs detection of hypoventilation by pulse oximetry. Chest 2004;126:1552-558. Crellin D, Sullivan TP, Babl FE, et al. Analysis of the validation of existing behavioral pain and distress scales for use in the procedural setting. Pediatric Anesthesia. 2007;720-33. Playfor S, Jenkins I, Boyles C, et al. Consensus guidelines on sedation and analgesia in critically ill children. Intensive Care Medicine.2006;32:1125-136. Cohen Mr. Chloral Hydrate Overdoses Implicated In Deaths. Nursing. 1993;23:25. Gibbins S, Stevens B. Mechanisms of sucrose and non-nutritive sucking in procedural pain management in infants. Pain Res Manag. 2001;6:21-28. Cravero JP, Blike GT, Beach M, et al. Incidence and nature of adverse events during pediatric sedation/anesthesia for procedures outside the operating room: report from the Pediatric Sedation Research Consortium. Pediatrics; 2006;118:1087-096. Meyer S, Grundmann U, Gottschling S, et al. Sedation and analgesia for brief diagnostic and therapeutic procedures in children. European Journal of Pediatrics: 2007;166:291-302. Cote CJ, Notterman DA, Karl HW, et al. Adverse sedation events in pediatrics: a critical incident analysis of Contributing factors. Pediatrics. 2000;105:805. Cote CJ, Karl HW, Notterman DA, et al. Adverse sedation events in pediatrics: analysis of medications used for sedation. Pediatrics. 2000;106:633-44. Pitetti RD, Singh S, Pierce MC. Safe and efficacious use of procedural sedation and analgesia by nonanesthesiologists in a pediatric emergency department. Arch Pediatr Adolesc Med. 2003;157:1090-096. Malviya S, Voepel-Lewis T, Eldevik OP, et al. Sedation and general anaesthesia in children undergoing MRI and CT: adverse events and outcomes. Br J Anaesth. 2000;84:743-48. Newman DH, Azer MM, Pitetti RD, et al. When is a patient safe for discharge after procedural sedation? The timing of adverse effect events in 1367 pediatric procedural sedations. Ann Emerg Med. 2003;42:627-35.
34
IP : 196.52.84.10
Diabetic Ketoacidosis
Figure 34.1: Protocolised approach and intensive monitoring of children with diabetes improve their quality of life.
Learning Objectives 1. Pathophysiology of DKA.
Introduction Diabetic ketoacidosis (DKA) a biochemical triad of hyperglycemia, ketonemia and acidemia is characterized by metabolic acidosis (pH < 7.3), plasma bicarbonate < 15 mEq/L, plasma glucose > 200 mg% and urine ketostix reaction 2+ or plasma ketostix > 1+.1 Refer Figure 34.1.
Pathophysiology Insulin deficiency, leads to increased secretion of counter-regulatory hormones (CRH). The imbalance causes alterations in the metabolism of fat, protein and carbohydrate (Figure 34.2). Lipolysis increases and leads to elevated circulating levels of free fatty acids (FFA). The latter is esterified to triglycerides and oxidized to ketone bodies in the liver resulting in a wide anion gap acidosis.
2. Use of the rapid cardiopulmonary cerebral assessment and the pediatric assessment triangle to implement the ISPAD guidelines. Excess CRH coupled with insulinopenia also stimulates hepatic gluconeogenesis, hepatic and skeletal muscle glycogenolysis and decreased peripheral utilization of glucose, culminating in severe hyperglycemia. The latter causes osmotic diuresis, polydipsia and polyuria. Dehydration and electrolyte loss ensues, which in course of time causes impaired renal perfusion. Renal glucose clearance is reduced, further exacerbating hyperglycemia. Thus a vicious cycle occurs wherein, hyperglycemia begets hyperglycemia. Osmotic diuresis leads to loss of sodium, potassium and magnesium. Sodium loss is aggravated by insulin deficiency and glucagon excess. The dilutional hyponatremia (low measured serum sodium) is caused by the osmotic shift of intracellular water to the extracellular compartment due to hyperglycemia. A rise in blood glucose of 100 mg/dL leads to a fall of 1.6 mEq/L of serum sodium.2
Chapter 34 n Diabetic Ketoacidosis
345
IP : 196.52.84.10
Figure 34.2: Flow chart showing the pathogenesis of DKA
Ù Serum Sodium Correction Add 1.6 mEq sodium for each 100 mg plasma glucose > 100 mg/dL to the measured serum sodium value. Corrected Na = Measured Na + 1.6 [(glucose – 100)/100]
Increased production of ketoanions exceed the capacity of existing buffer ions (HCO3–) to maintain physiologic pH. As a result DKA is characterized by metabolic acidosis.
Ù Retention of ketoanions after buffering is the cause for the increased anion gap acidosis.
The kaliuresis, which occurs in DKA is due to osmotic diuresis secondary to hyperaldosteronism caused by sodium depletion and the presence of negatively charged ketoanions in tubular fluid.
Hyperglycemia and ketoanions enhance the glomerular filtration rate. Progressive volume depletion decreases GFR, leading to worsening hyperglycemia and ketonemia.
Despite these losses, plasma potassium concentrations are typically normal or elevated at the time of diagnosis of DKA. This is a result of the shift of K+ from intracellular to extracellular compartment secondary to acidosis, hyperosmolarity, insulinopenia and intracellular lysis of proteins.
Simple rehydration itself can improve hyperglycemia, ketosis and anion gap acidosis.
Ù Normal or low serum potassium during initial evaluation should alert the clinician towards severely depleted total potassium stores.
Ù Signs and Symptoms DKA can be easily missed in a child presenting with new onset diabetes.3
Ù
To avoid missing DKA in the ED, routinely perform dextrostix in every critically ill child.
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Clinical signs and symptoms of DKA do not correlate with the severity of acidosis and dehydration. Classic signs and symptoms of DKAIP include: : 196.52.84.10 ●● Hyperglycemia: Polyuria, polydipsia, nocturia. ●● Acidosis: Hyperventilation, abdominal pain. ●● Abdominal pain mimicking an acute abdomen has been described in approximately 46% of patients with DKA. This symptom has been attributed to dehydration of muscle tissue, delayed gastric emptying and ileus secondary to acidosis.4 ●● Dehydration. ●● A fruity odor of the breath, akin to the odor of nail varnish remover is a clinical clue in a previously undiagnosed patient presenting with acidosis and dehydration. ●● Hypotension is a late finding in DKA, often associated with sepsis. ●● Fever is rare, though when present is usually indicative of underlying infection.
Ù Differential diagnosis of DKA include gastroenteritis with dehydration and hypovolemic shock, stress-induced hyperglycemia, bronchiolitis, asthma, pneumonia, meningitis, UTI and an acute ‘surgical abdomen’.
DKA can be classified as mild, moderate or severe based on the degree of acidosis. Table 34.1. Table 34.1: Classification of DKA Venous pH
Ù Mixed acid base abnormalities in DKA offer a clue to coexistent problems, e.g. respiratory alkalosis is suggestive of sepsis.
Management Therapeutic goals of the specific management of DKA include:
Classification of DKA
DKA
●● Measured hyponatremia is common in DKA. Normal or high measured sodium in face of severe hyperglycemia indicates hyperosmolarity and dehydration. ●● Leukocytosis with a shift to the left is often seen in DKA. This may not be due to infection, but warrants work-up if it fails to normalize after rehydration. ●● Majority of patients present with blood glucose level greater than 300 mg/dL. Patients who have received insulin before presentation may have reduced levels. ●● The diagnosis of DKA may be confounded by the coexistence of other acid base disturbances. Persistent vomiting and severe hypovolemia can sometimes give rise to metabolic alkalosis (Diabetic alkalosis).
Serum bicarbonate
Mild
< 7.3
< 15 mEq/L
Moderate
< 7.2
< 10 mEq/L
Severe
< 7.1
< 5 mEq/L
1. Correction of fluid and electrolyte deficits: Fluid therapy. 2. Decrement of blood glucose and the ongoing osmotic diuresis: Hydration and insulin therapy. 3. Halting of ketoacid production: Insulin therapy. 4. Assessment and treatment of precipitating cause (e.g. infection). 5. Close monitoring for complications (e.g. cerebral edema).
Laboratory Evaluation
Fluid Therapy
In addition to hyperglycemia, metabolic acidosis, ketonemia, ketonuria and an elevated anion gap, leukocytosis, hyponatremia, hypophosphatemia and hyperosmolarity may also be identified.
Volume depletion triggers release of CRH, which then activates the renin-angiotensin-aldosterone axis. The hormones, whose combined actions are directed towards preserving intravascular volume, also cause insulin resistance.
Elevation of ketone bodies is diagnostic of DKA. The sodium nitroprusside test, which identifies acetoacetate and acetone, does not recognize beta hydroxybutyrate making this a poor test for estimation of severity of ketonemia.
Fluid therapy, hence, results in significant improvement of hyperglycemia, hypertonicity and acidemia. Euvolemia or hydration, causes a decline in the counterregulatory hormones, enhances renal glucose clearance (following improved renal perfusion) and improves sensitivity to insulin.
Ù
Chapter 34 n Diabetic Ketoacidosis
Ù Hydration alone hasIPbeen shown to reduce glucose : 196.52.84.10 concentration by 25–50 mg/h in the first 1 hour. Fluid therapy though very important in DKA management, large volumes over short period of time has been found to be a probable factor in the development of overt cerebral edema.
CASE SCENARIO 1 (Figures 34.3 to 34.7) 8-year-old child presents with progressive lethargy and breathlessness. He has been having increased thirst and has been voiding urine excessively over the past 2 days.
347
Ù
Repeat fluids based on reassessment. Do not exceed 30 mL/kg.5 Rehydration phase begins after shock is corrected. Rehydration fluid: ●● Deficit correction + Maintenance fluids. ●● A standard water deficit of 100 mL/kg (10% dehydration) is assumed if the child presents with shock and a deficit of 85 mL/kg (8.5% dehydration) is assumed if the child presents with only dehydration and no shock. ●● Maintenance fluid. Ongoing losses—urinary losses are usually not replaced. ●● Assuming the patient’s weight as 20 kg in this case scenario, fluids are calculated as follows: Total fluid to be infused in 48 hours. ●● Shock correction: 200 mL (10 mL/kg NS) over 1 hour. ●● Maintenance fluid for 48 hours 1,500 × 2 = 3,000 mL. ●● Deficit: 100 mL/kg = 2,000 mL.
Ù
Figure 34.3 Physiological status: Airway stable, effortless tachypnea, tachycardia, shock with altered mental status.
Ù
Ketonemia itself can cause drying of oral mucosa and peripheral vasoconstriction mimicking dehydration and shock.
Shock: 1–2 Hours ●● Provide oxygen using the non-rebreathing mask. ●● Introduce NGT and decompress stomach. Gastric atony and dilation of the stomach are common in DKA. Nasogastric suction is important to prevent aspiration especially in obtunded patients. ●● Catheterize the bladder if unresponsive or in young infants and children. ●● Initiate 10–20 mL/kg of isotonic saline (0.9%) bolus over 1–2 hour. ●● If hypotensive shock: Administer 20 mL/kg using pull push technique.
Total fluid to be infused in 48 hours (including shock correction). Deficit + maintenance fluid for 48 hours – fluid bolus given for shock correction (during first hour). 3,000 + 2,000 – 200 = 4,800 mL (over 47 hours). ●● Plan to administer 100 mL/h of NS to which 40 mEq/L of potassium chloride is added.
Ù
Due to the inherent risk of cerebral edema, the first 24 hours total fluid intake is restricted to less than 4L/m2/24 h (1.5–2 times the maintenance fluid/day).5 Potassium is added to the maintenance fluid to counter insulin mediated shift of potassium into the intracellular compartment. Ensure that the total fluid is administered over 48 hours. ●● Use an infusion pump to administer fluids. Precision is necessary to ensure accuracy in the rate of fluid administration.
Ù
When blood glucose level falls below 250 mg/dL, change from 0.9 NS to 0.45 NS with 5% dextrose to which 40 mEq/L of KCl is added.
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Section XI n Special Topics
●● Switch to oral hydration as soon as the clinical condition permits, to avoid overhydration.
Ù
IP : 196.52.84.10
Hyperglycemia resolves faster than acidosis. Administration of 10% or 12.5% dextrose is necessary to prevent hypoglycemia during the management of DKA.
Insulin Therapy Insulin reverses proteolysis, lipolysis, suppresses ketone body and ketoacid formation. It also lowers blood glucose, by inhibiting glycogenolysis and gluconeogenesis and stimulates cellular glucose uptake.
Figure 34.5: Withdraw 40 units of plain insulin
Preparation of Insulin Infusion ●● Add 50 units of plain insulin to 50 mL of normal saline, such that each mL will contain 1 unit of insulin. Flush IV tubing thoroughly with 25 mL of this insulin solution to saturate binding sites before administering to the patient. ●● Insulin infusion is initiated at the rate of 0.1 U/kg/h after correction of shock. ●● For example, for a child weighing 10 kg, 0.1 mL/kg/h of this solution (1 mL/h) will deliver 0.1 U/kg/h. ●● Insulin should be delivered in a separate infusion and not mixed with the rehydrating solution.
Figure 34.6: Add insulin to the 50 mL syringe filled with NS
Figure 34.7: Insulin infusion line is primed by flushing. Insulin can adhere to plastic material. Flush out 25 mL of the solution. Initiate at the rate of 0.1mL/kg/h. Figure 34.4: Equipment needed to prepare an insulin infusion.
●● If hyperglycemia or acidosis is not improving within an hour of initiation of infusion, look for markers of sepsis, persistence of hypovolemia and review the dose and rate of insulin infusion. Check IV patency, it is possible that insulin has extravasated.
Ù
Error in insulin preparation is the commonest cause of failure to respond. End point of insulin therapy is resolution of ketoacidosis and not hyperglycemia. ●● Decrease infusion rate to 0.05 U/kg/h as acidosis starts to resolve and blood glucose declines to 250 mg/dL.
Chapter 34 n Diabetic Ketoacidosis
Case scenario 2 (Figures 34.8 to 34.9) 5-year-old girl (weight:15 kg) is brought with a history IP : 196.52.84.10 of polyuria and polydipsia for 15 days. She has been having abdominal pain and several episodes of vomit ing since morning. Her capillary blood glucose is 400 mg/dL and her urine is positive for ketones.
349
●● Initiate insulin therapy 1–2 hours after rehydration at the dose of 0.1 U/kg/h. ●● Change to subcutaneous insulin once acidosis resolves and patient starts to take oral feeds. ●● Continue intravenous insulin for 30 minutes (for rapid acting insulin) and 1 hour (for regular insulin) after the administration of first dose of subcutaneous insulin.
Ù
This overlap is essential, since the half-life of IV insulin is short (5–10 min). An abrupt discontinuation of IV insulin, coupled with a delayed onset of subcutaneous insulin regimen may lead to worsening of DKA.
Case scenario 3 6-year-old girl on treatment for insulin-dependent diabetes mellitus, missed her usual dose. Her routine capillary blood glucose (CBG) shows 510 mg/dL. Urine ketostix is positive (Figure 34.10). Figure 34.8 Physiological status: Moderate DKA with severe dehydration
Fluid therapy: A standard water deficit of 8.5% is assumed (only dehydration, no shock). Fluid is calculated based on this. ●● ●● ●● ●●
No bolus therapy is given. 48 hour maintenance = 1,250 × 2 = 2,500 mL. Deficit = 85 mL/kg = 85 × 15 kg = 1,275 mL. Total fluid to be given in 48 hour = 2,500 + 1,275= 3,775 mL or 79 mL/h.
Figure 34.10 Physiological status: Cardiopulmonary cerebral assessment normal with mild or uncomplicated DKA.
●● Initiate 0.1 U/kg of short acting or rapid acting insulin subcutaneous or IM every 1–2 hourly.5 Though the ISPAD guidelines suggest hourly or 2 hourly SC insulin, most patients in our setting can be managed well with 1 U/kg/day plain insulin given subcutaneously in 3–4 divided doses half an hour before each meal. ●● Oral feeds are given ad lib. Figure 34.9: Severely dehydrated child with DKA
●● Order 0.9 NS with 40 mEq/L of KCl at 79 mL/h for the initial 4–6 hours. ●● Once the blood glucose falls to < 250 mg change to 0.45 NS with 5% dextrose.
Rationale for Potassium Replacement Hydration and insulin therapy induces a rapid decline in plasma potassium during the initial hours due to the intracellular shift.
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Section XI n Special Topics
Serum potassium is a poor indicator of intracellular potassium status. Monitor potassium status indirectly using the ECG monitor. IP : 196.52.84.10
●● Monitor serum calcium during phosphate administration.10
Potassium Administration
●● Cardiopulmonary assessment.
●● Replace potassium only after correction of shock. Do not correct potassium if documented hyperkalemia or renal insufficiency exists. ●● Add 40 mEq/L potassium chloride to the rehydrating fluid. It can be increased up to a maximum of 60 mEq/L based on serum potassium levels and electrocardiogram (ECG). ●● Patients with ECG changes consistent with hypokalemia should receive rapid potassium correction at the rate of 0.3–0.5 mEq/kg/h till the ECG normalizes.6 ●● Use an infusion pump for potassium replacement under close cardiac monitoring.
