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Cambridge University Press 978-1-316-60886-9 — Pediatric Emergency Medicine Edited by Rebecca Jeanmonod , Shellie L. Asher , Blake Spirko , Foreword by Denis R. Pauze Frontmatter More Information

Pediatric Emergency Medicine Chief Complaints and Diferential Diagnosis

© in this web service Cambridge University Press www.cambridge.org Cambridge University Press 978-1-316-60886-9 — Pediatric Emergency Medicine Edited by Rebecca Jeanmonod , Shellie L. Asher , Blake Spirko , Foreword by Denis R. Pauze Frontmatter More Information

Pediatric Emergency Medicine Chief Complaints and Diferential Diagnosis

Edited by Rebecca Jeanmonod St. Luke’s University Health Network, Bethlehem, PA, USA Shellie Asher Albany Medical Center, Albany, NY,USA Blake Spirko Baystate Medical Center, Springield, MA, USA Denis R. Pauze´ Albany Medical Center, Albany, NY,USA

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Contents

List of Contributors page viii Preface xi List of Abbreviations xiii Reference Values xv

1 AStatement 1 Case 4 49 Denis R. Pauze´ Contributing Author: Amanda Shorette Case 5 52 2 Resuscitation 3 Contributing Author: M. Bryan Dalla Case 1 3 Betta Contributing Author: Erica Escarcega Case 6 55 Case 2 7 Contributing Authors: Daniel K. Pauze´ Contributing Author: Michael Leonard and Denis R. Pauze´ Case 3 10 Case 7 59 Contributing Author: Donald Jeanmonod Contributing Authors: Ben Church and Case 4 16 Rebecca Jeanmonod Contributing Authors: Denis R. Pauze´ Case 8 64 and William H. Hauda Contributing Authors: Natalie Moore and Case 5 19 Rebecca Jeanmonod Contributing Authors: John Tran and Rebecca Jeanmonod 4 Fever 68 Case 6 23 Contributing Authors: Ryan Fulton and Case 1 68 Melanie K. Prusakowski Contributing Author: Rebecca Jeanmonod Case 7 26 Case 2 71 Contributing Author: Edwin Layng Contributing Author: Shellie Asher Case 8 29 Case 3 73 Contributing Author: Erica Escarcega Contributing Authors: David H. Long and Case 9 32 Janet Young Contributing Author: Sean Zwiebel Case 4 76 Case 10 35 Contributing Author: Shellie Asher Contributing Author: Sean Zwiebel Case 5 78 Case 11 38 Contributing Authors: Kristine Marie J. Contributing Author: Ben Church Casal and Melanie K. Prusakowski Case 6 81 3 Breathing Complaints 42 Contributing Author: Taylor R. Spencer Case 1 42 Case 7 85 Contributing Author: Lauren Snyder Contributing Author: Sarah Hudgins Case 2 45 Case 8 88 Contributing Author: Natalie Moore Contributing Author: Rebecca Jeanmonod Case 3 47 Case 9 91 Contributing Author: Dorka M. Jimenez´ Contributing Authors: Keel Coleman and Almonte Khalief Hamden

Cambridge University Press 978-1-316-60886-9 — Pediatric Emergency Medicine Edited by Rebecca Jeanmonod , Shellie L. Asher , Blake Spirko , Foreword by Denis R. Pauze Frontmatter More Information

Contents

Case 3 206 Case 2 255 Contributing Author: Denis R. Pauze´ Contributing Author: Shellie Asher Case 4 209 Case 3 257 Contributing Author: Rebecca Jeanmonod Contributing Author: Abhishek Case 5 211 Chaturvedi Contributing Authors: Tom Williams, Case 4 260 Emily Miller, and Denis R. Pauze´ Contributing Author: Jennifer Pelesz Case 6 215 Case 5 263 Contributing Author: Rebecca Jeanmonod Contributing Author: Pamela Young Case 7 219 Case 6 266 Contributing Author: Kinsey Leonard Contributing Author: Leah A. Perez Case 8 221 Case 7 269 Contributing Author: Kinsey Leonard Contributing Authors: Shellie Asher and Rebecca Jeanmonod 10 Head and Neck Pain 224 Case 1 224 12 Skin Complaints 273 Contributing Author: Sonika Raj Case 2 226 Case 1 273 Contributing Author: Rebecca Jeanmonod Contributing Author: Efrat Rosenthal Case 3 230 Case 2 276 Contributing Authors: Tom Dittrich, Contributing Author: Efrat Rosenthal Denis R. Pauze,´ and Matthew Adamo Case 3 278 Case 4 234 Contributing Authors: Sundeep M. Contributing Authors: Anst Gelin and Shukla and Rebecca Jeanmonod Janet Young Case 4 282 Case 5 236 Contributing Author: Amanda Shorette Contributing Authors: Christine M. Case 5 286 George and Melanie K. Prusakowski Contributing Author: Benjamin Kitt Case 6 240 Case 6 288 Contributing Author: Carl Daniel Contributing Author: Rebecca Jeanmonod Case 7 243 Case 7 291 Contributing Authors: Michael Leonard Contributing Author: Dorka M. Jimenez´ and Rebecca Jeanmonod Almonte Case 8 247 Contributing Author: Jason Schwaber Case 9 249 Contributing Authors: Jamaine Ortiz Jr., Rebecca Jeanmonod, Carl Daniel, Denis Case Key 295 R. Pauze,´ and Matthew Adamo Index 296 11 Genitourinary Complaints 253 Case 1 253 Color plates are to be found between pages 152 and Contributing Author: Shellie Asher 153

vii

Contributors

Matthew Adamo Christine M. George Albany Medical Center, Albany, NY Carilion Clinic, Roanoke, VA Dorka M. Jimenez´ Almonte Khalief Hamden Baystate Medical Center, Springield, MA Carilion Clinic, Roanoke, VA Shellie Asher William H. Hauda Albany Medical Center, Albany, NY Inova Fairfax Hospital, Falls Church, VA M. Bryan Dalla Betta Sarah Hudgins Baystate Medical Center, Springield, MA St. Luke’s University Health Network, Bethlehem, PA Jason Black Donald Jeanmonod St. Luke’s University Health Network, Bethlehem, PA St. Luke’s University Health Network, Bethlehem, PA Kristine Marie J. Casal Rebecca Jeanmonod Carilion Clinic, Roanoke, VA St. Luke’s University Health Network, Bethlehem, PA Abhishek Chaturvedi Brian Kelly Pt. B.D. Sharma PGIMS, Rohtak, India St. Luke’s University Health Network, Bethlehem, PA Ben Church Benjamin Kitt Baystate Medical Center, Springield, MA Baystate Medical Center, Springield, MA Michelle Clinton Edwin Layng Carilion Clinic, Roanoke, VA St. Luke’s University Health Network, Bethlehem, PA Keel Coleman Kinsey Leonard Carilion Clinic, Roanoke, VA Baystate Medical Center, Springield, MA Carl Daniel Michael Leonard Albany Medical Center, Albany, NY St. Luke’s University Health Network, Bethlehem, PA Tom Dittrich David H. Long Roper St. Francis Hospital, Mount Pleasant, SC Carilion Clinic, Roanoke, VA Erica Escarcega Angela Mastantuono St. Luke’s University Health Network, Bethlehem, PA Carilion Clinic, Roanoke, VA Ryan Fulton Sade´ McKenzie Carilion Clinic, Roanoke, VA Albany Medical Center, Albany, NY Anst Gelin Alyssa Milano Carilion Clinic, Roanoke, VA St. Luke’s University Health Network, Bethlehem, PA

viii

List of Contributors

Emily Miller Efrat Rosenthal Albany Medical Center, Albany, NY Baystate Medical Center, Springield, MA Natalie Moore Jason Schwaber Baystate Medical Center, Springield, MA Ellis Hospital, Schenectady, NY Jonathan R. Morgan Amanda Shorette Carilion Clinic, Roanoke, VA Baystate Medical Center, Springield, MA Jonathan Nogueira Sundeep M. Shukla Carilion Clinic, Roanoke, VA Baystate Medical Center, Springield, MA Jamaine Ortiz Jr. Lauren Snyder St. Luke’s University Health Network, Bethlehem, PA Baystate Medical Center, Springield, MA Rachel A. Patterson Taylor R. Spencer St. Luke’s University Health Network, Bethlehem, PA Ellis Hospital, Schenectady, NY Daniel K. Pauze´ Holly Stankewicz Albany Medical Center, Albany, NY St. Luke’s University Health Network, Bethlehem, PA Denis R. Pauze´ Cara V. Tillotson Albany Medical Center, Albany, NY Carilion Clinic, Roanoke, VA Dorota Pazdrowska John Tran Carilion Clinic, Roanoke, VA St. Luke’s University Health Network, Bethlehem, PA Jennifer Pelesz Tom Williams Albany Medical Center, Albany, NY Albany Medical Center, Albany, NY Leah A. Perez Janet Young Albany Medical Center, Albany, NY Carilion Clinic, Roanoke, VA Melanie K. Prusakowski Pamela Young Carilion Clinic, Roanoke, VA Albany Medical Center, Albany, NY Sonika Raj Sean Zwiebel Albany Medical Center, Albany, NY St. Luke’s University Health Network, Bethlehem, PA

Preface

Textbooks abound, electronic resources are ubiqui- because every teenager is honest about substance use. tous, and there is an app for everything. Where But we know better. does this book it, as you struggle to “learn” clinical his book strives to ill the gap between tradi- medicine? tional textbooks and bedside medicine. Instead of he issue is always application. Most physicians, being organized by organ system, this book is orga- physicians-in-training, and physician assistants can nized by chief complaint, based on published frequen- takeatest.heyknowhowtolookataquestionwitha cies of the most common pediatric chief complaints list of closed possibilities and choose the right choice. seen in emergency departments. Each chapter repre- If given four possibilities, the correct answer is oten sents a chief complaint. Each case is presented as an obvious, or at least recognizable. Question banks and unknown, with a historical vignette and an examina- question books are designed to help learners with this, tion and ancillary tests, ater which we have provided and they work well. questions for thought. he reader should stop and Textbooks are generally, almost universally, orga- consider the case and really think about these ques- nized by organ system. his is a very rational way tions, the next steps, the dilemmas that are real, pre- to write a text book. It is straightforward from a sented by these patients that are real, written by the writing perspective, and allows the learner to get in- physicians who actually cared for them. his is fol- depth information about everything in a given organ lowed by the diagnosis, and a discussion of the dis- system in a step-by-step fashion. When you haven’t ease as well as the other diseases that you should have learned about gastrointestinal physiology, let alone considered, and how to distinguish them from one gastrointestinal pathophysiology, this makes sense, as another. well. Youcanusethisbookonyourown,oryoucanuse But the practice of medicine isn’t really like either it with a friend. he book can easily be used for case- of these things. Not really. Patients come in with com- based teaching for clerkships, residencies, or small plaints. heir complaints don’t come with a closed list group learning. of answers to choose from, and they don’t come with What you won’t ind is a chapter on “staph scalded their organ-system chapter. A complaint may seem skin syndrome,” or a chapter on “new onset dia- to be referable to a speciic organ system, but ulti- betes.” You will, however, learn when to worry about mately may be multifactorial. Take, for instance, the a rash, how to resuscitate a baby, which seizure complaint of “shortness of breath.” Your brain wants patient needs labs and what your diferential diagnosis youtothinkaboutthelungsandtheairwayasthe should be, and basically, how to think about illness in source of the problem. But maybe it’s symptomatic children. anemia. Maybe it’s cardiac. Maybe it’s acidosis from an If you happen to ind yourself wanting to read ingestion. Maybe it’s renal failure with luid overload. about a speciic disease without the mystery of the case, Maybe it’s a foreign body. Maybe it’s traumatic, even wedoprovideakeyatthebackofthebookto“cheat” with no history of trauma. It happens. andindadiscussiononintussusception,orreadingon But most written resources do not invoke the intracranial tumors. And it’s ok to do that, but remem- model of the patient as a mystery, the disease as an ber that human tradition was based on stories, handed unknown. hey presuppose you know it’sa GI problem down through generations by the telling and remem- because the complaint is vomiting, or that it’s a toxin bering. You will learn better from stories than from

Preface

tables and graphs. You will retain information when to close your diferential prematurely. You will be less youcareabouttheoutcome,andtheproviderswho likely to short-cut your examination or skip the impor- wrote these cases want you to care the way they do. tant questions on your history. And you will be a bet- If you use this book as it’s intended, you will have terdoctorandtakebettercareofourmostvulnerable broader diferential diagnoses. You will be less tempted population. And what could be better than that?

xii

Abbreviations

AAP American Academy of Pediatrics CSF cerebrospinal luid ABC airway, breathing, and circulation c-spine cervical spine ABG arterial blood gas CT computed tomography ACE inhibitor angiotensin-converting-enzyme CTA clear to auscultation inhibitor CVC central venous catheter ACLS Advanced Cardiac Life Support CXR chest X-ray ALL acute lymphoblastic leukemia DKA diabetic ketoacidosis ALT alanine transaminase EBV Epstein–Barr virus ALTE apparent life-threatening event ECMO extracorporeal membrane AML acute myeloid leukemia oxygenation ARDS acute respiratory distress syndrome ED emergency department AST aspartate transaminase EEG electroencephalogram ATLS Advanced Trauma Life Support EKG electrocardiogram BiPAP bilevel positive airway pressure ELISA enzyme-linked immunosorbent BLEEP bedside-limited echocardiogram by assay emergency physician EM emergency medicine BNP B-type natriuretic peptide EMS emergency medical services BP blood pressure (in millimeters of ENT otolaryngology mercury [mmHg]) EPO erythropoietin BRUE brief resolved unexplained event ESR erythrocyte sedimentation rate BUN blood urea nitrogen ET tube endotracheal tube CBC complete blood count FAST focused assessment with sonography c-collar cervical spine immobilization collar for trauma CHALICE Children’s Head Injury Algorithm FEV1 forced expiratory volume in 1 second for the Prediction of Important FVC forced vital capacity Clinical Events GCS Glasgow Coma Scale CHD congenital heart disease GERD gastroesophageal relux disease CDC Centers for Disease Control and GI gastrointestinal Prevention Hb hemoglobin CHF congestive heart failure ␤-hCG beta-human chorionic gonadotropin CI conidence interval HCT hematocrit Cl chloride HEENT head, ears, eyes, nose, and throat cm centimeter HIV human immunodeiciency virus CMV cytomegalovirus HR heart rate (in beats per minute) CNS central nervous system HSV herpes simplex virus CPAP continuous positive airway pressure ICU intensive care unit CPR cardiopulmonary resuscitation IgG immunoglobulin G Cr creatinine IgM immunoglobulin M CRP C-reactive protein IM intramuscular c-section caesarean section INR international normalized ratio

xiii

List of Abbreviations

IO intraosseous PCP primary care provider IU international units PCR polymerase chain reaction IV intravenous PECARN Pediatric Emergency Care Applied JVD jugular venous distension Research Network Kpotassium PEEP positive end expiratory pressure kg kilogram PERRL pupils equally round and reactive to LDH lactate dehydrogenase light LFT liver function test PGE1 prostaglandin E1 LP lumbar puncture PICC peripherally inserted central catheter LSD lysergic acid diethylamide PICU pediatric intensive care unit M/R/G murmurs, rubs, gallops Plt platelets mcg microgram PO per os, or by mouth MCHC mean corpuscular hemoglobin PTLD post-transplant lymphoproliferative concentration disease MCV mean corpuscular volume RBC red blood cells mEq milliequivalents RICE rest, ice, compression, elevation MIGB metaiodobenzylguanidine RR respiratory rate (in breaths per mL milliliter minute) ␮L microliter RSV respiratory syncytial virus mmHg millimeters of mercury SIDS sudden infant death syndrome MRI magnetic resonance imaging SIRS systemic inlammatory response MRSA methicillin-resistant Staphylococcus syndrome aureus Ttemperature MSSA methicillin-sensitive Staphylococcus TBI traumatic brain injury aureus TBSA total body surface area Na sodium TIBC total iron binding capacity NEXUS National Emergency X-radiography U/A urinalysis Utilization Study U/S ultrasound NICU neonatalintensivecareunit URI upper respiratory infection NKDA no known drug allergies USA United States of America NMDA N-methyl-D-aspartate UTD up to date NMS neuroleptic malignant syndrome UTI urinary tract infection NPO nothing per os (do not feed) UTO unable to obtain NSAIDs non-steroidal anti-inlammatory VBG venous blood gas drugs W/R/R wheezes, rales, rhonchi O2 sat oxygen saturation WBC white blood cells OR operating room WHO World Health Organization PaCO2 partial pressure of carbon dioxide in arterial blood

xiv

Reference Values

Pediatric normal laboratory values

Test Value Unit Age Complete blood count (CBC) White blood cells (WBC) 5,000–30,000 cells/µL 0–30 days 5,000–19,000 cells/µL 1–6 months 6,000–17,500 cells/µL 6–12 months 4,500–14,500 cells/µL1–16years Hemoglobin (Hb) 15.0–22.0 g/dL 0–30 days 9.5–15.0 g/dL Ͼ30 days Hematocrit (HCT) 44–70 % 0–30 days 29–45 % Ͼ30 days Mean corpuscular hemoglobin concentration (MCHC) 28–36 g/dL Mean corpuscular volume (MCV) 86–115 fL 0–30 days 72–100 fL Ͼ30 days Platelets (Plt) 150,000–450,500 platelets/µL

Serum chemistries Alanine aminotransferase (ALT) 6–50 U/L Albumin 2.9–5.5 g/dL Alkaline phosphatase 110–400 U/L Ammonia 47–94 µmol/L 0–30 days 15–48 µmol/L 30 days–16 years 9–26 µmol/L Ͼ16 years Amylase 30–115 U/L Aspartate aminotransferase (AST) 35–140 U/L 0–5 days 20–60 U/L Ͼ5 days Bilirubin 1–14 mg/dL 0–5 days 0.2–1.0 mg/dL Ͼ 5days Blood urea nitrogen (BUN) 5–28 mg/dL Calcium 8.0–10.7 mg/dL Chloride 95–105 mEq/dL C-reactive protein (CRP) Ͻ1.0 mg/mL Creatine phosphokinase (CPK) 60–365 U/L Creatinine (Cr) 0.12–1.06 mg/dL Erythrocyte sedimentation rate (ESR) 0–20 mm/hour Ferritin 36–391 ng/ml 0–6 months 36–100 7 months–5 years 36–311 Ͼ5years Glucose 30–80 mg/dL 0–3 days 70–110 Ͼ3days Iron 55–150 µg/dL Iron (transferrin) saturation 56–74 % 0–10 days 17–44 Ͼ10 days Lactate 0.2–2.0 mmol/L Lactate dehydrogenase (LDH) 934–2,150 U/L 0–5 days 420–900 5 days–9 years 313–750 Ͼ9years Lipase 15–300 U/L Magnesium 1.2–2.6 mg/dL

Reference Values

Test Value Unit Age Phosphorus 2.3–8.0 mg/dL Potassium (K) 4.5–7.0 mEq/L 0–30 days 4.0–5.5 Ͼ30 days Sodium (Na) 132–145 mEq/L Total iron binding capacity (TIBC) 100–400 µg/dL 0–11 months 250–425 Ͼ11 months Transferrin 200–360 mg/dL Arterial blood gas (ABG) pH 7.33–7.43 pH Partial pressure of carbon dioxide (PaCO2) 26–41 mmHg 0–12 months 33–46 Ͼ12 months Partial pressure of oxygen (PaO2) 65–76 mmHg 0–12 months 88–105 Ͼ12 months

Cerebrospinal luid (CSF) Glucose 50–70 % of serum glucose Protein Ͻ100 mg/dL 0–30 days 14–45 Ͼ30 days Red blood cells (RBC) Ͻ10 cells/␮L White blood cells (WBC) Ͻ30 cells/␮L 0–12 months Ͻ20 cells/␮L 1–4 years Ͻ10 cells/␮L Ͼ4years

Coagulation studies Prothrombin time (PT) 12.2–15.5 seconds International normalized ratio (INR) 0.8–1.2 Partial thromboplastin time (PTT) 26.5–35.5 seconds

Urine Specific gravity 1.001–1.035 pH 4–9 Bilirubin None Glucose Ͻ30 mg/dL Ketones None Protein None Urobilinogen Ͻ2.0 White blood cells (WBC) 0–4 cells/high-powered field Red blood cells (RBC) 0–4 cells/high-powered field Epithelial cells 0–4 cells/high-powered field

Reference: Gregory’s Pediatric Anesthesia, 5th edition. Gregory G, Andropoulos D (eds). Wiley-Blackwell, 2011.

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A 3-year-old boy with a bead stuck up his nose. A we didn’t have vaccines for measles or Haemophilus helpless 4-month-old girl with a devastating traumatic influenzae or Streptococcus pneumoniae,bacterial brain injury...from abuse. A 15-year-old with four meningitis was common and deadly, and the care of months of persistent headaches, countless healthcare the pediatric trauma patient was similar to that of the visits...andtoday...diagnosedwithabraintumor. dark ages. As an example, in 1946, Caffey described a Kids are unique. They are different. And most series of pediatric patients with subdural hematomas certainly...theyareincrediblyspecial. and long-bone fractures. He writes, “For many years Kids represent our future. we have been puzzled by the roentgen disclosure of As clinicians, we are entrusted with someone’smost fresh, healing and healed multiple fractures in the valuable possession, their child. We are entrusted to long bones of infants whose principal disease was take care of them, to fix them, to cure them. Some- chronicsubduralhematoma.”Atthetime,westill times,itmaybeassimpleasremovinganasalforeign hadn’t heard of the term “child abuse.” Several years body or reducing a nursemaid’s elbow. Very easy, yet later, in 1962, Kempe and colleagues introduced the incredibly satisfying. But for other children, the situa- term “The Battered Child Syndrome” in a landmark tion and consequences are much more dire. In critical JAMA article.1 Today, hundreds of articles, confer- situations,weareaskedtosavethem,to save their lives. ences, and teaching seminars discuss non-accidental Achildonabicyclehitbyacar...Aninfantincardio- trauma. genicshockfromacriticalcoarctation...Orateenager Technology has also changed pediatric care. with anaphylaxis from a peanut ingestion. We are there Seventy-five years ago we struggled to interpret to save their lives. low-quality X-rays. Today, we have pediatric X-ray Wewhotakecareofchildrenmustbereadyfor technicians and pediatric radiologists. The CT scan these dramatic and life-threatening encounters. But was not invented until 1972! Today, low-dose CT, we must also be prepared for the less obvious, the clinical indications for CT, PECARN traumatic brain less dramatic, the “subtle” presentation. A fussy 4- injury prediction rules, and “pan-scan” are ever month-old infant with abusive head trauma may har- so common medical vernacular for the pediatric bor only one small diagnostic clue, such as a small patient. Imagine a shift in the ED without a CT scan scalp bruise, which the astute physician must discover. machine?! And of course there is ultrasound, first Failure to identify equates to further abuse. A wheez- used for clinical purposes in the 1950s. Today, not ing 4-month-old infant during RSV season may actu- only is there three- and four-dimensional ultrasound, ally harbor an undiagnosed cardiomyopathy. Can we but also pediatric emergency medicine physicians pick out that needle in the haystack? That child with who perform point of care emergency ultrasound a persistent headache, could it be a brain tumor, car- and make life-saving treatment decisions based upon bon monoxide poisoning, or just a simple migraine theseimmediatebedsideimages. headache? And the ever so common sore throat that In this book, the authors present dozens of inter- you see day in and day out in Fast Track, will your next esting pediatric case vignettes. A pediatric story is fol- encounter be Lemierre’s syndrome? lowed by thought-provoking clinical questions, many Just think how vastly the care of the pediatric very “cool” images, and subsequently an engaging dis- patient has evolved in the past 75 years. In the mid- cussion of the diagnostic topic. The authors discuss dle of the last century, antibiotics were rarely used, a wide range of clinical situations, such as trauma,

16:08:58 1 02 Chapter 1: A Statement toxicology, resuscitation, orthopedics, and infectious As you read through this book, remember, you are disease. There are simple “bread-and-butter” cases the safety net for our children. described, things we see and do everyday. A nurse- Kids are unique, kids are special. maid’s elbow, a lodged foreign body, appendicitis, Kids represent our future. and pharyngitis. The reader will also experience critical scenarios, cases in shock, respiratory failure, Reference and multi-trauma. These are unique situations where 1. Kempe CH, Silverman FN, Steele BF, et al. The seconds count to save a young one’s life. battered-child syndrome. JAMA 1962; 181: 1–24.

16:08:58 02 Chapter2 Resuscitation

Table 2.1 Glasgow Coma Scale. A score of 15 is normal. A Case 1 score of 8 is considered comatose. A score of 3 is entirely unresponsive. In children Ͻ 4 years of age, modified verbal Contributing Author: Erica Escarcega response includes 5 - smiles/coos, 4 - cries and is consolable, 3 - cries inappropriately or persistently, 2 - grunting or moaning, History agitation, and 1 - no response. The patient is a 10-year-old male brought in by EMS Eyes open Voice response Motor response as a trauma alert after his bicycle was struck by a car at r r r r 4: spontaneous r 5: coherent speech 6: follows low speed. According to bystanders, the front wheel of r 3: voice r 4: confused r commands the bicycle was struck by the front end of the car while 2: pain 3: inappropriate 5: purposeful/ r 1: no opening words localizes the child was attempting to cross an intersection. The r 2: incomprehensible r 4: withdraws to child fell forward over the handlebars and then landed r sounds r pain on the street. The child was unhelmeted. There wasa 1: no speech 3: decorticate r 2: decerebrate loss of consciousness at the scene for approximately r 1: no movement 1 minute. He sustained significant facial injury, with soft-tissue swelling, and is unable to speak. He occa- r Primary survey: sionally spits out a moderate amount of blood, but is r A able to handle his secretions and does not appear to be irway: Child with swollen bleeding tongue, in respiratory distress. He was unable to ambulate at but able to spit. No pooling secretions. r B the scene and cries in pain with every touch. reathing: Good air entry, adequate effort and oxygenation. r Circulation: Tachycardic, good central and Past Medical History r peripheral pulses. None. He sees his pediatrician regularly and is r Disability: GCS 12 (eyes open spontaneously: UTD on vaccinations. 4, verbal is incomprehensible: 2, motor able to follow commands: 6) (see Table 2.1). Medications r Exposure: Multiple abrasions and contusions. r None. r Secondary survey: r HEENT: PERRL. Mucous membranes are Allergies moist. There is significant swelling to the right r NKDA. mandible with abrasions over the right cheek, chin, and forehead. A 2-cm laceration is present to the left side of the tongue, with Physical Examination and Ancillary Studies moderate active bleeding. Patient is currently r Vital signs: T 98.6 °F, HR 114, BP 110/68, RR 20, in a c-collar and cries with palpation of the O2 sat 100% on room air. posterior c-spine. Trachea is midline. r General: The patient is distressed, anxious, and r Cardiovascular: He is tachycardic, with normal crying. However, he is able to cooperate with rhythm and no M/R/G. Peripheral pulses are examination. normal. Capillary refill Ͻ 3 seconds.

16:09:45 3 03 Chapter 2: Resuscitation

r What injuries are common in children who have been victims of severe trauma? r How much blood volume can a child lose prior to becoming hypotensive?

Diagnosis r Multiple trauma.