Rationale for Avoiding Bicarbonate Acidosis can cause negative inotropy, central nervous system (CNS) depression, insulin resistance and hyperkalemia. However, bicarbonate therapy can aggravate hypokalemia, paradoxical CNS acidosis, hypernatremia, rebound alkalosis and hypocalcemia. More recently, bicarbonate therapy has been associated with increased risk of cerebral edema.7-9
Guidelines for Administering Bicarbonate ●● Administer Bicarbonate (1–2 mEq/kg) slowly over 1–2 hours10 if child presents with severe acidosis and impending cardiovascular collapse or imminent arrest.
Phosphate Enhanced urinary excretion of phosphate in DKA, commonly leads to hypophosphatemia.
Guidelines ●● Do not routinely replace phosphate. ●● Replacement is indicated in those with anemia, cardiac dysfunction, respiratory depression or muscle weakness or serum phosphate lower than 1–1.5 mg/dL. ●● Administer one third of calculated phosphate as potassium phosphate.11-13
Monitoring and Posthyperglycemic Care
Ù
Assess level of consciousness and document every 2 hourly. ●● Strict hourly input output chart. ●● SaO2, ECG . ●● Random blood sugar.
Ù
Monitor glucose every hour in the first 6 hours and thereafter every 2–4 hours until the patient is taking oral fluids. ●● Electrolytes. Serum electrolytes should be measured every 2–6 hours with special emphasis on potassium, corrected sodium and bicarbonate. ●● VBG: 4, 6, 8 hourly. Venous pH can be used to monitor acidosis; pH may improve, even when bicarbonate is low. ●● Monitor urea and creatinine every 12 hours. Measurement of blood or urinary ketones is not necessary either during treatment or during the recovery phase. Conversion of β-hydroxybutyrate to acetoacetate increases with improvement in circulatory status and hypoxia, giving rise to a paradoxical increase in ketones and may take 1 week to disappear in the postDKA period. ●● Search for hidden foci of infection. – Empiric broad spectrum antibiotics should be considered in children who appear sick. Sepsis may be a triggering event. – End tidal carbon dioxide measurements or newer home glucose meters with the ability to measure blood β-hydroxybutyrate concentration have been shown to be accurate and may be beneficial in guiding therapy in DKA.14,15 ●● Encourage oral feeding as early as possible, once the ketoacidosis resolves.
Criteria for DKA Resolution ●● Blood glucose < 200 mg/dL. ●● Serum bicarbonate level > 15 mEq/L.
Chapter 34 n Diabetic Ketoacidosis
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●● Venous pH 7.3. ●● Calculated anion gap of 12 mEq/L. Resolution of DKA switch to subcutaneous IPwarrants : 196.52.84.10 insulin therapy.
time to get dissipated. During this period, rapid decrease in extracellular osmolality draws fluid into the intracellular compartment resulting in cerebral edema because of the following causes.
Indication for Change to Subcutaneous Insulin
Iatrogenic Causes of Cerebral Edema
●● ●● ●● ●●
●● ●● ●● ●● ●●
Alert, tolerating oral feeds. Resolution of acidosis. Initiate subcutaneous insulin just before a meal. Continue intravenous insulin for 30 minutes (for rapid acting insulin) and 1 hour (for regular insulin) after the administration of first dose of subcutaneous insulin to prevent rebound hyperglycemia. The dose of subcutaneous plain insulin is 1 U/kg/day in three divided doses administered half an hour prior to meals. Continue for 2–3 days. Once blood glucose levels stabilize around 150–200 mg, initiate insulin in 2 doses using a combination of short acting and intermediate acting insulin. 2/3rd of the total dose is given in the morning of which 2/3rd is intermediate acting insulin (Monotard) and 1/3rd is short acting insulin (Actrapid). Another 1/3rd of the total dose is given in the evening, which again split into 2/3rd intermediate acting insulin (Monotard) and 1/3rd short acting insulin (Actrapid).
For example, for a child weighing 30 kg: ●● Morning: Total dose needed is 20 units: Lente (intermediate acting) 13 and plain (rapid acting) 7. ●● Evening: Total dose needed is 10 units; Lente (intermediate acting) 7 and plain (rapid acting) 3.
Complications in DKA Cerebral Edema15-22 Vasogenic cerebral edema has been noted even before initiation of therapy. It is caused by blood brain barrier endothelial injury due to hypoxia, ischemia, inflammation or metabolic stress. Cytotoxic cerebral edema is caused by brain swelling secondary to hyperosmolar state, which is largely related to therapy. ‘Idiogenic osmoles’ in the brain cells are generated in the face of hypertonic plasma, to guard against intracellular dehydration and shrinkage. These osmoles take
●● Rapid reduction of blood glucose. ●● Vigorous fluid replacement. ●● Failure of corrected sodium to rise with therapy. ●● Bicarbonate use. Recognition of cerebral edema, is based on a high index of clinical suspicion. Characterized by headache, behavioral changes and abrupt neurological deterioration 2–24 hours after starting therapy, it can rapidly progress to death. ●● Impaired sensorium persisting despite improvement in pH and blood glucose levels. ●● Early subtle neurological signs. ●● Fall in Glasgow coma scale (GCS). ●● Perform frequent cardiopulmonary cerebral assessment to detect early signs of cerebral edema.
Management of Cerebral Edema5,23 ●● Avoid rapid fall in glucose. When cerebral edema is suspected, the blood glucose decrements should be gradual in order to avoid aggravation of the osmotic disequilibrium. ●● Intubate for controlled ventilation. ●● Elevate the head end of the bed (avoid elevation if hypotensive). ●● Restrict fluids to two-third maintenance. ●● If not in shock, administer mannitol 0.25–1 g/kg IV over 20 minutes. A repeat dose may be given if no response is noted within 30 minutes to 2 hours. ●● 3% saline may be used at a dose of 5 mL/kg over 30 minutes and can be repeated 8th hourly as needed. ●● Order computed tomography (CT) brain after stabilization to rule out thrombosis and intracranial hemorrhage.
Acute Respiratory Distress Syndrome (ARDS) Non-cardiogenic pulmonary edema is generated by reduction in colloid osmotic pressure in pulmonary capillaries by exclusive crystalloid replacement in DKA. Hypoxemic patients with a widened pulmonary alveolar arterial gradient (PAO2PaO2) should be suspected to have pulmonary edema. ●● Avoid ARDS by judicious fluid replacement. ●● Use colloids to treat hypotension refractory to crystalloid replacement.24
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Hyperchloremic Acidosis A normal anion gap metabolic acidosis resulting from rela: 196.52.84.10 tive anion clearance andIPloss of potential bicarbonate from the tubules, it can also be secondary to excessive infusion of sodium chloride. It can last for up to 24–48 hours and has no adverse clinical effects.25
Steps to Prevent DKA in Diabetic Children Teach parents and children ‘sick day’ management: ●● Do not stop insulin completely. ●● Monitor blood glucose and urine ketones more closely during intercurrent illness. ●● Continue the usual carbohydrate intake. ●● Seek early medical help to avoid precipitating an attack of DKA. Table 34.2 shows the DKA monitoring chart.
ü
Key Points
1. 50% of DKA patients present with new onset diabetes. Hence a high index of suspicion is needed to diagnose DKA.
2. Check sugar with dextrostix in order to identify DKA early in the critically ill child. 3. Fluid therapy should be given evenly over 48 hours. Aggressive fluid correction may lead to cerebral edema. 4. Insulin infusion should be started only after shock correction or at least 1–2 hours of fluid therapy in the patient without shock. 5. Signs of cerebral edema should be closely watched for and managed aggressively if identified to prevent mortality.
common errors
û
1. The insulin dose and insulin infusion should be counter checked by two personnel. 2. Check if the calculated fluid is within 1.5–2 times daily maintenance. 3. Do not exceed 30 mL/kg for shock correction. Give boluses slowly over 1 hour in compensated shock. 4. Stopping insulin infusion before acidosis is fully corrected. 5. If glucose levels fall rapidly and acidosis persists, increase glucose concentration to 10%–12.5% and continue insulin infusion.
Table 34.2: DKA monitoring chart Date and time
HR
RR
BP
Pulses/ perfusion
GCS
Blood sugar
Corrected Na
IVF rate
Insulin rate
Remark/ intervention
Complete initial cardiopulmonary assessment, if no shock, calculate fluid requirements and correct over 48 hour.
Protocol 34.1: PEMC approach: Management of children with DKA
Chapter 34 n Diabetic Ketoacidosis
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References 1. ISPAD Clinical Practice Consensus Guidelines 2009 ComIP : 196.52.84.10 pendium, Diabetic ketoacidosis in children and Adolescents with diabetes. Pediatric Diabetes. 2009:10 (Suppl.12):118-33. 2. Katz MA. Hyperglycemia induced hyponatremia: calculation of expected serum sodium depression. N Engl J Med. 1973;289:843-44. 3. Jayashree M, Singhi S. Diabetic ketoacidosis: Predictors of outcome in a pediatric intensive care unit of a developing country. Pediatr Crit Care Med. 2004;5:427-33. 4. Umpierrez G, Freire AX. Abdominal pain in patients with hyperglycemic crises. J Crit Care. 2002;17:63-67. 5. Global IDF/ISPAD guideline for diabetes in childhood and adolescence, International diabetes federation. 2011. 6. Singhi S, Gautham KS, Lal A. Safety and efficacy of a concentrated potassium chloride solution infusion for rapid correction of hypokalemia. Indian Pediatr. 1994;31:565-70. 7. Allain V, Zeni F, Lafond P, et al. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? Crit Care Med. 1999;27:2690-694. 8. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:264-69. 9. Green SM, Rothrock SG, Ho JD, et al: Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. 1998;31:41-48. 10. Stuart A Weinzimer, Michael F Canarie, Edward Vincent S, et al. Disorders of glucose homeostasis. In: David G. Nicholas. Roger’s Textbook of Pediatric Intensive Care, 4th edition, Lippincott Williams and Wilkins; 2008. pp. 1599-602. 11. Fisher JN, Kitabchi AE. A randomized study of phosphate therapy in the treatment of diabetic ketoacidosis. J Clin Endocrinol Metab. 1983;57:177-70. 12. Wilson HK, Keuer SP, Lea AS, et al. Phosphate therapy in diabetic ketoacidosis. Arch Intern Med. 1982;142:517-20. 13. Keller U, Berger W. Prevention of hypophosphatemia by phosphate infusion during treatment of diabetic ketoaci-
14.
15.
16.
17.
18.
19.
20.
21.
22. 23.
24.
25.
dosis and hyperosmolar coma. Diabetic ketoacidosis and hyperosmolar coma. Diabetes. 1980;29:87-95. Fearon DM,Steele DW. End tidal carbondioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002;9:1373-378. Rewers A, McFann K, Chase HP. Bedside monitoring of blood beta hydroxyl butyrate levels in management of DKA in children. Diab Technol Ther. 2006:8:671-76. Duck SC, Wyatt DT. Factors associated with brain herniation in the treatment of diabetic ketoacidosis. J Pediatr. 1988;113:10-14. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:264-69. Edge JA, Hawkins MM, Winter DL, et al. The risk and outcome of cerebral edema developing during diabetic ketoacidosis. Arch Dis Child. 2001;85:16-22. Arief Al, Kleeman CR. Studies on mechanisms of cerebral edema in diabetic come, effects of hyperglucemia and rapid lowering of plasma glucose in normal rabbits J Clin Invest. 1973;52:571-83. Marcin JP, Glacer N, Barnett P, et al. Factors associated with adverse outcomes in children in diabetic ketoacidosis related cerebral edema. J Pediatr. 2002;145:793-97. Roberts M, Slover R, Chase H. Diabetic Ketoacidosis with intracerebral complication. Pediatr Diabetes. 2001;2:103-14. Levin DL. Cerebral edema in diabetic Ketoacidosis. Pediatr Crit Care Med. 2008;9:320-29. Dunger DB, Sperling MA, Acerini CL, et al. ESPE/LWEPS consensus statement on diabetic ketoacidosis in children and adolescents Arch Dis Child. 2004;89:188-94. Carrol P, Matz R. Adult respiratory distress syndrome complicating severly uncontrolled diabetes mellitus: Report of nine cases and review of the literature. Diabetes Care. 1982;5:574-80. Oh MS, Banerji MA, Carrol HJ. The mechanism of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. Diabetes. 1981;30:310-13.
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Figure 35.1: Organized pediatric emergency services can generate tremendous good will in the community
Learning Objectives 1. How to set up a pediatric resuscitation and emergency unit at the entrance of the hospital?
There is a critical and growing need for emergency physicians and emergency medicine resources worldwide. To meet this need, emergency services must be established and physicians must be trained to deliver time-sensitive interventions and life-saving emergency care. Society has a right to expect that at the completion of their medical school training all pediatricians must possess basic knowledge of emergency care and the skills to manage common acute problems. Emergency medicine is a core medical discipline and should be a required portion of the curriculum for every medical school and every medical student in the world (Figure 35.1). Every graduating pediatric medical student, should be able to provide care in an emergency situation without any faults or lack of confidence and should be independent at the site of the emergency. Every physician should be able to manage clinical decision-making under pressure of time when it is essential to save lives.
2. Organizing equipment for the emergency service. 3. The need for trained nursing personnel in pediatric emergency medicine. Competence in basic emergency medicine should be an outcome measure for all medical students and represent a criteria for completion of degree.1 Globally, the millennium goal for the year 2015 aims at reducing under 5 mortality by one third. Mortality has already fallen to 20%–30% in many states in India due to interventions such as immunization, appropriate antenatal, natal and postnatal care, breastfeeding, etc. to 25%–30%. Mortality can be further reduced by appropriate management of acutely ill children and neonates in the Golden hour. This is especially important, where the small family norm is being advocated. For both the pediatricians and children, the first step would be to establish pediatric emergency services in every district and medical college hospitals. ●● Create dedicated space in the casualty or outpatient department exclusively for a pediatric emergency care unit. ●● The pediatric emergency service should be used only for evaluation and management of children referred with
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●● ●●
●● ●●
●● ●● ●●
Section XI n Special Topics
‘bad’ histories suggestive such as breathlessness, convulsions, loss of consciousness, envenomation, trauma, etc. Avoid evaluation and of stable children in the IPtreatment : 196.52.84.10 emergency unit. These children must be referred to the OPD. Failure to do so will interfere with management of critically ill children in large volume hospitals. Round the clock availability of physician and nurse is a very important aspect of service provided by the emer gency unit. Avoid leaving the emergency unit when patients are not being treated. Acutely ill children may be rushed in at any time and absence of physician or nurse can result in serious medicolegal problems for the hospital. On the contrary, presence of personnel and immediate attention to a sick child earns a great deal of good will for the hospital. The casualty medical officer should be responsible for documentation of medicolegal entries, whilst the emergency physicians should be responsible for resuscitation of injured and poisoned children. ‘Brought dead’ should be certified by the casualty medical officers. Emergency services require a great deal of support from the hospital administration for its smooth running. Trained nurses, paramedical staff, easy accessibility to the radiology suite, blood bank and laboratory backup are essential to provide effective services.
Design and Floor Plan of the Resuscitation Unit ●● Place the resuscitation trolley perpendicularly to the wall and not alongside (Figure 35.2).
Ù
All sides of patient should be accessible for resuscitation. ●● Electrical points should be placed 3 feet above the ground (Figure 35.3).
Figure 35.3: Plug points are needed for pulse oximeter, infusion pumps, suction apparatus, warmer, light source and monitors.
Ù
This ensures that the wires connecting electrical devices such as monitors and infusion pumps do not prevent access to the patient. ●● 6–8 plug points of 5 and 15 amperes should be available on either side of the resuscitation trolley. ●● Centralized oxygen supply is preferable, if not available oxygen cylinders can be used, but have to be periodically checked and replaced. ●● Install a suction apparatus at the head end of the resuscitation trolley. ●● Attach a disposable Yankauer suction catheter to the suction equipment.
Ù Ideally, both electrical and vacuum suction should be available. In case of power failure, presence of the vacuum suction is lifesaving. ●● Place a bag-valve-mask at the head end of the resuscitation trolley at all times (Figure. 35.4). ●● Place a stool at the head end of the trolley. Figure 35.2: The resuscitation cot, as shown in this picture should not not have railings around its sides.
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services
Ù The airway stool is placed such that the airway manager
IP : 196.52.84.10 can sit as he initiates bag-valve-mask ventilation. Effective bag-valve-mask ventilation can be continued until other aspects of resuscitation such as intravenous access, intubation tray, etc. can be prepared. ●● Place an intravenous stand at the head end of the trolley. ●● Ensure that a saline bottle into which an infusion set has been inserted be available at all times.
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●● Age-appropriate Guedel’s airway devices (Figure 35.5). ●● Nasopharyngeal airways should also be available (Figure 35.6). ●● Age-appropriate disposable Jackson-Rees circuits (Figure 35.7) for children who present with respiratory distress or respiratory failure. ●● Three sizes of Jackson-Rees circuits are available in the Indian market: – Neonatal and infants < 1 year. – 1 year to 5 years. – Older than 5 years.
Figure 35.4: Place a self-inflating bag-valve-mask device at the head end of the resuscitation trolley.
Figure 35.6: Nasopharyngeal airway
Ù Struggling to open and prepare a saline bottle during an emergency should be avoided. ●● Install a pulse oximeter near the head end of the resuscitation trolley.
Airway Equipment (Figures 35.5 to 35.10) ●● Organize the following airway equipment for all age groups.
Figure 35.7: Jackson-Rees circuit
Ù Non-rebreathing masks help to administer up to 90% of oxygen compared to the simple facemask, which provides 40% of oxygen.
Figure 35.5: Oropharyngeal airways
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Section XI n Special Topics
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Figure 35.8: Disposable non-rebreathing masks
Ù
Respiratory or cardiopulmonary arrest is a catastrophic emergency in children. The first responder may not have the expertise in intubation. The easy to use laryngeal mask airway is an attractive alternative to endotracheal tube. Laryngeal mask airways (LMA), as compared with endotracheal tube (ETT), led to more rapid establishment of effective ventilation and fewer complications, when performed by prehospital providers.2
Figure 35.10: Stock, age-appropriate disposable masks, since these are as important as having the correct sized ET tubes
Equipments Chart, Vital Signs Chart and Protocols (Figures 35.11 to 35.13)
Figure 35.11: Display age-based equipment sizes near the crash cart. Display charts, which help to choose age-appropriate nasogastric tubes, ET tubes, urinary catheters, etc. Nurses and doctors should have easy access to this information to ensure that the right size is inserted during resuscitation.
Figure 35.9: Stock, weight appropriate laryngeal mask airways
Ù Straight blades < 2 year; Curved blades > 2 year; ET tubes : 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5 (cuffed and uncuffed tubes); Tincture benzoin for sticking the ET tube; Dynaplast cut and available as ‘trouser legs’; gloves, syringes and cotton; Anesthetic drugs for rapid sequence intubation.
Figure 35.12: Display vital signs chart at head end of resuscitation trolley
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services
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Figure 35.13: Display protocols for all common emergencies
Procedure Trays (Figures 35.14 to 35.16)
Figure 35.16: Organize the intraosseous tray with the following: Bone marrow needle, sand bag, gloves, hole towel, dynaplast, tincture of benzoin, betadine, stainless steel cups, gauze. Prior to insertion of needle, prepare 2 fluid-filled syringes (preferably 5 mL in small infants and 10 mL in older children).
Drugs and Dosages (Figures 35.17 to 35.19)
Figure 35.14: An intubation tray should be organized and ready at all times. Figure 35.17: Display drugs with labels for ease of retrieval during resuscitation. Replenish after the resuscitation is complete. Stock all resuscitation drugs. Organize drugs in an ‘easy to retrieve’ method by labeling. Stock adequate quantity of drugs.
Figure 35.15: Organize the intravenous tray with age -appropriate intravenous catheters, cotton balls, disinfectant, adhesive tapes and gloves.
Figure 35.18: Display drug dosages and methods of preparation close to the crash cart
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Section XI n Special Topics
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Figure 35.19: Prefilled epinephrine should be available at all times
●● Use a 10 mL syringe for mixing 1 mL of 1:1000 adrenaline in 9 mL of NS (1:10,000 dilution). ●● Discard unused epinephrine once in 24 hours. ●● Make note of date and time of reconstitution on the syringe. ●● When administering a bolus dose of epinephrine to the child, load in a separate 2 mL syringe, this ensures precise dosage.
Figure 35.21: Ultrasonography machine is very useful to detect fluid and blood (FAST—focussed abdominal sonography in trauma) in children with trauma.
Ù Avoid administering epinephrine directly from the 10 mL syringe. ●● Direct administration from the 10 mL syringe can lead to over dosage (lethal consequences).
Biomedical Equipment (Figures 35.20 to 35.22)
Figure 35.20: Equip the ED with syringe pumps. Ideally, 4 pumps are needed for every resuscitation trolley viz vasoactive medications, anticonvulsants, sedation and pain relief and maintenance fluids.
Figure 35.22: Equip the emergency service with cardiac monitor, end tidal CO2 monitor and a pulse oximeter
Special equipment—spinal immobilization board and cervical collar for management of head and spinal injuries. Refer Figure 35.23.
Figure 35.23: Spinal immobilization board and cervical collar are essential for managing head and spinal injuries
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services
Time Sensitive, Goal-directed Management and Documentation (Figures 35.24 to 35.26) IP : 196.52.84.10
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Biomedical Waste Disposal (Figure 35.27)
Figure 35.27: Organize biomedical waste disposal as per national guidelines. Wash area should also be available near emergency service. Figure 35.24: Install a digital clock to ensure time sensitive goal-directed management
Figure 35.25: Perform the rapid cardiopulmonary cerebral assessment and documentation following every intervention during resuscitation
Figure 35.26: Use the emergency case record for documentation after every assessment. Maximum information should be documented within a minimum time frame. The case record should be available at the foot end of every resuscitation trolley.
Education and Training of Paramedical Personnel (Figures 35.28 to 35.31)
Figure 35.28: Train nurses in emergency resuscitation. They should be able to recognize respiratory failure and initiate bagvalve-mask ventilation, initiate age-appropriate cardiac massage, quickly prepare drugs and infusions, and set up age-appropriate airway tray within minutes.
Figure 35.29: Emergency nurses should know how to perform backward and upward, rightward cricoid pressure (BURP) technique, Sellick’s maneuver and to assist airway manager.
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Section XI n Special Topics
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Figure 35.30: Train nurses to prepare age-appropriate anticonvulsant, inotrope infusions. Nurses should be aware of protocols for all common emergencies.
●● Encourage friendly behavior amongst all members of team (nurses, doctors, house officers, nursing attendants between resuscitation). ●● Work in the ED can be very stressful and rapport amongst all members is essential for good outcomes. Indeed, successful resuscitation depends on TEAM WORK. ●● Appreciating team members for all the right things done in right way and constructive criticism of their mistakes and further training to avoid them in future, will reinforce their confidence, help improve themselves and encourage them to perform even better. ●● Team members should be periodically updated on newer developments in the standards of care. ●● Encourage, parents and children who had been successfully resuscitated to come back and meet the ER team prior to discharge. This boosts morale and cultivates good team dynamics. ●● Celebrate successful resuscitation in the emergency room with parents, child and emergency team.
Figure 35.31: Ideally, nurses who are trained in resuscitation should be retained in the ED
●● House officers and junior doctors should be aware of resuscitation protocols modified for the Indian context. ●● Train medical officers and house officers to take correct therapeutic decisions during resuscitation in critical illness. ●● Train them to avoid errors, which precipitate cardiac arrest during resuscitation.
Figure 35.33: Happy mothers with their infants postresuscitation
“Emergency departments are places within the hospital where the greatest good can be done for the greatest number of people”—‘Foreword from the first edition of Pediatric Emergency Medicine Course- 2008 N. Kissoon’.
Figure 35.32: Team effort—Many hands... One goal
IP : 196.52.84.10 - Dr Govindappa Venkataswamy, Founder, Aravind Eye Hospitals, Tamil Nadu, India
ER MOTTO: “Intelligence and capability are not enough... there must be the joy of doing something beautiful”
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services
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Key Points
ü
1. Space for the ‘Pediatric and Emergency IP : Resuscitation 196.52.84.10 Services’ unit must be created inside the casualty. 2. The emergency service provides specialized care to get kids back on track. 3. Dedicated doctors and nurses are needed to man the emergency service. 4. Resuscitation equipment and drugs must be organized and replenished when used. 5. Training in the Pediatric Advanced Life Support, Basic Life Support are mandatory prior to working in this area.
common errors
û
1. Referring to the emergency service as ‘Casualty’! 2. Failure to implement current evidence-based protocols. 3. Failure to identify early signs of critical illness. 4. Failure to resuscitate until therapeutic goals of hypoxia, shock, myocardial dysfunction and seizures have resolved.
References 1. WP Burdick, et al. SAEM Education Committee, undergraduate subcommittee academic emergency medicine, 1998;(5):1105-110. 2. Chen L, Hsiao AL. Randomized trial of endotracheal tube versus laryngeal mask airway in simulated pre-hospital pediatric arrest. Pediatrics. 2008;122;e294; DOI: 10.1542/ peds.2008-0103.
Section XII
Procedures IP : 196.52.84.10
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Nebulizer Therapy
Introduction
Check List for Nebulization
The nebulizer is used to deliver medications directly into the lungs in the form of an aerosol mist. It ensures that the therapeutic dose is delivered within a short span of time right into the lungs via the mouthpiece or a face mask.
NEBULIZER: HOW IT WORKS? The Bernoulli’s principle (Venturi effect) is used to operate the jet nebulizer. Oxygen or compressed air is driven through a tube. This creates an area of subatmospheric pressure around the jet, as it exits the tube. As a result, the solution in the nebulizing chamber is sucked up and dispersed in the form of an aerosol. The size of the droplets are characteristically 1–20 microns. Droplets less than 5 microns get deposited in the distal airways. The baffle provided in the chamber ensures uniformity in the size of the particles. Larger sized particles are returned to the chamber and aerosolized.
Ù
Avoid using nebulizers that are driven by electricity in the emergency setting. Jet nebulizer that is driven by oxygen is the method of choice in hypoxic children.
nebulization Medications ●● Beta-agonists and Ipratropium in severe asthmatic exacerbation. ●● Epinephrine and steroids for acute stridor due to ALTB. ●● 3% sodium chloride for bronchiolitis.
Figure 36.1: Nebulization tray
Nebulizing kit (Figure 36.1) with appropriate sized face mask. ●● Mask: Used in ill children, less than 5 years of age. ●● Mouthpiece: Used in older children and adolescents. It increases drug deposition. ●● Oxygen source. ●● Medications. ●● 2 mL syringe. ●● Cardiac monitor and pulse oximeter.
How to Use a Nebulizer? ●● Assemble the tubing, nebulizer cup and mouthpiece (or mask). ●● Load the prescribed drug in a syringe. ●● Fill the nebulizing chamber with the medication. ●● Fill the chamber with 4–5 mL of normal saline. If lesser volume is used, nebulization may not be possible (avoid distilled water) (Figure 36.2A to F).
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Section XII n Procedures
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Figures 36.2A to F: A. Draw 0.5 mL of Salbutamol in a syringe; B. Empty the contents into the chamber; C. Draw 0.5–1 mL of Ipratropium Bromide solution separately; D. Add this to the chamber containing Salbutamol; E. Draw 4 mL normal saline and add to the chamber containing Salbutamol and Ipratropium; F. Avoid drawing all drugs and NS together in the same syringe.
Ù
The minimum volume needed for nebulization is 4 mL. Lower fill volumes can cause suboptimal drug delivery. The maximum volume that can be loaded is 10 mL. NS (normal saline) is the recommended diluent. Plain water can cause bronchospasm. ●● Connect the nebulizer chamber to the oxygen source and initiate nebulization using a flow rate of 8 mL/min. (NB: Domiciliary oxygen cylinders do not provide an adequate flow rate). ●● Nebulization should be stopped and the chamber tapped when spluttering occurs. ●● The delivery time should not exceed 10 minute. ●● Ensure that the child is seated comfortably on his mother’s lap, in an upright sitting position. ●● Ensure that the mask fits well such that minimal mist escapes.
Chapter 36 n Nebulizer Therapy
●● Monitor the patient throughout the nebulizer treatment. ●● Stop nebulization if child’s mental status worsens or IP : 196.52.84.10 saturations fall. ●● Ensure that the nebulizer chamber remains upright at all times.
Maintenance ●● Disconnect the nebulizer cup from the plastic tubing, wash with warm tap water, mild detergent and air dry. ●● Do not wash or rinse the plastic tubing. ●● Store the dry nebulizer cup and plastic tube in a plastic bag. ●● Once a week, soak the nebulizer cup and mouthpiece or face mask for 20 minutes, in a disinfecting solution. ●● Run the nebulizer empty for a few seconds before use.
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●● Replace nebulizers once every 3 months. ●● Ideally, each patient should have his own nebulizer.
Key Points
1. 2. 3. 4.
ü
Nebulizer should be driven using oxygen. Ensure a gas flow rate of 8 liter per minute. Avoid use of plain water. NS is the ideal diluent. The nebulizer must be rinsed after each use.
common errors
û
1. Drawing salbutamol, ipratropium and normal saline all together in the same syringe. 2. Administering nebulization for stable asthmatics with minimal wheeze.
37
Needle Thoracocentesis and Thoracostomy IP : 196.52.84.10
Pleural aspiration describes a procedure whereby pleural fluid or air may be aspirated via a needle or tube inserted into the pleural space (Figure 37.1).
Equipments ●● 16, 18, 20 gauge over the needle angiocatheter.
Ù
Avoid butterfly needle since the needle could lacerate the expanding lung. ●● 10 cc syringe half-filled with NS (aids in visualizing air bubbles, thus confirming underlying pneumothorax). ●● Betadine solution. ●● Sterile gloves. ●● Sterile intravenous set. ●● Saline bottle for underwater seal drainage. Figure 37.1: Right sided pneumothorax.
indications 1. 2. 3.
Trauma with possibility of chest injury. Severe pneumonia with pneumatocele. Desaturation in the intubated child: Rule out ‘DOPE’. Oxygen saturations not normalizing despite the following maneuvers: a. Confirmation of tube position. b. Ruling out obstruction by checking for adequacy of chest rise, bilateral air entry and suctioning the ET. c. Ruling out faulty equipment. 4. Congenital cystic adenomatoid malformation.
Needle Thoracocentesis ●● Monitor using a pulseoximeter and cardiac monitor. ●● Ensure that emergency medications are close at hand.
Technique (Refer Figure 26.16 in Chapter 26) ●● Identify the second intercostal space in the midclavicular line. ●● Prepare skin with Betadine solution. ●● Attach syringe filled with saline to the angiocath. ●● Insert perpendicular to chest wall above the third rib in the midclavicular line. ●● Aspirate, as the needle is advanced. ●● A rush of air/bubbles in the syringe denotes entry into pleural space. ●● Withdraw stillette of the angiocath and keep the hub closed with your thumb to prevent air entering the pleural space. ●● Connect an intravenous tube to a saline bottle such that an underwater seal drainage is provided. ●● Improvement in saturations and air bubbles in the saline bottle are confirmatory of tension pneumothorax. ●● Confirmatory CXR. ●● Prepare for definitive tube thoracostomy.
Chapter 37 n Needle Thoracocentesis and Thoracostomy
371
●● If fluid in the chest is causing respiratory embarrassment aspirate using the procedure mentioned above. ●● Use the 4th, 5th or 6th space in the midaxilIP :intercostal 196.52.84.10 lary line.
Postprocedure Care Prepare for thoracostomy insertion soon after CXR in suspected tension pneumothorax. In the instances where CXR may not be readily available, a second physician prepares to insert a chest tube while urgent needle thoracocentesis is being performed by the first physician.
Ù
Tension pneumothorax is a clinical diagnosis and needs urgent intervention. Continue to monitor and maintain the ABCs The commonest complications from pleural aspiration are pneumothorax, procedure failure, pain and hemorrhage. The most serious complication is visceral injury.
thoracostomy A chest drain is a tube, which is placed in the pleural space to drain its contents (fluid or air) and remains in place until drainage is complete.
Indications
1. Postoperatively, e.g. cardiac surgery, thoracotomy. 2. Pneumothorax. 3. Hemothorax. 4. Chylothorax. 5. Pleural effusions.
Figure 37.2: Thoracostomy kit
●● Scalpel with 11 size blade. ●● Curved artery forceps (for blunt dissection). ●● Antiseptic solution povidone iodine 10% or chlorhexidine in alcohol. ●● Appropriate sized chest tube. a. Newborn : 8–12 FG. b. Infant : 12–16 FG. c. Child : 16–24 FG. d. Adolescent : 20–32 FG. ●● Connecting tube. ●● Sterile dressing tray with Tegaderm. ●● Suture material with needle (‘1’ silk). ●● Closed drainage system (including sterile water if underwater seal is used) (Figure 37.2).
Technique of Chest Tube Insertion ●● Obtain written consent. ●● Connect cardiac monitor and pulse oximeter. ●● Administer ketamine 2 mg/kg and midazolam 0.2 mg/ kg IV for adequate pain relief and sedation. ●● Confirm the site of insertion clinically (Figure 37.3).
Empyema is a serious and avoidable complication of pleural aspiration, the risk of which is greater with multiple attempts. It is recommended that strict asepsis should be employed, especially when carrying out therapeutic aspirations.
Equipments ●● ●● ●● ●●
Sterile gloves and gown. Drape. 1% or 2% lignocaine. Syringes with needle (21–25 gauge).