Discussion r Epidemiology: It is estimated that 12,175 children die every year in the USA due to traumatic Figure 2.1 FAST examination with free fluid. injuries, with the largest percentage of fatal injuries related to motor vehicle accidents.1 Of motor vehicle-related fatalities, an average of r Lungs:CTAbilaterally,withnoW/R/R.No 3,724 children die each year as occupants of the chest-wall tenderness. vehicle, 724 of annual fatalities are pedestrians, r Abdomen: The patient’s abdomen is diffusely and 162 children are struck by a vehicle while tender; however, soft and non-distended riding their bicycles.1 Seatbelt and bicycle helmet without rebound or guarding. There are no laws are measures that have been taken to attempt palpable masses on examination. to reduce the number of childhood fatalities; r Extremities and skin:Therearemultiple however, pediatric trauma continues to be a major abrasions including a large abrasion over the concern for public health, both in the USA and right flank, right arm, bilateral palms, bilateral internationally.2 knees, and shins. Abrasions are dirty, r Pathophysiology: Trauma presents a different impregnated with asphalt, and have minimal diseasespectruminchildrenascomparedto venousoozingatthetimeofexamination. adults. The bones of children are generally more There is tenderness to palpation over the right pliable than those of the more calcified adult hip. The patient is unable to tolerate range of skeleton; therefore, fractures are often sustained motion of the right leg secondary to pain. He in the setting of higher force mechanisms and has tenderness over the left knee and cries internal injuries may occur despite an absence of with attempts at range of motion. He has fractures.2,3 The proportionally larger and softer fullrangeofmotionofbilateralupper skullinsmallchildrenresultsinanincreasedrisk extremities. of traumatic brain injuries as well as facial r Neurologic: He has tenderness over the injuries. Additionally, the ligaments of the child’s c-spine. No thoracic or lumbar spine c-spine have an increased laxity, which may tenderness. No step-offs present on palpation increase the risk of c-spine injury that may not be of the spine. seen on radiography. In regards to the circulatory r Ancillary studies:FASTexaminationwithfree system,achild’shearthasafixedstrokevolume, fluid (Figure 2.1). which results in a reliance on an increase in heart rate in order to improve cardiac output. The low cardiopulmonary reserve in small children may result in a rapid, precipitous progression into Questions for Thought shock. Hypothermia may also occur more quickly in children due to their higher relative body r What steps should be taken to evaluate and surface area. stabilize a pediatric trauma victim? r r How do pediatric trauma patients diﬀer from Presentation: Children are often unable to provide adult trauma patients? history and may not be able to cooperate with examination, which makes evaluation for the

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extent of injuries challenging. Significant injuries hematuria, and elevated liver enzymes.5 Signs may exist despite an inability to elicit tenderness which should increase suspicion for intrathoracic on physical examination, especially in the setting injuries include hypotension, tachypnea, of a decreased mental status. Indeed, the most abnormal mental status, and abnormal lung common cause of pediatric trauma mortality is in sounds on auscultation and should prompt the fact head injury, and specific decision rules exist performance of CXR.4 CXR, however, may miss to guide the clinician in determining when up to 40 percent of intrathoracic injuries and if neuroimaging is indicated. This is covered in suspicion remains high despite negative CXR, Case2inthischapter. further studies should be considered such as chest Neckandspineinjuriescanbedevastating,but CT.4 FAST examinations are often performed are relatively uncommon in children. Children are quickly at the bedside to evaluate for the presence more likely to have a ligamentous injury than a of free fluid in the abdomen as well as around the c-spine fracture. Decision rules exist for heart; however, a negative FAST does not obviate neuroimaging in neck injury, as well, and this is the need for further imaging. covered in Case 3 in this chapter. r Treatment:Casesofseveretraumaareideally The most common intrathoracic injury in managed by a multidisciplinary team consisting significant blunt trauma is pulmonary contusion of emergency providers, surgeons, nurses, and the most common immediately respiratory therapists, intensivists, radiologists, life-threatening injury in children is tension and subspecialists. Treatment of all pediatric pneumothorax.4 Children may also sustain rib traumas should begin with a primary survey and fractures, simple pneumothorax, hemothorax, stabilization, as taught in ATLS courses, and pneumomediastinum, as well as injuries to the should follow the ABCDE mnemonic (Airway, heart, aorta, and diaphragm in the setting of blunt Breathing, Circulation, Disability, Exposure).3 trauma. Children may have significant This algorithm applies to all causes of shock, not intrathoracic trauma in the absence of rib just shock related to trauma. In traumatized fractures. patients, the c-spine should remain immobilized Abdominal injuries are common after severe until the child has been completely assessed. blunt trauma with highest risk of injury to the liver and spleen.5 Be wary of signs of injury related to seatbelts (such as abdominal bruising) as this Airway: orotracheal intubation is the preferred may be an indication of significant underlying method of securing the airway in the absence of injury.3,4 Fractures of the lumbar spine (Chance facial or laryngeal trauma if there are signs of fracture) are caused by a flexion-distraction injury respiratory distress, apnea, airway obstruction, associated with lap belts and are often or decreased mental status resulting in an 3 accompanied by GI injuries. Children presenting inability to protect the airway. In the rare cases with femur fractures may also have concomitant where orotracheal intubation is contraindicated intra-abdominal and intrathoracic injuries as or unable to be established, a surgical airway is these fractures are generally associated with a necessary. Needle cricothyroidotomy is a high impact mechanism.3 temporizing measure which can be used in r Diagnosis: Many decision rules have been young children. Standard cricothyroidotomy formulated with the goal of reducing radiation may be performed in children over the age of 12 exposure in children. Although as many as 58 in which the cricothyroid membrane can be 3 percent of intra-abdominal injuries present with palpated. Nasotracheal intubation is not abdominal pain, significant injuries may be recommended in children. Hoarseness or missed due to the unreliability of the patient’s crepitus may suggest a laryngeal injury that is examination; therefore, providers should have a best managed in consultation with ENT. In low threshold for CT of the abdomen in patients these cases, cricothyroidotomy may with significant mechanism, especially in the worsen the patient’s injury, and stabilization of setting of hypotension and laboratory the airway in an operating suite may be abnormalities, including decreased HCT, required.

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Breathing: The patient should be evaluated for findings during examination of the child. bilateral breath sounds, the absence of which Children with multiple severe injuries may need should prompt immediate intervention with to be managed in a staged approach, addressing placement of chest tubes to relieve suspected the most life-threatening injuries first followed by pneumothorax or hemothorax.3 The most further stabilization prior to subsequent common cause of cardiac arrest in children is interventions.6 hypoxia, so it is vital to establish appropriate r Disposition: Children presenting to a center ventilation in pediatric trauma victims using without PICU capabilities, who are seriously weight-based lung volumes and titrating to injured, should be stabilized and transferred to a oxygenation and end-tidal carbon dioxide or trauma center. It is appropriate for EMS to bypass using serial ABGs. a non-trauma center to bring children who are Circulation: Evaluation of the circulation of a hemodynamically stable to the appropriate child is best performed by assessing peripheral nearest trauma facility. perfusion (capillary refill and quality of peripheral pulses) as patients may lose more than 25 percent of their blood volume before Historical Ancillary becoming hypotensive.3 Crystalloid fluid clues Physical findings studies boluses of 20 mL/kg (preferably warmed) r r r High impact r Tachycardia Positive FAST should be given initially, followed by boluses of r mechanism External signs of 10 mL/kg of blood if needed. IV access in small Loss of trauma (abrasions, consciousness contusions, children can be challenging, and IO access lacerations, crepitus, should be obtained if peripheral access cannot r deformities) be obtained after two attempts.3 Tenderness to abdomen, spine, and Disability: The disability portion of the ABCDE lower extremities mnemonic refers to the patient’s neurologic status.TheGlasgowComaScale(GCS),which is commonly used in adult trauma, may also be Follow-Up used in the evaluation of mental status in Although the patient had a positive FAST, he was pediatric trauma with modification of the hemodynamically stable to undergo CT scanning to verbalscoreinchildrenundertheageof4.This further assess his injuries. CT chest, abdomen, and score contributes to imaging decisions in the pelvis performed with IV contrast showed a grade head-injured patient. III splenic laceration without active extravasation. Exposure: Be sure to fully expose and inspect CT facial bones revealed a non-displaced mandibu- the patient for external signs of injury. Palpate lar fracture. CT head showed no intracranial hem- for deformity, swelling, and crepitus. During the orrhage or skull fractures and CT c-spine was neg- assessment, care should also be taken to keep ative for fractures or dislocations. An X-ray of his the child as warm as possible to avoid left knee showed a non-displaced patellar fracture. hypothermia, which can worsen coagulopathy The tongue laceration was sutured and his jaw was and acidosis. If the child’s condition worsens at banded shut by ENT. The patient was admitted to the any point during the assessment, the primary PICU for airway monitoring as his tongue had swollen survey should be repeated, beginning with significantly and there was concern of potential air- reassessment of the patient’s airway. way compromise. He also underwent serial abdominal examinations and hemodynamic monitoring for Once the primary survey is complete and the his splenic laceration. His patellar fracture was man- child is stable, a careful head-to-toe examination, aged conservatively by orthopedics with splinting. The called the secondary survey, takes place. Every bands for his mandibular fracture were exchanged for inch of the child should be examined to avoid wires when the swelling resolved. After an unevent- missing injuries. ful stay in the ICU, he was eventually discharged Imaging should be performed in a stabilized home with ENT, general surgery, and orthopedics patient after the primary survey as directed by follow-up.

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References Physical Examination and Ancillary Studies r 1. Borse N, Gilchrist J, Dellinger A, et al. CDC Vital signs: T 98.6 °F, HR 115, RR 18, BP 100/60, Childhood Injury Report: Patterns of Unintentional O2 sat 100% on room air. Injuriesamong0–19YearOldsintheUnitedStates, r General:Confusedandagitated,resistingany 2000–2006. Atlanta (GA): Centers for Disease Control effort to examine him. and Prevention, National Center for Injury Prevention r Primary survey: and Control, 2008. r 2. Sharar S. The ongoing and worldwide challenge of Airway: Patent, no pooling secretions. pediatric trauma. Int J Crit Illn Ing Sci 2012; 2: 111–13. r Breathing: Clear and equal breath sounds. 3. American College of Surgeons. Pediatric trauma. In r Circulation: Intact central and peripheral Advanced Trauma Life Support Student Course pulses. Manual, 9th edition. Chicago, IL: American College of r Disability:GCS13(eyes= 4, speech = 4, Surgeons, 2012, pp. 246–70. motor = 5), non-focal. 4. Homes J, Sokolove P, Brant W, et al. A clinical decision r Exposure: Bleeding laceration to right parietal rule for identifying children with thoracic injuries area, with palpable bony depression and after blunt torso trauma. Ann Emerg Med 2002; 39: numerous facial abrasions. Abrasion to right 492–9. elbow. No bony deformity. Bleeding is 5. Homes J, Sokolove P, Brant W, et al. Identification of controlled. children with intra-abdominal injuries after blunt r trauma. Ann Emerg Med 2002; 39: 500–9. Secondary survey: 6. Wetzel R and Burns C. Multiple trauma in children: r HEENT: Lacerations and abrasions as noted. Critical care overview. Crit Care Med 2002; 30: Normal ear examination without evidence of S468–77. hemotypanum or periauricular ecchymosis. Normal funduscopic examination without Case 2 evidence of hyphema and with apparently normal extraocular movements from a limited Contributing Author: Michael Leonard examination due to patient cooperation. r Neck: Non-tender, child spontaneously ranging History neck, with no apparent pain. A 5-year-old male presents to the ED after being struck r Cardiovascular:Heartwithregularrateand by a bicycle ridden by another child. The child had rhythm, no M/R/G, good capillary refill. been playing on the sidewalk. The child struck his r Lungs:CTAbilaterally,withnoW/R/R. head on the pavement. Bystanders rushed to the scene r Abdomen:Soft,notenderness,noreboundor and EMS was contacted immediately, who note the guarding, no masses. patient was briefly unconscious. Upon arrival, abra- r Extremities:Nodeformity.Abrasiononelbow sion is noted to the right parietal area, and the child is as noted. Normal range of motion. confused and agitated. He does not follow commands r Axial skeleton: No back tenderness or step-offs, but appears to be moving all extremities. pelvis stable to rock and compression. r Neurologic: Confused, disoriented, and Past Medical History uncooperative. Examination appears non-focal r Full-term birth with no complications, and symmetric. developmentally normal, immunizations are UTD. Questions for Thought r What is the diﬀerential diagnosis of pediatric Medications head injuries? r r None. What additional testing or imaging would be useful in this patient? r What instructions should be given to the parents Allergies of children with less severe injuries? r Strawberries.

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Diagnosis or nausea. Elicit further details from the patient’s r Fall with depressed parietal skull fracture, dural parents regarding whether the child is acting tear with surrounding brain edema but without normally and at his or her baseline. evidence of intracranial hemorrhage. Initial assessment of the child should be focused on the ABC algorithm instituted with ATLS training to identify and intervene upon any Discussion potentially life-threatening conditions. An initial r Epidemiology: The incidence of ED visits for neurologic assessment of the child must account TBI-related issues has been increasing over the for age-specific variation in relation to expected last several years with the highest incidence (1,889 findings. Following primary assessment, the visits/100,000 person-years) occurring in children secondary survey, including a head-to-toe less than 3 years old.1 Fortunately, the vast examination, should be completed. Specific focus majority of pediatric head trauma is benign and on scalp examination for any hematoma, the resultant rate of TBI-related deaths is lowest in lacerations, or other signs of trauma should be the 0–4 year (4.3/100,000) and 5–14 year performed. Hemotympanum, posterior auricular (1.9/100,000) age groups.2 Hence, the challenge ecchymosis (Battle’s sign), or periocular for the EM provider relates to identifying the rare ecchymoses that spare the tarsal plates (Raccoon cases of a potentially devastating condition eyes) are potential signs of a basilar skull fracture within an exceedingly common presenting that, although rare, should be promptly evaluated complaint. by a trauma surgeon. Funduscopic examination, r Pathophysiology: The majority of pediatric head including evaluation for retinal hemorrhages, and injuries are due to blunt traumatic mechanisms. complete eye examination, assessing for hyphema, Significant injuries are rare but can result in skull globe rupture, and corneal injury, should be fractures or intracranial injuries, including completed; if there is concern for non-accidental epidural, subdural, or subarachnoid hemorrhages. trauma, a formal examination by an Additionally, the increasing emphasis on the ophthalmologist should be performed to assess long-term effects of concussion has contributed to for retinal hemorrhages. the increasing number of ED visits. The r Diagnosis: Although ultrasound has been pathophysiology of concussions or mild TBI is evaluated for the diagnosis of skull fractures, complex and incompletely understood and intracranial evaluation typically requires CT remains an area of evolving research. imaging, and recent efforts have been focused on r Presentation: Key components of the history limiting the exposure to ionizing radiation, include details of the mechanism of injury, any particularly in the pediatric population.3 To this reported loss of consciousness, vomiting, or extent, identifying which children are most at risk headache following the incident, and any change becomes a critical component of the evaluation in behavior. In the case of a motor vehicle and diagnosis of a potentially serious injury while accident, acquire details from EMS or witnesses limiting the risks from testing. Several decision about the location of the child in the car, the aids have been developed and when compared in extentandlocationofdamagetothevehicle, prospective trials, the PECARN clinical decision whether the child was restrained and secured rules were found to be superior to other appropriately in a car seat, and any history of guidelines.4 The PECARN consortium evaluated vehicular ejection. If the child fell, obtain 42,412 children (less than 18 years old) information about the height of the fall or if the presenting to 25 North American EDs, to develop fall was from standing. If the child was on a a set of highly sensitive clinical decision aids that bicycle, identify whether a helmet was worn at the predict which children are at risk for intracranial time of the incident. Any history that seems injury and may benefit from imaging.5 The implausible or does not fit with the injury pattern decision aids include separate algorithms for demonstrated on physical examination raises the children less than 2 years old and for older possibility of abuse. Whenever practical, query children. Each algorithm stratifies patients into the patient directly about mechanism, headache, three distinct groups:

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Table 2.2 PECARN high- and intermediate-risk definitions for children with head injury5 Children less than 2 years old Children greater than 2 years old High risk (CT recommended) Palpable skull fracture Signs of basilar skull fracture GCS ࣘ 14 including any signs of altered mental status (agitation, somnolence, repetitive questioning, or slow responses to verbal communication) Intermediate risk (observation Loss of consciousness greater than 5 seconds Loss of consciousness any period versus CT) Occipital, parietal, or temporal scalp hematoma History of vomiting Not acting normally per parent Severe headache Severe mechanism of injury, including: a motor vehicle collision where the patient was ejected, the collision involved the death of another passenger, or a rollover; the patient was a pedestrian or a bicyclist without helmet and was struck by a motor vehicle; or the patient’s head was struck by a high-impact object Fall Ͼ 3 feet Fall Ͼ 5 feet

r High-risk patients warranting immediate managing these injuries. Additional interventions, imaging, with a greater than 4 percent risk of such as the use of osmotic agents (including clinically important TBI (ciTBI). hypertonic saline and mannitol) and seizure r Intermediate-risk patients who may be observed prophylaxis, may be warranted based upon the or may warrant imaging based upon additional severity of the injury and the potential for factors (approximately 1 percent risk of worsening due to evolution of the initial injury. ciTBI). Theseagentsshouldbegiveninconsultationwith r Low-risk patients who are unlikely to benefit a neurosurgeon, and in cases where a child shows from imaging (Ͻ0.05 percent risk of evidence of increased intracranial pressure ciTBI). (hypertension, bradycardia, worsening of mental status), osmotic agents may be life-saving. These Low-risk patients are those who do not meet agents, though, are only temporizing, and any criteria for high or intermediate risk. Based definitive care is surgical. There is further upon the high sensitivity demonstrated in discussion of these topics in Chapter 10, Case 3. multiple validation studies, the risk of clinically r significant TBI is exceedingly low in these Disposition: The majority of pediatric patients patients, and the risks of imaging likely outweigh presenting to the ED can be safely discharged any benefit. The different risk categories are home. Any patient identified as an intermediate showninTable2.2. risk, who is not undergoing imaging, should be For those children in the intermediate-risk observed in the ED for several hours and group, the decision whether to observe or reassessed throughout that period and prior to perform imaging on the patient should be discharge. All patients and their parents should be considered in consultation with the child’s parents given detailed return instructions for repetitive and in accordance with the physician’s experience vomiting, worsening pain, or alterations in mental and comfort. Observation allows the opportunity status.Itisalsocriticaltoeducatepatientsand to assess for symptom evolution, which might families on injury prevention, focusing on the warrant a change in care. Ultimately, like any inciting event. In particular, seatbelt and helmet decision aid, the use of the PECARN algorithm is safety should be addressed. meant to be a guideline and should not supersede For patients diagnosed with a concussion, the clinician judgment. current evidence supports a limited period of rest (1–2 days) with stepwise return to activity.6 Due r Treatment: After initial resuscitation of a patient to the developing arena of concussion with a traumatic head injury, the identification of management and the potential for long-term any clinically significant TBI warrants immediate monitoring, the patient should be referred to a consultation with an appropriately trained physician specially trained in this area, such as a neurosurgeon or transfer to a center capable of sports medicine physician.

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Historical clues Physical findings Ancillary studies obviously deformed right femur. The child was admin- ␮ r High-risk r Altered mental r Child warrants CT istered 1 g/kg of fentanyl pre-hospital. mechanism status/GCS r Loss of r Palpable skull Past Medical History consciousness fracture r Unknown. Medications r Follow-Up Unknown. The child underwent CT scanning and, due to dural Allergies violation, had operative elevation of his depressed skull r Unknown. fracture. He was hospitalized for 10 days and then Physical Examination and Ancillary Studies transferred to a rehabilitation center, where he has r ° recovered with no deficits. Vital signs:T97 F, HR 146, RR 32, BP 96/54, O2 sat 94% on room air. References r Primary survey: r 1. Marin JR, Weaver MD, Yealy DM, et al. Trends in visits Airway: The child is somnolent and there is for traumatic brain injury to emergency departments blood noted at the oropharynx. in the United States. JAMA 2014; 311: 1917–19. r Breathing: Respirations are sonorous but 2. Centers for Disease Control and Prevention, Traumatic present bilaterally. brain injury & concussion. See http://www.cdc.gov/ r Circulation: The child is tachycardic and has traumaticbraininjury/data/ (accessed June 22, 2016). intact distal pulses in four extremities. 3. Rabiner JE, Friedman LM, Khine H, et al. Accuracy of r Disability:GCSis9(eyes= 2, speech = 3, point-of-care ultrasound for diagnosis of skull motor = 4), and the child seems to respond to fractures in children. Pediatrics 2013; 131: e1757–64. pain in all four extremities. 4. Easter JS, Bakes K, Dhaliwal J, et al. Comparison of r Exposure: Right-femur deformity, 12-cm scalp PECARN, CATCH, and CHALICE rules for children wound with venous oozing, bruising to with minor head injury: A prospective cohort study. Ann Emerg Med 2014; 64: 145–52. abdomen. r 5. Kuppermann N, Holmes JF, Dayan PS, et al. Secondary survey: Identification of children at very low risk of r HEENT: 12-cm full-thickness laceration to the clinically-important brain injuries after head trauma: right parietal-occipital area with venous A prospective cohort study. Lancet 2009; 374: 1160–70. oozing. The skull beneath appears to be intact. 6. Thomas DG, Apps JN, Hoffman RG, et al. Benefits of No hemotympanum. Eyes open to pain. Pupils strict rest after acute concussion: A randomized 4 mm and reactive bilaterally. Blood noted controlled trial. Pediatrics 2015; 135: 213–23. within oropharynx from an unknown source. r Neck: Neck is immobilized in a c-collar. Case 3 Trachea is midline, without subcutaneous emphysema appreciated. Contributing Author: Donald Jeanmonod r Chest: Clavicles intact, but ecchymosis noted History over the right shoulder. Lungs are rhonchorous A 4-year-old female presents to the trauma bay via bilaterally. Chest wall is stable without EMS. She was the restrained passenger-side rear-seat subcutaneous emphysema. passenger in a booster seat in a car involved in a r Heart: Tachycardic and regular. multicar accident on the interstate at highway speeds. r Abdomen: Non-distended and soft, without There was a fatality within her vehicle. It is unknown apparent tenderness. There is an ecchymosis if she had loss of consciousness. EMS immobilized over the lower abdomen. the child on a pediatric immobilization board and r Pelvis: Stable to rock and compression. No initiated IV access. Their primary survey has identi- perineal hematoma. fied a significant scalp laceration, whose bleeding they r Extremities: There is deformity of the right have attempted to control with direct pressure, and an femur with moderate thigh hematoma. The

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remainder of the extremities are unremarkable. 5–20 percent of injuries in those less than 21 years Back is without step-offs. of age, being increasingly common with r Neurologic: GCS is 9 and the child withdraws decreasing age. Luckily, spinal cord injury is fairly all four extremities to painful stimuli. uncommon, representing 5–7 percent of all injuries. The majority of pediatric c-spine injuries are the result of motor vehicle accidents, followed Questions for Thought by falls. r What are the appropriate steps in the initial r Pathophysiology: There are a number of anatomic stabilization of this child? r features of the pediatric c-spine that result in In evaluating this child for traumatic injury, what unique injury patterns. To start, the pediatric are the appropriate imaging studies to obtain head is relatively large compared to body size, and and why? Are there risks to obtaining these the neck musculature is proportionally studies? r If the child has negative imaging studies but underdeveloped, potentially causing greater force remains obtunded, can the c-collar be removed? of motion. In younger children, the incompletely ossified c-spine is characterized by horizontally oriented facets and intervertebral joints, anterior vertebral body wedging, and ligamentous laxity, Diagnosis allowing for significant flexion motion of the C-spine dislocation, femur fracture, cerebral c-spine and a propensity to dislocate. The spinal contusion. cord,however,isrelativelyanchoredbythe brachial plexus, so while the pediatric c-spine can Discussion moveupto2inches,thespinalcordcanbe r Epidemiology:Spinalinjuryinchildrenis significantlydamagedwithaslittleas1cmof relatively rare. In 2009, the estimated incidence of movement,4,5 putting it at risk to be pinched or spinal injury of all kinds was 170 per 1 million crushed, resulting in higher rates of SCIWORA in population less than 21 years of age and the children. Younger pediatric patients are more incidence of spinal cord injury was 24 per 1 likely to have higher c-spine injuries, from the million population.1 In the very youngest of base of the skull to C4, but because the developing patients (0–2 years) the majority of injuries are to spine reaches adult proportions by age 10, after the c-spine, while older children more commonly this age, c-spine mechanics and injury patterns injure the lumbar spine. C-spine injuries are mirror adults.6 Several congenital abnormalities relatively rare in children, occurring in less than 1 in children, including Down’s syndrome, juvenile percent of children who were imaged for injury in rheumatoid arthritis, Morquio syndrome, and the NEXUS study2 andinlessthan2percentof Grisel syndrome, predispose to increased seriously injured children in trauma databases.3 ligamentous laxity and increased rates of injury. The mortality rate for children with c-spine injury r Presentation: As with any trauma patient, the has been reported to be between 13 percent and systematic examination will help to identify any 28 percent, likely reflecting the association with potentially life-threatening injury first, and then head injury, rather than significant mortality from anyinjurythatwillpotentiallycausesignificant the spine injuries.4 morbidity. Although we believe that appropriate Most commonly, injuries are simple fractures immobilization is important to prevent without spinal cord involvement. However, progression of injury in unstable fractures and because of the anatomic differences noted below, ligamentous disruptions, the data supporting dislocations of the pediatric spine are also these assumptions are scarce. Furthermore, relatively common, accounting for approximately because of the wide variety of sizes in children, 15–25 percent of injuries in patients less than 12 c-spine immobilization in a hard collar can be years of age.1 As well, because of the relatively difficult. That said, during the primary and increased flexibility of the pediatric spine, spinal secondary survey, spinal precautions should be cord injury without radiographic abnormality maintained while rolling the child. If a child is (SCIWORA) is responsible for approximately immobilized in a c-collar, it is important to have a

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bolsterbehindtheshoulderstocompensatefor Table 2.3 NEXUS low risk criteria7 the relatively large occiput in children, which will r tend to cause neck flexion if not supported. Normal mentation r No neurologic deficit After the primary assessment with the ABC r Non-tender neck algorithm, assessment of mental status should be r r No distracting injury obtained. Multiple studies have demonstrated that No alcohol intoxication the presence of altered mental status both precludestheabilitytobeabletoadequatelyclear ac-spine,aswellaspotentiallyincreasesthe patient from appreciating significant neck probability that there is a fracture, because tenderness. The presence and absence of significant head injury is a well-established risk ecchymosis, the presence of neck hematomas, and for significant neck injury. Additionally, the the position of the trachea and airway should be disability portion of the primary assessment noted. Additionally, a detailed neurologic should be able to identify if the child is moving all examination, including strength and sensation, four extremities, identifying patients with can help to illicit any neurologic abnormalities paraplegia or quadriplegia from significant which may be attributable to an injured c-spine. c-spine spinal cord injuries. r Diagnosis:Inordertobalancetheverylowrisksof The secondary survey then proceeds from missing a significantly disabling condition with head to toe. Injuries to the head and face should the risks of medical radiation-induced cancer be noted, as these are often associated with from over-testing, a number of investigators have cervical injury. The significant findings pertaining sought to produce c-spine clearance rules. The to the neck include neck tenderness and the NEXUS criteria7 (Table 2.3) and the Canadian presence of injuries which might distract the C-spine Rule8 (Figure 2.2) are large multicenter

Figure 2.2 Canadian c-spine Rule. Any high risk factors? • GCS < 15 Ye s • ≥ 65 years • Dangerous mechanism • Paresthesias

Any low risk factors? • Simple rear-end motor vehicle crash No • Sitting in the department Radiography • Ambulatory at any time • Delayed-onset neck pain • No midline tenderness

Ye s No Able to rotate 45°?