Figure 37.3: Selection of site for ICD insertion (Courtesy: Dr Gunda Srinivas)
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Section XII n Procedures
●● Take universal precautions. ●● Infiltrate skin, underlying tissue up to the periosteum using lignocaine (Figure 37.4). IP : 196.52.84.10
Figure 37.4: Local anesthetic administration around the site of ICD insertion (Courtesy: Dr Gunda Srinivas).
●● Position the child in the supine position or affected side up with the arm above the head. ●● Choose the 4th, 5th or 6th intercostal space in the posterior or midaxillary line. ●● Make a small incision parallel to intercostal space over the skin above the desired insertion point. ●● Insert an artery forceps through the tissues above the rib, taking care to avoid damaging the neurovascular bundle in the inferior aspect of the rib. ●● Push the artery forceps (not > 1 cm) through the intercostal muscles and pleura applying steady pressure to the blades. ●● Forcefully spread the blades to enlarge the hole wide enough to accommodate the chest tube. ●● Clamp the tip of the chest tube parallel to the blades of the artery forceps. ●● Use your forceps, to guide insertion of the chest tube through the dissected pathway, until it is safe inside the pleural space (Figure 37.5).
Figure 37.5: Controlled pressure during ICD insertion (Courtesy: Dr Gunda Srinivas).
●● Unclamp the forceps and insert the chest tube till all the holes are inside the pleural cavity (Figure 37.6).
Figure 37.6: ICD inserted in 4th intercostal space (Courtesy: Dr Gunda Srinivas).
●● Connect the other end of the tube to the underwater seal sterile drainage system or suction pump (Figure 37.7). ●● Suction is not always required, and may lead to tissue trauma and prolongation of an air leak in some patients. ●● Suction on the drainage unit should be set to the prescribed level. – -5 cm H20 is commonly used for neonates. – -10– -20 cm H20 is usually used by convention for children.
Figure 37.7: Underwater seal with air column moving (arrow) (Courtesy: Dr Gunda Srinivas).
Chapter 37 n Needle Thoracocentesis and Thoracostomy
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Figures 37.8A and B: Sutures to fix ICD (Courtesy: Dr Gunda Srinivas).
●● Apply two sutures (Figures 37.8A and B). ●● The first suture is to close the skin (mattress suture) after drainage removal and second one is a stay suture. ●● To prevent the tube from slipping, an omental tag of tape has been described, which allows tube to lie a little away from chest wall to prevent kinking and tension at the insertion site. ●● Dress the site of insertion using sterile dressing or Tegaderm (Figures 37.9A to C).
Figures 37.9A to C: Fixing of ICD (Courtesy: Dr Gunda Srinivas)
●● Check for bubbling of air and movement of air column (Figure 37.7).
Care After the Thoracostomy ●● Take a chest X-ray to confirm position of the tube and lung expansion after thoracostomy. ●● Watch for complications such as bleeding from intercostal vessels causing subcutaneous hematoma or hemothorax, subcutaneous emphysema, infection and puncture of lung, liver or spleen. ●● Monitor hemodynamic status. ●● Adequate pain relief. ●● Never lift drain above chest level. ●● The unit and all tubing should be below patient’s chest level to facilitate drainage. ●● Tubing should have no kinks or obstructions that may inhibit drainage. ●● Ensure all connections between chest tubes and drainage unit are tight and secure. ●● Connections should have cable ties in place. ●● Tubing should be anchored to the patient’s skin to prevent pulling of the drain.
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Section XII n Procedures
●● In PICU and NICU, the tubing should also be secured to patient bed to prevent accidental displacement. ●● Ensure the unit is securely positioned on its stand or IP : 196.52.84.10 hanging on the bed. ●● Suction on the drainage unit should be set to the prescribed level as mentioned earlier.
Removal of the Thoracostomy Tube Indications
1. Absence of an air leak (pneumothorax). 2. Drainage diminishes to little or nothing. 3. No evidence of respiratory compromise. 4. Chest X-ray showing lung re-expansion. By clamping the chest drain for several hours followed by a chest X-ray, a recurrence of a pneumothorax may be ruled out. The clamped drain should be closely supervised by nursing staff who are familiar with the management of chest drains and who should unclamp the chest drain in the event of any clinical deterioration. CXR should be performed post drain removal Clinical status is the best indicator of a reaccumulation of air or fluid. CXR should be performed if patient deteriorates. Remove sutures 5 days post drain removal.
Key Points
ü
1. Use the 2nd intercostal space for needle thoracocentesis. 2. Needle thoracocentesis is performed when saturations fail to improve following less invasive maneuvers to rule out DOPE. 3. If saturations improve following needle thoracocentesis, plan thoracostomy. 4. Perform thoracostomy only after adequate pain relief and sedation. 5. Avoid injury to the neurovascular bundle.
common errors
û
1. Using butterfly needle (scalp vein set), large bore IV needles for thoracocentesis. 2. Wasting valuable time for taking the chest X-ray to confirm pneumothorax in a ventilated child who is desaturating. 3. Not providing underwater seal. 4. Not closing the hub after entry into the pleural space. 5. Failing to fix the tube securely after insertion.
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Pericardiocentesis
Pericardiocentesis is a procedure by which pericardial fluid is removed by needle from the pericardial cavity for diagnostic or therapeutic purposes, also called as pericardial paracentesis.
Indications ●● Life-threatening hemodynamic changes in a patient with suspected pericardial effusion (Figure 38.1). ●● Aspiration of pericardial fluid for diagnostic and therapeutic purposes (Figure 38.2).
3. Gross ascites, massive hepatomegaly and elevated diaphragm can alter landmarks for subxiphoid approach.
Equipment ●● ●● ●● ●● ●● ●● ●● ●● ●●
Antiseptic solution. Sterile drapes, gown and mask. Local anesthetic (lidocaine 1%). 5, 10 and 50 mL syringes. No. 11 blade. Needles 18 gauge and 25 gauge. Spinal needle 18 gauge. Emergency resuscitation drugs and intubation trolley. Ultrasound machine (if available) and sterile ultrasound probe cover.
Procedure ●● Obtain written consent. ●● Ensure secure airway and vascular access. ●● Attach the patient to the cardiac monitor and pulse oximeter. ●● Ideally, use ultrasound to visualize the heart and pericardial space.
Figure 38.1: Chest X-ray showing pericardial effusion (Courtesy: Dr Gunda Srinivas)
CONTRAINDICATIONS There are no absolute contraindications. Relative contraindications: 1. Blood dyscrasias. 2. Cutaneous infection at the site most feasible for peri cardiocentesis.
Figure 38.2: Echocardiogram showing fluid in pericardial space (marked by star) (Courtesy: Dr Gunda Srinivas)
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Section XII n Procedures
●● Position the patient in a semirecumbent position at a 30°–45° angle. This position ensures that the heart is closer to the anterior chest wall. IP : 196.52.84.10 ●● Take universal precautions. ●● Clean the area with antiseptic solution (Figure 38.3).
Figure 38.5: Pericardial cavity entered by needle
●● Connect 20 mL or 50 mL syringe to needle and aspirate. Slowly advance needle until a return of fluid is visualized or you notice ECG changes (arrhythmia) (Figure 38.6).
Figure 38.3: Preparation of patient for pericardiocentesis
●● Infiltrate with local anesthetic solution at the site by first creating a skin wheal and then infiltrating the subcutaneous and deeper tissues. ●● Enter the skin 1 cm to the left and inferior to the xiphoid process at 45° angle to the skin (Figure 38.4 and 38.5).
Figure 38.6: Pericardial fluid being aspirated
●● Withdraw as much fluid as possible attaching a 3-way stopcock. When the syringe is filled, stabilize the needle, remove the filled syringe and replace it with another one (Figure 38.7).
Figure 38.4: Site of insertion of needle
If the subxiphoid approach might be difficult (due to an unusually located heart or elevated diaphragm), consider preparing the left sternal border.
Figure 38.7: Pericardial fluid being aspirated through catheter under ECHO guidance (Courtesy: Dr Gunda Srinivas)
Chapter 38 n Pericardiocentesis
●● Remove the needle, when fluid can no longer be aspirated (pericardial fluid does not clot). ●● Apply dressing overIPthe: 196.52.84.10 site. ●● Continue monitoring hemodynamic status. ●● Confirm resolution of pericardial effusion by ultrasonogram. ●● Send pericardial fluid aspirated for relevant investigations.
Complications ●● ●● ●● ●● ●● ●●
Dysrhythmias. Damage to vascular structures. Hemothorax and pneumothorax. Pneumopericardium. Hepatic injury. Reaccumulation of pericardial fluid.
Key Points
377
ü
1. Take care of the ABCs during the pericardiocentesis. 2. Always connect the child to the ECG monitor to visualize electrical changes during the procedure. 3. Provide adequate pain relief and sedation.
common errors
û
1. Improper position of patient. 2. Delaying pericardiocentesis can cause obstructive shock, which will not improve with fluids or inotropes. 3. Delay in relieving pericardial effusion urgently, can often result in constrictive pericarditis.
IP : 196.52.84.10
Cannulation of External Jugular Vein
The external jugular vein, a large peripheral vein, offers quick access to the central circulation when other smaller veins have collapsed and central venous (internal jugular, subclavian or femoral) access could not be obtained immediately (Figure 39.1).
Indications ●● Venous access when other peripheral veins are collapsed especially in a shocked child. ●● Placement of a large-bore venous catheter (16–20 gauge) in an emergent situation to deliver fluid, blood products and inotropes.
39
Contraindications ●● Infection over the insertion site. ●● Lack of anatomic landmarks due to neck size, shape or deformities. ●● Suspected or proven fracture of the cervical spine. ●● Bleeding diathesis. ●● Unsuccessful attempt at insertion with resultant hematoma.
equipments ●● Universal precaution. ●● Tape and dressings.
Figure 39.1: Anatomical landmark of external jugular vein and cannulation; lower head position (by 10°–20°) than thorax by placing a towel under the spine.
Chapter 39 n Cannulation of External Jugular Vein
●● Lidocaine (4%). ●● Syringe (5 cc) and 25 gauge needle. ●● 10% betadine solution chlorhexidine wipes or alIP :and 196.52.84.10 cohol swab. ●● Large bore IV catheter over needle (16–20 gauge). ●● IV fluid and IV tubing.
Procedure ●● Use universal precautions and sterile technique. ●● Attach the IV tubing to the IV fluids and place at the bedside on the IV pole. ●● Place the patient in a Trendelenburg position (10°–20° head down) to enable of neck vein and also to reduce risk of air embolism. ●● Place the roll along the axis of the spine such that the child’s neck is hyperextended. ●● Turn the patient’s head away from the side chosen for insertion. ●● Prepare and drape the entire side of the neck chosen. ●● Identify the vein. Usually, the vein can be visualized running from the angle of the mandible inferolaterally to the clavicle, crossing the sternocleidomastoid muscle above the clavicle. ●● If not visualized, occlude the vein by placing the index finger of your left hand in the supraclavicular space parallel to the long axis of the clavicle. This will result in engorgement of the vein enabling better visualization. ●● Simultaneously, stretch the overlying skin with the thumb of the same hand. With the bevel of the needle facing upward, puncture the skin at an angle of 30°. ●● The needle-tip should enter midway between the clavicle and angle of mandible and should be aimed towards
379
the shoulder on the same side. Advance the cannula, while simultaneously applying suction. ●● When a flash of blood returns, advance the catheter over the needle and remove the needle. ●● Attach the IV tubing to the catheter and secure the catheter to the neck with transparent dressing or dynaplast. Turn on the IV fluids to ascertain that there is good flow.
Complications ●● ●● ●● ●●
Local hematoma. Laceration of the deeper internal jugular vein. Infection. Air embolism: Place the patient in the left lateral decubitus in the head down position to minimize the chance of an air embolism.
Key Points
ü
1. Position the head such that it is 10°–20° below the level of the chest. 2. Cover the hub of the angiocath to avoid air embolism. 3. Stringent aseptic precautions need to be taken. 4. No blind sticks. If you cannot see it, do not stick it.
common errors
1. 2. 3. 4.
û
Improper position of patient. Improper selection of patient. Inadequate fixation of the IV catheter. Use of local anesthetics, which may be harmful, if injected into the superficially placed external jugular vein.
IP : 196.52.84.10
Foley Catheter Insertion
Indications ●● Monitoring of urine output in a child with hemodynamic compromise. ●● Acute urinary retention.
40 ●● Generously coat the distal portion (2–5 cm) of the catheter with lubricant.
Equipments
Figure 40.2: Insertion of Foley catheter
Figure 40.1: Bladder catheterization tray
●● ●● ●● ●● ●● ●● ●●
Universal precautions. Sterile gloves. Sterile drapes. Cleansing solution, e.g. povidone iodine. Cotton swab forceps. Sterile water (usually 10 cc). Foley catheter (according to age), syringe (usually 10 cc), lubricant (lignocaine jelly). ●● Collection bag and tubing (Figure 40.1).
Procedure ●● Get written consent. ●● Strict aseptic precautions. ●● Position the patient supine; males with legs extended and females with frog-leg posture (Figure 40.2). ●● Choose age-appropriate catheter.
●● If female, separate labia using non-dominant hand. ●● If male, hold the penis with the non-dominant hand. Maintain hand position until preparing to inflate balloon. Lift the penis to a position perpendicular to patient’s body and apply light upward traction (with nondominant hand). ●● Using dominant hand to handle forceps, cleanse periurethral mucosa with povidone iodine. Clean anterior to posterior, inner to outer, one swipe per swab, discard swab away from sterile field. ●● Pickup catheter with gloved (and still sterile) dominant hand. Hold end of catheter loosely coiled in palm of dominant hand. ●● Identify the urinary meatus and gently insert until 1–2 inch beyond where urine is noted. ●● Inflate balloon, using correct amount of sterile liquid (usually 10 cc, but check actual balloon size). ●● Gently pull catheter until inflation balloon is snug against bladder neck.
Chapter 40 n Foley Catheter Insertion
●● Connect catheter to drainage system. ●● Secure catheter to abdomen or thigh, without tension on tubing. IP : 196.52.84.10 ●● Place drainage bag below the level of bladder. ●● Evaluate catheter function and amount, color, odor and quality of urine. ●● Remove gloves, dispose of equipment appropriately, wash hands. ●● Document the size of catheter inserted, amount of water in balloon, patient’s response to procedure and assessment of urine.
Contraindications ●● Urethral trauma. ●● Urethral stricture.
Complications ●● ●● ●● ●● ●●
Trauma and bleeding. Infection. Creating false track. Renal inflammation. Pyelonephritis (if left in for prolonged periods).
Catheter not draining/patient oliguric ●● Check catheter/tubing not kinked. ●● Check catheter is still secured to patient leg and has not migrated out of bladder. ●● Checking patency by irrigating catheter with 2–3 mL of sterile 0.9% normal saline. Do not use force to instill fluid. This is an aseptic procedure. Catheter leaking ●● Remove catheter. If indication for bladder catheterization remains, then follow insertion procedure with new catheter.
Key Points
381
ü
1. Choose size based on weight and age of the child as per the ready reckoner. 2. Push the Foley until the bifurcation is reached and inflate with distilled water. Pull gently such that the bulb is seated on the neck of the bladder. 3. If correctly placed, urine will start filling the uro bag. Do check ultrasound, if the catheterization is dry. 4. Distal end should be strapped to the medial aspect of the thigh.
common errors
û
1. Failing to insert the Foley up to the bifurcation in male children and prematurely inflating the balloon can cause ureteral rupture. 2. Confusion and erroneous passage of catheter into vagina in the female child. 3. Failing to retract prepuce and clean well with Betadine in a male child. 4. Using smaller tubes can cause urinary leak and ammoniacal dermatitis. 5. Using larger tubes can traumatize and lead to stricture urethra.
REFERENCES 1. Gary R Fleisher, Stephen Ludwig. Text Book of Pediatric Emergency Medicine. 6th edition. Lippincott Williams & Wilkins. 2. Christopher King. Text Book of Pediatric Emergency Procedures. 2nd edition. Lippincott Williams & Wilkins.
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Spinal Stabilization
Cervical spine injuries occur in about 2% of patients with polytrauma. Since the consequences of cervical cord in jury are devastating, stabilization of the cervical spine should be continued along with immobilization of the en tire spinal column, while attending to the ABCs of trauma resuscitation. While head and facial injuries (due to rela tively large head) are common in children, soft tissue, neck and airway injuries are thankfully uncommon due to the shorter, protected neck. All trauma patients with a cervical spinal column in jury or with a mechanism of injury having the potential to cause cervical spine injury should be immobilized at the scene, throughout extrication, transport and transfer.
STEPS IN SPINAL STABILIZATION ●● Manual stabilization of cervical spine. ●● Cervical collar application. ●● Immobilizing the entire spine.
Cervical Spine Stabilization is Recommended in the Following Situations Dangerous mechanisms of injury: ●● Fall from a height of ≥ 1 meter or 5 stairs. ●● Axial load to head. ●● Injury sustained in a high speed motor vehicle (crash/ roll over/ejection). ●● Injury sustained, while using motorized recreational vehicles. ●● Bicycle collision. ●● Struck by motor vehicle. ●● Diving and submersion injuries. ●● Sports injuries. ●● Objects falling over head accidentally indoor/outdoor
Other situations that mandate cervical spine immobilization: ●● Unconscious child with significant injury. ●● Any child who has suffered traumatic respiratory arrest. ●● Preverbal children (should automatically be considered high risk). ●● Trauma associated with abnormal neurological exami nation. ●● Alert child with neck pain/tenderness/restricted neck movements. ●● Polytrauma with significant ‘distracting’ injury (anoth er injury, which may ‘distract’ the patient from com plaining about a possible spinal injury).
Manual Stabilization of the Cervical Spine ●● Manually immobilize the head and neck in neutral po sition as the first step. ●● Maintain a clear airway with jaw thrust or head tilt (if jaw thrust is not achievable) if patient is unconscious or has breathing difficulties. ●● Limit side to side movement of the head. ●● Manually stabilize the cervical spine, whether the pa tient is lying/sitting/standing (Figures 41.1A and B).
Ù
Even after application of cervical collar, maintain manual stabilization until securing the victim to the spinal board.
Technique of Manual Stabilization ●● Spread your fingers across the side of the child’s head to obtain maximum contact. ●● Stabilize your hands by resting your elbows firmly on the ground (supine position) or by locking the elbows.
Chapter 41 n Spinal Stabilization
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Figures 41.1A and B: Steps of manual cervical spine stabilization (Courtesy: Dr Radhika R)
●● Align the head in the neutral position and fit the cervi cal collar (The external acoustic meatus must be in line with the anterior shoulder).
Ù
Trapezius grip or Vice grip are the other techniques of manual stabilization.
Selection and Fixing of Appropriate Cervical Collar
●● If patient is seated, apply chin support first and then fasten the collar. ●● Maintain neutral position of head throughout the pro cedure.
Immobilizing the Entire Spine ●● If the patient is prone, log roll patient to the supine po sition.
Log Rolling 1. Use spinal immobilization devices to achieve spinal stability during extrication and transport. 2. Use a combination of: ●● Rigid cervical collar immobilization. ●● Supportive blocks on either side of the head. ●● Rigid back board with straps to secure the entire body of the patient (Figure 41.3).
Figure 41.2: Applying cervical collar
●● Examine neck for hematomas/subcutaneous emphy sema/open wounds/tracheal shift. ●● Avoid flexion or hyperextension of neck. ●● Measure distance between top of shoulders and bottom of chin. ●● Single or two piece hard collar can be used. ●● Tallest collar that does not hyperextend the neck is most appropriate. ●● Assemble the collar and slide collar behind neck with Velcro folded (to avoid Velcro attachment to child’s clothing or hair) and fit the chin piece (Figure 41.2).
Figure 41.3: Log rolling (Courtesy: Dr Radhika R)
384
Section XII n Procedures
All three methods in combination are needed to limit motion of the cervical spine effectively.
IP : 196.52.84.10 Cervical Spine Immobilization
lowed out or a blanket is placed under the torso, there by maintaining a neutral position of the head and neck (Figures 41.5A and B).
Ù
Cervical spine immobilization using sandbags and tape alone is not recommended. 1. Secure the patient preferably in the supine position to a long hard spine board by tape or straps across bony points (Figure 41.4). ●● Forehead. ●● Chin. ●● Bony prominences of the shoulders, pelvis and ex tremities. ●● Chest straps. ●● Hip and leg straps. All are secured in that order to minimize cervical spine mobility. 2. Assess the straps periodically for adequate and safe restraint. 3. In the event of that the child needs to vomit, the back board may be rapidly rotated 90°, while the patient remains fully immobilized in a neutral position. 4. Provide analgesia, if patient has been lying on a hard backboard for an extended period. 5. For victims in sitting or standing position, cervical collar application and spine immobilization should be done in the same position using techniques for manual cervical spine stabilization and sliding the spine board.
Figure 41.4: Spine stabilization (Courtesy: Dr Radhika R)
6. Occiput in infants and toddlers is prominent. Hence, ensure that the head end of the spine board is hol
Figures 41.5A and B: Spine board maintaining neutral position of head and neck (reproduced from Copley LA, Dorman’s JP: Cervical spine disorders in infants and children Am Acad Orthop Surg. 1998;6: 204-14).
Airway Management Immobilization techniques may agitate and distress the child, thus increasing movement of the cervical spine. It is important to be gentle, but firm and institute manual re straint first. The presence of parents and close relatives is vital to calm the child. If immobilization attempts appear to cause more move ment of the cervical spine, than if it is not applied, abandon attempts. 1. While managing the airway in the setting of spinal cord injury, maintain the cervical spine in neutral alignment at all times. 2. Clear oral secretions and/or debris to maintain airway patency and to prevent aspiration. 3. Use modified jaw thrust and insertion of an oral airway or intubation, as required to maintain airway patency. 4. Failure to intubate when needed, due to the potential risk of worsening cervical cord injury must be avoid ed. 5. Open cervical collar anteriorly and maintain manu al inline spinal stabilization to facilitate mandibular movement for intubation (Figures 41.6A and B). 6. Secure surgical airway through the opening in the an terior part of the collar, if situation warrants.
Chapter 41 n Spinal Stabilization
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3. Imaging the spine does not take precedence over lifesaving diagnostic and therapeutic procedures.
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Box 41.1: Preconditions that rule out cervical spine injury The following history rules out cervical cord injury: • Fully alert and orientated • No head injury • No drugs or alcohol • No neck pain • No abnormal neurology • No significant other ‘distracting’ injury (another injury, which may ‘distract’ the patient from complaining about a possible spinal injury)
If these preconditions are met, the neck may be exam ined (Box 41.1). If there is no bruising, deformity or tenderness and a pain free range of active movements, the cervical spine can be cleared. It is important to remember that children are at in creased risk for traumatic cervical instability with no os seous injury [Spinal cord injury without radiological ab normality (SCIWORA)].
Order Lateral Cervical Spine X-ray The lateral cervical spine X-ray can be difficult to inter pret:
Figures 41.6A and B: Manual stabilization of cervical spine during intubation.
Problems During Cervical Spine Immobilization ●● Worsening of injury due to application of collar in a struggling child. ●● Worsening of injury due to incorrect size of collar. ●● Limited access to internal/external jugular vein. ●● Limited visualization of neck injury/hematoma/subcu taneous emphysema/distorted anatomy.
Spinal Clearance 1. Spinal immobilization is a priority in multiple trauma. 2. The spine should be assessed and cleared after taking into account, the severity of injury, neurological defi cits and physiological status of the ABCs.
1. 2. 3. 4.
Alignment. Bone. Cartilage and joints. Soft tissue.
Pitfalls in Cervical Spine Radiology 1. SCIWORA ●● Spinal cord injury without radiological abnormality may occur in 20%–30% of younger children due to increased ligamentous laxity, relatively large head, poorly developed cervical musculature, anterior wedging of vertebral bodies, vulnerable growth zones at vertebral end-plates and shallow facet joints. 2. Physeal lines. ●● Physeal lines may give the appearance of fractures. 3. Psuedosubluxation. ●● C2/C3 and C3/C4. Cervical spinal immobilization devices should be re moved as soon as definitive evaluation is accomplished and/or definitive management is initiated.
386
Section XII n Procedures
Key Points
ü
1. Consider cervical IP spine precautions and spinal im : 196.52.84.10 mobilization in trauma victims. 2. 3–4 trained personnel are needed to perform these maneuvers. 3. C-spine precautions may withdrawn only after com plete neurological and radiological clearance. 4. The purpose of spinal immobilization is prevent secondary quadriplegia or paraplegia.
common errors
û
1. Trauma victims being carried into hospitals by par ents. 2. Lack of trained manpower results in panic and fail ure to follow protocols. 3. Failing to provide spinal stabilization (starting at the site of accident).
REFERENCES 1. Jeremy Dewall. The ABCs of TBI. Evidence-based guide lines for adult traumatic brain injury care. JEMS a journal of emergency medical services. 2010;35(4):54-61. 2. Hadley MN, Walters BC, Grabb PA, et al. Management of pediatric cervical spine and spinal cord injuries, Neurosur gery. 2002; 50:S85-99. 3. Cindy GR, Peter SD, Bruce L, Klein. Acute care of the victim of multiple trauma.In: Robert M, Kliegman, Bonita, Stanton, Joseph SG, Nina Schor, Richard EB (Eds). Nel
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6. 7.
8.
9. 10. 11.
son Textbook of Pediatrics, 19th edition. Chapter 66. USA: Saunders;10 Jun 2011 ISBN: 9781437707557. Fred M Henretig, Christopher King. Textbook of Pediat ric Emergency Procedures. 2nd Revised edition. Wolters Kluwer/Lippincott Williams and Wilkins; United States: 2007. Joseph JT, Mary EF, Thomas M. Trauma. APLS: The Pe diatric Emergency Medicine resource. American Academy of Pediatrics. American College of Emergency Physicians. Jones & Bartlett Learning; USA: 4th edition; 2007. pp. 274-75. Julie L, Jeffry RL, Gary RS, et al. Pediatric cervical spine injry. Pediatric emergency medicine, 3rd edition. Section iv . Chapter 30.USA: McGraw-Hill; 2011. American association of neurological surgeons (Spine Uni verse homepage). Management of Pediatric Cervical Spine and Spinal Cord Injuries. The Spine Section of the AANS and CNS 2012. www.spineuniverse.com/professional/ acute-cervical-spine-injury-guide. Gary RF, Stephen Ludwig. Textbook of Pediatric Emer gency Medicine, 6th edition. Philadelphia: Wolters Klu wer/Lippincott Williams & Wilkins; 2010. ISBN-13:9781-6054-7159-4. Initial assessment of spinal injury, Spinal injury assessment and clearance, 2002. Trauma.org. (Internet) www.trauma. org/archive/spine/spine-conscious.htm Christopher WR. Pediatric Spine Trauma. J Bone Joint Surg Am. 2007; 89(suppl 1) :98-107 doi:10.2106/ JBJS.F.00244. Australian Life Saving Academy. Australian lifesaving academy learners guide IRB crew certificate. SLSA Ver sion. 2011. Pg 11 www.tamaramaslsc.org/twiki/bin/view file/IrbTraining.guide.
Appendices IP : 196.52.84.10
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Appendices
Appendix 1: VITAL SIGNS AND EQUIPMENTS Age (kg)
Resp. rate
Heart rate
Systolic BP
ET tube size*
ET tube distance at lip
Laryngoscope blade
Suction catheter
NGT (Fr)
Foley (Fr)
Chest tube (Fr)
Preemie (1–2)
30–60
90–180
50–70
2.5–3.0
8
0
5–6
5
5
8–10
New born (3.5)
30–60
90–180
50–70
3.0–3.5
8–9.5
1
6
8
5
8–10
6 month (7)
24–40
85–170
65–106
3.5–4
9.5–11
1
8
8
5
12–16
1 year (10
20–40
80–140
72–110
4.0–4.5
11–12.5
2
8
10
8
14–20
3 year (15)
20–30
70–120
78–114
4.5–5.0
12.5–14
2
8
10
10
18–22
6 year (20)
18–25
65–110
80–116
5.0–5.5
14–15.5
2
10
12
10
20–28
8 year (25)
18–25
70–110
84–122
6.0–6.5 (cuff )
17–18.5
2
10
12
10
28–32
10 year (30)
16–20
65–110
90–130
6.5–7.0 (cuff )
18.5–20
3
12
14
12
28–32
12 year ( 40)
14–20
60–110
94–136
7 (cuff )
20
3
12
4
12
28–32
15 year (50)
12–20
55–100
100–142
7.0–7.5 (cuff )
20–21.5
3
12
16
14
32
ET selected in Indian children should be 0.5 size lesser than that recommended by PALS guidelines
*
Appendix 2: EMERGENCY INFUSIONS TITRATED TO PATIENTS RESPONSE Medication
Preparation
Dose
Epinephrine (1:1,000)
0.6 × body weight (kg) equals mg to add to 50 mL D5W/NS
1 mL/h delivers 0.2 μg/kg/min (0.2–2 μg/kg/min IV Infusion)
Norepinephrine
0.6 × body weight (kg) equals mg to add to 50 mL D5W/NS
1 mL/h delivers 0.2 μg/kg/min (0.2–2 μg/kg/min IV Infusion)
Dopamine Dobutamine
6 × body weight (kg) equals mg to add to 50 mL D5W/NS
1 mL/h delivers 2 μg/kg/min (5–20 µg/kg/min infusion)
Lignocaine (1%)
60 mg × body weight (kg) equals mg to add in 50 mL D5W
1 mL/h delivers 20 μg/kg/min (15–50 µg/kg/min)
Prostaglandin E1 (alprostadil)
1 vial (500 mg) added to 99 mL D5W yielding 5 μg/mL
0.1 mL/kg/h delivers 0.01 µg/kg/min (0.05–0.1 µg/kg/min)
Appendices
390
Appendix 3: ANESTHETIC AGENTS USED TO ASSIST INTUBATION
a. Hemodynamically stable* IP : 196.52.84.10 Medication
Dose
Route
Comments
Fentanyl
2–5 μg/kg
IV
Slow push over 3–5 minute, flush well.
Midazolam
0.05–0.2 mg/kg
IV
Slow push, flush well.
Rocuronium
1 mg/kg
IV
Quick push. Ventilation must be supported.
Vecuronium
0.1–0.2 mg/kg
IV
Normal BP for age, normal mental status, good perfusion
*
b. Hemodynamically unstable* Medication
Dose
Etomidate or Ketamine
Route
0.3 mg/kg; 1–2 mg/kg
Comments
IV
Not with raised ICP.
Midazolam ( not needed if Etomidate is used) 0.1 mg/kg
IV
Slow push, flush well.
Rocuronium or Vecuronium
IV
Quick push, ventilation must be supported.
1 mg/kg; 0.1–0.2 mg/kg
Abnormal BP for age, abnormal mental status, poor perfusion
*
c. Hemodynamically stable, suspected increased ICP Medication
Dose
Route
Lidocaine
1 mg/kg
IV
Thiopental or Etomidate
5 mg/kg; 0.3 mg/kg
IV
Rocuronium or Vecuronium
1 mg/kg; 0.1–0.2 mg/kg
IV
Comments
Quick push, ventilation must be supported.