Ye s Dangerous mechanism • Fall from ≥ 3 ft/5 stairs Clinically cleared • Axial load (i.e. diving) • High-speed motor vehicle crash, rollover, ejection • Motorized recreational vehicle • Bicycle collision

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studies of adults and children that were Table 2.4 PECARN model10 prospectively derived and validated and r demonstrate very good sensitivities (99.0 percent Altered mental status r Focal neurologic findings [95% CI 98.0–99.6%] and 100 percent sensitivity r Complaint of neck pain [95% CI 98–100%], respectively)7,8 for identifying r r Torticollis clinically significant injuries in a predominantly r Substantial torso injury adult population. One of the criticisms of Predisposing conditions r Diving applying these rules in the pediatric population r High-risk motor vehicle crash has been the low numbers of children with significant injuries from which to derive and validate their decision points. Nine percent (n = (95% CI 95% to Ͼ99%) for any injury requiring 3,065) of the NEXUS cohort were aged less than neurosurgical intervention.10 18, including only 88 children who were less than Using the protocol outlined in Figure 2.3, 2yearsofage.1 Of the NEXUS cohort of Anderson et al.11 prospectively evaluated 575 adolescents and children, there were only 30 children aged 0–3 who were trauma activations in injuries in the 3,065 included patients. Although a level 1 trauma center, identifying 19 ligamentous in the pediatric subset the NEXUS criteria injuries, 9 fractures, with 4 patients requiring demonstrated an excellent sensitivity of 100 stabilization. Although the protocol required percent, the relatively small number of injuries plain X-ray in 100 percent of patients, there were resulted in the lower limit of the 95% CI of no missed injuries in this cohort. 87.8%.2 A case-matched cohort study where the Although CT is more sensitive for the NEXUS criteria and the Canadian C-spine Rule identification of c-spine injury, plain radiography were retrospectively applied to a cohort that was remains the imaging modality of choice in imaged and a cohort that was not imaged found children to minimize radiation exposure. Because that neither rule had adequate sensitivity, but was childrenusuallyarenotobeseanddonothave limitedbothinstudydesignandthelownumbers degenerative spine disease, plain films may be of clinically important injuries.9 Asimilar easier to interpret. The reported sensitivity of a retrospective application of NEXUS criteria to a single-view, lateral neck X-ray is 74 percent and cohort of imaged injured (all had fractures and/or maybehigherinchildrenolderthanage8,witha ligamentous injuries) pediatric trauma patients reported sensitivity of 93 percent.4 Open-mouth revealed 100 percent sensitivity in the detection of odontoid views may improve the ability to fracture in 158 patients older than age 8, but only recognize burst fractures of C1, but are very a 94 percent sensitivity in those under age 8. The difficult to obtain in the smallest of children. American Association of Neurosurgical Surgeons Flexion–extension views and oblique views are have endorsed the use of NEXUS criteria in not routinely recommended. children above 9 years of age, and likely it is Evaluation of plain radiographs in pediatric applicable in any communicative child when there patients can be challenging due to anatomic is a low likelihood of ligamentous disruption in differences in the c-spine. The most common the proximal spine. variant seen on plain radiographs is Several investigators have sought to clarify the pseudosubluxation of C2 on C3, and sometimes of appropriate way to evaluate the c-spine in younger C3 on C4. To differentiate pseudosubluxation children. The PECARN collaboration performed a from real subluxation, one should draw a line retrospective case–control study which identified through the anterior portion of the posterior arch eight variables (Table 2.4) associated with from C1 to C3 (Swischuk’s line). In physiologic increased risk of cervical injury in children under pseudosubluxation, the line should be within 1 16 years of age. Comparing their cohort of 540 mm of the posterior arch. A distance of ࣙ 1.5 mm patients with injuries with 1,060 matched is concerning for true injury. In children under 8 controls, they found that the presence of any one years of age, the atlanto-dens interval (the space of the eight criteria had a sensitivity of 98 percent between the anterior portion of the dens to the (95% CI 96–99%) for any injury and 98 percent posterior aspect of the anterior ring of the atlas)

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Figure 2.3 Algorithm for clearing the cervical spine in children ࣘ 3 years of age.

may be up to 5 mm as opposed to 3 mm seen in of the increased radiation exposure with CT, the older children and adults. Finally, wedging of the risk to the thyroid is increased with a theoretical anterior portion of the vertebral body is common excess risk of CT of 13 percent for males and in children as the vertebral body changes shape 25 percent for females. This results in an absolute from a more oval appearance to the classic risk of 5.87 in 100,000 in males and 19 in 100,000 rectangular appearance of the developed spine.5 in females. When patients have severe mechanism of SCIWORA is the term used to describe an injury, significant head injury, or continued pain acute spinal cord injury that results in sensory despite normal radiographs, CT can be obtained. and/or motor deficits without radiographic In the youngest of patients, some recommend abnormalities being present on plain radiographs only scanning from the base of the skull to or CT scans. SCIWORA is more common in C3, to evaluate the areas most commonly younger children, representing as much as 20 injured.4 percent of the spinal injuries in these patients. The Whenever possible, it is imperative to decrease patterns of neurologic presentation can vary and radiation exposure from unnecessary imaging. depend on which portion of the cord is injured The incidence of thyroid cancer has doubled since but may include partial cord syndrome (55 1985, and is not thought to be just the result of percent), complete cord syndrome (27 percent), increased diagnostic yield.12 The baseline central cord syndrome, (10 percent), prevalence of thyroid cancer is 5.2 in 100,000 Brown–Sequard syndrome (5 percent), and males and 15.2 in 100,000 females and the anterior cord syndrome (3 percent).13 If theoretical excess relative risk of developing SCIWORA is suspected, the patient should thyroid malignancy after plain radiographs is 0.24 undergo further imaging with an MRI while percent for males and 0.51 percent for females, maintaining adequate cervical immobilization. resulting in an absolute risk of 5.21 in 100,000 for Most SCIWORA will spontaneously resolve with males and 15.3 in 100,000 for females. Because 8 to 12 weeks of cervical immobilization.

16:09:45 03 Chapter 2: Resuscitation r Treatment: Once an injury is identified, it is Historical clues Physical findings important to maintain spinal immobilization. r High-speed trauma r Traumatic injury to head Consultation with the appropriate specialist and r r r Death in vehicle r Bruising to shoulder transfer to a pediatric tertiary care facility with Cannot be cleared by Altered mental status/GCS NEXUS or PECARN r Cannot be cleared by NEXUS specialization in the management of pediatric or PECARN cervical injuries is important to deliver the appropriate continued care for these patients. In patients with significant paralysis, continual Follow-Up reassessment of breathing mechanics is essential Because of concerns of potential airway compromise to identify possible hypoventilation. Likewise, in given the blood at the oropharynx and the sonorous patients with high-up cervical injuries, loss of respirations, the child was intubated using video- vascular tone may lead to neurogenic shock with assisted laryngoscopy and rapid sequence intubation. associated hypotension, which requires treatment The child underwent trauma-bay evaluation with a with fluid resuscitation and appropriate CXR that demonstrated aspiration versus contusion in weight-based vasopressors like norepinephrine. the right lung and a FAST examination that was neg- Although once recommended for spinal cord ative. With IV fluid and pain medication, the post- injury, the most recent guidelines from the intubation HR improved to 128. American Academy of Neurological Surgeons The child underwent CT imaging of the head, neck, advise against use of methylprednisolone for abdomen, and pelvis, which demonstrated a small spinal cord injury.14 right parietal cerebral contusion and atlanto-occipital Although the c-spine remains the most dislocation. The abdomen and pelvis were uninjured. commonly injured structure in the pediatric neck, ThechildwasadmittedtothePICUwhereshewas one needs to consider injury to other structures seen in consultation by neurosurgery and treated with including superior tracheal injuries and blunt a halo-vest. Her femur was operatively repaired. vascular injuries to the carotid arteries in children who have had direct trauma to the References neck from a clothes lining mechanism or 1. Piatt JH. Pediatric spinal injury in the US: inappropriately positioned shoulder portion of a Epidemiology and disparities. JNeurosurgPediatr seatbelt. 2015; 16: 463–71. Airway injury may be suggested by change in 2. Viccellio P, Simon H, Pressman BD, et al. A voice or significant respiratory distress. On prospective multicenter study of cervical spine injury examination, the patient may present with blood in children. Pediatrics 2001; 108: E20. in the airway, noisy breathing, deviated trachea, or 3. Pieretti-Vanmarcke R, Velmahos GC, Nance ML, et al. subcutaneous air in the anterior neck. In a patient Clinical clearance of the cervical spine in blunt trauma with suspected airway injury or signs of patients younger than 3 years: A multi-center study of significant distress, endotracheal intubation the American Association for the Surgery of Trauma. J should be performed by the most experienced Trauma 2009; 67: 543–9. provider using either direct laryngoscopy or 4. Tat ST, Mejia MJ, Freishtat RJ. Imaging, clearance, and video-assisted laryngoscopy. controversies in pediatric cervical spine trauma. PediatrEmerCare2014; 30: 911–18. Vascular injuries to the pediatric neck are exceedingly rare with a reported incidence of 5. Jones TM, Anderson PA, Noonan KJ. Pediatric 0.035 percent in 57,659 pediatric blunt trauma cervical spine trauma. JAmAcadOrthopSurg2011; 19: 600–11. patients. There is limited experience with CTA of the neck in pediatric patients, but the reported 6. Lustrin ES, Karakas SP, Ortiz AO, et al. Pediatric cervical spine: Normal anatomy, variants, and trauma. sensitivity of CTA is 100 percent for penetrating Radiographics 2003; 23: 539–60. trauma to the neck and 50 percent for blunt 7. Hoffman JR, Mower WR, Wolfson AB, et al. Validity of trauma.15 r a set of clinical criteria to rule out injury to the cervical Disposition: Children with c-spine or cord injury spine in patients with blunt trauma. National should be admitted to a PICU with neurosurgery Emergency X-Radiography Utilization Study Group.N consultation. Engl J Med 2000; 343: 94–9.

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8. Stiell IG, Wells GA, Vandemheen KL, et al. The diarrhea or rash. The infant has been eating with good Canadian c-spine rule for radiography in alert and urine output. There is occasional labored breathing stable trauma patients. JAMA 2001; 286: 1841–8. andcough.Noreportedseizures,cyanosis,orfeeding 9. Ehrlich PF, Wee C, Drongowski R, et al. Canadian difficulties. C-spine Rule and the National Emergency X-Radiography Utilization Low-Risk Criteria for Past Medical History c-spine radiography in young trauma patients. J r Pediatr Surg 2009; 44: 987–91. Significant for prematurity at 35 weeks; spent 2 10. Leonard JC, Jaffe DM, Olsen CS, et al. Age-related days in the NICU for jaundice with phototherapy differences in factors associated with cervical spine treatment. injuries in children. Acad Emerg Med 2015; 22: 441–6. Medications 11. Anderson RC, Kan P, Vanaman M, et al. Utility of r None. cervical spine clearance protocol after trauma in children between 0 and 3 years of age. JNeurosurg Pediatr 2010; 5: 292–6. Allergies r 12. Muchow RD, Egan KR, Peppler WW, et al. Theoretical None. increase of thyroid cancer induction from cervical spine multidetector computed tomography in Physical Examination and Ancillary Studies pediatric trauma patients. J Trauma Acute Care Surg r ° 2012; 72: 403–9. Vital signs: T 99.6 F, HR 179, RR 48, O2 sat 94% on room air, weight 5.3 kg. 13. Kreykes NS, Letton RW Jr. Current issues in the r diagnosis of pediatric cervical spine injury. Semin General: Infant is non-toxic and in no acute Pediatr Surg 2010; 19: 257–64. distress. Occasional crying that is consolable. r 14. Hurlbert RJ, Hadley MN, Walters BC, et al. HEENT: No evidence of head trauma. No facial Pharmacological therapy for acute spinal cord injury. bruising or scalp hematoma. PERRL. Right sclera Neurosurgery 2015; 76 Suppl 1: S71–83. has small lateral subconjunctival hemorrhage. 15. Hogan AR, Lineen EB, Perez EA, et al. Value of Unable to perform adequate funduscopic computed tomographic angiography in neck and examination. Oropharynx moist and normal. No extremity pediatric vascular trauma. JPediatrSurg lesions or signs of oral trauma. 2009; 44: 1236–41. r Cardiovascular: Tachycardic. S1, S2. No S3. Strong and equal distal pulses. Good capillary Case 4 refill. r Lungs: Decreased breath sound bilateral. Bilateral Contributing Authors: Denis R. Pauzeand´ rhonchi. Otherwise good air movement. No labored breathing or accessory muscle use. William H. Hauda r Abdomen: Soft and non-distended. No History hepatomegaly. No masses. r A 4-month-old male is brought in by his grandmother Skin: Bruising on the posterior aspect of right for redness of both eyes. The grandmother describes shoulder, significant for three circular reddish and several weeks of cough and nasal congestion along purple areas approximately 2 × 2 cm each, and a with periodic breathing. There have been intermittent linear progression along the right posterior low-grade fevers. The infant was seen by his PCP sev- shoulder. r eral times during this period, as well as having a prior Neurologic: Awake and alert. Interactive. Moves all ED visit for these cold symptoms where he was diag- four extremities. Good tone. r nosed with a URI. The patient’s mother also notes that Pertinent laboratory values: WBC 27,300, Hb 9.5, her son’s “chest makes popping sounds” over the past chemistry unremarkable other than AST 106 and fewweeks.Motherandgrandmotherbothdenyfalls, ALT 154. trauma, or sick contacts. r Pertinent radiologic studies: CXR with scattered The child has had a couple of episodes of vomit- interstitial infiltrates and clavicle fracture. CT ing in the past, but not recently. There has been no chest with rib fractures (Figure 2.4).

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were responsible for nearly 80 percent of child abuse fatalities.2 Only 17 percent of fatalities were from non-parents, and in approximately 4 percent of the cases, the perpetrator was unknown.2 There are many more children who suffer non-fatal injury every day, and up to one-third of patients with abusive head trauma are misdiagnosed at their first visit to a healthcare provider.3 r Presentation: Non-accidental trauma and abusive head trauma have many different presentations duetotheseverityandorgansinjured.Some presentations are dramatic – seizures, lethargy, respiratory distress, or apnea. These dramatic presentations are recognized by parents and cause parents to seek medical care, but may not be recognized as being caused by non-accidental Figure 2.4 CT chest reconstruction: Lateral view showing multiple injury. As a result, these symptoms often are rib fractures. For the color version, please refer to the plate section. ascribed to other medical conditions such as reflux disease, BRUE, gastroenteritis, or respiratory infections.4,5 However, some infants Questions for Thought with non-accidental trauma may present with r Does this infant need brain imaging? Which common and non-specific symptoms. They often modality would be appropriate? r arrive looking well and in no acute distress. They Does this child need abdominal imaging? Which may come in with a common complaint, such as modality would be appropriate? r vomiting, ear infection, fever, or URI. Their Why do you think this infant was seen multiple examination may be normal if done quickly, but a times before a diagnosis was made? careful and detailed examination may identify r What are the risk factors for this diagnosis? r What are some “red ﬂags” in your history and seemingly minor findings which herald the physical examination for this diagnosis? presence of abuse, such as a bruise, subconjunctival hemorrhage, nosebleed, or petechiae. They may appear neurologically Diagnosis well, even if suffering from abusive head trauma.3 r Non-accidental trauma. r Diagnosis: A high index of suspicion is paramount to diagnosing many cases of non-accidental Discussion trauma.Theyoungertheage,theharderitcanbe r Epidemiology: According to the National Child to make a diagnosis. The history may be Abuse and Neglect Data System, over 1,500 fabricated or deliberately misleading. The children died in 2013 from child abuse in the caregiver presenting with the child may have no USA.1 Nearly three-quarters of these pediatric knowledge of injuries caused by someone else, fatalities were children of 3 years of age and such as another family member or a daycare younger, and nearly half were less than 1 year of provider. Failure to diagnose non-accidental age.1 This equates to four children dying every day trauma allows the child to return to their from abuse. Not every case of non-accidental- dangerous environment, and repeated abuse will injury-related death is diagnosed or reported, likely occur.3 A detailed and thorough history and especially in cases of asphyxia or smothering physical examination are crucial to look for red deaths, so these statistics likely under-represent flags. Historical red flags include inconsistencies the extent of the problem. Abusive head trauma is in the described mechanism and the physical the most common cause of child abuse death. findings, injuries that do not fit with the According to childwelfare.gov, in 2013 parents developmental stage of the child (for instance,

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when a child has been said to have rolled off a bed, butexaminationrevealsthatthechildis developmentally unable to roll), delay to presentation for injuries, or history of repeated visits for injuries. Redflagsonphysicalexaminationinclude bruises on non-ambulatory children (“if you don’t cruise, you don’t bruise”), bruises in areas not typical for ambulatory trauma (for instance, buttock bruises or bruises to the back of legs), mouth injuries including dental injuries or frenulum tears, retinal hemorrhages, bony deformity, apnea, seizures, altered mental status, or epistaxis in children prior to fine motor control.6,7 The physical examination can be Figure 2.5 Retinal hemorrhages. For the color version, please refer to the plate section. non-specificorevennormalincasesof non-accidental trauma. follow-up with a child abuse physician and CPS Helpful diagnostic tools include neuroimaging can be arranged. (CT or MRI) with CT usually being done first in the ED. Evaluation for retinal hemorrhages and skeletal survey are typically part of an inpatient Historical clues Physical findings Ancillary studies evaluation, but can be accomplished in the ED at r Numerous prior r Bruising to r Elevated LFTs times. For patients undergoing an LP, visits shoulder suggesting xanthochromia or fresh red blood cells may be r r Convoluted and Subconjunctival r abdominal injury discovered, signifying abusive head trauma. In confusing hemorrhage Anemia medical history suggesting cases of concern for abdominal trauma, CT is blood loss appropriate in the ED. Although it is important to r CXR with rib be conscious of the untoward effects of excessive fractures radiation exposure in infants, the risk of missed injury in an abused child is far greater than the risk of CT scanning. Unfortunately, there are no Follow-Up current biomarkers for abuse, although The infant was admitted to the PICU after CT wasper- biomarkers for traumatic brain injury are being formed demonstrating subdural hemorrhage. Pedi- studied. atric ophthalmology assessed the child and found r Treatment: Treatment of these children varies bilateral multilayered extensive retinal hemorrhages depending upon the injuries discovered. In all (Figure 2.5). Abdominal CT revealed a grade II cases, the provider should manage the patient’s liverlaceration.Askeletalsurveywasperformedand physical discomfort and ensure the child’s safety. showed the above-mentioned chest trauma as well r Disposition: Infants with suspected non-accidental as metaphyseal corner fractures of the left tibia and trauma should be admitted to the hospital for fibula. Shortly after admission, the infant had neuro- both safety planning and for further diagnostic logic deterioration, requiring tracheal intubation and evaluation. Further studies, such as brain imaging neurosurgical evacuation of the subdural hematoma. by MRI, funduscopic evaluation by Social workers, CPS, and the police were involved. The ophthalmology, and skeletal survey should be child was eventually discharged into foster family care. performed. CPS, social workers, and law enforcement should be involved. The infant will References typically be admitted to the hospital until he or 1. The Children’s Bureau. The National Child Abuse and she is stabilized and a safe discharge environment Neglect Data System (NCANDS). See www.acf.hhs is confirmed. Some children can be discharged .gov/cb/research-data-technology/reporting-systems/ from the ED safely if CPS is involved and ncands (accessed November 2016).

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2. The Children’s Bureau. Child Abuse and Neglect Physical Examination and Ancillary Studies Fatalities 2015: Statistics and Interventions. See www r Vital signs: HR 125, BP 105/70, RR 55, O2 sat 95% .childwelfare.gov/pubPDFs/fatality.pdf (accessed on 2 L nasal cannula, T 99.5 °F, 20 kg. November 2016). r General: The patient is drowsy. She opens her eyes 3. JennyC,HymelKP,RitzenA,ReinertSE,HayTC. to her name and follows commands, moving all Analysis of missed cases of abusive head trauma. extremities. JAMA 1999; 281: 621–6. r 4. Guenther E, Powers A, Srivastava R, Bankowsky JL Primary survey: Abusive head trauma in children presenting with an r Airway: Patent airway, soot in and around the apparent life-threatening event. JPediatr2010; 157: mouth, no pooling secretions. 821–5. r Breathing: Rapid shallow respirations, with 5. Altman R, Brand D, Forman S, et al. Abusive head minimal chest-wall excursion, O2 sat 88%, injury as a cause of apparent life-threatening events in corrects to 95% with 2 L nasal cannula. infancy. Arch Pediatr Adolesc Med 2003; 157: r 1011–15. Circulation: Tachycardic, strong central and peripheral pulses. 6. Sugar NF, Taylor JA, Feldman KW. Bruises in infants r = = and toddlers: Those who don’t cruise rarely Disability:GCS13(eyes 3, verbal 4, motor = bruise. Arch Pediatr Adolesc Med 1999; 153: 6), moves all four extremities. 399–403. r Exposure: The child is completely exposed, 7. McIntosh N, Mok JY, Margerison A. Epidemiology of revealing numerous burns. She is placed on a oronasal hemorrhage in the first 2 years of life: sterile sheet. Implications for child protection. Pediatrics 2007; 120: r Secondary survey: 1074–8. r HEENT: Cranial nerves are intact, PERRL. The child has dry mucous membranes with Case 5 soot in and around her mouth. No eye involvement. Contributing Authors: John Tran and r Neck: Non-tender with no signs of trauma. Rebecca Jeanmonod Trachea midline, no JVD. r History Cardiovascular: Tachycardic and regular, with normal heart sounds, good pulses, and The patient is a 4-year-old girl who is brought in to the capillary refill throughout. ED by ambulance after being rescued from a burning r Lungs/Chest: Anterior chest wall with house. While she was trying to escape from her room, cutaneous burns. No stridor. Lungs sound her nightgown caught on fire, but was put out by one clear, but with shallow rapid breaths. of the firefighters. En route, EMS state she was sleepy r Abdomen: There are cutaneous burns involving and confused. Her parents were able to escape with- the superior region of the abdomen. The out any significant injury. The patient arrives to the ED abdomen is mildly tender diffusely, with no complaining of pain to her torso and limbs as well as peritoneal signs or distention. Bowel sounds difficulty breathing. She has received fentanyl for pain are normal. from EMS en route. r Extremities: No deformity, moves spontaneously. Past Medical History r r Skin: There are burns involving the front of the The child had a normal uneventful birth history patient’s neck, her upper chest, upper back, and is fully immunized. bilateral shoulders, and right upper arm. All burn areas are erythematous, with bullous Medications blisters both intact and unroofed. There is a r None. small area at the sternum with a pale appearance that is non-blanching. The Allergies total burn surface area (TBSA) is r None. approximately 22 percent.

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r Neurologic: GCS 13, follows commands, no epidermis (whose primary function is to protect lateralizing findings. against water loss and bacterial invasion) and r Back and pelvis: Non-tender, no step-offs, dermis (whose primary function is temperature pelvis stable to rock and compression. regulation).3,4 Cell damage occurs at temperatures ° r Pertinent laboratory values: CBC, electrolytes, higher than 113 F, with the temperature, as well renal function, and U/A are unremarkable. as time of exposure, ultimately dictating the degree of damage. In addition to local damage, r Radiographs: Normal CXR. extensive cutaneous burns can lead to electrolyte abnormalities, increased systemic vascular Questions for Thought resistance, metabolic acidosis, increased blood 3 r When is it necessary to intervene in the airway of viscosity, and depressed cardiac function. aburnvictim? Burns are classified as superficial, superficial r How do you choose the volume of resuscitative partial-thickness, deep partial-thickness,and ﬂuids to deliver? How do you monitor its full-thickness burns. Superficial burns involve only adequacy? r the epidermal layer. Skin is red, painful, and What is the appropriate way to care for burn tender, but without blisters, similar to a sunburn. wounds? Superficial partial-thickness burns involve the r When is it necessary to transfer a patient to a epidermis and superficial dermis. Skin is painful burn center? and has blisters with a moist/erythematous base. Both superficial and superficial partial-thickness burns typically heal without scarring, and are Diagnosis treated with resuscitation and pain control. These r Superficial partial-thickness, deep are medically managed. partial-thickness, and full-thickness burns Deep partial-thickness burns involve the deep involving greater than 20 percent of the TBSA. dermis, with resulting damage to hair follicles, sweat and sebaceous glands, and nerves. Blisters Discussion may form, and the dermis is pale white to yellow r Epidemiology: Approximately two million burn without blanching, and with absent pain injuries occur annually in the USA, with half of sensation. Full-thickness burns involve the entire these in children.1 Although most burns are dermal layer and may involve deeper structures minor, each year, 50,000 burns require admission (such as fat, muscle, and bone), with charred skin to the hospital. There are 2,500 pediatric deaths that is pale, painless, and leathery. Both deep attributable to burns annually.1,2 Children have partial-thickness and full-thickness burns often worse outcomes, morbidity, and mortality require surgical intervention. compared to adults with similar burns.1 This may Systemic derangement occurs with superficial be due to physiologic differences, such as thinner partial-thickness or deeper burns involving skin, difficult vascular access, less margin for error greater than 15 percent of the TBSA. There can be in fluid management, and greater hesitancy for cardiovascular collapse, termed “burn shock,” burn surgeries. which occurs from fluid loss, increased capillary Scaldburnsaremorecommoninchildren permeability, and vasodilation. This leads to younger than 5 years of age, and flame burns are decreased cardiac output and, without adequate usually seen in older children.2 Most burns occur fluid resuscitation, it will continue to decline. at home. Non-accidental trauma should be Renal function may deteriorate from considered in all cases of pediatric burns, but most vasoconstriction of the renal arteries. Metabolism burns are accidental. The provider should suspect is increased in burn patients, up to 150–200 child abuse in the setting of bilateral, symmetric percent of the normal rate. This can lead toa burn patterns, injuries to the dorsum of the hand, decrease in body weight, a negative nitrogen and burns presenting in a delayed fashion.1,3 balance, and a decrease in energy stores. r Pathophysiology: Depending on their depth, r Presentation: In addition to the obvious injuries cutaneous burns can disrupt the function of the evident in burn patients, the emergency provider

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should consider the possibility of blunt trauma relatedtotheburn.Somepatientsmayhave jumped from a height to escape, and sometimes there is a component of the burn injury that involves blast trauma, for instance from an exploding gas can, which causes the patient to be thrown or struck by flying objects. Therefore, the provider should be cognizant of the possibility of occult blunt and penetrating traumatic injury associated with the burn. Additionally, the patient may present with altered mental status or respiratory compromise. Some patients are intoxicated before the burn injury takes place, but the provider should also Figure 2.6 Rule of 9s for older children, depicting relative values for calculated TBSA involved in burn. consider the possibility of inhalational intoxicants/poisons, such as carbon monoxide and cyanide, which occur not uncommonly in 18 percent, the posterior as 18 percent, the head burn victims in enclosed spaces. If the patient is counts as 9 percent, and the genitalia count as 1 knowntohavecomeinfromanenclosedfire,a percent (Figure 2.6). This rule does not accurately carbon monoxide level should be checked. If the represent the burn area in smaller children. For patient has an unexplained lactic acidosis, the them, the most accurate method for TBSA burn provider should consider the possibility of determination is using a standardized commercial cyanide exposure, as well, and could consider chart, such as Lund and Browder, to estimate burn initiating treatment. area by age. If a chart is not available, a modified r Treatment: It is important to evaluate the patient’s rule of 9s can be used (Figure 2.7). If there is ABCs and remove any clothing or potential greater than 15 percent TBSA burn, initial fluid sources of heat. If there is a chemical burn, resuscitation is guided by the Parkland formula (4 decontamination should be performed × TBSA burned × weight in kg). This estimates immediately. If the patient appears to have airway the fluid volume necessary for the first 24 hours involvement from the burn injury, such as after the burn. Half of this volume is given in the stridorous breathing, burns involving the oral first8hoursstartingfromthetimeoftheburn, cavity, or circumferential burns of the neck, it is andthesecondhalfisgiveninthenext16hours. important to secure the airway sooner rather than This is only an approximation, and resuscitation later, as later swelling may preclude orotracheal should be titrated to adequate urine output of 1 intubation and require surgical airway. mL/kg per hour. For infants younger than 1 year Continuous oxygen supplementation and or less than 25 kg, maintenance fluids should be monitoring is important, as well as added to the initial 24-hour resuscitation. carboxyhemoglobin levels, if appropriate. Because Patients should have aggressive pain of fluid shifts in the burn victim, patients without management, typically with narcotic analgesics. airway burns may need to be intubated from Cooling the patient and wet dressing applications ARDS, especially if the burn involves more than must be avoided to prevent additional heat loss 30 percent of the TBSA. and vasoconstriction. IV or IO access is essential early in the initial Laboratory work including electrolytes and assessment to begin fluid resuscitation. The renal function are useful to guide electrolyte provider should determine the depth and TBSA of replacement and resuscitation. CXR may the burn to guide fluid resuscitation. To calculate demonstrate ARDS or inhalational injury. In theTBSAinchildrenwhoareclosetoadult electricalburns,EKGmustbedone.Ifthereis size/age, the rule of 9s can be employed. For this concern for muscle damage or rhabdomyolysis, a rule, each leg counts as 18 percent, each arm myoglobin and creatine kinase level may help counts for 9 percent, the anterior torso counts as guide therapy.