Appendix 4: SEIZURES Medication
Dose
Route IV, IO Rectal
Comments
Diazepam (Valium)
0.1–0.3 mg/kg 0.5 mg/kg initial 0.25 mg/kg subsequent
Lorazepam (Activan)
0.05–0.1mg/kg
IV
Slow push over 2 minute
Phenobarbital
20 mg/kg
IV
Max dose = 500 mg/kg Push over 5 minute
Phenytoin
15–20 mg/kg, slow over 20–30 min
IV
Max dose = 1 g Max rate = 1 mg/kg/min
Levetiracetam
20–30 mg/kg at 5 mg/kg/min
IV
Max dose = 3 g
Sodium valproate
15–20 mg/kg at 5 mg/kg/min
IV
Max dose = 40 mg/kg Infusion = 1–4 mg/kg/h
Midazolam
0.1–0.2 mg/kg
IV, PR
Max rate = 1 mg/min Push over 5 minute
Max dose = 0.15 mg/kg Infusion = 1 μg/kg/min to max 30 μg/kg/min
Fluid Replacement, Electrical Intervention, Resuscitation Medications
391
Appendix 5: FLUID REPLACEMENT Fluid bolus in shock NS/RL* (20 mL/kg)
Packed Red Blood Cells (10 mL/kg)
Preemie
10–20 (10 mL/kg)
5–10 (mL/kg)
New born
35 (10 mL/kg)
17 (5 mL/kg)
6 month
140
70
1 year
200
100
3 year
300
150
6 year
400
200
8 year
500
250
10 year
500
300
12 year
500
400
15 year
500
500
Age
IP : 196.52.84.10
5–10 mL/kg of fluid boluses can be given to titrate response
*
Appendix 6: ELECTRICAL INTERVENTION Initial
No response
Defibrillation
2.0 Joule/kg
4.0 Joule/kg
Cardioversion
0.5–1.0 Joule/kg
1.0–2.0 Joule/kg
Appendix 7: RECUSCITATION MEDICATIONS Age (kg)
Epinephrine 1:10,000
Atropine 0.1 mg/mL
Bicarbonate (1meq/l)
Glucose
Lidocaine 2% (0.5 mL/kg)
Crystalloid Bolus
Preemie(1–2)
0.2 mL
1 mL
2 mL (4.2%)
5 mL (D10)
0.1 mL
20 mL
New born (3.5)
0.35 mL
1 mL
3.5 mL (4.2%)
10 mL (D10)
0.18 mL
35 mL
6 month (7)
0.7 mL
1.4 mL
7 mL
14 mL (D25)
0.35 mL
140 mL
1 year (10)
1 mL
2 mL
10 mL
20 mL (D25)
0.5 mL
200 mL
3 year (15)
1.5 mL
3 mL
15 mL
30 mL (D25)
0.75 mL
300 mL
6 year (20)
2 mL
4 mL
20 mL
40 mL (D25)
1 mL
400 mL
8 year (25)
2.5 mL
5 mL
25 mL
50 mL (D25)
1.25 mL
500 mL
10 year (30)
3 mL
6 mL
30 mL
30 mL (D50)
1.5 mL
500 mL
12 year (40)
4 mL
8 mL
40 mL
40 mL (D50)
2 mL
500 mL
15 year (50)
5 mL
10 mL
50 mL
50 mL (D50)
2.5 mL
500 mL
392
Appendices
Appendix 8: DRUGS AND DOSAGES IP : 196.52.84.10
DRUGS USED IN PEDIATRIC EMERGENCIES
Activated charcoal
1–2 g/kg through NG tube
Adenosine
SVT 0.1 mg/kg IV/IO rapid push (ma× 6 mg), 0.2 mg/kg IV/IO rapid push (max 12 mg)
Albumin
Shock, Trauma, Burns 0.5–1 g/kg (10–20 mL/kg of 5% solution) IV/IO rapid infusion
Albuterol (Salbutamol)
Asthma, Anaphylaxis (bronchospasm), Hyperkalemia MDI : 4–8 puffs INH q 20 min PRN with spacer (OR ET if intubated) Nebulizer: 2.5 mg/dose (weight < 20 kg) OR 5 mg/dose (weight > 20 kg) INH q 20 minute PRN Continuous nebulizer: 0.5 mg/kg/h INH (max 20 mg/h)
Alprostadil (PGE1)
Ductal-dependent Congenital Heart Diseases (all forms) 0.05–0.1 µg/kg/min IV/IO infusion initially, then 0.01–0.05 µg/kg/min IV/IO
Amiodarone
SVT, VT ( with pulses) 5 mg/kg IV/IO load over 20–60 minute (max 300 mg), repeat to daily max 15 mg/kg (or 2.2 g) Pulseless Arrest (i.e. VF/pulseless VT) 5 mg/kg IV/IO bolus (max 300 mg), repeat to daily max 15 mg/kg (or 2.2 g) 8–10 vials in 100 mL NS over 1–2 hour (max 20 vials)
Aminophylline
Refractory Near Fatal asthma 5 mg/kg loading (1 mg/kg/h IV infusion)
Antisnake venom
Snake bite with signs of envenomation 8–10 vials in 100 mL NS over 1-2 hour (maximum 20 vials)
Atropine sulfate
Bradycardia (symptomatic) 0.02 mg/kg IV/IO (min dose 0.1 mg, max single dose child 0.5 mg, max single dose adolescent 1 mg), may repeat dose once, max total dose child 1 mg, max total dose adolescent 2 mg 0.04–0.06 mg/kg ET Toxin overdose (e.g. organophosphate, carbamate) 0.02–0.05 mg/kg ( 12 year) IV/IO initially, repeat q 20–30 minute until atropine effect (dry mouth, tachycardia, mydriasis) is observed or symptoms reverse
Blood
10 mL/kg over 4 hour
Calcium gluconate 10%
Hypocalcemia, Hyperkalemia, Hypermagnesemia, Calcium Channel Blocker Overdose 200 mg/kg (0.2 mL/kg) IV/IO slow push during arrest or if severe hypotension, repeat PRN
Dexamethasone
Croup 0.6 mg/kg PO/IM/IV (max 16 mg)
Dextrose (Glucose)
Hypoglycemia 0.5–1 g/kg IV/IO (D25 W 2–4 mL/kg; D10 W 5–10 mL/kg)
Diazepam
0.05–0.3 mg/kg, (Max < 5 year: 5 mg; 5 year: 10 mg) PR: 0.5 mg/kg, Infusion: 0.1 mg/kg/min
Diphenhydramine
Anaphylactic Shock 1–2 mg/kg IV/IO/IM q 4–6 hour (max 50 mg) Congestive Heart Failure, Cardiogenic Shock 2–20 µg/kg/min IV/IO infusion; titrate to desired effect
Dopamine
Cardiogenic Shock, Distributive Shock 5–20 µg/kg/min IV/IO infusion; titrate to desired effect
Contd...
Drugs Used in Pediatric Emergencies
393
Contd... DRUGS USED IN PEDIATRIC EMERGENCIES Epinephrine
IPPulseless : 196.52.84.10 Arrest, Bradycardia (symptomatic)
0.01 mg/kg (0.1 mL/kg) 1:10, 000 IV/IO q 3–5 minute (max 1 mg; 1 mL) 0.1 mg/kg (0.1 mL/kg) 1:1,000 ET q 3–5 minute Hypotensive Shock 0.1–1 µg/kg/min IV/IO infusion (consider higher doses if needed) Anaphylaxis 0.01 mg/kg (0.01 mL/kg) 1:1,000 IM in thigh q 15 minute PRN (max 0.5 mg) or Auto-injector 0.3 mg (weight ≥ 30 kg) IM or Child Jr Auto-injector 0.15 mg (weight 10–30 kg) IM 0.01 mg/kg (0.1 mL/kg) 1:10,000 IV/IO q 3–5 minute (max 1 mg) if hypotension 0.1–1 µg/kg/min IV/IO infusion in hypotension despite fluids and IM injection Asthma 0.01 mg/kg (0.01 mL/kg) 1:1,000 SQ q 15 minute (max 0.5 mg; 0.5 mL) Croup 0.25–0.5 mL racemic solution (2.25%) mixed in 3 mL NS INH OR 3 mL 1:1,000 INH
Epinephrine (continued)
Toxins/overdose (e.g. β- adrenergic blocker, calcium channel blocker) 0.01 mg/kg (0.1 mL/kg) 1:10,000) IV/IO (max 1 mg); if no response consider higher doses up to 0.1 mg/ kg (0.1 mL/kg) 1: 10,000 IV/IO 0.1–1 µg/kg/min IV/IO infusion (consider higher doses)
Fos-phenytoin
Status Epilepticus refractory to 2 doses of benzodiazepines 20–30 mg/kg, IV, IM, 5 mg/kg/min (Max: 225 mg/min), [7.5 mg of Fos-phenytoin ~ 5 mg of Phenytoin]
Furosemide
Pulmonary Edema, Fluid Overload 1 mg/kg IV/IM (usual max 20 mg if not chronically on loop diuretic)
Hydrocortisone
Adrenal Insufficiency 2 mg/kg IV bolus (max 100 mg)
Inamrinone
Myocardial Dysfunction and Increased SVR/PVR Loading dose: 0.75–1 mg/kg IV/IO slow bolus over 5 minute (may twice to max 3 mg/kg), then 5–10 µg/ kg/min IV/IO infusion
Ipratropium Bromide
Life-threatening asthma 250–500 µg INH q 20 minute PRN × 3
Labetolol
0.25–0.5 mg/kg IV over 2 minute, can be repeated every 10 minute if required
Lidocaine
VF/Pulseless VT, Wide-Complex Tachycardia (with pulses) 1 mg/kg IV/IO bolus Maintenance: 20–50 µg/kg/min IV/IO infusion (repeat bolus dose if infusion initiated > 15 minute after initial bolus) 2–3 mg/kg ET
Levetiracetam
Refractory Status epilepticus, SE complicated with cardiac dysfunction 20–30 mg/kg IV at 5 mg/kg/min (maximum, 3 g) Intravenous NGT route if IV preparation not available
Lorazepam Magnesium sulfate
0.05–0.1 mg/kg (Max: 4 mg) IV Infusion: 0.1–0.01 mg/kg/h Asthma (refractory status asthmaticus), Torsades de Pointes, Hypomagnesemia 25–50 mg/kg IV/IO bolus (pulse less VT) or over 10–20 minute (VT with pulses) OR slow infusion over 15–30 minute (status asthmaticus) (max 2g)
Contd...
394
Appendices
Contd...
Mannitol 20%
DRUGS USED IN PEDIATRIC EMERGENCIES IP : 196.52.84.10 0.25–0.5 g/kg/dose (1.25–2.5 mL/kg/dose) IV every 8 hour
Methylprednisolone
Asthma (Status asthmaticus), Anaphylactic Shock Load: 2 mg/kg IV/IO/IM (Max 80 mg) use acetate salt Maintenance: 0.5 mg/kg IV/IO q 6 hour (max 120 mg/d)
Midazolam
Seizures (pre-hospital), initial management of status epilepticus, Refractory SE 0.1–0.2 mg/kg (Max: 0.15 mg/kg) IV, PR, infusion 1 μg/kg/min to max 30 μg/kg/min
Milrinone
Myocardial Dysfunction and Increased SVR/PVR Loading dose: 50–75 µg/kg IV/IO over 10–60 minute followed by 0.5–0.75 µg/kg/min IV/IO infusion
Morphine
0.1–0.2 mg/kg/dose IV
Naloxone
Narcotic (opiate) Reversal Total reversal required (for narcotic toxicity secondary to overdose): 0.1 mg/kg IV/IO/IM/SQ bolus q 2 minute PRN (max 2 mg) Total reversal not required (e.g. for respiratory depression associated with therapeutic narcotic user): 1–5 µg/kg IV/IO/IM/SQ; titrate to desired effect Maintain reversal: 0.002–0.16 mg/kg/h IV/IO infusion
Neostigmine
0.05 mg/kg/dose IV
Nitroglycerin
Congestive Heart Failure, Cardiogenic Shock 0.25–0.5 µg/kg/min IV/IO infusion, may increase by 0.5–1 µg//kg/min q 3–5 minute PRN to 1–5 µg/kg/ min (max 10 µg/kg/min) Adolescents: 10–20 µg/min, increase by 5–10 µg/min every 5–10 minute PRN to max 200 µg/min
Norepinephrine
Vasodilatory shock refractory to fluids and dopamine 0.1–2 µg/kg/min IV/IO infusion; titrate to desired effect
Oxygen
Hypoxia, Hypoxemia, Shock, Trauma, Cardiopulmonary Failure, Cardiac Arrest Administer 100% O2 via high-flow O2 delivery system (if spontaneous ventilations) or ET (if intubated); titrate to desired effect
Phenytoin
Status Epilepticus refractory to 2 doses of benzodiazepines 15–20 mg/kg (Max: 1 g) Slow IV over 20–30 minute @ 1mg/kg/min Max : 50 mg/min
Phenobarbitone
Refractory status epilepticus, Neonatal status epilepticus 15–20 mg/kg up to max 1 g/dose IV, 1 mg/kg/min up to a maximum of 60 mg/min
Procainamide
SVT, Atrial Flutter, VT (with Pulses) 15 mg/kg IV/IO load over 30–60 minute (do not use routinely with amiodarone)
Pralidoxime
25–50 mg/kg/dose IV
Prazosin
30 μg/kg/dose PO
Sodium bicarbonate
Metabolic Acidosis (servere), Hyperkalemia 1 mg/kg IV/IO slow bolus Sodium Channel Blocker Overdose (e.g. tricyclic antidepressant) 1–2 mEq/kg IV/IO bolus until serum pH is > 7.45 (7.50–7.55 for severe overdose) followed by IV/IO infusion of 150 mEq NaHCO3/L solution to maintain alkalosis
Sodium nitroprusside
Cardiogenic Shock (i.e. associated with high SVR), Severe Hypertension 1–8 µg/kg/min (weight < 40 kg) OR 0.1–5 µg/kg/min (weight > 40 kg) Iv/IO infusion
Sodium valproate
Refractory status epilepticus 15–20 mg/kg up to max 40 mg/kg IV 5 mg/kg/min infusion: 1–4 mg/kg/h
Terbutaline
Asthma (status asthmaticus), Hyperkalemia 3–6 μg/kg/min over 1hour, then 0.4-1 μg/kg/min
Sample Case Record: Status Epilepticus
Appendix 9 IP : 196.52.84.10
Sample documented pediatric emergency case record of status epilepticus—assessment sheet
395
396
Appendices
IP : 196.52.84.10
Sample documented pediatric emergency case record of status epilepticus—monitoring sheet
Sample Case Record: Drowning
Appendix 10 IP : 196.52.84.10
Sample documented pediatric emergency case record of drowning victim—assessment sheet
397
398
Appendices
IP : 196.52.84.10
Sample documented pediatric emergency case record of drowning victim—monitoring sheet
Sample Case Record: Near Fatal Asthma
Appendix 11 IP : 196.52.84.10
Sample documented pediatric emergency case record of near fatal asthma—assessment sheet
399
400
Appendices
IP : 196.52.84.10
Sample documented pediatric emergency case record of near fatal asthma—monitoring sheet
Sample Case Record: Head Injury (Raised ICP)
Appendix 12 IP : 196.52.84.10
Sample documented pediatric emergency case record of raised ICP due to head injury—assessment sheet
401
402
Appendices
IP : 196.52.84.10
Sample documented pediatric emergency case record of raised ICP due to head injury—monitoring sheet
Sample Case Record: Septic Shock
Appendix 13 IP : 196.52.84.10
Sample documented pediatric emergency case record of septic shock—assessment sheet
403
404
Appendices
IP : 196.52.84.10
Sample documented pediatric emergency case record of septic shock—monitoring sheet
Sample Case Record: Septic Shock
IP : 196.52.84.10
Sample documented pediatric emergency case record of septic shock—monitoring sheet continued...