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Figure 2.7 Modified rule of 9s for infants and toddlers. Subtract 1 percent from the head for each year of life over age 1 year, add 1 percent for both legs for each year of life over age 1 year.

In patients with circumferential burns, the need debridement unless they overlie large joints. provider should consider escharotomy to avoid Topical antimicrobial should be lathered compartment syndrome. This should be done in generously on the wounds. This includes consultation with a surgeon to ensure the bacitracin ointment or 1% silver sulfadiazine appropriate technique and to minimize risk. cream (except on the face). Synthetic occlusive r Disposition: Transfer criteria to a burn center dressingsshouldbeusedtocoverburnedareas, include the following: followed by gauze dressings. Ideally, dressings r Greater than 20 percent partial-thickness should be changed twice a day. Some patients may burns in patients Ͼ 10 years old, and greater require surgical intervention, which should be than 10 percent in patients Ͻ 10 years old; done at burn centers. Discharged patients should be prescribed r Burns involving face, hands, feet, perineum, adequate analgesics and should follow up with a genitalia, major joints; burn specialist. Antihistamines may be used for r Circumferential burns; significant pruritis during the healing process. r Full-thickness burns; With appropriate care, most children with burns r Electrical burns and chemical burns; survive, even with extensive burns in smaller r Inhalational injury; children.5 r Preexisting significant comorbidities; r Suspected child abuse; Historical clues Physical findings If a patient has minor burn wounds and does r Extricated from burning r Soot in mouth notmeetthecriteriafortransfertoaburncenter, r r building r Hypoxia and tachypnea the wound can be managed in the ED. This Confused en route Burns on examination involves debridement of the burn wounds, after proper analgesia. This should be done with mild soap and water or dilute antiseptic solution. Follow-Up Scissors should be used to cut loose skin that is Thechildwasintubatedbecauseofherrelative still attached to healthy skin. Intact blisters do not hypoxia, dyspnea, tachypnea, and evidence of soot in

16:09:45 03 Chapter 2: Resuscitation her mouth. She was resuscitated with 1,600 mL lac- Past Medical History tated Ringer’s over the next 24 hours (4 × 20 kg r Seasonal allergies. × 20 TBSA) and maintained adequate urinary output. Her carbon monoxide level was not significantly Medications elevated. She had bronchoscopy, which revealed no r lower-airway burns, and was ultimately extubated on Cetirizine. hospital day 3. She has undergone skin grafting over her chest and right arm since, and has otherwise had Allergies an uneventful recovery. r None.

References Physical Examination 1. Gonzalez R, Shanti C. Overview of current pediatric r Vital signs:T92°F, HR 40, RR 5, BP 50/20, O sat burn care. Semin Pediatr Surg 2015; 24: 47–9. 2 80% on 100% oxygen. 2. Kramer CB, Rivara FP, Klein MB. Variations in US r General:Unresponsiveandintubated. pediatric burn injury hospitalization using the r National Burn Repository Data. JBurnCareRes2010; Primary survey: 31: 734–9. r Airway: 4.0uncuffedtube,15cmatthelip, 3. Merz J, Schrand C, Mertens D, et al. Wound care of the airway confirmed with waveform capnography pediatric burn patient. AACN Clin Issues 2003; 14: and auscultation. There is an air leak. 429–41. r Breathing: Decreased breath sounds on the left 4. Reed J, Pomerantz W. Emergency management of versus the right, bilateral crackles with pediatric burns. Pediatr Emerg Care 2005; 21: 118–29. decreased air entry at bases. 5. Sheridan R, Remensnyder J, Schnitzer J, et al. Current r Circulation: Bradycardia, poor capillary refill, expectations for survival in pediatric burns. Arch cool extremities, thready pulses. Pediatr Adolesc Med 2000; 153: 245–9. r Disability: GCS 3. r Exposure: Wet clothing removed and patient fully exposed, no signs of trauma. Case 6 Resuscitative Measures Contributing Authors: Ryan Fulton and Based on the child’s primary survey, further Melanie K. Prusakowski examination is deferred. The child’s examination suggests that the ET tube is likely the wrong size, as History the child has a large air leak. The examination also A 2-year-old boy presents after his mother found him suggests that the tube may be placed too deeply, unconscious in the backyard swimming pool. The likely in the right mainstem bronchus. The child’s patient had been otherwise healthy prior to presen- bradycardia may be secondary to his hypoxia and tation. Upon EMS arrival, CPR was initiated and the hypothermia. patient was intubated in the field. The patient remained Thechild’sETtubeischangedoutfora4.0-mm comatose with GCS 3 during transportation. Once the cuffedtubeandaPEEPvalveisattached. patient was attached to a monitor, asystole was discov- Consideration is given to placing an uncuffed ered and CPR was continued. Initial vitals showed no 4.5-mm tube instead, but because of the anticipated discernible heart rate, hypotension, and hypothermia. high airway pressures, the provider recognizes that Peripheral IV access was obtained and a bolus of lac- the cuff will provide a better seal for adequate PEEP. tated Ringer’s (20 cc/kg) was administered. The patient The tube is advanced to 13 cm. During this, the had copious amounts of fluid suctioned from the ET child is given IV 1:10,000 epinephrine at the dose tube during resuscitation efforts. Four minutes prior recommended by the Broselow tape. The ET tube is to arrival, following suctioning, appropriate oxygena- confirmed by auscultation and waveform tion, and two doses of weight-based epinephrine, he capnography. Rewarming is begun with heated air had return of spontaneous circulation. blankets and warmed IV saline at 20 cc/kg.

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Repeat Physical Examination and Ancillary Studies Diagnosis r Vital signs:T93°F, HR 110, RR 25 (bagged), BP r The patient experienced a non-fatal drowning. 85/60, O2 sat 94% on 100% oxygen. r Primary survey:

r Discussion Airway: Tube position confirmed, no air leak. r r Breathing: Equalchest-wallexcursion,equal Epidemiology: Drowning is defined as respiratory breath sounds, bibasilar crackles, adequate impairment from submersion or immersion in a 1,2 oxygenation. liquid media. If a patient is rescued at any r Circulation: Good central pulses, poor point, drowning is interrupted and is considered peripheral capillary refill. non-fatal drowning. Older terminology includes “near drowning” and “dry drowning.” In the USA, r Disability: GCS 3. drowning is the leading cause of death among r Exposure: Child covered with warming blanket. children of 1 to 4 years of age, and the second r Secondary survey: leading cause of death in children 1 to 18 years of 1,2 r HEENT:Noevidenceofheadtrauma.AnET age. Male sex, young age, low socioeconomic tubeistapedinplace.Nohemotympanum. status,andriskybehaviors(e.g.alcoholuse)are Pupils are not reactive. the most common risk factors associated with 1,2 r Neck: No JVD. Trachea is midline, c-collar is drowning. r placed. Pathophysiology:Thephysiologicresponseto r Cardiovascular: Regular rate and rhythm, no drowning is the same regardless of age or the M/R/G. media of submersion. The first response is to hold r Lungs: Equal with bilateral crackles. No one’s breath in an attempt to maintain an airway. chest-wall crepitus or bruising. Eventually, the drive to breathe overcomes this r Abdomen: Hypoactive bowel sounds, response and aspiration occurs. Water in the non-distended abdomen without alveoli results in a significant osmotic gradient, organomegaly. which leads to increased permeability, fluid shifts, 1,3 r Extremities: No deformity or bruising. Pulses and electrolyte disturbances. These electrolyte present throughout. irregularities are similar in both saltwater and freshwater drowning.3 The increased fluid in the r Skin: Cool to touch, no bruising or rashes. lung also causes a wash-out effect of the surfactant r Neurologic: No spontaneous respirations, no in the alveoli, resulting in poor lung compliance response to pain, pupils non-reactive. andamismatchbetweenventilatedandperfused r Pertinent laboratory tests: pH 7.20, PaCO2 43, lung tissue (V/Q mismatch).1,3 As more bicarbonate 15, Na 135, K 3.5, Cl 110, BUN 10, Cr aspiration occurs, hypoxemia develops, leading to 0.8, glucose 110. loss of consciousness. A typical progression of r Radiographs: CXR shows diffuse airspace tachycardia, bradycardia, pulseless electrical infiltration, consistent with pulmonary edema. activity, and asystole is documented in the literature.1,4,5 The first stage of drowning is measured in Questions for Thought seconds to minutes, but for those who drown in ice water this process can last an hour or longer.1 r What concomitant illnesses or injuries must be Electrical and metabolic activity of the brain is considered in children presenting with drowning? reduced in the hypothermic patient, with a r What is the pathophysiology of drowning? reduction of cerebral oxygen consumption by r What role does induced hypothermia play in 5percentforeach1.8°F drop in body post-drowning care? temperature.1 Therefore, drowning in ice water is r Does the liquid media in which drowning occurs protective, and the medical provider should not aﬀect outcome or treatment? terminate resuscitative efforts in an ice-water drowning victim until his or her temperature has

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surpassed 86 °Fwithnoreturnofvitalsigns.1,4–6 respiratory membranes, fluid may appear in the Warm-water drowning victims with ET tube, causing oxygenation to become cardiopulmonary arrest have a much more dire challenging. Due to this, a fine balance between prognosis. suctioning and oxygenation must be obtained.1 In r Presentation and diagnosis:Inanycaseof cases of hypotension not responsive to drowning, the medical provider must consider the appropriate ventilation, rapid crystalloid infusion context in which it occurred. Drowning is often is recommended. immediately preceded by traumatic injuries, In the ED, attention to the ABCs should especially head and c-spine injuries. Therefore, in continue. The next steps include CXR and addition to resuscitative efforts, the provider measurement of ABG.1 The most common should evaluate for multi-system trauma. finding on ABG is a metabolic acidosis. This can Underlying seizure disorder is known to be a risk be overcome by the patient’s innate tachypneic factor for drowning, and the provider should response if spontaneous respirations occur. If the evaluate for this possibility in the right clinical patient is intubated, a metabolic acidosis can be circumstance (for instance, drowning in a youth treated by increasing the ventilator rate, or with who knows how to swim). Toxic ingestions are an elevation of the peak inspiratory pressure. Poor also common in the older drowning victim. response to mechanical ventilation and typical ED Finally, the clinician should weigh the possibility care should raise concern for alternate pathology.1 of non-accidental trauma in young drowning ACTscanoftheheadandevaluationoftoxic victims. exposure can be helpful in such a case. r Treatment: Resuscitation of drowning victims can Electrolytes should be obtained but are minimally be described in five categories: In-water useful and are usually normal, regardless of the resuscitation, resuscitation on land, pre-hospital media in which drowning occurred.1 r care, care in the ED, and in-hospital care. The key Disposition: A patient with a history of minor to in-water resuscitation is stabilization and submersion, no vital sign abnormalities, and getting the patient to safety on land. normal mental status may be observed for Immobilization of the c-spine is necessary only in 6–8 hours in the ED and then discharged events in which spinal injury is suspected, such as home.1 All others should be admitted for diving or accidents involving watercrafts.1 Once observation. on land, the patient should be evaluated for People who have been stabilized and admitted responsiveness. Since drowning is classically a to the hospital are not clear of complications. respiratory arrest there may be gasping or apnea Signs and symptoms similar to ARDS are with a maintained heart rate, in which case only common, although recovery tends to be faster.1,3 supported ventilation is necessary.1 If the patient The literature does not support the use of requires CPR, the traditional ABC approach of broad-spectrum antibiotics, glucocorticoids, airway–breathing–circulation and not the new artificial surfactant, or inhaled nitric oxide in sequence of circulation–airway–breathing is typical drowning victims.1 While rewarming is a recommended.1,4,5 New recommendations also key goal in all cases of drowning, induced suggest five rescue breaths instead of the original hypothermia with temperatures between 89.6 and two, due to the increased resistance found in the 93.2 °F for 24 hours may be neuroprotective.6 r airway.1,4,5 Prevention: Prevention is the most important step In nearly 86 percent of drowning cases in managing victims of drowning. More than 85 requiring CPR, regurgitation and aspiration of percent of cases can be prevented by supervision, stomach contents occurs.1 This aspiration swimming instruction, technology, regulation, compounds the poor lung compliance and and public education.1 Key prevention measures worsens oxygenation. If the patient is include: always swimming with others, use of life deteriorating or showing signs of fatigue, early jackets, and swimming in areas with lifeguards. intubation and mechanical ventilatory support is Areas that have lifeguards on duty show improved recommended. Due to fluid shifts across statistics on drowning outcomes. Less than

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6 percent of all rescued persons need medical Case 7 attention and only 0.5 percent need CPR in areas where lifeguards function.1 New regulations on Contributing Author: Edwin Layng swimming pools include having a four-sided fence The patient is a 4-year-old boy with a history of vomit- with a self-closing, self-latching gate. Having a ing and diarrhea. Symptoms began 3 days ago, shortly fence that meets these guidelines has been shown after being picked up from daycare. The patient has had to reduce incidence of drowning by 50–70 non-bloody/non-bilious vomiting about four times percent.1 per day and has had eight non-bloody bowel movements per day since symptom onset. He has tried eat- Historical clues Physical findings Ancillary studies ing bland foods, such as bananas, rice, toast, as well r Found r Cardiorespiratory r CXR with as drinking clear liquids, but vomits shortly thereafter and has overall had very poor PO. Mom reports that he r submerged r arrest r pulmonary edema Known risks: Increased ABG with has also had a low-grade fever and cramping abdom- Male, age 1–4 secretions metabolic acidosis inal pain. The child states his pain is made worse by attempts to eat or drink. Of note, his older sister, who attendsthesamedaycare,hadsimilarsymptomsbefore Follow-Up the patient began feeling ill. He denies chest pain, The child was admitted to the PICU with ongoing shortness of breath, or headache. resuscitative support. He later underwent confirmatory testing and was ultimately declared brain dead. Past Medical History His organs were harvested for transplant. r Otherwise healthy, immunizations are UTD. References Medications r Acetaminophen for fever. 1. Szpilman D, Bierens J, Handley A, et al. Drowning. N r EngJMed2012; 366: 2102–10. Bismuth subsalicylate for nausea/vomiting. 2. Van Beeck EF, Branche CM, Szpilman D, et al. A new Allergies definition of drowning: Towards documentation and r prevention of a global public health problem. Bull Penicillin – patient gets hives. WorldHealthOrgan2005; 83: 853–6. 3. Orlowski JP, Abulleil MM, Phillips JM. The Physical Examination and Ancillary Studies r hemodynamic and cardiovascular effects of Vital signs: T 99.5 °F, HR 130, BP 75/45, RR 30, O2 near-drowning in hypotonic, isotonic, or sat 100%. Per his mother, his weight at his last hypertonic solutions. Ann Emerg Med 1989; 18: appointment several months ago was 28 kg, and 1044–9. the measured weight in the ED is 26.5 kg. Per the 4. Soar J, Perkins GD, Abbasc G, et al. European Broselow tape, he is in the “orange” category. Resuscitation Council guidelines for resuscitation r General:Heisawake,butdrowsy.Heis 2010. Section 8. Cardiac arrest in special uncomfortable, holding his abdomen. circumstances: Electrolyte abnormalities, poisoning, r drowning, accidental hypothermia, hyperthermia, HEENT:Thepatient’seyesaresunken.PERRL. asthma, anaphylaxis, cardiac surgery, trauma, Cranial nerves are intact. The patient’s mucous pregnancy, electrocution. Resuscitation 2010; 81: membranesaredry.Hisneckissupplewitha 1400–33. midline trachea. 5. International Life Saving Federation Medical r Cardiovascular: Tachycardic, no M/R/G. Committee. Clarification Statement on ExtremitiescoolandpalewithϾ 3second Cardiopulmonary Resuscitation for Drowning.Leuven: capillary refill. International Life Saving Federation, 2008. r Lungs: CTA bilaterally, without W/R/R. 6. Warner D, Knape J. Recommendations and consensus r brain resuscitation in the drowning victim. In Bierens Abdomen: Child has hyperactive bowel sounds. JJLM, ed. Handbook on Drowning: Prevention, Rescue, His abdomen is soft with diffuse generalized and Treatment. Berlin: Springer-Verlag, 2006, tenderness to palpation, with no rebound or pp. 436–9. guarding. There are no masses.

16:09:45 03 Chapter 2: Resuscitation r Extremities and skin: Extremities are cool. There reduced stroke volume and low cardiac output. are no rashes or skin changes. Tachycardia, increased systemic vascular r Ancillary studies: Na 145, K 3.3, Cl 90, bicarbonate resistance, and increased cardiac contractility are 30, BUN 30, Cr 1.3, albumin 3.3, remaining LFTs the main compensatory mechanisms. In addition, normal. WBC 13,000, Hb 15.0, Plt 200,000. tachypnea is often seen once a metabolic acidosis Lactate 2.0. U/A with elevated specific gravity, ++ develops. ketones, negative glucose, nitrite, leukocyte The shock syndrome is characterized bya esterase, and blood. continuum of physiologic stages, beginning with an initial inciting event that causes a systemic disturbance in tissue perfusion. Subsequently, Questions for Thought shock may progress through three stages, which r How much and what type of ﬂuid is indicated for include compensated shock, hypotensive shock, treatment of this child? r and irreversible shock. The shock progression is Does the ﬂuid resuscitation process change with often an accelerating process, and pediatric malnourished children? patients in particular can decompensate very r What is the best way to obtain IV access in quickly. While it may take hours for compensated patients like this? r What therapeutic endpoints should be obtained shocktoprogresstohypotensiveshock,itmay to assess for adequate resuscitation? only take minutes for hypotensive shock to progress to cardiopulmonary failure and arrest. During compensated shock, the body’s homeostatic mechanisms are able to counteract Diagnosis the diminished perfusion, and systolic blood r Hypovolemic shock secondary to intravascular pressure is maintained within the normal range. volume loss from viral gastroenteritis. The heart rate is initially increased. Signs of peripheral vasoconstriction, such as cool skin, Discussion decreased peripheral pulses, and oliguria can be r Epidemiology:Hypovolemiaisthemostcommon noted as perfusion becomes further cause of shock in children worldwide and is compromised.2,3 During hypotensive shock, broadly divided into hemorrhagic and compensatory mechanisms are overwhelmed. non-hemorrhagic causes. Fluid loss from diarrhea Signs and symptoms of organ dysfunction, such as is the leading cause of hypovolemic shock and is a altered mental status, appear. Systolic blood major cause of infant mortality worldwide.1 Other pressure falls, although children who have lost as causes of hypovolemic shock include vomiting, much as 30–35 percent of circulating blood inadequate fluid intake, diabetic ketoacidosis, volume can typically maintain normal systolic third-space losses, and large burns. Hemorrhagic blood pressures. Once hypotension develops, the shockinchildrenismostoftentheresultofmajor child’s condition usually deteriorates rapidly to trauma. Less common causes include GI bleeding, cardiovascular collapse and cardiac arrest. post-operative bleeding, and pulmonary During irreversible shock, progressive hemorrhage. end-organ dysfunction leads to irreversible r Pathophysiology:Shockisaphysiologicstate, organ damage and death despite resuscitative characterized by a significant, systemic reduction efforts.2,3 in tissue perfusion, resulting in decreased tissue r Presentation: When patients present with oxygen delivery. Although the effects of hypovolemicshock,itcanbeanywhereonthe inadequate tissue perfusion are initially reversible, continuum from compensated to non- prolonged oxygen deprivation leads to generalized compensated. For non-hemorrhagic cases, cellular hypoxia and derangement of critical patients often present with tachycardia and are biochemical processes.2 normotensive.2 However, they can progress to Hypovolemic shock is the result of an absolute hypotension quickly, if not addressed. For deficiency of intravascular blood volume. It is hemorrhagic causes, patients often present as a characterized by decreased preload leading to trauma alert and can be mildly tachycardic or

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unresponsive, depending on the quantity of the causes of hypoalbuminemia). However, volume lost/severity of the inciting event. randomized trials and meta-analyses have failed r Diagnosis: When diagnosing hypovolemic shock to consistently demonstrate a difference in clinical in pediatrics, physical examination findings are outcomes for adults and children receiving colloid critical. Common examination findings for therapy for shock when compared to crystalloid hypovolemic shock include tachycardia, narrow infusion. Vasoactive medications have no place in pulse pressure, weak peripheral pulses, cool skin, the treatment of isolated hypovolemic shock. capillary refill Ͼ 2 seconds, oliguria, and altered These interventions do not address the underlying mental status.2–4 Children who are hypotensive, problem of inadequate circulating blood volume with histories of trauma, are likely in hemorrhagic and may worsen tissue hypoxia. shock. They must be carefully evaluated in order In patients with hypovolemic shock who have to identify sources of bleeding and associated a history of severe malnutrition, there is a risk that injuries. the malnutrition will cause sodium and water r Treatment: It’s important to initially do a primary retention. Once resuscitation begins, there can be assessment in a pediatric patient with shock to an over-expansion of the extracellular fluid and address airway, breathing, and circulation. If the myocardial dysfunction. The WHO cites a risk of patient is not protecting the airway, is cyanotic, or fluid overload, heart failure, and pulmonary has signs of increased work of breathing and edema and recommends against rapid fluid impending compromise, you should intubate the bolusesof20mL/kginthesechildren.6 Current patient before proceeding with the resuscitation.2 recommendations are that severely malnourished If active bleeding is seen, attempt to stop it with children should receive 15 mL/kg of isotonic direct pressure. Fluid administration is the crystalloid fluids combined with 5% dextrose over primary therapy for hypovolemic shock. Timely 1hour.6 Furthercaredependsuponthepatient’s administration of fluid is key to preventing response. A recent study in Kenya comparing metabolic decompensation.2–5 Children with resuscitation with 30 mL half-strength hypovolemic shock who receive an appropriate Darrows/5% dextrose over 2 hours to 40 mL volume of fluid within the first hour of Ringer’s lactate over 2 hours found lower resuscitation have the best chance for survival and mortality and better response to therapy in the recovery. Ringer’s lactate group that received more fluid.7 Start fluid resuscitation for shock with Furthermore, there were no cases of pulmonary 20 mL/kg of isotonic crystalloid administered as a edema or cardiogenic failure in any of these bolus over 5 to 20 minutes.2,3 For children in patients. Further research needs to be conducted shock, IO cannulation should be performed if IV in order to make conclusions to optimize care for access cannot be established quickly.2 When patients with severe malnutrition in hypovolemic administering fluid boluses, it’s important to use shock. either a pressure bag, deliver aliquots using a large It is important to monitor the patient’s syringe that is refilled through a three-way responsetothefluidbolusaswellasreassess stopcock (“push–pull” method), or a rapid endpoints to decide whether or not there is a need infuser, in order to ensure adequate delivery. In a for additional fluid boluses. Some physical study comparing three methods of IV fluid examination signs for fluid responsiveness include resuscitation, delivery by gravity was measured to strong distal pulses, capillary refill less than 2 be6.2mL/kgin5minutes,incomparisonto seconds, warm skin, normal mental status, urine 20.9 mL/kg for the pressure bag and 20.2 mL/kg output above 1 mL/kg per hour, correction of for the push–pull method.5 The patient’s weight or blood pressure with systolic at least in the 5th theBroselowtapeshouldbeusedtodecide percentile for age, slowing of heart rate, decreased volume and dosing of fluid and medications respiratory rate, and normalization of lactate. It is during resuscitation. Colloid administration may also important to monitor for signs of detrimental be an option for patients with decreased arterial effects of fluid overload in the patient, such as volumerelatedtolowintravascularoncotic pulmonary edema. If the condition does not pressure (as in nephrotic syndrome or other improve or worsens after fluid boluses, try to

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identify the cause of shock to help determine the 2. Chameides L, Samson RA, Schexnayder SM, Hazinski next interventions. Oftentimes, pediatric patients MF. Pediatric Advanced Life Support Provider Manual. come in with shock that has a multifactorial Dallas, TX: American Heart Association, 2011, etiology. For instance, children in septic shock pp. 69–99. may have concurrent hypovolemic shock from 3. Brierley J, Carcillo JA, Choong K, et al. Clinical intravascular volume loss due to fever, diarrhea, practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from or third-spacing. the American College of Critical Care Medicine. Crit With patients in hemorrhagic shock, blood is Care Med 2009; 37: 666–88. recommended for replacement of volume loss if 4. Raimer PL, Han YY, Weber MS, et al. A normal the child’s perfusion is inadequate despite capillary refill time of ࣘ 2 seconds is associated with administration of a bolus of 20 mL/kg isotonic superior vena cava oxygen saturations of ࣙ 70%. J crystalloid fluid. Administer 10 mL/kg packed red Pediatr 2011; 158: 968–72. blood cells as soon as possible using a rapid 5. Stoner MJ, Goodman DG, Cohen DM, et al.Rapid infuser. fluid resuscitation in pediatrics: Testing the American r Disposition: Children with hypovolemic shock College of Critical Care Medicine guideline. Ann warrant inpatient admission and ongoing Emerg Med 2007; 50: 601–7. evaluation, monitoring, and treatment. Those who 6. World Heath Organization. Initial treatment of have traumatic hemorrhagic shock require dehydration for severe acute malnutrition. See www management by a surgical team with expertise in .who.int/elena/titles/bbc/dehydration sam/en/ pediatric trauma. Use endpoints and response to (accessed November 11, 2016). treatment to guide whether or not an ICU 7. Akech SO, Karisa J, Nakamya P, et al. Phase II trial of admission is warranted. isotonic fluid resuscitation in Kenyan children with severe malnutrition and hypovolaemia. BMC Pediatr 2010; 10: 71. Historical clues Physical findings Ancillary studies r r r Prolonged Tachycardia Elevated lactate Case 8 vomiting and r Dry mucous r Hypochloremic diarrhea membranes metabolic r Sunken eyes alkalosis Contributing Author: Erica Escarcega r Decreased urine r Acute kidney output injury from History dehydration The patient is a 12-year-old male brought in by his mother for evaluation of a persistent, low-grade fever and worsening weakness and fatigue over the past 2 Follow-Up weeks. The patient is usually very active and enjoys This patient had hypovolemic shock secondary to playing soccer, but has not been able to participate in intravascular volume loss from a viral gastroenteritis. the past two games due to his symptoms. He denies After three boluses of 20 mL/kg crystalloid fluid over recent cough, chest pain, abdominal pain, nausea, or thecourseof1hour,thepatient’svitalsignsnormal- vomiting, but has had a diminished appetite. He com- ized, urine output increased, and his lactic acid fell plains of aching in his bilateral lower extremities. He to a value within normal limits. His nausea resolved denies any recent sick contacts. with administration of ondansetron and he was able to tolerate clear liquids as well as an ice pop. He was Past Medical History admitted to the inpatient pediatric floor to be observed r None. overnightandwasdischargedtohomeinthemorning. Medications References r None. 1. Centres for Disease Control and Prevention. Global Water, Sanitation, & Hygiene (WASH). See www.cdc .gov/healthywater/global/wash statistics.html Allergies r (accessed November 11, 2016). NKDA.

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Physical Examination and Ancillary Studies shock is much less frequent in children; however, r Vital signs: T 100.8 °F, HR 134, BP 85/58, RR 26, a multitude of both congenital and acquired O2 sat 100% on room air. conditions predispose a child to the development r General: The patient is not in any acute distress of cardiogenic shock, including congenital heart and is cooperative. defects, arrhythmias, cardiomyopathies, r HEENT: PERRL. Mucous membranes moist. myocarditis, endocarditis, toxin exposures, and 1,2 Tympanic membranes normal. ischemia. About 12,000 children in the USA r Neck: Supple, with no lymphadenopathy and no suffer from heart failure, the majority of which are JVD. the result of congenital heart diseases (usually presenting within the first year of life), followed r Cardiovascular: His heart rate is tachycardic and by acquired dilated cardiomyopathy.1–3 regular. He has a grade 4/6 crescendo– r decrescendo murmur best appreciated at the Pathophysiology: The pathophysiology of upper-right sternal border. There are no gallops or cardiogenic shock depends upon the underlying rubs.Peripheralpulsesarepalpable,butthready. disease process. In infants with congenital heart Capillary refill Ͼ 3 seconds. defects dependent upon a patent ductus arteriosus, the closing of the ductus as the infant’s r Lungs:CTAbilaterally,withnoW/R/R.No circulation matures over the first days of life chest-wall tenderness. precipitates shock rapidly. Children with r Abdomen:Thepatient’sabdomenissoft, congenital defects causing volume- or non-tender, and non-distended, without rebound pressure-overload may present in the first few or guarding. There are no palpable masses. r months to years of life with slowly progressive Extremities:Nodeformity,nobruising,fullrange heart failure. Additionally, children who have of motion. r undergone repair of a congenital heart defect are Skin: Pale and diaphoretic, without rashes or signs at higher risk of arrhythmias or other of trauma. r complications from the repair which compromise Neurologic:Awakeandinteractive,butsomewhat pump function. listless and fatigued. Heart failure from acquired sources is most commonly infectious in origin. Myocarditis is Questions for Thought usually of viral origin, but may also be caused by r In what kind of shock is this child? bacteria, fungi, rickettsia, spirochetes, r How can this shock be diﬀerentiated from other autoimmune diseases, hypersensitivity reactions, 4 forms of shock? and toxic exposures. Endocarditis may involve r What are some of the common causes of this the myocardium as well, or may cause valvular kind of shock in children? incompetency leading to cardiac pump failure.5 r How can cardiac output be improved in this kind Myocardial infarction is rare in children, but may of shock? r occur as the result of Kawasaki disease, which What clues within a patient’s history and physical typically presents in children under the age of 5.3 examination help in the determination of the r Presentation: Infants with underlying congenital underlying cause of the patient’s shock? heart defects may initially have non-specific signs of congestive heart failure, such as feeding difficulties, failure to thrive, tachypnea, and Diagnosis agitation.3 Children diagnosed with heart failure r Cardiogenic shock secondary to endocarditis. early in life tend to progress gradually in their illness despite medical interventions until Discussion inotropic support becomes necessary. r Epidemiology: Cardiac arrest in children is rarely In acquired cases of heart failure, such as caused by cardiac causes, but instead is more often myocarditis, the progression may be more secondary to respiratory failure and shock. In sudden, with as many as 57 percent of myocarditis cases of shock, the most common cause in the patients diagnosed on autopsy after sudden pediatric population is hypovolemia. Cardiogenic death.3,4 Infective endocarditis often presents

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with a new or changing murmur, fever, malaise, as r Treatment: Prostaglandin may be considered in well as chest and abdominal complaints.3,5 In infants with cardiogenic shock and suspected patients with an underlying arrhythmia, episodes ductal dependent lesions, to help maintain an of syncope may precede their presentation.3 open ductus arteriosus. These infants present Regardless of cause, in the initial stages of precipitously in the first days to weeks of life. This cardiogenic shock, the patient often becomes therapy is not effective in older infants and tachycardic with prolonged capillary refill, children with cardiogenic shock. Arrhythmia cool/pale extremities, and weak peripheral pulses. management should be initiated in patients with At this point the body is able to compensate; shock from cardiac arrhythmia. however, as time progresses the patient’s In suspected cases of endocarditis, blood condition deteriorates with signs of decreased cultures should be drawn and broad-spectrum mental status, reduced urinary output, metabolic antibiotics should be initiated. Emergency acidosis, tachypnea, hypotension, mottling of the echocardiography may help define the extent of skin, and weak central pulses with absent or weak disease and need for operative repair. peripheral pulses. In all cases of cardiogenic shock, including r Diagnosis: The diagnosis of cardiogenic shock is a those with myocarditis, patients require clinical one, requiring emergent recognition and resuscitation with respiratory support and resuscitation with inotropes to improve cardiac inotropes such as dopamine.6 These patients output. A thorough history and physical generally will not respond to fluid resuscitation as examination should be performed after the initial this form of shock is not caused by redistribution resuscitation of the patient. A hallmark of or loss of volume, but is instead due to the cardiogenic shock that distinguishes it from diminished contractility of the heart. At some hypovolemic or distributive shock is that centers, severe cases of refractory cardiogenic cardiogenic shock is generally unresponsive to shock may be treated with ECMO and ventricular fluid resuscitation. Children will receive multiple assist devices as a temporizing measure, prior to boluses but will often have ongoing tachycardia heart transplantation.7 Therefore, when the and hypotension and may even develop diagnosis of cardiogenic shock is made in a child, worsening respiratory status from volume consideration should be given to transferring the overload. Therefore, the clinician should suspect child to a center with these capabilities. cardiogenic shock when fluid resuscitation fails to r Disposition: All children with cardiogenic shock improve or worsens the child’s clinical status.3,4 require admission to a PICU, preferably at a In terms of bedside and diagnostic testing, facility with capacity for ECMO, pediatric chest radiography may aid in the diagnosis of an cardiology, and pediatric cardiothoracic surgery abnormal size or shape to the heart, suggestive of capability. cardiomyopathy or congenital defects. Blood pressure should be taken in all four extremities as Historical clues Physical findings a discrepancy may indicate obstruction along the r r r Fever r Murmur on auscultation aortic arch. An EKG should be performed to r Fatigue r Tachycardia evaluate for ischemic changes and arrhythmias. Exercise intolerance Tachypnea r Diaphoresis An echocardiogram is useful in determining the r r Delayed capillary refill ejection fraction of the heart, the extent of r Hypotension dilation or hypertrophy of the ventricles, the Weak peripheral pulses presence of pericardial effusion as well as the presence of lesions, stenosis, or regurgitation of heart valves. Biomarkers such as BNP and Follow-Up troponin may help in the determination of the The patient was given two fluid boluses at 20 mL/kg, causeofcardiogenicshockasBNPisoften with no improvement in his tachycardia or hypoten- elevated in cases of heart failure and an elevation sion.Hewasstartedonadopaminedrip,which in troponin may be seen in cases of myocarditis, improved his blood pressure. Broad-spectrum antibi- anthracycline toxicity, or cardiac ischemia.4 otics were initiated for suspected endocarditis. An

16:09:45 31 03 Chapter 2: Resuscitation echocardiogram revealed a large vegetation on his aor- fevers, ear tugging, change in bowels or bladder func- tic and mitral valves, with a diminished ejection fraction, or rashes. No recent travel, sick contacts, or day- tion.HewasadmittedtotheICUwherehereceivedIV care. antibiotics. After a prolonged hospital stay, the patient had a full recovery and was discharged home. Past Medical History r Born at term with uncomplicated birth history. References r Immunizations are UTD. r 1. Rossano J, Shaddy R. Heart failure in children: GERD. Etiology and treatment. JPediatr2014; 165: 228–33. 2. Hsu D, Pearson G. Heart failure in children part I: Medications History, etiology and pathophysiology. Circ Heart Fail r 2009; 2: 63–70. Ranitidine. 3. Woods W, McCullock M. Cardiovascular emergencies in the pediatric patient. Emerg Med Clin N Am 2005; Allergies 23: 1233–49. r Sulfa-containing medications (rash). 4. Canter C, Simpson K. Diagnosis and treatment of myocarditis in children in the current era. Circulation 2014; 129: 115–28. Physical Examination and Ancillary Studies r 5. Baltimore R, Gewitz M, Baddour L, et al. Infective Vital signs: T 100.5 °F, HR 184, BP 82/58, RR 80, endocarditis in childhood. 2015 Update: A scientific O2 sat 78% on room air. statement from the American Heart Association. r General: She appears ill, drowsy, and fatigued, Circulation 2015; 132: 1487–515. with marked increase in work of breathing. 6. Kleinman ME, Chameides L, Schexnayder S, et al. Part r Primary survey: 14: Pediatric advanced life support – 2010 American Heart Association Guidelines for cardiopulmonary r Airway: Intact airway, no drooling or pooling resuscitation and emergency cardiovascular care. of secretions, no stridor. Circulation 2010; 122 Suppl 3: S876–908. r Breathing: Tachypneic, with intercostal, 7. Hetzer R, Potapov E, Alexi-Meskishvili V, et al. supraclavicular, and suprasternal retractions Single-center experience with treatment of cardiogenic and decreased breath sounds. shock in children by pediatric ventricular assist r Circulation: Tachycardic, with intact pulses and devices. JThoracCardiovascSurg2011; 141: 616–23. capillary refill 2 seconds. r Disability: Listless and lethargic, poor tone. Case 9 r Exposure: The child is fully exposed. There are no signs of trauma. Contributing Author: Sean Zwiebel r Secondary survey: History r HEENT: Her head is atraumatic, PERRL, The patient is a 15-month-old female brought in by her tympanic membranes clear, dry mucous mother for difficulty breathing. The mother notes that membranes, her oropharyngeal structures are the child has had 2 days of a moderate, non-productive midline, without erythema or swelling. cough and profuse anterior rhinorrhea. The patient r Neck: Supple and non-tender, without was brought to the ED because her mother was con- adenopathy. Trachea is midline. cerned that the child’s lips appeared blue and that r Cardiovascular:Thepatient’sheartis she was breathing quickly. The mother states that the tachycardic, without appreciable murmurs, patient was otherwise in her usual health yesterday, rubs, or gallops. Her capillary refill is with noted cough and runny nose, and that her respi- 2seconds. ratory symptoms have progressed rapidly over the last r Lungs: Tachypneic, with increased work of severalhours.Themotheraddsthatthepatienthashad breathing, decreased air movement. She has decreasedoralintaketoday.Thechildhasnohistoryof diffuse mild expiratory wheezing with cardiopulmonary or infectious problems. Mom denies scattered rhonchi.

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r Abdomen:Thepatient’sabdomenissoft, hypercarbic (failure to ventilate). Hypoxic non-tender, non-distended, with bowel sounds respiratory failure is from inadequate delivery of throughout. oxygen from the alveoli to the pulmonary r Skin and extremities: The patient is diaphoretic, capillaries or from intrapulmonary shunting. This her lips and tongue are cyanotic, her skin is results in diminished oxygen dissolved in blood, warm peripherally and centrally. or hypoxemia. Hypercarbic respiratory failure is r Neurologic:Thechildmovesallfour from decreased minute ventilation and results in extremities spontaneously. She has intact increased CO2 dissolved in the blood, which reflexes. Her mental status is depressed. causes acidemia and can suppress respiratory drive at higher levels. These two distinct processes r Pertinent ancillary studies: WBC 12,000; CXR coexist on a spectrum. For example, severe demonstrates diffuse patchy infiltrates throughout hypoxemia can cause increased work of breathing, both lung fields. which leads to fatigue and hypoventilation. This hypoventilation in turn results in hypercarbia, and Questions for Thought as the PaCO2 climbs, respiratory drive declines r further, causing the PaO2 to drop, and ultimately What steps would you take initially to stabilize causing death. The underlying cause for these two this patient? entities is vast as further pathophysiology is r When do you decide to establish a definitive dependent upon the underlying cause of airway in a patient like this? r respiratory distress and failure. What are some therapeutic, procedural, and r anatomic considerations to reflect upon before Presentation: Respiratory distress and respiratory attempting to intubate a sick child or infant? failure represent a broad spectrum of clinical r After establishing a definitive airway, what type presentations, depending on the underlying of settings will this patient require for mechanical disease process. Children may be tachypneic or ventilation? bradypneic, they may be hypoxic or have normal oxygen saturation, they may be alert or have altered mental status. Children may have Diagnosis abnormal lung sounds or essentially normal r auscultation. Acute respiratory failure secondary to pneumonia. Although the patient in the case above had a pneumonia causing respiratory distress, the Discussion differential should be broad and can be broken up r Epidemiology: The epidemiology of pediatric into the following categories: central or respiratory distress and respiratory failure is upper-airway obstruction, peripheral or difficult to define as it largely depends onthe lower-airway obstruction, alveolar or interstitial underlying cause. In general, two-thirds of all airway disease, thoracic cage dysfunction, cases of respiratory failure occur in the first brainstem abnormality, spinal cord process, or postnatal year, with one-half occurring in the neuromuscular disorder. 1 neonatal period. This is attributed primarily to r Diagnosis: The diagnosis of respiratory distress anatomic and physiologic differences in young and failure is primarily a clinical one. The infants, who have developing airways and clinician should focus on careful history and 1 immature respiratory drive mechanisms. physical examination, with particular attention to However, respiratory failure is a broad category work of breathing. The respiratory rate is the most and is difficult to further define without misreported vital sign in a patient’s chart and discussing specific disease processes. should be counted during physical examination r Pathophysiology: Respiratory failure occurs when with careful attention for tachypnea, nasal flaring, the rate of gas exchange between the atmosphere stridor, grunting, and retractions. Inspiratory and the blood is unable to keep up with the body’s stridor suggests an upper-airway obstruction metabolic demands. Respiratory failure can be while expiratory wheezes suggest lower-airway subdivided into hypoxic (failure to oxygenate) or involvement. A decreased level of consciousness

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or being poorly interactive can suggest and the rest of his/her body. This often requires hypercarbia and impending failure. special positioning, with a towel roll beneath the Although history and physical examination child’s shoulders to align the oral, pharyngeal, and can provide clues to the underlying cause of laryngeal axes. Regardless of child’s age, the respiratory distress and ancillary testing can appropriate positioning places the child’s earlobe confirm a diagnosis, recognizing respiratory at the level of the sternal notch, parallel to the distress is based on clinical impression and can be floor. Children tend to have large tongues, with a subtle. For example, it is easy to take a history large floppy epiglottis, often necessitating the use from a parent as her 3-year-old sits on her lap of a Miller blade for laryngoscopy, and their with URI symptoms and the monitor reads 97% airways tend to be anterior. The narrowest portion on room air and quickly listen to his lungs, which of the airway is the cricoid ring, as opposed to the are clear but near silent. A careful clinician would vocal cords in adults. Rapid sequence intubation note that same patient is breathing shallowly at 60 may be safely employed using pediatric specific per minute, that removing the patient’s shirt may equipment and weight-based medication dosing. reveal significant retractions and belly breathing, Pretreatment with atropine has shown no benefit that the chest and back are diaphoretic, and that and should not be used.2 the lungs appear clear because the patient is so During intubation, the clinician should tachypneic he is not exchanging air. That same anticipate that the child has a decreased safe apnea child cannot maintain that work of breathing for period as compared to an adult. This is because long without failure. It is important to identify children consume more oxygen per kilogram than those in distress and to act and intervene early to adults, and therefore desaturate faster.2 Once prevent failure. Although the diagnosis is intubated, the child should be placed on primarily clinical, an ABG can help define mechanical ventilation which is set to match the impending failure, with an acute PaO2 Ͻ 60 or patient’s minute ventilation, preferably on PaCO2 Ͼ 50 in the setting of new acidemia, and pressure control settings. can also help guide therapy and aid in Circulation should be supported with fluids or decision-making. pressors as needed. A Broselow tape or reliable r Treatment: The patient in this case was in pediatric dosing application should be utilized to respiratory distress from pneumonia. The reference airway and resuscitation medications approach to all sick patients should include rapid for all sick pediatric patients. After stabilizing the IV access, oxygen administration, and patient, treatment is supportive and therapy cardiopulmonary monitoring. The child’s airway, should be aimed at the underlying cause. If the breathing, and circulation should be assessed patient fails mechanical ventilation rescue, almost simultaneously. therapies include ECMO or bypass if available. A patient’s work of breathing and oxygenation r Disposition:Childreninrespiratoryfailure, may improve with simple nasal cannula and regardless of cause, should be admitted to an ICU medical management aimed at the underlying setting. cause. This may be escalated to high-flow nasal cannula, BiPAP, or CPAP. It is important to keep Historical clues Physical findings the child as calm as possible, as when children cry, r r not only do their metabolic demands increase, but Lips turning blue Hypoxia r Report of fast breathing r Tachypnea/retractions the increased turbulence of airflow correlates to r Cough/runny nose r Altered mental status increased resistance to airflow. If these measures fail, the child should be intubated. Indications to provide a definitive airway Follow-up include failure to oxygenate, failure to ventilate, or The patient was in severe respiratory distress, hypoxic, anticipated clinical decline. The clinician should with clinical evidence to suggest hypercarbia and anticipate that children’s airways differ from impending respiratory failure. A high-flow nasal can- adults in that the child’s head and occiput is nula was used for pre-oxygenation to increase the disproportionately large compared to his/her neck working intubation time. Because the patient was

16:09:45 03 Chapter 2: Resuscitation severely hypoxic despite pre-oxygenation and she had r Asthma, mild intermittent, well-controlled. a very high minute ventilation, ketamine was chosen r ALL, diagnosed 6 weeks ago. without a paralytic drug to perform an awake intuba- r Right internal jugular port, placed 4 weeks ago. tion. The child was intubated with an uncuffed 4.5-mm ET tube, secured, and mechanically ventilated, matching her minute ventilation with pressure control set- Medications r tings.ShewastransferredtoaPICUandremained Induction chemotherapy regimen via port, last intubated for 5 days. She was discharged from the dose8daysago. r hospital after 8 days with a diagnosis of rhinovirus Dexamethasone. r pneumonia. Ondansetron. r Albuterol. References 1. Nitue ME, Eigen H. Respiratory failure. Pediatr Rev Allergies 2009; 30: 470–7. r NKDA. 2. Walls RM, Murphy MF. Manual of Emergency Airway Management. Philadelphia (PA): Lippincott Williams Physical Examination and Ancillary Studies & Wilkins, 2012. r Vital signs: T 101.7 °F, HR 145, BP 62/38, RR 22, O2 sat 97% on room air. r Case 10 General: He appears ill, fatigued, but able to answer questions appropriately. Contributing Author: Sean Zwiebel r HEENT:Headisatraumatic,PERRL,tympanic membranes clear, dry mucous membranes, History oropharyngeal structures are midline without The patient is a 5-year-old male presenting with par- erythema or swelling. r ents for chief complaint of generalized weakness and Neck: Supple and non-tender, without fatigue. The parents note that the patient was recently adenopathy. Trachea is midline. No nuchal diagnosed with acute lymphoblastic leukemia (ALL) rigidity or meningismus. and had his last dose of induction chemotherapy 8 r Cardiovascular: Tachycardic, without appreciable days ago. He has mild persistent nausea with several murmurs, rubs, or gallops. Warm skin, capillary episodes of non-bloody, non-bilious vomiting over the refill 5 seconds. last week but has otherwise been doing well, without r Lungs: Clear and equal, with good breath sounds. focal complaint. They went to wake him this morn- r Abdomen: Soft, non-tender, non-distended, with ing, and found him poorly responsive. After rousing bowel sounds throughout. him, he complained of being fatigued and feeling gen- r Extremities and skin:Theskiniswarmanddry. erally unwell. The parents recorded an oral temper- There is a 1 cm area of erythema with induration ° ature of 102 F and brought him to the ED for fur- surrounding the port in the right chest, without ther evaluation. The patient is ill-appearing but inter- fluctuance or purulence. The incision is well active and states that he does not feel well and has healed. There are no other rashes or other skin ongoing nausea. The patient and parents otherwise lesions noted, including the perirectal and deny headache, neck pain, URI symptoms, chest pain, perineal regions. cough, shortness of breath, abdominal pain, change in r Neurologic: The child is somewhat listless, but has bowels/bladder,rashes,orsickcontacts.Theydonote normal mentation and a non-focal neurologic there is increasing erythema around the port in his examination. right chest. r Pertinent ancillary studies: WBC 600, polymorphonuclear cells 52%, bands 6%, absolute Past Medical History neutrophil count 348, Hb 10.1, Plt 22,000, BUN r Born at term with uncomplicated birth history. 32, Cr 2.2, INR 1.8, lactic acid 4.3, U/A negative, r UTD on immunizations. CXR negative.

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Questions for Thought and smooth muscle relaxation, which cause worsening vasodilation and release of further r What are some potential sources of infection in inflammatory mediators; this can result in this patient? r What is the deﬁnition of septic shock and how is multi-organ failure and fulminant cardiovascular it managed? collapse despite appropriate therapy and 4,5 r What are some diﬀerences between pediatric hemodynamic support. r and adult septic shock? Presentation: Sepsis and septic shock encompass a r How would you resuscitate this patient and broad spectrum of disease, dependent largely on support his blood pressure? the type of infection and how far into the disease process the patient presents, ranging from well-appearing children with mildly deranged or normal vital signs to toxic-appearing children Diagnosis with multi-organ failure and cardiovascular 5 r Septic shock secondary to presumed line collapse. Well-appearing pediatric patients with infection. early sepsis can progress very rapidly; the child can decompensate over the course of the provider’s history and physical examination. Discussion Pediatric patients with severe sepsis and septic r Epidemiology: Severe sepsis is a leading cause of shockwithclinicalorlaboratoryevidenceof deathininfantsandchildrenwithmorethan end-organ dysfunction are well advanced into the 44,000 cases annually in the USA.1 Almost 50 clinical spectrum, and are at risk for increased percent of all pediatric sepsis involves infants less morbidity and mortality.2,5 The clinician must than 1 year of age, with 49–74 percent of children have a high index of suspicion for sepsis. A careful diagnosed with severe sepsis suffering from an history and physical examination, taking note of underlying systemic disease process.1,2 Mortality subtle signs of organ dysfunction or shock, has improved significantly in recent decades in such as tachypnea, delayed capillary refill, or developed countries but the overall mortality is complaints of decreased wet diapers, are still estimated at 25 percent.2 In the USA, imperative. mortality rate is still around 15–20 percent r Diagnosis: For the emergency care provider, the depending on the source cited with respiratory, diagnosis of severe sepsis and septic shock in a bloodstream, and genitourinary infections pediatric patient is primarily a clinical one. accounting for the overwhelming majority of Traditionally, sepsis is defined as a presumed 2,3 cases. If the child survives to discharge, source of infection and the patient should meet approximately 17 percent will have at least SIRS criteria, with two or more of the following: a 2 moderate disability. temperature less than 96.8 °Forgreaterthan r Pathophysiology: Septic shock is truly a 100.4 °F, a HR greater than 90 BPM, a RR greater combination of distributive, hypovolemic, and than 20 breaths per minute or PaCO2 less than 32, cardiogenic shock.4 The distributive component is or WBC less than 4,000 or greater than 12,000.4,6 from an inflammatory cascade or toxin-mediated However, all children under 5 years of age could decrease in systemic vascular resistance resulting satisfy SIRS criteria using their normal in capillary leak and third-spacing, with age-appropriate vital signs. Furthermore, normal intravascular losses and ensuing hypovolemia.4,5 WBC also vary by age. For the pediatric The cardiogenic component is from the population, a less stringent definition of sepsis myocardial-depressant effects from sepsis, the includes a presumed source of infection with two systemic inflammatory cascade, and acidosis. The or more of the following: temperature less than resultant effect is hypoperfusion and end-organ 96.8 °F or greater than 101.3 °F, age-specific dysfunction, which can be evident clinically or tachycardia or bradycardia not from secondary through laboratory values. Hypoperfusion and causes (pain, fever), age-specific tachypnea, or an tissue hypoxia result in further cell damage, abnormal leukocyte count or greater than 10% release of intracellular contents, lactic acidosis, bands.2,5,7

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There is less consensus on the definition of significant improvement in mortality in adults severe sepsis and septic shock in pediatric with severe sepsis and septic shock by early patients, as children have excellent physiologic antibiotic administration and aggressive compensatory mechanisms. Age-specific hemodynamic support with invasive monitoring hypotension is generally a late finding and should to meet predefined resuscitative endpoints.4 This cause concern for impending cardiovascular was the standard for over a decade until the collapse. Pediatric severe sepsis can be defined as ProCESS trial in 2014 refuted this and found that sepsis with evidence of cardiovascular early identification of severe sepsis and septic dysfunction, ARDS, or evidence of involvement of shock along with early administration of two or more organ systems.2,5,7 This can include antibiotics and aggressive fluid resuscitation was altered mental status, an acutely elevated Cr, INR, as effective in improving outcomes without the or liver enzymes, acute thrombocytopenia, or the need for invasive monitoring. There is less robust need for increasing supplemental oxygen. Septic information in the treatment and management in shockissepsiswithevidenceofongoing the pediatric population; however, early cardiovascular dysfunction despite adequate fluid recognition is paramount and again the provider resuscitation in the first hour. This is defined as must maintain a high clinical suspicion to identify hypotensionlessthan5thpercentileforageor early sepsis.5,7 Furthermore, antibiotics should be requiring pressors to support blood pressure, or at administered based on age, risk factors, and least two of the following: urine output less than presumed source as soon as sepsis is identified. 0.5 mL/kg per hour, capillary refill Ͼ 5 seconds, The patient should have an adequate IV/IO/CVC, base deficit greater than 5 or lactic acid twice the and aggressive fluid resuscitation should be upper limit of normal, or core to peripheral initiated in 20 mL/kg aliquots, with up to temperature gap of greater than 5.4 °F. 2,5,7 60mL/kggiveninthefirsthourbeforepressors Presumed sources of infection can include are initiated. Ongoing fluid resuscitation may be bacteria, viruses, fungi, and parasites. In the acute continued until the patient develops care setting, blood, urine, and viral cultures are hepatomegaly, or respiratory distress with rales, not immediately available for clinical and some children may require as much as decision-making. Therefore, during the initial 200 mL/kg intially. Although norepinephrine is encounter with an ill pediatric patient, careful recommended as a first-line pressor in adult septic attentionshouldbemadetoidentifypotential shock, most sources cite dopamine as the first-line sources of infection, including meningitis, upper agent for blood pressure support if the pediatric or lower respiratory infections, intra-abdominal patient has clinical signs of shock, which are not sources, the skin (including perineal and responsive to fluid boluses. Norepinephrine and peri-rectal areas), cardiac for new murmurs or epinephrine are recommended for hypotensive stigmataofembolicphenomena,orriskfactors patients with warm or cold shock, respectively, or for clinically significant viremia or fungemia. It is for shock refractory to dopamine. Consider imperative to carefully take note of these patients’ hydrocortisone in patients with refractory vital signs and perform a thorough history and hypotension on pressors or those with known physical examination to evaluate for evidence of adrenal insufficiency or prior steroid use. end-organ dysfunction. Laboratory values may be Careful monitoring of blood glucose and of benefit in borderline-appearing or higher-risk serum calcium is also crucial during resuscitation. children, but hypotension or lactic acidosis are Resuscitative endpoints in the acute care setting often late findings and should not alone be should include maintaining urine output Ͼ 1 relied upon to define severe sepsis or septic mL/kg per hour, improving capillary refill to Ͻ 2 shock. seconds, improving mentation, no difference r Treatment: Treatment of severe sepsis and septic between central and peripheral pulses, and the shock should focus on source control, if possible, maintenance of an adequate blood pressure. and antibiotics directed towards presumed source r Disposition: All pediatric patients with severe of infection. The landmark study of early sepsis and septic shock have the potential for goal-directed therapy in 2001 demonstrated a rapid decompensation, and should be evaluated