405
Epilogue IP : 196.52.84.10
IP : 196.52.84.10
Way back in 1997, when I was invited to take charge of the Pediatric Emergency Room, little did I expect that this would be the beginning of the most exciting chapter in the history of the institute. Seriously ill children and neonates were flooding its gates. Brought late by their parents, these children had received little prehospital resuscitation, were recognized late and were from the most under-privilaged sections of the population. This was compounded by the fact that pediatric emergency medicine was relatively new and few doctors were formally trained in this sub-specialty during their under-graduation. A large proportion of severely hypoxic and shocked children were presenting with features of pulmonary edema, cardiac dysfunction with eyes signs of non-convulsive status epilepticus. To our surprise, response to apparently innocuous interventions such as fluids, brochodilators and anticonvulsants were often detrimental! Why was this happening? Little published evidence supported these observations. Perhaps, children reaching western hospitals were not so sick?! Perhaps, these children were intubated earlier, resulting in failure to develop these findings and hence never documented. Protocols were modified to incorporate this information. Residents were drilled to perform the rapid assessment within 60 seconds. Evaluation of liver span and eye movements was enforced in every assessment. Response to each intervention was vigorously assessed for improvement and deterioration. Anticipation for the development of pulmonary edema and cardiac dysfunction were built into protocols in order to avoid deterioration to cardiac arrest. The innovations started paying rich dividends and hospital mortality dropped dramatically. Pursuit to seek the truth never ends. Only history can truly judge the impact of these innovations in the care of the seriously ill child during the initial minutes of resuscitation. Indumathy Santhanam md dch
Index IP : 196.52.84.10 A Abdominal distension 286 pelvic trauma 285 respiration 79 sonogram for trauma 286 tenderness 286 Abnormal cardiopulmonary cerebral assessment 10 movements 7 respiratory rates 11 Abrasions 286 Acetaminophen 254 IP : 196.52.84.10 Acidosis 135, 199 Acneiform rash 252 Acoustics of the stridor 63 Activated charcoal 242, 255 Acute accidental ingestion of kerosene 250 ataxia and nystagmus 240 cardiogenic pulmonary edema 55, 80, 81, 136, 150 cardiogenic shock 124, 136, 140 clinical syndrome 170 diarrhea 129 epiglottitis 65, 67 FB obstruction 69 gastroenteritis 130 infectious disease 45 laryngotracheal bronchitis 62, 65 lung injury 82, 144, 299, 300 respiratory distress syndrome respiratory distress syndrome (ARDS) 101, 351 tubular necrosis 199 urinary retention 380 viral croup 63 Administration of anticonvulsant drugs 7 digoxin 177 neuromuscular blockage 32 Administration of premedication 32 sedation 32 Adrenaline 92
Adrenergic receptor dysfunction 134 Advanced cardiac life support 300 Aggravate hypoxia 62 Aggravating factors 62 hydration 90 Agitation 86 Air bronchogram 314 embolism 379 Airway assessment 45 breathing 171, 189, 249, 292, 306 cervical spine protection 281 equipment 33, 357 experts 50 management 384 manager manipulating 47 obstruction 63, 141 positioning is warranted 104 stable 130 unmaintainable 253 Albuminuria 260 Alkalinization of urine 255 Allergies 33 Alpha-adrenergic 102 Alteration in mental status 80 Altered autoregulation 199 level of consciousness 3 mental status 130 Aminophylline 89, 90, 92 Ammoniacal dermatitis 381 Analgesics 67 Anaphylactic shock 123, 170 Anaphylaxis 111, 135, 138, 171, 232 Anatomical landmark 378 Anemia and congenital heart diseases 11 Anesthetic agents of choice 36 Angioedema 65 Anomalous left coronary artery 135 Anoxemia 199 Anoxic spell and blue spell 174 Anteriorly placed pediatric larynx 47 Anthracyclines 135 Antibiotic prophylaxis 285 Antibiotics 67
Anticholinergic activity 240 derivative 88 signs 252 Anticholinesterase 233 Anticipation 104 Anticonvulsant drugs 31, 110 Antidote 253, 255, 257 Antiemetics 219 Antiepileptic drugs 207 Antihistamines 172 Antihypertensive drugs 179 Antisnake venom 231 Antitussives and decongestants 67 Antivenom administration 234 serum 111 Apneustic breathing 270 Approach to decreased level of consciousness 187 GI bleeding in the ED 306 kerosene 247 PEMC 112 respiratory distress 77 traumatic brain injury 265 Appropriate sized laryngoscope 33 oral airway 33 Armamentarium 50 Arrhythmias 111, 134 Arterial blood gas 85, 139 carbon dioxide 200 catheter 125 oxygen 200 bed pulsates 96 Aseptic procedure 381 Aspiration of pericardial fluid 375 Assessment of heart rate 9, 148 urine 381 Assisted tracheal intubation 25 Asthma acute severe 84 exacerbation 84 mimics 85 moderate 84 near fatal 84
410
IP : 196.52.84.10
Pediatric Emergency Medicine Course (PEMC)
ASV administration 232 dose 231 Ataxic 270 Atelectasis 299 Atropine 36 Autoaugmentation 102 Autonomic activity 200 system disturbance 199 Autoregulation of cerebral blood flow 266
B Bacterial tracheitis 65, 68 Bag-valve-mask ventilation 25, 26, 46, 198 Barbiturate poisoning 251 Basic airway management 25, 31 Basic life support 301 Basilar skull fracture 269 Belladonna alkaloids 253 IP : 196.52.84.10 Benzodiazepines 40, 199, 204, 219, 203 Bernoulli’s principle 367 Beta blockers 176 Bilateral abductor palsy 70 chest rise 37 hilar opacities 318 Bimanual laryngoscopy 45 Bipyridines 124 Bladder catheterization 380, 381 Bleeding diathesis 378 from scalp lacerations 268 Blood culture 193 dyscrasias 375 pressure 11, 200 transfusion 153 Blood-brain barrier 265 Body surface area 291 Boggy swelling 284 Bolus therapy 117 Bone marrow needle 114 Boon in the ED management of acute pulmonary edema and shock 53 Bougie 50 Bradycardia 9, 14, 19, 37, 40, 135, 275, 299 Bradypnea 19 Brassy cough 62 Breathing airwary 14, 112, 104, 150 Breathlessness 7
Brochospasm 87 Bronchilitis 7, 79, 80, 81 Bronchodilator intervention 85 therapy 111 Bronchorrhea 248 Bronchospasm 248 Broselow tape 14 Budesonide 66 Bullard laryngoscope 50 Bungarus caeruleus 225 Burns and polyuria 107 around mouth 293 classification 291 facial 293 hand 293 minor 294 scal 293 specific secondary survey 294
C Calculation of burns percentage 292, 293 Camphor poisoning 260 Cannulation of external jugular vein 378 Capillary blood glucose 202 leak 8, 145 refill time 10, 11 Carbamates 250 Carbamazepine 243 Carbon monoxide poisoning 103 Cardiac arrest 123, 135, 199 diseases 141 dysfunction or acute lung injury 80, 144, 152 failure 199 function 145 index 145 rhythm 120 surgery 371 tamponade 109, 111, 135 Cardiogenic shock 31, 80, 81, 103, 120, 121, 132, 134, 135, 187, 188 Cardiomyopathy 135 Cardioprotective effect 219 Cardiopulmonary assessment 124 bypass surgery 135 cerebral assessment 80, 129, 130, 132, 139, 143, 144, 231, 240 cerebral status 131, 298 resuscitation 297, 300
Cardiorespiratory cerebral assessment 233 monitoring 33, 95 Cardiovascular dysfunction 143 response to shock 102 Carotid artery 269 Cartilaginous support 61 Case scenarios illustrating indications 30 Catastrophic deterioration 187 Catecholamine release 217 Catecholamine resistant cold septic shock 125 Cathartic agents 243 Catheter leaking 381 Causative factors of myocardial dysfunction 134 Causes of cardiac arrest 299 cardiogenic shock 134 cardiogenic shock in children 135 coma 193 hospital mortality 143 respiratory failure 299 Caveat 4 Cellulitis and hemostatic abnormalities 234 Central nervous system depression 350 pulse (femoral) 9 Cerebral blood flow 200, 265 edema 351 metabolic rate for oxygen 199 perfusion pressure 266 Cerebrospinal fluid leak 269 Cervical collar application 382 Cervical spine immobilization 384 injuries 382 precautions 386 stabilization 301, 382 Check list for nebulization 367 Chest injury 370 radiographs 85 wall rigidity 40 X-ray (CXR) in the ED 312 Cheyne-Stokes breathing 199 Children with airway abnormalities 337 diarrhea 132 iron deficiency anemia 174 polytrauma 284 Chloral hydrate 339 Cholinergic activity 240
Index
IP :
Cholinesterase reactivator 250 Chronic congestive heart failure 120 heart failure 136 Chylothorax 371 Classification of breathing patterns 77 DKA 346 196.52.84.10Clinical stages of acetaminophen toxicity 254 therapeutic goals of shock resolution 143 Closed head trauma 265 Coagulopathy 308 Colonoscopy 310 Coma with raised ICP 187 Common herbal medications and adverse/toxic effects 260 household things of low toxicity 251 iron preparations 255 Comparison of central and peripheral pulses 10 IP : 196.52.84.10 femorals and dorsalis pedis 10 pulses 9 Compartment syndrome 298 Compensated shock 161 Complete blood count 139, 181, 208 Completion of degree 355 Complication of pleural aspiration 371 severe sepsis 145 renal diseases 151 Components of status epilepticus 5 Congenital anomalies 85 craniofacial abnormalities 45 cystic adenomatoid malformation 370 heart disease 81, 122, 135 lobar emphysema 321 malformations obstructing the airway 65 malformations of the airway 62 Congestive heart failure 103 Conjugate deviation of eyes 206 tonic eye movement 270 Consumption of the respiratory muscles 136 Continuous epileptiform electroencephalogram 12 positive airway pressure ventilation 136 sedation and paralysis 32
Contrecoup injury 271 Convulsive status epilepticus 199, 206, 297 Cool the burn 294 Corneal reflex absent 270 Correct hypoxia and shock 6 Correction of hypovolemia 125 shock 137 Corrosive agent ingestion 242 Corticosteroids 89 Costophrenic angle 314 Cotton swab forceps 380 Counter-regulatory hormones (CRH) 344 Cranial nerves 269 Craniofacial injuries 281 trauma 282 Cricoid pressure 32, 45 Cricothyrotomy 45 Crisis of hypertension 179 Criteria for DKA resolution 350 Critical illness 3 Crystalloids 106 CSF drainage 276 Cuff being inflated 50 Cumulative anoxia 199 Cut off levels for hypertension 179 Cute cardiogenic pulmonary edema 55 Cyanosis diaphoresis 86 Cyanotic congenital heart diseases 174 spell 174 spell with cardiogenic shock 176 Cystic fibrosis 81, 85 Cytotoxic 145
D Damage control surgery 287 Dangerous mechanisms of injury 382 Decreased cerebral perfusion pressure 192 myocardial contractility 145 portal pressure 308 De-fasciculating 30 Dehydration and electrolyte loss ensues 344 Delayed administration of epinephrine 173 Dengue virus 158 Dengue with or without warning signs 159 Depressed mental status or respiratory failure 242 skull fracture 269
411
Derangement of the hemocoagulation system 158 Deterioration in respiratory function 79 Determine physiological status 14 Development of pulmonary edema 152 Dextrostix 112, 202 Diabetic ketoacidosis (DKA) 344 Diaphoresis 86 Diaphragmatic hernia 103 Diarrhea and hypovolemic shock 129 Diastolic blood pressure 11 dysfunction 134 Diazepam 209 Diazoxide 183 Difficult airway algorithm 45 equipment 44 kit 45 protocol 44 Digital rectal exam 310 Digoxin 221, 243 Direct laryngoscopy 32 Disability 14, 112, 151 Disseminated intravascular coagulation 101, 199, 308 Dissociative shock 103 Distal pulses 9 Distributive shock 103 Divert portal blood flow 308 Dobutamine 109, 121 Dobutamine for cardiogenic shock 297 Dopamine refractory hypotensive vasodilatory shock 124 Dorsum of the foot 9 Drooling and dysphagia 62 Drowsiness 4 Drugs induced gastritis 306 interactions with herbal products 261 therapy 203 used for asthmatic exacerbation in the ED 92 used in emergency room for management of status epilepticus 209 Dynaplast 114 Dyselectrolytemia 129 Dysmorphic facial features 33 Dysphagia 62, 68 Dysphonia 85 Dysrhythmias 377
412
Pediatric Emergency Medicine Course (PEMC)
E
IP : 196.52.84.10
Ecchymosis 286 EC-clamp: appropriate 28 EC-double clamp 28 EC-inappropriate clamp 27 Ectopic gastric mucosa 310 Effortless tachypnea 130 Electrical injury 296 Electrocardiography 301 Electroencephalography 193 Emergency medicine 355 services 355 Emesis 248 Empyema 80, 371 Enalapril 183 Endogenous catecholamine 124 Endotracheal 46 Endotracheal tube (ETT) 47, 50, 334, 358 Ensure oxygenation 45, 46 Entry wound in the forearm 298 Envenomation 111, 141 IP : 196.52.84.10 Enzyme acetylcholinesterase 247 Epidural hematoma 270 Epiglottitis 45, 63, 85 Epilepticus 31, 120 Epinephrine 66, 109, 111, 122, 172 Episodes of diarrhea and vomiting 129 Esmolol 183 Esophageal injury 242 Esophagitis 308 Etiology of shock 110 Etomidate 39, 40, 340 Euvolemic restrict fluids 202 Evidence of facial and neck trauma 33 respiratory distress 132 warm shock 132 Excessive catecholamine state 135 cricoid pressure 36 sweating 199 Expiratory pressure valve 55 External auditory meatus 35 portion 97 Extravascular fluid shifts 299
F Faces pain scale-revised (FPSR) 335 Failure of the cardiovascular system 134 Failure to decompress stomach contents 34
Failure with tachycardia 144 Fasciculations 41 Fasciotomy 230 Fatal attack of asthma 86 FB obstruction in the ED 69 Features of pulmonary edema 138 severe sepsis 144 Febrile children 6 infants 5 Fenoldopam 183 Fentanyl and atropine 64 Fiberoptic intubating laryngoscope 45 laryngoscope bronchoscope 45 scopes 50 Fibrinolytics 226 Fighting the mask 86 Fixation of tracheal tube 38 Flexible devices 50 Floor plan of the resuscitation unit 356 Flow inflating ventilation device 53, 55, 56 Fluid bolus therapy 150 correct shock 106 management in severe dengue 161 resuscitation of septic shock 143 resuscitation of shock 139 unresponsive 124 Flumazenil 341 Focus of infection 143 sepsis 153 Foley catheter insertion 380 Forced neutral diuresis 245 Foreign body (FB) obstruction 65, 68 Fosphenytoin 205, 209 Fracture of cervical spine 378 ribs 282 Free fatty acids (FFA) 344 Fresh whole blood preferable 282 Functional residual capacity 30
G Gag and cough reflexes 270 Galea aponeurosis 267 Gastric decompression via NGT 26 Gastric lavage 241, 253, 261, 307 Gastritis 308 Gastrointestinal bleeding 305 decontamination 241
GIT duplication 308 Glasgow coma scale (GCS) 187, 273 Glossopharyngeal nerve 32 Glottic edema 66 Glottic obstruction 62 Glottis 62 Glucocorticoids 66 Glucose normal saline 153 Grunting 79 Guedel airways 45 Gum elastic bougie 45 Gustilo classification of open fractures 285 grade 285
H Hazards of intubation 32 salbutamol nebulization 87 Head and skull 282 Head bobbing 84 Heart disease 120 Heart rate abnormalities 135 Hemangiomas 63 Hematemesis 305 Hematocrit 159 Hematoma accumulation 271 causes mass effect 271 Hemodialysis 245 Hemodynamic interventions 143 Hemostatic bites 233 resuscitation 287 Hemothorax 371, 377 Henoch-Schönlein purpura 310 Hepatic injury 286, 377 Hepatomegaly resolved 6 Herniation syndromes 192 Hexaethyltetraphosphate 247 High tension wire 297 History of breathlessness in children 144 chronic respiratory distress 140 diving 300 respiratory distress 137, 141 Hoarse voice 62 Hyaline membrane disease 120 Hydralazine 183 Hydrocortisone 92 Hyperacute respiratory distress 81 Hyperchloremic acidosis 352 Hypercyanotic spell 174 Hyperdynamic circulation 9
Index
IP :
Hyperglycemia and ketoanions 345 Hypernatremia 199 Hyperpyrexia 199 Hypersecretion 199 Hypertension in children 179 Hypertensive emergency 179 encephalopathy 181 196.52.84.10 urgency 180, 183 Hypocalcemia 65, 70, 135, 138 Hypoglycemia 129, 135, 202 Hypokalemia 9, 138 Hypoperfusion 145 Hypopharynx 48 Hypotensive cardiogenic shock 136, 218 intra-abdominal injury 282 septic shock 123 shock associated with SE 201 warm shock 124 Hypothermia 9, 135, 143, 242 Hypotonia 4 Hypovolemic shock 129, 132, 135, 300 IP : 196.52.84.10 Hypoxic asthmatics 87 Hypoxic injury 29 Hypoxic ischemic encephalopathies 80
I Iatrogenic causes of cerebral edema 351 Immediate antimicrobial coverage 194 Immobilizing the entire spine 383 Impending respiratory failure 61 Inability to recognize 5 Inadequate oxygen flow 55 Inappropriate technique 28 Increased cerebral blood flow 199 production of ketoanions 345 pulmonary blood flow 177 pulmonary vascular resistance 145 Indian National Snakebite Protocol (2007) 226 Indications for activated charcoal 242 CT brain 279 initiating inotropes 109, 126 intubation in comatose children 189 intubation in SE 201 Induction agents 33, 39 Ineffective cough 62 Infant or neonate 45 Inflammatory mediators 101 Infra-auscultate axillary 8 Ingestion of corrosives 262