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for ICU-level admission, especially if pressors Case 11 have been initiated. Contributing Author: Ben Church Historical clues Physical findings Ancillary studies History r Underlying r Fever r Leukopenia immunosup- r Tachycardia r Elevated Cr The patient is a 16-year-old male who initially pre- r r sentedtothelocalfiredepartmentwithshortnessof r pression r Tachypnea r Lactic acidosis Fatigue Hypotension Elevated INR breath, which began approximately 20 minutes after r Altered mental r Skin changes at status line site beingstungbyabee.Hehasaknownanaphylac- r Indwelling line tic bee allergy but did not have an epinephrine auto- injector with him. IM epinephrine and IV diphen- Follow-Up hydramine and steroids were immediately given by paramedic staff, after which emergency transport was The patient was in septic shock, with evidence of car- initiated. Associated symptoms include nausea, vomit- diovascular dysfunction, end-organ failure, and lactic ing, extreme anxiety, and diaphoresis. The child arrives acidosis. He was persistently hypotensive despite three at the ED minimally responsive after decompensating 20 mL/kg boluses of normal saline in the first hour. in the ambulance bay. He was immediately started on weight-based cefepime, tobramycin, and vancomycin. Dopamine was initiated to support his blood pressure, in addition to aggres- Past Medical History r sive fluid resuscitation, and the patient was transferred Poorly controlled asthma. r to a PICU with his oncologists consulting. His blood Immunizations are UTD. cultures grew out MSSA. His port was removed and a PICC line was placed. The patient’s antibiotics were changed to cefazolin and he improved clinically, ulti- Medications r mately being discharged after 7 days in the hospital. Albuterol. r Fluticasone. References 1. Watson RS, Carcillo JA. Scope and epidemiology of Allergies pediatric sepsis. Pediatr Crit Care Med 2005; 6 Suppl 3: r Bees and shellfish. S3–5. r 2. Weiss SL, Fitzgerald JC, Pappachan J, et al. Global No known drug allergies. epidemiology of pediatric severe sepsis: The sepsis prevalence, outcomes, and therapies study. Am J Respir Crit Care Med 2015; 191: 1147–57. Physical Examination and Ancillary Studies r ° 3. Ruth A, McCracken CE, Fortenberry JD, et al. Vital signs: T 98.8 F, HR 116, BP 97/61, RR 34, O2 Pediatric severe sepsis: Current trends and outcomes sat 75% on room air per pre-hospital staff and from the Pediatric Health Information Systems 98% on 15 L O2 non-rebreather in the ED. database. Pediatr Crit Care Med 2014; 15: 828–38. r General: The patient has labored respirations and 4. Rivers E, Nguyen B, Havstad S, et al. Early is responsive to painful stimuli only. goal-directed therapy in the treatment of severe sepsis r Primary survey: and septic shock. NEnglJMed2001; 345: 1368–77. r Airway: Child has drooling and some airway 5. BibanP,GaffuriM,SpaggiariS,etal.Early recognition and management of septic shock in swelling, no stridor, gag intact. Vomitus is children. Pediatr Rep 2012; 4: e13. present on his cheek. r 6. Yearly DM, Kellum JA, Huang DT, et al. A randomized Breathing: Tachypneic, with severe intercostal trialofprotocol-basedcareforearlysepticshock.N and supraclavicular retractions. He has diffuse Engl J Med 2014; 370: 1683–93. rhonchi and expiratory wheezing and little to 7. Sepanski RJ, Godambe SA, Magnum CD, et al. no air movement. Designing a pediatric severe sepsis screening tool. r Circulation: Tachycardic, with intact pulses and Front Pediatr 2014; 2: 56. capillary refill 2 seconds.

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r Disability: Responsive to painful stimuli only, Questions for Thought no focal deficits appreciated. r r Should you have obtained laboratory tests prior Exposure: The child is fully exposed. There are to initiating therapy? no signs of trauma. He has diffuse urticaria and r How would you interpret this child’s ABG? is grossly diaphoretic, flushed, and warm. r What are the treatment options for this disease entity? r How would you monitor response to therapy in Questions for Thought this patient? r Are there interventions you should perform prior r What anatomic diﬀerences unique to the to continuing with your examination? pediatric airway must be considered? r How urgent is airway management in anaphylaxis? Diagnosis r r You intubate the child prior to continuing with Anaphylaxis secondary to insect envenomation. your examination, because you recognize that, although the child does not have stridor and is Discussion breathing spontaneously, he is at high risk for r Epidemiology: Insect envenomation leading to losing his airway from ongoing edema or anaphylaxis can result from the sting of many vomiting. You use ketamine as an induction agent different Hymenoptera species including Vespidae because you know it is a bronchodilator, and you (wasps/hornets), Apidae (bees), and Formicidae also use succinylcholine because you know that (fire ants). Second only to antibiotic-related his airway may be difficult, and you want the best anaphylaxis, Hymenoptera anaphylaxis is the next chance of success. You use a size 3 glidescope and most common etiology causing just under 100 a7.5-mmcuffedtube,confirmingairway deathsperyearintheUSA.1,2 Food allergies affect positioning with end-tidal capnography. You also 4–6 percent of children.3 Surveys aimed at recognize the most likely diagnosis and start gauging anaphylactic reactions within the USA treatment. estimate that 1–3 percent of the general r Secondary survey: population will be affected in their lifetimes, with 1,4 r HEENT:PERRL,tympanicmembranesclear, a mortality rate of 1 percent. Limited data exist moist mucous membranes, increased for the exact prevalence of insect stings within the secretions. USA. Those that spend more time outdoors and those living in rural areas are more prone to r Neck: Supple, with midline trachea. disease exposure. Poorly or uncontrolled reactive r Cardiovascular: Tachycardic, regular rhythm, airway disease, namely asthma, is a major risk with no M/R/G. Radial and carotid pulses are factor involved in increased morbidity and present. He has erythematous skin, with brisk mortality of patients experiencing anaphylaxis.4–6 capillary refill. r Pathophysiology: Anaphylaxis develops via an r Lungs: Tachypneic with rhonchi and wheezing, immediate type I hypersensitivity reaction. breath sounds are symmetric. Sensitization occurs when patients are initially r Abdomen: The patient’s abdomen is soft and exposed to an allergen triggering increased non-distended, with hyperactive bowel sounds. production of Immunoglobulin E antibodies. There is no guarding. Early phase reaction then results from subsequent r Skin and extremities: The patient is diaphoretic, allergen exposure and massive degranulation of and has diffuse erythroderma and urticaria. mast cells and basophils via receptor-mediated r Neurologic: The child moves all four extremities binding of antigen and preformed spontaneously. He responds to pain. Immunoglobulin E complexes. Degranulation of r Pertinent ancillary studies: WBC 19,100, ABG (pH histamine, leukotrienes, prostaglandins, and 6.8, pCO2 63, pO2 241, bicarbonate 14), Na 141, K tumor necrosis factor-␣ are some of the many 3.9, Cl 101, serum bicarbonate 12, lactate 11.3. immunologic mediators implicated in the disease.

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Late-phase reaction finally involves the continued compromise, hypotension or associated production and release of additional symptoms (presyncope/syncope), and/or inflammatory mediators. This all then leads to persistent GI symptoms. massive vasodilation and distributive shock. r Criteria 3 suggests anaphylaxis if hypotension r Presentation: Symptoms of anaphylaxis stem from occurs in association with exposure to a known the widespread vasodilatory effects of allergen. Laboratory testing in such a rapid and immune-cell degranulation and fall into a incredibly lethal disease is generally not spectrum of mild to very severe disease. helpful. Histamine levels, which are elevated Presentation of symptoms can be categorized for approximately 5–30 minutes post-reaction, according to the organ system affected. For begintodeclinebythetimepatientspresentto instance, patients may complain of pruritus and the ED. display diffuse urticaria with cutaneous r Treatment: As with all emergencies, a focus on 2,7,8 involvement. Respiratory-system signs and airway, breathing, and circulation is paramount. symptoms include dyspnea, rhinorrhea, stridor, In anaphylaxis, IM epinephrine is the next most 2,7,8 and wheezing. GI involvement includes important treatment in life-saving therapy.2,4 nausea, vomiting, diarrhea, and abdominal Epinephrine is the cornerstone of anaphylaxis 2,7,8 pain. Presyncope or syncope, tachycardia or treatment, with other therapies being bradycardia, hypotension, and altered mental complementary at best. Common pitfalls in status should all raise red flags of cardiovascular anaphylaxis management include delayed or involvement and the possibility of impending failed epinephrine administration, leading to 2,7,8 cardiovascular collapse. A complaint of “a significantly worsened outcomes. Preferred lump in my throat” or of hoarseness may indicate dosing is 0.01 mg/kg IM with an initial maximum impending and potentially lethal laryngeal edema. dose of 0.3 mg of the 1:1,000 concentration in The vast majority of patients will experience children.2,4 IV epinephrine should be reserved for symptom onset within 60 minutes of exposure, those with severe disease as the majority of with those experiencing more rapid onset adverse outcomes stem from IV administration. It carrying a significantly higher rate of morbidity is important to realize that compensated pediatric 2,7,8 and mortality. The overwhelming majority of shock may initially present with tachycardia patients will experience symptoms within 6 alone, as hypotension can occur quite late in the hours.2,7,8 r disease process. Diagnosis: There has been much controversy Steroids, antihistamines, and inhaled regarding the diagnosis of anaphylaxis as it is bronchodilators comprise the list of adjunctive largely a clinical diagnosis. The most recent therapies only.2 Steroids are used to dampen the guidelines which outline a diagnosis of continued production and release of anaphylaxis come from the 2005 joint inflammatory mediators, and adjunct therapy collaboration between the National Institute of with a histamine blockade includes both H1 and Allergy and Infectious Disease and the Food H2 receptor blockers, such as diphenhydramine Allergy and Anaphylaxis Network, and have been and famotidine, respectively.2 None of these drugs 2,9 updated recently. They describe three criteria act within a time frame to make them appropriate for making the diagnosis. Fulfillment of one out of primary therapies for anaphylaxis.2 Inhaled the three criteria is highly sensitive but not albuterol can be given to help correct 2,9 specific in recognizing the disease. bronchospasm, especially in light of the large r Criteria 1 includes the rapid onset of symptoms proportion of these patients that have underlying (minutes to hours) involving skin, mucosa, or bronchospastic disease/asthma. both in addition to respiratory compromise or r Disposition:Theappropriatedispositionof hypotension. patients experiencing anaphylaxis can be difficult. r Criteria2suggeststhediagnosisiftwoofthe Those with a rapid and severe onset of symptoms following are present after exposure to a likely or those requiring airway interventions should be allergen:skininvolvement,respiratory admitted to the hospital for further treatment and

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observation. Those with very mild disease can in-line bronchodilators as well as IV antihistamines safely be discharged home. The difficulty arises as and steroids. He was admitted to the PICU where his most patients fall somewhere in between these epinephrine drip was weaned off over the course of two extremes. Other aspects of the patient’s 6hoursandhewasextubatedandultimatelydis- presentation that may warrant admission include charged home in good condition. He was instructed a history of severe or protracted anaphylaxis, a to carry an epinephrine auto-injector with him at all history of poorly controlled asthma, as well as times. various barriers to care or poor parental understanding of discharge instructions. There is References no universally agreed-upon observation period in 1. Centers for Disease Control and Prevention. Insects the ED but 6 hours is used as a general rule, to and scorpions. See www.cdc.gov/niosh/topics/insects/ evaluate for any disease refractory to treatment or (accessed February 2017). re-emergence of symptoms, known as the biphasic 2. Campbell RL, Li JTC, Nicklas RA. Emergency reaction.2 A biphasic reaction has been reported department diagnosis and treatment of anaphylaxis: A to occur in approximately 11 percent of pediatric practice parameter. Ann Allergy Asthma Immunol patients and can occur as far out as 72 hours. 2014; 113: 599–608. Those patients identified appropriate for 3. Centers for Disease Control and Prevention. Food outpatient treatment should receive an allergies in schools. See www.cdc.gov/healthyschools/ epinephrine auto-injector device, return foodallergies/index.htm (accessed February 2017). precautions, education regarding allergen 4. McLean-Tooke APC, Bethune CA, Fay AC, et al. avoidance, indications for epinephrine Adrenaline in the treatment of anaphylaxis: What is administration, and outpatient follow-up the evidence? BMJ 2003; 327: 1332–5. instructions.2 Traditionally, steroids and 5. Bilo` MB, Bonifazi F. The natural history and antihistamines have also been recommended. epidemiology of insect venom allergy: Clinical implications. Clin Exp Allergy 2009; 39: 1467–76. 6. Bock SA, Munoz-Furlong A, Sampson HA. Fatalities Historical clues Physical findings due to anaphylactic reactions to foods. JAllergyClin r r Immunol 2001; 107: 191–3. r Known allergy to bees r Hypoxia r Vomiting r Tachypnea/retractions 7. Lieberman P, Nicklas RA, Oppenheimer J, et al. The Difficulty breathing Altered mental status diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol 2010; 126: 477–80. Follow-Up 8. Golden DBK, Moffit J, Nicklas RA. Stinging insect The child was intubated. His ABG showed evidence hypersensitivity: A practice parameter update 2011. J of respiratory and metabolic acidosis, with elevated Allergy Clin Immunol 2011; 127: e1–23. carbon dioxide as well as lactate. He was started on 9. Lieberman P, Nicklas RA, Randolph C, et al. an epinephrine drip which was titrated to 0.3 ␮g/min Anaphylaxis: A practice parameter update 2015. Ann per kg. This improved his symptoms. He was given Allergy Asthma Immunol 2015; 115: 341–84.

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Case 1 r General: The patient is alert, smiling, playful, and in no acute distress. Contributing Author: Lauren Snyder r HEENT: The patient’s head is atraumatic and normocephalic. PERRL. No conjunctival injection History or discharge. Tympanic membranes normal The patient is a healthy 3-year-old male who presents bilaterally. Nares are patent with small amount of to the ED after a choking episode just prior to arrival. clear rhinorrhea. Oral examination shows mucosa The child’s mother reports that they were at home that is pink and moist, no tonsillar swelling or getting ready for church when she felt the child tap exudates, and no foreign body. the back of her leg. The mother turned around and r Neck: Supple and non-tender, with no masses. found the child unable to breathe. She swept the r Cardiovascular:Heartwithregularrateand child’s mouth with her finger, but didn’t feel anything rhythm, no M/R/G. The patient has normal so she began to implement the Heimlich maneuver. peripheral perfusion, with brisk capillary She delivered approximately five thrusts without refill. dislodging anything from the child’s airway. When r Lungs: CTA, with non-labored breathing and she turned the child around, she noticed the child equal breath sounds bilaterally. No W/R/R. No was blue in the face. She again placed her finger in retractions with respiration. the child’s mouth and this time felt an object. She was r Abdomen: Soft and non-tender, with normal unable to get a hold of the object in order to remove it, active bowel sounds and without distension. so instead she pushed the object downwards. The child r Skin and extremities: Warm, dry, and intact, with begantobreathe,mothercalled911fortransportto no signs of trauma and no rashes. the ED. Mother reports that the child has been acting r Neurologic: No focal neurologic deficits. normally since the event, without respiratory distress r and without additional choking episodes. Pertinent ancillary studies:CXRandabdominal series both normal. Past Medical History r No significant medical history, immunizations are Questions for Thought UTD.Heliveswithbothparents. r What is the importance of a normal CXR in this case? Medications r What is the disposition of this child, now that he r None. is in the ED with a normal examination and CXR? r What services (if any) should be consulted? r Allergies What is the deﬁnitive procedure to diagnose and treat this condition? r NKDA.

Physical Examination and Ancillary Studies r Vital signs: T 97.4 °F, HR 92, RR 22, O2 sat 98% on Diagnosis room air. r Foreign-body aspiration.

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Discussion triad of wheezing, cough, and diminished breath r Epidemiology: Foreign-body aspiration is a sounds is not always present. In patients with common occurrence in children, especially in subacute or chronic foreign body, the child may toddlers, due to increasing mobility and oral develop infection (such as post-obstructive exploration. Foreign-body aspiration can occur at pneumonia) and may present with fever. Some any age; however, peak incidence is between 1 and children present with no symptoms at all, and a 2 years of age, with 80 percent of foreign-body foreign body is only suspected based on history, aspiration occurring in children less than 3 years or after an extensive work-up excluding other old.1,2 Commonly aspirated objects include small pathologies. r toys and food items, such as peanuts and Diagnosis: Historical clues that can help lead to a sunflower seeds.2,3 diagnosis of airway foreign body include a sudden Pathophysiology: Children have immature or onset of respiratory distress, cough, or wheezing. incomplete dentition and an imature swallowing Parents or caretakers may also report a choking reflex, predisposing them to an aspirated foreign episode, defined as a sudden onset of any of the body.2 Young children also have a smaller- following symptoms in a previously healthy child: diameter airway, which puts them at increased cough, dyspnea, and/or cyanosis. A witnessed risk for partial or complete obstruction if a choking episode is very sensitive for the diagnosis foreign body is aspirated. Depending on the of foreign-body aspiration. In a child with object, the child may have an inflammatory respiratory symptoms and a history of choking, reaction, particularly with lipophilic foreign foreign-body aspiration should be assumed bodies (for example, peanuts).2 Organic material, regardless of radiologic findings, and rigid such as popcorn or items with high starch bronchoscopy should be performed.4 content, may absorb water over time, converting a In some cases, the aspiration of a foreign partial obstruction to a complete one.2 Aspirated objectisunwitnessed,andthechildiswithout foreign bodies are most often located in the severe respiratory symptoms, making the bronchial tree, with laryngeal and tracheal foreign diagnosis difficult. For any pediatric patient with bodies occurring less frequently. The location of a a respiratory complaint and no obvious etiology, foreign body partially determines the patient’s the practitioner should consider foreign-body presentation. aspiration and inquire about choking or r Presentation: The clinical signs of foreign-body coughing episodes. For children with aspiration are highly variable, and depend on the confirmed foreign-body aspirations, a history of location of the object in the respiratory tract and choking is found in the majority of cases 2 whether the object is mildly or severely (80–90 percent). obstructing the airway. Additionally, an unwitnessed aspiration with Severe obstruction includes complete or minimal symptoms may go unnoticed by near-completeblockageoftheairway.Children caregivers, so that by the time the child presents with severe airway obstruction by a foreign object for medical evaluation, the foreign body may have will present in respiratory distress that may been in the airway for days or weeks, causing include the inability to speak or cough, cyanosis, secondary infection or inflammation. These cases and abnormal behavior, most commonly lethargy of unwitnessed aspiration may have additional or listlessness from their inability to adequately symptoms of fever, sputum production, and other oxygenate. signs and symptoms of pneumonia, which often 2 r More commonly, aspirated foreign bodies will not leads to misdiagnosis. Therefore, it is imperative cause severe airway obstruction, and the child to consider foreign-body aspiration in a child with may have little or no acute distress. Children will unusual respiratory symptoms (i.e. sudden onset have various respiratory symptoms, which may coughing fits in the absence of nasal congestion include cough, stridor, or wheezing.2 Wheezing, if and fever), failure of treatment for another present, can be localized to a specific area or diagnosis (i.e. asthma, pneumonia), or multiple generalized throughout the lung fields. The classic healthcare visits (pediatrician office or ED) with

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little or no resolution of symptoms after canbemadetoremovetheobjectwithMagill treatment.2 forceps. If an object is not visualized or the Radiographs may be helpful in the evaluation removal is unsuccessful, intubation should be ofachildwithasuspectedairwayforeignbody, attempted, with dislodgement of the object although this is dependent on whether the distally, usually into the right mainstem bronchus. aspiratedobjectisradiopaqueandthedegreeof This will allow partial ventilation of the airway obstruction present.2 Abnormalities, when unobstructed lung while awaiting rigid they exist, are usually visualized foreign bodies or bronchoscopy for definitive removal of the foreign an area of hyperinflation, best seen in bilateral body. decubitus CXR. In most cases, CXR will be Foreign bodies in the lower airway are usually normal, without visualization of a foreign body. removed via rigid bronchoscopy. Therefore, a Therefore, the diagnosis of airway foreign body consult to pulmonology or surgical services should come primarily from historical clues and proficient at bronchoscope should be placed. physical examination findings. Rigid bronchoscopy under general anesthesia r Treatment: For children presenting with severe allows airway control, good visualization of the airway obstruction and active respiratory distress, airway and any foreign objects, and allows for attempts to dislodge the object must be made manipulation/removal of the object with a variety immediately. As with any critical patient, the of forceps. The procedure is both diagnostic and practitioner should follow the ABC method of therapeutic, as it can identify and remove foreign primary assessment, evaluating the airway and bodies from the airway successfully in 95 percent breathing of the patient first. Look inside the of cases.4 In rare instances, thoracotomy is mouthofthechildtoevaluateforavisibleforeign indicated for foreign-body removal, if body. If an object is visualized and appears easy to bronchoscopy is unsuccessful. remove, an attempt should be made to retrieve the r Disposition: Once an aspirated foreign body is object.5 The American Heart Association does not suspected based on history or examination, recommend sweeping the mouth blindly with a consultation with pulmonology or surgical finger, as this could move a foreign object further services that are proficient at bronchoscope into the airway or worsen obstruction.5 Per should be obtained. Hospital admission might American Heart Association recommendations also be required for additional medical care for patients with foreign-body airway obstruction, relatedtocomplicationssuchaspneumoniaand infants less than 1 year of age should have five continued respiratory distress. back slaps followed by five chest thrusts administered to attempt to dislodge the foreign body, repeating this pattern until the object is Historical clues Physical findings Ancillary studies 5 dislodged or the child becomes unresponsive. r Sudden onset r Normal r Normal CXR Forchildrenover1yearofage,theHeimlich of difficulty in examination maneuver (abdominal thrusts) should be done breathing r Visualized until the object is dislodged or the child becomes foreign body by 5 unresponsive. Of note, these maneuvers (back r mom slaps and chest compressions) should only be High-risk age group attempted in children that are unable to speak or cough. In children with mild airway obstruction, these maneuvers have the potential to convert a mild obstruction into a severe Follow-Up obstruction. Thechildunderwentrigidbronchoscopy,andapiece If these maneuvers are unsuccessful in of red crayon was removed from the child’s right main- dislodging the foreign body, direct laryngoscopy stem bronchus. The child was kept in the hospital for should be performed, in an attempt to visualize observation for 23 hours and discharged home with no the object. If an object is visualized, an attempt sequelae.

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References Allergies r 1. Centers for Disease Control and Prevention. Non-fatal NKDA. choking-related episodes among children – United States, 2001. MMWR Morb Mortal Wkly Rep 2002; 51: Physical Examination and Ancillary Studies r 945–8. Vital signs: T 98.9 °F, HR 168, RR 54, O2 sat 99% 2. Salih AM, Alfaki M, Alam-Elhuda DM. Airway foreign on room air. bodies: A critical review for a common pediatric r General:Awakeandalert. emergency. World J Emerg Med 2016; 7: 5–12. r Skin: Warm, dry, and intact. She has milia on her 3. Foltran F, Ballali S, Passali FM, et al. Foreign bodies in nose. the airways: A meta-analysis of published papers. Int J r HEENT: Her head is normocephalic. Her anterior Pediatr Otorhinolaryngol 2012; 76 Suppl 1: S12–19. fontanelle is soft and flat. PERRL. Normal 4. Martinot A, Closset M, Marquette CH, et al. oropharynx, with moist mucous membranes. Indications for flexible versus rigid bronchoscopy in r Neck:Normal. children with suspected foreign-body aspiration. Am J r Respir Crit Care Med 1997; 155: 1676–9. Cardiovascular: Regular rate and rhythm. Ͻ 5. Neumar RW, Shuster M, Callaway CW, et al. Part 1: Peripheral pulses normal throughout. 2second Executive summary. 2015 American Heart Association capillary refill. Guidelines Update for Cardiopulmonary Resuscitation r Lungs:Thepatient’slungsoundsareCTAand and Emergency Cardiovascular Care. Circulation 2015; respirations are non-labored. She has symmetric 132 Suppl 2: S315–67. chest-wall expansion. r Abdomen: Non-tender and non-distended. Case 2 r Neurologic: Moro, grasp, and suck reflexes normal and symmetric. Good tone. Contributing Author: Natalie Moore Questions for Thought History r What is the differential diagnosis? The patient is an 11-day-old female born at 34 weeks r What is the definition of apnea? via spontaneous vaginal delivery, who was brought r What should the disposition be for the child? into the ED because her mom was worried about r What specific characteristics of these episodes “abnormal breathing spasms.” Mom noted that while support admission for observation? the infant was sleeping today, she had several episodes of breathing quickly followed by 4–5 seconds of apnea. The breathing spells have been intermittent but mostly Diagnosis while she is sleeping. Mom has otherwise not noted r Periodic breathing. any changes in color, tone, or mental status. The baby has not had any fevers, cough, rhinorrhea, vomiting, Discussion or diarrhea. She has been breastfeeding well every r Epidemiology: Periodic breathing is defined as three hours. Mom called her pediatrician after the fifth recurring cycles of regular respiration interrupted breathing spasm and was told that, given the child’s by short pauses in respiration, which typically last prematurity, the child should be evaluated in the ED. somewhere between 3 and 10 seconds and are followed by bursts of rapid shallow breaths.1 Then Past Medical History r breathing returns to normal. It is termed periodic The patient was born prematurely via breathing if these episodes occur at least three spontaneous vaginal delivery at 34 and 2/7 weeks times within a minute. Periodic breathing is to a group B streptococci-negative mother. There considered to be a normal respiratory pattern in were no significant perinatal complications and both preterm and full-term infants although it is the pregnancy was uncomplicated. reported more frequently in preterm infants.1,2 Thisbreathingpatternisestimatedtooccurin Medications almost all preterm infants and between 70 and r None. 95 percent of full-term infants.1,2 The episodes are

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observed more frequently when the infant is CHD; carefully assess the infant’s tone and sleeping. This normal respiratory pattern must be perform an abdominal examination; always assess distinguished from an ALTE or apnea, which is for signs of non-accidental trauma. defined as the cessation of breaths for over 20 r Diagnosis: Periodic breathing is a clinical seconds at a time or if the infant has a skin color diagnosis. Differential diagnosis includes apnea change (pale or blue), becomes bradycardic, has a (and characteristics associated with an ALTE), drop in oxygen saturation, becomes limp, or respiratory disease (bronchiolitis, pneumonia), requires stimulation for the episode to end.3 These sepsis, CNS pathology, meningitis, seizures, signs are not considered normal and do not increased intracranial pressure, metabolic happen in periodic breathing. If these are noted, derangements, CHD, upper-airway obstruction, further work-up should be pursued to assess for aspiration, and GI pathology.3–5 When the history an underlying pathologic etiology, such as is consistent with periodic breathing and the infection, CHD, metabolic derangements, airway patient has a normal physical examination, the obstruction, child abuse, or GI pathologies, diagnosis can be made clinically. However, if any among other causes.4,5 alternative diagnoses are considered, further r Pathophysiology:Periodicbreathingisthoughtto diagnostic work-up should be performed. If the be a manifestation of immature ventilatory patient is having a significant amount of periodic control and thus is common in preterm infants breathing, the pediatrician may consider and occurs less frequently as the infant matures.2 home-monitoring or polysomnography to assess Periodic breathing typically begins around the the frequency of events and associated first week of age, which corresponds to when the bradycardia or hypoxia, but these do not need to infant’s peripheral chemoreceptors begin to be performed in the ED. mature. When the infant is born, the peripheral r Treatment: None. chemoreceptors are not sensitive, and as the r Disposition: Patients with a normal physical chemoreceptors begin to mature, they become examination and a clinical picture, consistent with highly sensitive to changes in blood oxygen and periodic breathing, can be discharged home to carbon dioxide concentrations.2 This leads to follow up with their pediatrician. If any of the fluctuating breathing patterns of short periods of characteristics of apnea (cessation of breaths for apnea followed by hyperventilation. over 20 seconds, skin color change, bradycardia, r Presentation: The classic presentation for periodic hypoxia, or change in tone) are present, or signs of breathing is a preterm infant presenting with underlying infection or other pathology are noted, “abnormal breathing,” or the chief complaint of further work-up should be pursued. “my infant stopped breathing.” The caregiver describes a brief cessation of breathing, usually less than 10 seconds, followed by rapid, shallow Historical clues Physical findings r r breaths. This is normally observed while the Otherwise healthy preterm infant Normal examination r Brief apnea with hyperventilation infant is sleeping and occurs more often in rapid r Recurrent episodes eye movement sleep and in a recurrent fashion. A patient with periodic breathing will have a completely normal physical examination. It is Follow-Up important to remember that this is a diagnosis of Mom was reassured and the child was discharged exclusion, and an assessment for other underlying home. There were no sequelae at follow-up. pathology is required. A complete physical examination must include the following: assess References vital signs for fever, bradycardia or tachycardia, 1. Glotzbach SF, Baldwin RB, Lederer NE, et al. Periodic and observe for an abnormal oxygen saturation; breathing in preterm infants: Incidence and assess skin color and condition carefully for pallor characteristics. Pediatrics 1989; 84: 785–92. or cyanosis; assess for nasal flaring, retractions, or 2. Mohr MA, Fairchild KD, Patel M, et al. Qualification any signs of increased respiratory difficulty; listen of periodic breathing in premature infants. Physiol for murmurs and look for other signs of CHF and Meas 2015; 36: 1415–27.

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3. American Academy of Pediatrics Policy Statement, Allergies Committee on Fetus and Newborn. Apnea, sudden r NKDA. infant death syndrome, and home monitoring. Pediatrics 2003; 111: 914–17. Physical Examination and Ancillary Studies 4. Semmekrot BA, van Sleuwen BE, Engelberts AC, et al. r Vital signs: T 98.9 °F, HR 110, RR 35, O sat on Surveillance study of apparent life-threatening events 2 room air 100%, weight 5.4 kg. (ALTE) in Netherlands. Eur J Pediatr 2010; 169: r 229–36. General:Awake,alert,andinnodistress.She 5. Tieder JS, Altman RL, Bonkowsky JL, et al. appears very comfortable in her mother’s arms, Management of apparent life threatening events in turns toward mother’s voice and smiles. infants: A systematic review. JPediatr2013; 163: 94–9. r HEENT: Anterior fontanelle is soft and flat. PERRL. Moist mucous membranes. There is no Case 3 pharyngeal erythema, no whitish membranes, and no oral lesions. Tympanic membranes are clear. Contributing Author: Dorka M. Jimenez´ There is no nasal discharge. Mild audible upper-airway sounds, no stridor. Almonte r Cardiovascular: Heart has regular rate and History rhythm, with no M/R/G. Patient has equal femoral pulses. Capillary refill Ͻ 2 seconds. A 2-month-old baby girl presents with noisy breath- r Lungs: Chest expansion symmetric. No ing after feedings for the past 2 weeks, worsening retractions. CTA bilaterally, no W/R/R. over the last few days. The mother reports that the r baby becomes fussy, sometimes appears breathless Abdomen: The abdomen is not distended. The andsoundscongestedafterfeedings.Shedeniesany patient has normal bowel sounds. Her abdomen is fever, cough, nasal discharge, or cyanosis. The mother soft and depressible. There is no tenderness to palpation and no masses or organomegaly. describes that the infant has had spit-ups with every r feed since birth, but that more recently the amount Extremities and skin:Thepatienthasnorashor edema. she spits up has increased. She is very concerned that r the baby appears to be in pain and has not been nurs- Neurologic:Infantmovesallfourextremitieswell. ingaswellinthelastfewdays.Thechildlatchesto Her tone is appropriate for her age. She has the breast and then unlatches before completing the symmetric Moro reflex and has adequate head feed and cries. The infant has also been arching her control for her age. back during feedings. She has had no change in urination or stools. Mom specifically reports approximately eight wet diapers and two to three soft, yellowish, seedy Questions for Thought bowel movements per day. The mother denies any skin r What is the diﬀerential diagnosis for this patient’s rash or blood in the stool. There are no sick contacts at symptoms? r home. What diagnostic modalities, if any, could you use to evaluate this patient? r How would you describe this patient’s airway? Past Medical History r r What interventions should be done in the ED? The patient was born to a first-time mother via r What is the prognosis for this condition? spontaneous vaginal delivery at 39 weeks’ gestation, without complications. Mother had adequate prenatal care and denies any Diagnosis complications during pregnancy. The birth weight r was 3.5 kg. The newborn screen was normal and GERD. the immunizations are current. Discussion r Epidemiology:Gastroesophagealrefluxisthe Medications passage of stomach contents into the esophagus r Vitamin D drops. with or without regurgitation (spitting up) or

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vomiting. Gastroesophageal reflux is a normal Table 3.1 Reflux differential diagnosis and associated red flags physiologic process that occurs in more than Differential diagnosis Red flags two-thirds of healthy infants. The frequency of r r reflux episodes and the proportion of episodes Pyloric stenosis Projectile vomiting r Malrotation, volvulus r Bilious vomiting, distension that result in regurgitation peak at the age of r Cow milk protein r Perianal rash, blood in the stool, 4 months and then resolves with age in most intolerance diarrhea 1,2 r r cases. Physiologic spitting up affects only r Gastroenteritis r Fever, diarrhea 5–10 percent of infants at 12 months of age and is r UTI r Fever 1–3 Urinary obstruction Failure to thrive, recurrent UTIs very rare in children older than 18 months. r Pneumonia, bronchiolitis r Fever, cough, nasal discharge, Gastroesophageal reflux disease (GERD) is wheezing, crackles, rhonchi, significantly less common than gastroesophageal r r respiratory distress reflux and is characterized by troublesome Meningitis Fever, altered mental status, petechial rash, bulging symptoms or complications associated with the r r fontanelle, seizures passage of stomach contents into the esophagus. Hydrocephalus Rapid increase in head Children with certain underlying conditions such circumference, downward deviation of eyes (“sun setting”), as neurologic impairment, developmental delay, seizures, developmental delay prematurity, anatomic abnormalities (esophageal r Metabolic/genetic r Failure to thrive, developmental atresia, hiatal hernia), and chronic respiratory disorders delay, seizures, hepatomegaly, disorderssuchasbronchopulmonarydysplasia, macro/microcephaly idiopathic interstitial fibrosis, and cystic fibrosis, are at high risk for developing severe chronic GERD.1,2 or wheezing. Rarely, infants may present with r Pathophysiology: The primary mechanism in ALTEs and Sandifer syndrome (abnormal refluxistransientloweresophagealsphincter posturing or spells of generalized stiffening, relaxation, unaccompanied by swallowing. In occurring within 30 minutes following a feeding). addition, gastric distension due to large volume r Diagnosis: The diagnosis of physiologic feeds in small stomachs, and delayed gastric gastroesophageal reflux in infants is a clinical emptying, increases the frequency of lower diagnosis based on a thorough history and esophageal sphincter relaxation in infants. Also physical examination.1–3 In older children, the gravitational/positional factors (lying in a flat clinical diagnosis of GERD is usually made when supine position) may predispose infants to the characteristic symptoms of heartburn, gastroesophageal reflux. Alterations in protective regurgitation, and epigastric pain are present. A mechanisms, such as the clearance of regurgitated 2–4 week empiric treatment trial with acid gastric contents and gastric epithelium repair, suppressants is recommended for these children enable physiologic reflux to develop into and a positive response to treatment is considered GERD.1–3 Clustering of GERD symptoms in diagnostic.1,2 No specific group of symptoms has families suggests some heritability of the disease. beenfoundtobereliableforthediagnosisof r Presentation: The most common presentation for GERD in infants, however; it is still generally a gastroesophageal reflux is spitting up. Infants with clinical diagnosis. Laboratory studies are not physiologic reflux present with a history of necessary for the diagnosis of GERD but are regurgitation but have no signs of discomfort and utilized to investigate possible causes of failure to no problems with weight gain.1 These babies are thrive in infants with a history of weight loss typically described as “happy spitters” as they despite adequate caloric intake. Diagnostic appear happy and undisturbed by spitting up evaluation is indicated only if there are the although the caregivers often have significant presence of red flags, concerns with complications concerns about it. Infants with GERD usually related to GERD, or if the diagnosis is uncertain present with regurgitation or vomiting associated (Table 3.1).1–3 Diagnostic methods most with irritability, feeding difficulties, poor commonly used are barium upper GI series, weight-gain, arching of the back during feedings, esophogeal and/or impedance pH monitoring, or respiratory symptoms such as cough, gagging, and upper endoscopy with biopsy.

16:12:31 04 Chapter 3: Breathing Complaints r Treatment: Lifestyle modifications are emphasized changes in vital signs were noted and the physical as treatment of gastroesophageal reflux and examination was unchanged from previous. Lifestyle GERD. In infants, feeding changes such as modifications (smaller, more frequent feedings and reducing the feeding volume, increasing the keeping the baby upright during and after feedings) frequency of feedings, and positional changes were recommended. The patient was discharged with such as keeping infants upright during feedings outpatient follow-up. and for 30 minutes after feedings are recommended.1–3 Semi-supine positioning References (seating in a carrier or carseat) should be avoided 1. Vandenplas Y, Rudolh CD, DiLorenzo C, et al. 2 as it may exacerbate reflux. Prone position Pediatric gastroesophageal reflux clinical practice compared to supine position has been shown to guidelines: Joint recommendations of the North decrease the number of episodes of American Society for Pediatric Gastroenterology, gastroesophageal reflux in infants but infants Hepatology, and Nutrition (NASPGHAN) and the should not sleep in the prone position because of European Society for Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN). JPediatr the increased risk of sudden infant death Gastroenterol Nutr 2009; 49: 498–547. syndrome (SIDS).1,2 Current guidelines strongly recommend that infants should sleep in the 2. Lightdale JR, Grense DA, Section on Gastroenterology, Hepatology and Nutrition. Gastroesophaegeal reflux: supine position until the age of 12 months. For Management Guidance for the Pediatrician. Pediatrics formula-fed infants, modifications including 2013; 131: 1684–95. thickening the formula with rice cereal or 3. Sullivan JS, Sundaram SS. Gastroesophageal reflux. changing to a commercially thickened formula Pediatr Rev 2012; 33: 243–53. may have some benefit.1–3 First-line pharmacologic therapy for GERD consists of acid suppressants, specifically histamine 2-receptor antagonists and proton pump inhibitors.1,2 Case 4 Prokinetic agents and surface agents are also used in the treatment of GERD but are not as effective Contributing Author: Amanda Shorette as acid suppressants. Finally, patients with severe History symptoms or severe complications from GERD may benefit from surgical intervention The patient is a 5-week-old full-term infant female (funduplication). who presents by ambulance to a community hospital with difficulty in breathing. Her mother describes 2 days of fussiness followed by 1 day of cough, sneezing, watery eyes, and increased nasal and oral Historical clues Physical findings secretions. She has had two episodes of non-bloody, r r History of regurgitation Normal examination non-bilious emesis over the past couple days but r Presence of troublesome r Normal weight gain for symptoms associated with age (1 kg per month in otherwise has been breastfeeding and eliminating regurgitation: irritability, the first 3 months of life) normally. Her mother denies fevers, cyanosis or color discomfort with feedings, change, rash, or diarrhea. Per EMS, the child was feeding refusal, respiratory symptoms in the absence of noted to be tachypneic with grunting respirations and mild hypoxia (O sat 91–92% on room air). r signs of infection 2 No red-flag historical items They placed her on a non-rebreather mask with improvement in oxygen saturations to 99%.

Follow-Up Past Medical History The patient was observed during a feeding cycle and r The patient was born full-term via c-section for nursedwell;however,shefrequentlyunlatchedfrom non-reassuring fetal heart rate tracings but had no the breast. She was observed to occasionally arch her significant perinatal complications. She has no back when unlatching and did have a few non-bilious chronic medical problems and lives at home with spit-ups. No signs of respiratory distress or significant her parents.

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Medications Diagnosis r None. r RSV bronchiolitis with impending respiratory failure. Allergies r NKDA. Discussion r Epidemiology: Bronchiolitis is an acute Physical Examination and Ancillary Studies inflammatory disease caused by a viral, lower r Vital signs: T 98.7 °F, HR 182, RR 62, BP 109/66. respiratory tract infection in infants. It is a clinical O2 sat 82% on room air. She is placed on syndrome seen almost exclusively in children high-flow nasal cannula oxygen at 5 L/min and younger than 2 years of age and is the leading 30% oxygen, with improvement of her saturation cause of hospitalization in infancy in the USA, to 96%. accounting for about 3 percent of all r General: The patient is awake and alert but hospitalizations in the first 12 months of life.1,2 ill-appearing. She appears uncomfortable with There are approximately 100,000 admissions for laboredrespirations.Sheispinkincolorandshe bronchiolitis in the USA annually, with an has good tone. estimated cost of 1.73 billion dollars.1 A r HEENT: Mucous membranes are moist with thick CDC-sponsored study reported an average RSV nasal secretions. There are no oropharyngeal hospitalization rate of 5.2 per 1,000 children lesions or exudates. under 24 months of age, with younger infants r Cardiovascular: The heart rate is tachycardic, with (30–60 days of age) and very preterm infants a regular rhythm. No M/R/G. (born Ͻ 30 weeks’ gestation) having the highest r Lungs: The child is grunting, tachypneic, and has age-specific rate of RSV hospitalization.1 intercostal retractions. Diffuse rhonchi are heard Bronchiolitis has a seasonal pattern, with the bilaterally as are transmitted upper-airway highest rates of infection occurring between sounds. December and March in North America; however, r Abdomen: The abdomen is soft, non-tender, and regional variations do occur. RSV is the most non-distended, with normal bowel sounds. common etiology of bronchiolitis, accounting for r Skin: The skin is warm and well-perfused, without approximately 70 percent of all cases; however, central or peripheral cyanosis. There is no rash other viruses can cause bronchiolitis. These visualized. include, but are not limited to, human rhinovirus, r Neurologic: Alert and interactive, with good tone, human metapneumovirus, influenza, adenovirus, intact reflexes. Fussy. coronavirus, and parainfluenza viruses. Infection with RSV does not confer permanent or r Pertinent laboratory values: WBC 6,400 with a long-term immunity so re-infections are common differential of 77% lymphocytes. Hb 10.6. Plt throughout life. 438,000. PCR positive for RSV. r Pathophysiology: Bronchiolitis is characterized by acute inflammation, edema, and necrosis of the Questions for Thought epithelial cells which line small airways, with r subsequent sloughing, accumulation of What are the typical presenting features of this intraluminal debris, and increased mucous diagnosis? production.1,2 Because non-ciliated cuboidal r Is ancillary testing helpful in the evaluation of this epithelial cells initially replace ciliated epithelial patient? r When should more aggressive airway support be cells, there is inadequate mobilization of considered? secretions and cellular debris, resulting in r Is there any beneﬁt to beta-agonist therapy, increased small airway obstruction and mucous hypertonic saline, or systemic glucocorticoids? plugging. This variable obstruction throughout r When should inpatient admission for this the airways results in ventilation/perfusion condition be considered? mismatching, with resultant hypoxia and compensatory hyperventilation. In addition, air

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trappingandatelectasiscanoccurdistalto symptoms of lower-airway-tract involvement in a bronchiole obstruction. Hypercarbia may occur childlessthan2yearsold.Inaddition,an and is a very concerning finding, indicating that assessment of disease severity should be made on the obstructive process is severe and/or that the a clinical basis. Specific variables have not been patient is experiencing respiratory fatigue. reliably correlated with outcomes but, in general, Functional regeneration of ciliated epithelium a child’s respiratory rate, degree/persistence of usually requires approximately 2 weeks, and hypoxia, work of breathing, mental status, and children may continue coughing for over a month perfusion should be assessed. In addition, it is after infection.2 imperative that the clinician performs serial r Presentation: Regardless of the infectious etiologic examinations in order to more accurately assess a agent, infants and children with bronchiolitis child’s respiratory status given the substantial generally have a similar disease course, which temporal variability in physical findings in infants typically begins as a viral upper respiratory tract with bronchiolitis; at any given moment, a child’s prodrome followed by wheezing and increased degree of agitation, mucous plugging, upper- respiratory effort. Symptoms include rhinorrhea, airway obstruction, and even positioning can alter cough, low-grade fever, and anorexia in the first a respiratory examination. 1–2 days. As the lower airways become involved Ancillary tests, including laboratory studies, and obstruction occurs, this prodromal phase is viral serology, and chest radiography, are then followed by tachypnea, wheezing, rales, and generally not helpful in either the diagnosis or the increased work of breathing, which can manifest assessment of disease severity and are therefore as use of accessory muscles (intercostal not routinely recommended per the AAP practice retractions, substernal retractions, diaphragmatic guidelines.1–4 CXR in particular has not been breathing, tracheal tugging), grunting, head demonstrated by current evidence to correlate bobbing, and/or nasal flaring. Shallow with disease severity. CXR is likely to be abnormal respirations and a hyperinflated chest may be in bronchiolitics, with findings including appreciated due to air trapping. Hypoxia is also a hyperinflation, peribronchial cuffing, and frequent finding. Children with bronchiolitis may subsegmental atelectasis. Such findings may result be dehydrated due to a combination of limited in inappropriate antibiotics use, as suggested by oral intake from increased work of breathing and one study cited by the AAP guidelines.1 The AAP increased insensible losses from fever and recommends CXR be reserved only for cases of tachypnea. Disease severity, however, can be quite severe respiratory distress, warranting ICU level variable, ranging from minimal cough to of care, or where signs of airway complications progressive respiratory distress, resulting in (i.e. pneumothorax, foreign body) exist. respiratory failure. r Treatment: Therapy is supportive with analgesia, Apnea is also associated with the disease antipyretics, rehydration, and airway support.1–4 process. Interestingly, apnea generally occurs very The AAP does not recommend using beta-agonist early on in the illness and often prior to the onset therapy, antibiotics, systemic glucocorticoids, or of other respiratory symptoms. Among patients chest physiotherapy in the treatment of infected with RSV, apnea occurs in about 1 bronchiolitis.1–4 Hypertonic saline (3%) has been percent of healthy term infants, with rates as high shown to have some benefit in the inpatient as 24 percent in those with risk factors such as setting but has not been shown to reduce very young age and prematurity.3 The acute phase hospitalization rates in the ED setting.1 of bronchiolitis tends to be short-lived, with Suctioning of the nasopharynx is a common disease severity peaking around day 5–7 of illness; practice, and may transiently improve nasal however, residual symptoms may persist for congestion and upper-airway obstruction; weeks.2 however, evidence is lacking to support routine r Diagnosis: The diagnosis of bronchiolitis isa use of this. Supplemental oxygen is indicated for clinical one based on history and physical SpO2 persistently Ͻ 90% in previously healthy examination, specifically the history of viral URI infants.1–3 The AAP recommends discontinuing 1 prodromal symptoms followed by signs/ supplemental oxygen for SpO2 Ͼ 90%.

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Increasing evidence suggests that continuous Follow-Up pulse oximetry monitoring is not required, This patient was stabilized in the ED after brief suc- especially in stable and overall well-appearing tioning of copious thick, yellow secretions and place- bronchiolitics. This may lead to unnecessary ment on high-flow nasal cannula. Despite supportive hospital stays and prolonged length of stay given therapy and titration of her high-flow settings on the that normal, healthy infants often have transient floor, her work of breathing progressively worsened. desaturations into the low 80s. If indicated, there Approximately 12 hours after admission, the patient are multiple methods of oxygen delivery including went into hypercarbic respiratory failure due to fatigue nasal cannula, non-rebreather, and high-flow and severe mucous plugging, ultimately requiring nasal cannula. There are retrospective studies intubationandtransfertothePICU.Shewasweaned showing that a high-flow nasal cannula reduces from the ventilator 1 week later and quickly transi- the work of breathing through generation of tioned to room air. She was discharged in good health CPAP, with a decline in the need for intubation; from the hospital without need for further respiratory however, given the lack of data, the AAP cannot support after a 2-week hospital stay. make specific recommendations regarding its use.1 There are no absolute criteria for Further reading endotracheal intubation and mechanical 1. Ralston SL, Lieberthal AS, Meissner HC, et al. Clinical ventilation; however, the following indicators practice guideline: The diagnosis, management, and should prompt consideration for more aggressive prevention of bronchiolitis. Pediatrics 2014; 134: airway management: hypercarbia greater than 1474–89. 60–65 mmHg, poor respiratory effort or fatigue, 2. Joseph M, Witt M, Sharieff GG. Evidence-based depressed mental status, recurrent apneic spells, assessment and management of acute bronchiolitis in and persistent hypoxia despite oxygen therapy.1–4 the emergency department. Emerg Med Pract 2011; 8: r Disposition: The clinician should assess both 1–20. disease severity and risk for apnea. Full-term 3. Ravaglia C, Poletti V. Recent advances in the infants Ͻ 1 month of age, preterm infants Ͻ 2 management of acute bronchiolitis. F1000Prime Rep months of age, children with underlying 2014; 6: 103. neuromuscular disorders, those with chronic lung 4. Johnson LW, Robles J, Hudgins A, et al. Management disease or congenital heart disease, and children of bronchiolitis in the emergency department: Impact with a history of previous apneic events are at a of evidence-based guidelines? Pediatrics 2013; 131 Suppl 1: S103–9. higher risk for apnea and warrant admission and monitoring.1,2 Other indications for admission include recurrent apneic episodes, persistent Case 5 tachypnea greater than 70, severe work of breathing, alterations in mental status, inability to Contributing Author: M. Bryan Dalla Betta tolerate feeds as a result of work of breathing, and poor hydration status.1–3 In addition, it is History important to assess the ability of the family to care A6-year-oldmalepresentstotheEDwithshortnessof for the child and their ability to return for further breath and wheezing for the last day. His mother states evaluation if needed. Children with unreliable that he began having nasal congestion, cough, and rhi- follow-up may need to be observed in the hospital. norrhea 3 days ago. She notes that he has had similar difficulty in breathing in the past that has sometimes been associated with changes in temperatures Historical clues Physical findings Ancillary studies or “colds.” Symptoms became worse overnight and the r r r patient had difficulty sleeping due to increasing cough. Viral prodromal r Tachypnea PCR positive for r symptoms Increased work of RSV There has been no fever, nausea, vomiting, rash, or Progressive breathing complaints of abdominal discomfort. The mother says respiratory r Retractions r the child has been less active over the last day but r distress r Hypoxia High-risk age Diffuse rhonchi has been eating and drinking normally. The cough is group and wheezing non-productive and there are no known family sick

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contacts, although she notes some of the child’s class- Questions for Thought mates have had similar symptoms recently. The child r What about this patient’s physical examination is has been using an albuterol inhaler over the last day concerning? every four hours, which provides only temporary relief r What therapies are indicated immediately? of his symptoms. r How would you treat this patient if he worsens or does not respond to initial treatment? Past Medical History r Does a CXR need to be done in all children with r The patient has a history of both asthma and these symptoms? eczema. Immunizations are UTD.