Inhalational induction 47 injuries due to burns 281 Inhaled ipratropium bromide 89 salbutamol 91 Initiate bag-valve-mask ventilation 46 Inotrope initiated 6 Inotrope infusion 55 Inserting the laryngoscope 46 Insertion of Foley catheter 380 Inspiratory stridor 85 Insulin deficiency 344 infusion line 348 resistance and hyperkalemia 350 therapy 348 Interictal coma 199 Internal jugular vein 379 Interpretation of chest radiographs 312 critical illness 16 Interrupt ASV infusion 232 fluids 203 Intestinal obstruction 131 Intra-abdominal injury 286 organs 286 Intra-arterial pressure monitoring 125 Intracellular concentration 88 Intracompartmental pressure 230 Intracranial infections 14 lesions 270 pressure 266 tension 40 Intramuscular route if intravenous 205 Intranasal route 200 Intraosseous access 105, 114 route 205 tray 114 Intraparenchymal bleeds 271 hemorrhage and edema 272 Intrapulmonary shunting 299 Intrathoracic airway 62 pressure 79 Intravascular catheters 105 fluid loss 299 volume 137 Intravenous hydrocortisone 89 lines prior to intubation 34 salbutamol 90 Intubating laryngeal mask 45 medications 46 Intubation triggers 152
413
Investigations in management of coma 187 Ipratropium bromide 86, 88, 92 Ipsilateral conjugate lateral gaze palsy 270
J Jackson-Rees circuit 34, 55, 104, 105, 357 Jerky respirations 200 Jet ventilation set 45 JR circuit in an apneic child 56
K Kawasaki’s disease 122, 135 Kehr’s sign 286 Kerosene ingestion 242 Ketamine 36, 39, 40, 64, 91, 92, 340 Ketonemia and acidemia 344
L Labetalol 183 Laboratory analysis of serum 241 Lacrimation 248 Large volume pediatric emergency 3 Larygnoscope handle 36 Laryngeal mask airway 44, 45, 48, 358 papilloma 65, 70 stridor 70 Laryngomalacia 63, 65, 70 Laryngoscope blades 35, 45 Laryngoscopic examination 68 Laryngoscopy and intubation 45, 46 Laryngospasm 45 Leakage of plasma 158 Lethal oral dose 255 Leukocytosis 143, 251 Level of consciousness 187 Levetiracetam 205 Lidocaine 36, 39 Life-asthma threatening 84 Life-saving emergency care 355 Liver function test 139 injury 254 span 12 Localization of head injury 270 Lorazepam 201, 209 Lorazepam controls seizures 203 Loss of cutaneous barrier 291 surfactant 299
414
IP : 196.52.84.10
Pediatric Emergency Medicine Course (PEMC)
Low systemic vascular resistance septic shock 124 Lower GI bleed 309 Lower nephron necrosis 199 Low-set ears 33 Lubricate the posterior surface 48 Lumbar puncture 193 Lung fluid 200 Lung parenchyma 78, 314 Lytic cocktail 221
M Macroglossia 63 Magic drugs 119 Magnesium sulfate 89, 92 Maintain electrolyte balance 255 euglycemia 138 fluid requirements 137 hematocrit 137 normal temperature 137 IP : 196.52.84.10 Major burns 292 Maldistribution 145 Malignant hypertension 180 Mallampati classification 336 Malrotation 308 Management of acute diarrhea 129 exacerbation of asthma 84 adverse events 341 anaphylactic shock 170 cardiogenic shock 134, 141 cerebral edema 351 dengue with warning signs 158, 160 drowning victim 299 eye signs 13 fluid overload 166 hypertensive emergency 179, 181 shock 148 intracranial hypertension 191 local and systemic effects 219 non-traumatic coma 187 pain in children 335 raised intracranial pressure 275 severe dengue 158 status epilepticus 198 Mandibular hypoplasia 33 Manual stabilization of cervical spine 382 Massive empyema 109 Match fluid resuscitation 129 Maxillofacial and intraoral trauma 282 Mean arterial pressure (MAP) 12, 266 Mechanical ventilation 143
Mechanism of working of Jackson-Rees circuit 55 Mecoprop poisoning 245 Mediastinal shift 314 Medical complications of status epilepticus 199 Mental status in children 129 Mepiridine (demerol) 341 Metabolic abnormalities 136, 138 acidosis 138, 199, 240 biochemical abnormalities 199 demands of tissues 134 derangements 101 disorders 203 effects 123 fat 344 Metered dose inhalers 91 Methemoglobinemia 103, 240, 261 Method of administration of ASV 232 Methylprednisolone 92 Microbial invasion 143 Micrognathia 33, 45, 63 Midazolam 39, 105, 207, 209, 339 Middle finger down 49 Mild traumatic brain injury 265 Milrinone 109 Minimal mucosal edema 62 Minor head trauma 267 Minor symptoms 4 Miosis 248 Monitor serum sodium 202 Monitoring equipment 33 Monitoring of urine output 380 Monroe-Kellie doctrine 267 Morphine 221, 340 Motor vehicle accidents 265 Mpending respiratory failure 218 Mucolytics 90 Muffling of voice 62 Multidose regimen 88 Multiorgan failure 101 Multiple organ dysfunction 199 Muscarinic acetylcholine receptors 248 Muscarinic effect 240 Muscarinic effects of acetylcholine 248 Muscular twitching 252 Mydriasis 270 Myocardial contractility 138 depressant factor 134 disease 121 dysfunction 134, 144, 147, 188, 203, 300 edema 134 function 5, 134 ischemia 125 oxygen demand 136 performance 136
Myocarditis 81, 122, 134 Myopathies and muscle necrosis 40 Myotoxins 226
N N-acetylcysteine 255 Naloxone 341 Nasal flare 84 Nasogastric tube (NGT) 27, 34, 200, 242, 307 Nasogastric tube emerging 28 Nasogastric tube insertion 34 Nasopharyngeal airway 45, 357 Nasopharynx 63 Nasotracheal intubation (NTI) 32 Near fatal asthma 86 Nebulization 367 Nebulization tray 367 Nebulizer therapy 86, 367 Nebulizing kit 367 Neck of the bladder 381 Need to ventilate cannot intubate 39 Needle cricothyrotomy 45 thoracocentesis 109, 282, 370 Needle thoracocentesis 374 Neem oil ingestion 259 Neostigmine test 233 Nephrotoxins 226 Neurogenic etiologies 81 functional stridor 8 pulmonary edema 199 stridor 71, 188 Neurohormonal responses 102 Neurological assessment 12 evaluation 283, 285 Neuromuscular blockade agents 33, 36, 40 Neuronal excitability 207 Neuropeptide activity 198 Neurotoxic bites 233 Neurotoxicity secondary 218 Neurotoxins 226 Neurovascular bundle 374 Nicardipine 183 Nicotinic effect 240 Nifedipine 183 Nitroprusside 182 Non-cardiogenic pulmonary edema 31, 81, 217, 145, 301 Non-convulsive status epilepticus 7, 110, 136, 143, 188, 206 Non-invasive positive pressure ventilation 55
Index
IP :
Non-steroidal anti-inflammatory drugs (NSAIDs) 170 Norepinephrine 109, 120, 124 Normal pulse pressure 150 respiratory rate for age 79 Normalization of blood 150 heart rate 150 span 151 196.52.84.10 liver mental status 151 peripheral pulses 150 respiratory rates 150 saturations 177 Normotensive shock 148 Nystagmus 12, 81
O Obesity 45 Obstructed airway and hypotensive shock secondary to anaphylaxis 32 Obstructive shock 103 Ocular movements 270 Oculogyric crisis 7 IP : 196.52.84.10 Oculomotor 218 Oliguria 199 Omeprazole 258 Ominous sign 79 Opioids 247 Oral rehydration salts 131 therapy 4 Organ dysfunction 144 Organization of the intraosseous tray 115 Organophosphates 248 Organophosphorus poisoning 250 compounds 247, 262 Orogastric tube 272 Oropharyngeal airways 357 bleeding 310 secretions 205 suctioning 249 Oropharynx 48 ORS administration with body weight 160 Orthopedic trauma 283 Osmotic diuresis 344 Osmotic therapy 276 Oxygen delivery 103 inhalational therapy 86 saturation 26 source 33
P Pain management in children 335 Painful procedures 336 Palliative shunt procedure 176 Palpable bony fragments 286 Pancuronium 41 Papilledema 270 Paradoxical chest wall movements 84 Paralytic drugs 33 Paranasal sinuses 63 Parasympathetic blockade 253 Parenchymal bleeding 271 Parkland resuscitation formula 294 Paroxysmal hyperpnea 174 Parts of laryngeal mask airway 48 Pasmodic croup 65 Pathophysiology of anaphylaxis 170 cyanotic spell 174 DKA 344 shock 101 snake venom 225, 226 Patients with polytrauma 382 Peak expiratory flow rate 90 Pearls and pitfalls 25, 53 Pediatric accident and emergency group 187 advanced life support 297, 300 assessment triangle (PAT) 129, 134, 143, 158 bain circuit 53 emergency medicine 39 resuscitation and emergency services 364 PEMC approach: respiratory distress 83 Penicillins 135 Pentobarbital 340 Pericardial cavity 375, 376 effusion 314, 334, 375 fluid 375, 376, 377 paracentesis 375 Pericardiocentesis 109, 375 Perinatal depression 120, 141 Perineum 282 Peripheral perfusion 150 utilization of glucose 344 vasoconstriction 9 Permissive hypotension 287 Petechial hemorrhages 270 Pharmacologically assisted intubation 30, 32
415
Pharmacotherapy of hypertensive emergencies 182 Phenobarbital 207 Phenothiazine group of drugs 7 Phentolamine 183 Phenytoin 204, 209 Phosphate 350 Photodetector picks up R/IR light source 95 Pitfalls in cervical spine radiology 385 Plaster for securing tube 33 Platelet dysfunction 158 Pleural aspiration 370 effusions 371 space 370 Pneumatocele 370 Pneumonia and asthma 7 Pneumopericardium 377 Pneumoperitoneum 334 Pneumothorax 111, 334, 370, 371, 377 Poison syndromes 241 Poisoning: general approach 239 Poisons 111 Polydipsia and polyuria 344 Polytrauma 281 Polyuria and polydipsia 349 Portal hypertension 307 Positioning of airway 35 Positive end-expiratory pressure 145 Posterior oropharynx 49 Postintubation management 37 Postsynaptic neurotoxins 233 Potassium administration 350 Pralidoxime and atropine 250 Prazosin 219, 220 Prehospital management 299 setting 69 Premedication agents 33 Premorbid sign 9 Preoxygenate on arrival 41 Preoxygenation of patient 34 Preoxygenation with non-rebreathing mask prior 39 Preparation of airway tray 35 insulin infusion 348 Prevalence of hypertension 179 Primary survey and initial management 283 Principles of prehospital care 299 Probable dengue 159
416
IP : 196.52.84.10
Pediatric Emergency Medicine Course (PEMC)
Problems during cervical spine immobilization 385 Procedural sedation 335 Procedures requiring sedation 336 Procoagulants 226 Progression of edema 228 status epilepticus 198 Progressive fall in mental status 86 Prolonged hypoxia 135, 299 seizures 141 Propofol 340 Pull push technique 129 Pulmonary artery 135 blood flow (PBF) 174 edema 80, 143, 145, 217, 218, 299, 300, 318 embolism 103 hydrostatic pressure 145 response 103 IPvascular resistance 136 : 196.52.84.10 Pulse oximeter 33, 55, 95, 96 Pulsus paradoxus 65 Pupillary examination 13 response 12 Push enteroscopy 310 Pyelonephritis 381 Pyrethroids 261 Pyridoxine 205
Q Quiet tachypnea 81
R Raised intracranial pressure 9, 36, 191, 188 Randomized controlled trials 55 Rapid cardiopulmonary assessment 82 cerebral assessment 14, 84 mechanism in shock 102 Rationale for avoiding bicarbonate 350 potassium replacement 349 Recognition of abdominal trauma 281 coexisting septic shock 129 early signs 3 septic shock 155 shock 143
Recognize cardiogenic shock 134 pulmonary edema 144 ‘red flag’ signs during 45 Recovery from water 300 Rectum 282 Recurrence of pulmonary edema 153 Refractory cardiogenic shock 124 status epilepticus 206 Rehydration fluid 347 Renal failure 199 function test 139 glucose clearance 344 inflammation 381 response 103 Resolution of hepatomegaly 151 hypotensive shock 150 ketoacidosis 348 myocardial dysfunction 151 Respiratory acidosis 199 distress 136, 144, 158, 177, 300 emergencies 312 failure 29, 79, 120, 136, 188, 252, 253 rate and work of breathing 78 system failure 199 Responsive to pain or unresponsive 281 painful stimulus 4 voice 4 Restoration of tissue perfusion 101 Resultant hematoma 378 Resuscitation in critically ill children 101 Resuscitation of acute cardiogenic shock 140 Retention of ketoanions 345 Retropharyngeal abscess 63, 65, 68 Reversal agents 341 Rhabdomyolysis 199 Right infraclavicular region 38 Right ventricular 136 Risk of air embolism 379 drowning in water bodies 299 pulmonary edema 177, 300 tachyarrhythmias 120 Rocuronium 33, 40, 41 Rothromboplastin time 208
S Salbutamol nebulization 84, 85, 88 Salivation 248
Sand bag 114 Scalp injuries 275 Scalp lacerations 267 Scorpion antivenom 221 envenomation 218, 220 sting envenomation 221 Seat belt injury 286 Secondary brain injury 266 Sedative analgesics 338 hypnotic overdose 252 hypnotic poisonings 261 paralytic agents 32 Seizure control neuropeptides 199 Selection and fixing of appropriate cervical collar 383 Selection of LMA 48 Sellick’s maneuver 36 pressure 36 Semirigid 50 Septic cardiogenic shock 81 neurogenic shock 102 Sequence of intubation 36 Sequential steps of PAI 30 Serious sepsis 143 Serology for dengue 139 Serum electrolytes 139 potassium 200 sodium correction 345 Severe bradycardia 301 cardiotoxic reactions 204 chest retractions 65 dehydration 129, 130, 132 dengue 159, 308 hyperglycemia 344 hypertension 179 parenchymal lung disease 31 peripheral vasoconstriction 299 pneumonia 370 sepsis 81, 103, 141 trauma 40 traumatic brain injury 268 Shaken baby syndrome 270 Shock correction 158 persists 108 resolution 149 with normal blood pressure 163 Short trachea predisposes 25
Index
IP :
Signs of acute lung injury 101 cardiac dysfunction 136 dehydration 131 hypoxia 134 pulmonary edema 108, 125, 137, 139, 151, 152, 300 refractory shock 151 196.52.84.10 shock 131 shock resolution 150 Simultaneous administration 32 Site of insertion of needle 376 Size of hemithorax 314 Skeletal muscle glycogenolysis 344 Skull fractures 268 Small endotracheal tubes 47 infants neonates 27 pupil 270 volume etiologies 108 Snake bite envenomation 225 envenomation 31 IP : 196.52.84.10 Soft stridor 62 tissue injury 285 Somnolence and obtundation 80 Spasmodic croup 68 Spectrum of difficult airway 44 gastrointestinal bleeding 305 Speed of fluid administration 106, 148 Spinal clearance 385 immobilization in trauma victims 386 injury 284 stabilization 382 Spleen and liver 282 Splenic injury 286 Stabilization of the cervical spine 382 Stable cardiorespiratory function 342 Status epilepticus 7, 198 Steps of manual cervical spine stabilization 383 procedural sedation 335 spinal stabilization 382 Sterile drapes 380 gloves 380 technique 379 water 380 Sternal retractions 63 Steroids 153, 172 Stimulation of the sympathetic system 218 Stricture urethra 381 Stridor due to structural abnormality of the airway 33 with respiratory distress 67
Structural diseases of the larynx 85 heart disease 135, 139, 140 Subcutaneous adrenaline 89 insulin 351 Subgaleal hematomas 268, 276 Subglottic regions 61 Submersion injury 7, 135, 299 Subpulmonary outflow tract 174 Succinylcholine 39, 40, 41, 64, 249 Suction oropharyngeal secretions 200 Suctioning pressure 27 Sudden unresponsiveness 7 Supine position 63 Supraglottic airway devices 45 Supraglottis 61, 62 region 61 Supraventricular tachycardia 126, 135 Surface irrigation with saline 285 Suspicion of shigellosis 130 Suxamethonium 6, 33 Swelling in front of the neck 64 Systemic hypersensitivity reaction 170 inflammatory response syndrome 143, 291 vascular resistance 126, 135, 137, 139 Systolic blood pressure 11
T Tachycardia 9, 79, 132 Tachypnea 8, 78, 132, 143, 199 Technique of chest tube insertion 371 manual stabilization 382 Tension pneumothorax 103, 109 Tetanus prophylaxis 283 Tetralogy of Fallot (TOF) 174 Theophylline 243 Therapeutic goals of shock resolution 108 Thiopental 36, 39, 207, 339 Thoracostomy kit 371 Time of onset of anaphylactic reactions 171 Tincture benzoin soaked cotton 33 Tonic-clonic activity 200, 207 Tourniquet made of rope 226 Toxic reactions 135 Toxicity of iron by amount ingested 256 Toxidromes 240, 241 Toxin screen 194 Tracheal narrowing 85 Tracheobronchomalacia 85 Tracheoesophageal fistula 63
417
Train nurses in emergency resuscitation 361 Transjugular intrahepatic portosystemic shunt (TIPS) 308 Traumatic brain injury in the ED 272 Treatment of intracranial pressure 193 Type of venom action 226 venom component 226 shock 103, 135
U Uncal herniation 187, 188 Unequal pupils 13 Unilateral fixed dilated 270 LMN 270 Unique odors 252 Unmaintainable airway 199 Unstable and obstructed airway 201 Upper abdominal organs 286 airway foreign bodies 85 airway obstruction 47 Ureteral rupture 381 stricture 381 trauma 381 Urinary tract infections 144 Urine alkalinization 243, 245 output 109, 151 Urological injury 286 Use of Jackson-Rees circuit 158 rapid cardiopulmonary cerebral assessment 344 sedative and analgesic drugs 335
V Vagal-induced bradycardia during laryngoscopy 47 Vallecula 36 Valproic acid 205, 209 Valvular pulmonic stenosis 174 Variable absorption of light 96 Vascular access 64 endothelial cell dysfunction 158 examination 284 malformation 308 structures 377
418
IP : 196.52.84.10
Pediatric Emergency Medicine Course (PEMC)
Vasoactive medications 119 Vasoconstrictors 176 Vasodilatory shock, diagnosis of 150 Vasopressin 125 Vasopressors and inodilators 109 Vecoronium 33, 36, 41 Venodilation 145 Venous return falls 37 Ventilation device 136 perfusion 299 Ventricular dysrhythmias 135 ectopy 125 fibrillation 299 premature contractions 126 Venturi effect 61 Video laryngoscope 45 Videoscopic techniques 50 Viperine envenomation 234
IP : 196.52.84.10
Viral infections 130 upper respiratory tract infection 88 Visual abnormalities 218 Vocal cord dysfunction 85 paralysis 65 Vomiting and diarrhea 103 during intubation 36 of gastric contents secondary 27
W Waiting for confirmatory blood gas analysis 105 Wavelength spectrum 96 Wheezing attacks 85 loudest 85
Whole bowel irrigation 243, 257 Wide pulse pressure 132 Wong-Baker faces pain scale (WPFPS) 335 Worsening hypoxia 56, 87, 88
X X-ray clues to diagnosis 320 severe traumatic brain injury 278 X-whilst abdominal ray 286
Y Yankauer suction catheter 26 Young infants 9