Medications Diagnosis r Intermittent albuterol. r Acute asthma exacerbation. Allergies Discussion r NKDA. r Epidemiology: Asthma affected 25 million people in the USA in 2010, including 7 million children 1 Physical Examination and Ancillary Studies under 18 years of age. Asthma prevalence in the USA increased from 5.5 percent in 1996 to 8.4 r Vital signs:T99°F, HR 115, RR 28, BP 122/78, O 2 percent in 2010.1 In pediatrics, asthma prevalence sat 91% on room air. is highest in males of 5–14 years of age, and is r General: Awake and alert, looking around the more prevalent in African Americans than any room. He is well-nourished but tired-appearing, other race.1 Geographically, the Northeast and sitting forward slightly and appearing mildly Midwest have the highest prevalence of asthma in anxious. He has a normal body habitus for his the USA. age. r Pathophysiology: Much remains to be learned r HEENT: Posterior pharyngeal erythema but no about the exact mechanism of airflow obstruction exudate. There is slight cobble-stoning to the in asthma. Asthma is an obstructive process that posterior pharynx. There is clear rhinorrhea about often begins when a stimulus or “trigger” the nares. r precipitates inflammatory change in the Neck: Supple, with no JVD or subcutaneous air. peripheral airways. Triggers can range from Trachea is midline. r exercise to viral respiratory infection, exposure to Cardiovascular: The heart rate is increased but the pharmacologic agents, or contact with rhythm is regular. No M/R/G. 2,3 r allergens. These triggering molecules activate Lungs: The respiratory rate is increased and there mast cells, eosinophils, and other cells of the are intercostal retractions bilaterally, with some immune system that cause the release of suprasternal retractions. There is bilateral histamine, cytokines, and other inflammatory inspiratory and expiratory wheezing on mediators into the lung vasculature. auscultation, without rhonchi. r r Build-up of inflammatory mediators causes Abdomen: Abdomen is soft, non-tender, and mucous hypersecretion, increased bronchial non-distended, without masses or scars. blood flow, and increased vascular permeability. r Skin and extremities: No rashes or pallor. No As the tissues around the bronchioles swell and peripheral edema, swelling, or deformity. smooth muscles around the airways contract, r Neurologic: PERRL. Cranial nerves intact. No mucous plugs form in the bronchioles.2–4 focal deficit. Normal alertness. Air-trapping in the distal airways causes impaired r Pertinent laboratory values: WBC 13,300, Hb exhalation and eventually dyspnea, as less and less 13.9, Plt 234,000, bicarbonate 21, all others air is able to enter the alveoli. normal. r Presentation: Acute asthma exacerbations can r Pertinent radiologic studies: CXR with present with great variability. Some patients will hyperinflation, no pneumothorax, no infiltrate. have only dry cough, variable wheezing, and

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subjective difficulty breathing or chest tightness foreign body, and to assess for complications of with normal vital signs.2,3 Others present in asthma such as pneumothorax. Most of the time, extremis, with tachycardia, decreased oxygen CXR during an acute asthma exacerbation will be saturation, increased respiratory rate, and normal or demonstrate hyperinflation. accessory muscle use.2,3 Patients with severe r Treatment: There are multiple treatment options exacerbations typically have poor air movement for children presenting to the ED with asthma on auscultation and appear anxious. Wheezing exacerbation, with the mainstays being inhaled can be variable and does not necessarily correlate beta-agonists and systemic glucocorticoids.5–8 with the severity of airway compromise. Inhaled beta-agonists are the most effective means Typically, children will present with a history for rapidly improving symptoms, and they should of dry, non-productive cough, chest tightness, and be started as soon as possible in the child worsening shortness of breath. Symptoms are presenting with respiratory difficulty due to frequently worse at night and wheezing is asthma exacerbation.4–7 Administration via common,butnotalwayspresent.Inpatientswith metered-dose inhaler, intermittent nebulizer, and an established diagnosis of asthma, it can be continuous nebulizer are all acceptable, but helpful to ask about exacerbating factors or continuous nebulization is usually reserved for triggers. Symptom onset after respiratory children with symptoms refractory to initial infections, exercise, allergen or smoke exposure, treatment with a metered-dose inhaler or or a history of seasonal allergy symptoms can aid intermittent nebulized albuterol. in diagnosis when the presentation is atypical. Glucocorticoids should also be started as soon r Diagnosis:Asthmashouldbesuspectedbasedon as possible in the child with asthma the presence of typical symptoms and suggestive exacerbation.9,10 Prednisone and dexamethasone physical examination findings such as retractions are both reasonable choices and have been shown or wheezing.2–4 Elements of history supporting to be similarly effective as treatment options.9,10 the diagnosis consist of non-productive cough Dosing is weight-based and duration of treatment that can be nocturnal or seasonal, with chest is typically 3–5 days for prednisone. There does tightness and dyspnea. Many patients will have not seem to be added benefit of IV administration symptom onset after precipitating factors or over oral administration if the child is capable of “triggers.” Examples include respiratory tolerating oral steroids. infections, smoke, allergens (dust, pollen), Another treatment option for asthma exercise, or changes in weather and temperature. exacerbations includes inhaled ipratropium, an Characteristically, cough is accompanied by anticholinergic agent that can be given with wheezing – a high-pitched musical sound – that albuterol. This drug facilitates relaxation of can be heard on auscultation. Patients with more smooth muscles and decreases bronchospasm. severe symptoms will have retractions. When co-administered with albuterol it can When asthma is suspected, spirometry is improve lung function and decrease admission commonly used to confirm the diagnosis.2–4 ratesinchildrenwithmoderatetosevere Spirometry measurements of interest include the exacerbations.8 forced expiratory volume in 1 second (FEV1), and Additional treatment options exist for more the forced vital capacity (FVC).2–4 It is important serious exacerbations, or if initial interventions to note that spirometry plays virtually no role in fail to significantly improve symptoms. One such the ED management of a child with suspected agent is IV magnesium sulfate. It is thought to aid asthma exacerbation, and should be done smooth muscle relaxation and bronchodilation, outpatient, after the acute exacerbation has been and may decrease the need for hospital managed. admission.11 When inhaled beta-agonists fail, IV In patients with suspected or known prior or IM beta-agonists like epinephrine or asthma and typical symptoms, CXR is not terbutaline can be used.6,7 Both can be given as an necessary. When patients fail to improve with IM injection to patients presenting with severe appropriate therapy, CXR is reasonable to rule out symptoms who may be anxious, uncooperative, or comorbid processes, such as pneumonia or have poor inspiratory flow, preventing effective

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inhaled beta-agonist treatment. Patients with following day after significant improvement in respi- rapid deterioration or persistent worsening of ratory status. symptoms may require intubation and sedation for continued treatment or respiratory support. r References Disposition: Several factors are involved when 1. Centers for Disease Control and Prevention. Most deciding to discharge a patient home or admit to recent asthma data. http://www.cdc.gov/asthma/most the hospital following an asthma exacerbation. recent data.htm (accessed February 2016). Chief among these is the amount of clinical 2. Wood PR, Hill VL. Practical management of asthma. improvement the patient has made, and the Pediatr Rev 2009; 30: 375–85. amount of therapy required in the ED. Patients 3. Bush A, Fleming L. Diagnosis and management of requiring high doses of inhaled beta-agonists, IM asthma in children. BMJ 2015; 350: h996. or IV beta-agonists, or those who have had 4. National Heart, Blood, and Lung Institute. National minimal or transient improvement should be Asthma Education and Prevention Program. Expert admitted for further therapy. However, use of Panel Report 3: Guidelines for the Diagnosis and second-tier therapies like magnesium sulfate do Management of Asthma. Bethesda, MD: National not always mandate admission. Clinicians should Institutes of Health, 2007. use clinical judgment when determining the 5. Scarfone RJ, Friedlaender EY. ␤2-Agonists in acute disposition of these patients. asthma: The evolving state of the art. Pediatr Emerg Conversely, patients presenting with mild to Care 2002; 18: 442–7. moderate symptoms that respond well to inhaled 6. Sellers WF. Inhaled and intravenous treatment in beta-agonists and glucocorticoids should be acute severe and life-threatening asthma. Br J Anaesth 2013; 110: 183–90. considered for discharge home if they appear clinically improved. Social factors, such as the 7. Suau SJ, DeBlieux PM. Management of acute abilitytoreturnforworseningsymptoms,the exacerbation of asthma and chronic obstructive pulmonary disease in the emergency department. Med reliability of parents to notice worsening Clin North Am 2016; 34: 15–37. symptoms, and the means to obtain and reliably 8. Griffiths B, Ducharme FM. Combined inhaled follow an outpatient treatment plan, should also anticholinergics and short-acting beta 2-agonists for be assessed when attempting to determine initial treatment of acute asthma in children. Cochrane disposition. Also important is the ability for Database Syst Rev 2013; 8: CD000060. discharged patients to be seen in follow-up for 9. Rowe BH, Spooner C, Ducharme F, et al. Early reassessment and continued treatment by their emergency department treatment of acute asthma with clinician. systemic corticosteroids. Cochrane Database Syst Rev 2001; 1: CD002178. Historical clues Physical findings Ancillary studies 10. Keeney GE, Gray MP, Morrison AK, et al. r r r Dexamethasone for acute asthma exacerbations in Recent URI Dry cough Hyperinflated children: A meta-analysis. Pediatrics 2014; 133: 493–9. r Exposure to r Wheezes CXR r r 11. Rowe BH, Bretzlaff JA, Bourdon C, et al. Intravenous r known trigger Retractions/ Respiratory Non-productive accessory muscle alkalosis magnesium sulfate treatment for acute asthma in the r cough r use emergency department: A systematic review of the Cough worse at Tachypnea literature. Ann Emerg Med 2000; 36: 181–90. night r Relative hypoxia

Follow-Up Case 6 Thepatientinthiscasereceivedoralsteroidsandtwo treatments of 7.5 mg nebulized albuterol as well as Contributing Authors: Daniel K. Pauzeand´ ipratropium in the ED. After interventions he was still Denis R. Pauze´ found to be wheezing diffusely and slightly tachypnic, with no improvement in oral intake or activity. He was History admitted to the pediatric ward for further treatment The patient is a 25-day-old girl who presents after of his asthma exacerbation and was discharged the having an episode where she stopped breathing and

16:12:31 55 04 Chapter 3: Breathing Complaints changed color. This child was born 4 weeks early by and grasp reflex. The patient has normal tone and spontaneous vaginal delivery. She has been completely suck. well until today, when the father noticed that the child had an episode where she stopped breathing, turned blue, and went limp. This lasted for about 30 seconds Questions for Thought and then the baby returned back to normal. This has r What are the possible etiologies of this condition? never occurred before. The episode occurred about r What are some components of history that could an hour after her noon feed. The dad notes she has help narrow the diagnosis? r no fever, irritability, lethargy, vomiting, diarrhea, or What are some considerations to guide the use of diagnostic modalities? cough. She has been eating normally and has had good r urine output. She has no history of trauma, no previ- What is the appropriate disposition of this child? ous ED visits, and no family history of similar events.

Past Medical History Diagnosis r r The patient was born at 36 weeks and has no Brief resolved unexplained event (BRUE), significant past medical history. The mother has formerly known as apparent life-threatening event no significant perinatal history. (ALTE).

Medications Discussion r r The patient takes no medications. Epidemiology: In 2016, the AAP offered a clinical practice guideline for infants with an ALTE.1 They Allergies decided to replace the ALTE term with BRUE. The new AAP specific BRUE guideline offers an r NKDA. approach to patient evaluation and Physical Examination and Ancillary Studies recommendations for management. Under the prior definition of ALTE, the r Vital signs: T 97.9 °F, HR 148, RR 40, BP 80/40, O 2 incidence of children with similar events varied sat 99% on room air. 2 r between 0.05 and 1 percent. The incidence under General: The patient is a well-developed female, in thenewdefinitionofBRUEisunknown.ABRUE no apparent distress. r typically occurs in the first 2 months of life and HEENT: No facial bruising or scalp hematoma. most often occurs between 8 am and 8 pm.1 Risk The anterior fontanelle is soft and flat. Mucous factors for occurrence include apnea history, membranes are moist and tympanic membranes feeding difficulties, and younger age are clear. The oropharynx is without erythema (Ͻ 10 weeks).1–5 Prematurity may also contribute exudate, or ulcers. PERRL. No conjunctival to risk.1–5 injection or scleral icterus. r Pathophysiology:Thereisnotonesingleunifying r Neck: Supple and with no cervical adenopathy. r pathophysiology for a BRUE as the cause depends Cardiovascular:Theheartisregular,withno upon the underlying disease process. In M/R/G.Briskcapillaryrefillandequalpulses. extrapolating causality from the prior definition r Lungs:CTAbilaterally,withnoW/R/R.No of ALTE, BRUEs may commonly be caused by retractions. gastroesophageal reflux, clinically non-apparent r Abdomen: Soft, non-distended, with no masses or respiratory tract infections, and seizures.1,4–10 organomegaly. Normal bowel sounds. Other less-common but serious causes of BRUEs r Skin and extremities: Normal range of motion, no include bacterial infections, congenital cardiac joint swelling or redness, well-perfused without abnormalities, poisoning, and inborn errors of rashes. No contusions, ecchymoses, or abrasions. metabolism.1,11 Non-accidental trauma, r Neurologic: Facial muscles activate symmetrically. especially abusive head trauma, should always be Extraocular movements are intact with midline considered in these patients.1,7,12 tongue. Spontaneously moves all four extremities r Presentation: An ALTE was initially defined by a with no obvious focal weakness. Normal Moro consensus panel of experts at the National

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Institutes of Health in 1986 as “an episode that is in this population. In one study of children frightening to the observer and that is admitted for an ALTE, 13.6 percent had a characterized by some combination of apnea subsequent extreme cardiorespiratory event.4 (central or occasionally obstructive), color change Other prospective studies where all children with (usually cyanotic or pallid but occasionally an ALTE were admitted showed that up to 12 erythematous or plethoric), marked change in percent of children had recurrent episodes as well muscle tone (usually marked limpness), choking as 9 percent needing stimulation and 3 percent or gagging.”13 Such a definition provides a large requiring resuscitation.15 Risk factors for umbrella for potential presentations. Today, this subsequent and serious events include term has been replaced by BRUE - a brief resolved prematurity, prior history of an ALTE, and unexplained event. The AAP defines a BRUE as suspected child abuse.1,3 Additional concerning “an event occurring in an infant younger than 1 findings included prolonged unresponsiveness year when the observer reports a sudden, brief, and/or cyanosis during the episode or a history of and now resolved episode of ࣙ1ofthefollowing: resuscitation by the caregiver.3 (1) cyanosis or pallor; (2) absent, decreased, or Therefore, for low-risk infants, the guidelines irregular breathing; (3) marked change in tone recommend monitoring, observation, and (hyper- or hypotonia); and (4) altered level of potentially EKG and pertussis testing.1,6,9 Patients responsiveness.”1 The AAP goes on to say that a may be observed and, when appropriate, BRUE may only be diagnosed after a history and monitored with pulse oximetry. Laboratory work, physical examination do not yield an explanation. LPs, chest radiographs, echocardiograms, and r Diagnosis: Patients presenting with BRUEs are a hospital admission are not recommended for significant diagnostic challenge to the practitioner these low-risk patients.1 Additionally, parents as symptoms are brief and have resolved by the and/or caregivers can be offered resources for time the child arrives at the ED. New diagnostic CPR training. The child should receive a repeat criteria mandate that a BRUE is only diagnosed assessment by their physician within 24 hours to after a complete and reassuring history and evaluate for developing illness.1 High-risk infants physical examination. Children who are unwell or should have the same evaluation as their low-risk present with systemic findings do not qualify for counterparts, but should be admitted to the the definition of a BRUE.1 Therefore, obtaining a hospital for monitoring because of their higher careful history and examination is imperative and risk for adverse events.1 may either elicit a diagnosis without unnecessary Infants with a non-reassuring history or an testing or drive further investigation. If the infant’s abnormal physical examination no longer complete history and physical examination do not represent the BRUE population, and are high-risk identify causality, infants are then evaluated to be infants who should be cared for based upon classified as “low risk” or “high risk.” historical and physical examination findings. Low-risk patients are those who have a Potential etiologies of BRUE are multifold. reassuring history and a normal physical Infections, including those from a respiratory examination, are greater than 60 days old, have a etiology, are common and may be not clinically gestational age of greater than 35 weeks, and did evident, especially in the younger and premature not have CPR performed by a medical child.1 Pertussis may be present without provider.1,14 The event must be brief (less than 60 respiratory symptoms or other findings on seconds) and must be a first-time event for the examination. If available, testing may be done to infant.1 confirm this etiology. Gastroesophageal reflux Higher-risk patients are those less than 2 may be suggested by episodes occurring during or months old, premature babies with a gestational after feeding.1 Seizures may be associated with ageoflessthan32weeks,andthosewithmultiple tonic-clonic type activity, as well as events.1 CPR by medical providers also places an unresponsiveness and poor muscle tone.1 infant into the high-risk category. Congenital arrhythmias, such as neonatal r Treatment: While most episodes of BRUE have supraventricular tachycardia, ventricular good outcomes, serious adverse events can occur tachycardia, and abnormal conduction pathways

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such as Wolff–Parkinson–White syndrome are Follow-Up 1 also possible causes in this population. Family This 25-day-old girl did not meet low-risk criteria due history of similar events, sudden death, long QT to the child’s age being less than 60 days. She had lab- syndrome, or Wolff–Parkinson–White syndrome, oratory evaluation, EKG, and pertussis swab. Because should be obtained. EKG and cardiac monitoring sheappearedwellandwasafebrile,aspinaltapwasnot may be considered. performed. She was admitted to the hospital, where all Non-accidental trauma must always be on the diagnostic testing was negative. differential diagnosis, and may be manifested as abusive head trauma, suffocation, or even poisoning. Previous studies have found up to References 10 percent of ALTEs may be caused by some form 1. Tieder JS, Bonkowsky JL, Etzel RA, et al. Clinical 1 of abuse. A high index of suspicion and careful practice guideline: Brief resolved unexplained events dissection of the presenting story is required in (formerly apparent life-threatening events) and these patients as physical findings are not always evaluation of lower-risk infants. Pediatrics 2016; 137: evident. Was there a previous event or 911 call? Is e20161487. the story consistent with the developmental 2. Kiechl-Kohlendorfer U, Hof D, Pupp Peglow U, et al. abilities of the infant? Does the story change? Is Epidemiology of apparent life threatening events. Arch there a prior injury? A thorough physical Dis Child 2004; 90: 297–300. examination should evaluate for bruising, as 3. Tieder JS, Altman RL, Bonkowsky JL, et al. bruises in non-ambulatory infants are a red flag Management of apparent life-threatening events in for potential abuse. The examination should infants: A systematic review. JPediatr2013; 163: 94–9. further look for bulging fontanelles, irritability, blood from the nose/mouth, or extremity 4. Al-Kindy HA, Gelinas JF, Hatzakis G, et al. Risk factors for extreme events in infants hospitalized for apparent swelling. Funduscopic examination can also life-threating events. JPediatr2009; 154: 332–7. detect retinal hemorrhages. Additionally, poisoningispossibleinachildwhohasaltered 5. Monti MC, Borrelli P, Nosetti L, et al. Incidence of apparent life-threatening events and post-neonatal risk sensorium. Over-the-counter medicines or factors. Acta Paediatr 2017; 106: 204–10. doi: 10.1111/ ethanol may be the offending culprits. One study apa.13391. Epub 2016 Apr 22. found over 18 percent of children with ALTE had 6. Santiago-Burruchaga M, Sanchez-Etxaniz J, a positive toxicology screen, many of these from Benito-Fernandez J, et al. Assessment and over-the-counter preparations such as ephedrine, management of infants with apparent life-threatening pseudoephedrine, and diphenhydramine.11 events in the paediatric emergency department. Eur J Appropriate toxicologic testing is indicated in Emerg Med 2008; 15: 203–8. these situations. 7. Guenther E, Powers A, Srivastava R, et al. Abusive r Disposition: Low-risk infants with BRUE may be head trauma in children presenting with an apparent discharged after EKG and pertussis swab with life-threatening event. JPediatr2010; 157: 821–5. close follow-up precautions, shared 8. Esani N, Hodgman JE, Ehsani N, et al. Apparent decision-making with the caregivers, and a life-threatening events and sudden infant death recheck at 24 hours.1 Additionally, resources and syndrome: Comparison of risk factors. JPediatr2008; 152: 365–70. information for learning CPR should be made available to the parents or caregiver. High-risk 9. De Piero AD, Teach SJ, Chamberlain JM. ED evaluation of infants after an apparent life-threatening infants should be admitted for monitoring event. Am J Emerg Med 2004; 22: 83–6. because of their higher risk of events. 10. Doshi A, Bernard-Stover L, Kuelbs C, et al. Apparent life-threatening event admissions and gastroesophageal reflux disease: The value of Historical clues Physical findings hospitalization. Pediatr Emerg Care 2012; 28: 17–21. r r r Apnea Entirely normal examination 11. Pitteti RD, Whitman E, Zaylor A. Accidental and r Color change (cyanosis) non-accidental poisonings as a cause of apparent r Limp tone life-threatening events in infants. Pediatrics 2008; 122: Less than a year old e359-62.

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12. McGovernMC,SmithMB.Causesofapparentlife threatening events in infants: A systematic review. Arch Dis Child 2004; 89: 1043–8. 13. LittleGA,BallardRA,BorooksJG,etal.National Institutes of Health consensus development conference on infantile apnea and home monitoring, Sept 29 to Oct 1, 1986. Pediatrics 1987; 79: 292–9 14. Claudius I, Keens T. Do all infants with apparent life threatening events need to be admitted? Pediatrics 2007; 119: 679–83. 15. Mittal MK, Sun G, Baren JM. A clinical decision rule to identify infants with apparent life-threatening event who can be safely discharged from the emergency department. Pediatr Emerg Care 2012; 28: 599–605. Case 7 Contributing Authors: Ben Church and Figure 3.1 CXR demonstrating enlarged cardiac-mediastinal Rebecca Jeanmonod silhouette. The lungs are clear with no evidence of effusion, History infiltrate, or pneumothorax. A 4-week-old boy is brought into the ED by his mother r HEENT: Anterior fontanelle soft and flat. No because of “breathing really fast.” Mom reports that signs of trauma. Mucous membranes moist. the child has had fussiness for the last day and “seems Oropharynx clear. to be working hard when he breathes.” She reports r Neck: Supple, with midline trachea. that he felt cold at home, especially in his hands and r Cardiovascular: The heart has a regular rate and feet, which prompted her visit. Mom denies decreased rhythm, without murmurs, rubs, or gallops. feeding or change in urine output. There have been no Pulses are intact. Capillary refill Ͼ 3 seconds. fevers, vomiting, or rash. He has been stooling nor- r mally. He has had some difficulties with weight gain Lungs:ThelungsareCTAbutthepatientis tachypneic, with mild supraclavicular retractions. since birth, and is on high-calorie formula for this. He r isnotindaycareandisanonlychild. Abdomen: Soft and non-tender. Normal bowel sounds. Past Medical History r Skin and extremities: No bony deformity. Skin is r cool, pale, and intact. The patient’s mother has a history of depression r and lupus. There were no complications with the Neurologic: Intact reflexes. Poor overall tone. patient’s birth, and prenatal vitamins were taken Weak suck. r throughout the entire pregnancy. The patient was Pertinent ancillary studies:CXRandEKGshown born full-term at 39 weeks via c-section. in Figures 3.1 and 3.2, respectively.

Medications Questions for Thought r None. r How does this patient’s EKG help you determine Allergies pathology? How does the EKG help you in r NKDA. general when considering congenital heart disease (CHD)? r Physical Examination and Ancillary Studies What are the diagnostic modalities you need to make a diagnosis of CHD? r ° Vital signs: T 91.6 F, HR 154, RR 40, BP 96/56, O2 r What treatment would you initiate on this sat 100% on 0.5 L nasal cannula. patient? r General: Mild respiratory distress, weak cry.

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Figure 3.2 EKG with normal sinus rhythm, some evidence of right ventricular hypertrophy, right-axis deviation, and right atrial enlargement. There are ST elevations in the inferolateral leads and inverted T waves in the lateral leads.

hypertension and diabetes, maternal r How would you monitor response to therapy in alcohol/tobacco/drug use, certain in utero this patient? r What is the deﬁnitive treatment for this infections including rubella, medications like condition? ACE inhibitors and lithium, as well as various genetic syndromes.1 r Pathophysiology: CHD can be roughly divided into cyanotic (“blue”) and acyanotic (“pink”) lesions. Diagnosis Blue CHD typically involves one of the following: r Congestive heart failure (CHF) secondary to large right-sided obstructive processes with shunting septal defect and volume overload. (for example, Tetralogy of Fallot, in which subpulmonic stenosis obstructs right ventricular outflow, and there is some degree of right-to-left Discussion shunting through either a ventricular septal defect r Epidemiology: CHD, including both cyanotic and or a patent ductus arteriosus) or mixing of acyanotic lesions, is the most common congenital oxygenated and deoxygenated blood (for example, disease in newborns, occurring in an estimated 6 in truncus arteriosus, where a single outflow tract to 13 per every 1,000 live births.1,2 Although there provides both right- and left-sided circulation). have been major advances in the management of Pink CHD most commonly involves anatomic the disease, CHD remains the leading cause of derangements that result in either pressure perinatal and infant death. The most common overload (such as in coarctation of the aorta, malformation is a ventricular septal defect with where the left ventricle must pump against the Tetralogy of Fallot being the most commonly obstruction posed by the narrowed aorta) or occurring cause of cyanotic CHD. There are many volume overload with left-to-right shunting (as in risk factors involved with the development of the case of this patient, where a large septal defect CHD, including prematurity, first-degree relative results in increased volume delivery to the right with CHD, maternal comorbidities such as heart).

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Figure 3.3 Differentiating features of cyanosis.

CHF, defined as inability of the heart to meet generalized edema as infants usually do not the blood supply demands of the body, can occur display these physical examination findings like with any kind of CHD. CHF can also result from adult patients. arrhythmia or from acquired cardiomyopathy, as r Diagnosis: In cases of cyanotic infants, the can occur from viral or bacterial etiologies. In provider should first determine if the cyanosis is childrenwhodonothaveevidenceof centralorperipheral.Acoolordehydratedinfant cardiovascular compromise at birth and who are may have peripheral cyanosis with neither cardiac discharged home with undiagnosed or nor pulmonary abnormality. Central cyanosis is asymptomatic CHD, the typical presenting age for typically cardiac or pulmonary in etiology. Some CHFis4–6weeks.Thisisbecausethereis distinguishing factors are that cardiac cyanosis persistently high pulmonary resistance does not typically improve with administration of immediately following birth (reducing the oxygen (because of shunt physiology), and pressure gradient for left-to-right flow), which typically worsens with crying (which increases slowly decreases over time, reaching its nadir at cardiac work), while pulmonary cyanosis often about 6 weeks. At this point, the decrease in improves with crying (because of increased pulmonary pressure may hit a tipping point, with recruitment of alveoli) and improves with oxygen high left-sided pressures causing pulmonary (Figure 3.3). Once cyanosis is suspected to be of overcirculation through septal defects. Our cardiac origin, the provider should perform a patient suffered from CHF due to increases in CXR and an EKG to support or refute the preload from left-to-right shunting secondary to diagnosis and to potentially narrow down the an atrial septal defect and ventricular septal defect diagnosis to specific pathologic entities causing ventricular hypertrophy and eventual (Figure 3.4). heart failure. Pink babies with CHD may present in more r Presentation: Patients with CHD with CHF often subtle fashion. Cardiac disease should be display lethargy and poor or prolonged considered in any neonate or child presenting with feeding.3–6 There may also be increased cyanosis poor feeding, diaphoresis, respiratory distress, or and sweating with feeding.5,6 The extremities can hepatomegaly.5 All these children should undergo be cool and mottled, with delayed capillary refill.5 CXR and EKG, as well. In addition to assisting in Tachypnea from metabolic acidosis is common diagnosis of specific cardiac lesions, these tests and tachycardia is frequently profound.5,6 Other can help rule out other diagnostic possibilities, common findings include murmurs, failure to such as pneumonia or arrhythmia (Figure 3.5). thrive, and hepatomegaly.5,6 These patients may Although laboratory testing is non-specific, it may appear septic but will only worsen with IV fluid reveal hyponatremia, renal dysfunction, or resuscitation. Do not rely on peripheral and elevated LFTs secondary to hepatic congestion.

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Figure 3.4 Differential of cardiac cyanosis based on CXR and EKG findings.

Echocardiography is the modality used to make a entire differential diagnosis for the unwell infant, definitive diagnosis of CHD by providing THE MISFITS (Trauma, Hypovolemia/heart, information regarding both cardiac anatomy and Endocrine, Metabolic, Intestinal disasters, function.3–5 Seizures, Formula misadventures, Inborn errors r Treatment: The EM provider does not need to of metabolism, Toxicologic, and Sepsis), and know the specific cardiac lesion in order to begin simultaneously treat for sepsis during evaluation. treating the child with symptomatic CHD. Definitive treatment for patients with CHD is Generally, in any ill-appearing child, the provider emergent consultation with a pediatric willbeginwiththeABCalgorithmandaddress cardiologist and eventual operative repair of the respiratory and circulatory issues. If the diagnosis underlying defect, but this can clearly not be is uncertain, the provider should consider the accomplished in every ED. Emergency

Figure 3.5 Differential of acyanotic cardiac lesions based on CXR and EKG findings.

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therapeutic modalities important to pediatric endotracheal intubation should be considered CHF management include airway control, before transport.8 diuretics, and vasopressor support.6,7 Oxygen administration for the most part is helpful in the Historical clues Physical findings Ancillary studies majority of cyanotic babies but keep in mind that r r r r Failure to thrive r Poor perfusion EKG with right oxygen is a potent vasodilator and can actually Dyspnea r Tachypnea ventricular lead to increased pulmonary vascular flow leading Hypothermia hypertrophy and r Ill-appearing right atrial to “steal” from the systemic circulation in those r hypertrophy patent ductus ateriosus-dependent patients.6,7 CXR with Patients with evidence of shock or heart failure cardiomegaly should initially be thought to be septic and treated with weight-based IV fluid administration, as well Follow-Up asantibiotics,assepsisisbyfarmuchmore common than CHD. Those with CHF will likely The child’s echocardiogram demonstrated moderate worsen clinically with IV fluid administration, to severely depressed left ventricular function, with a andthismaybethecluetotheproviderthatheor moderately dilated left ventricle. There was a moder- she is dealing with CHD. In patients in shock who ate muscular ventricular septal defect and a moderate- are unresponsive to other therapies, a trial of IV sized secundum atrial septal defect, both with left-to- 6–8 prostaglandin E1 therapy should be initiated. right flow, and bilateral dilated atria. There was mod- These refractory infants, who most commonly erate tricuspid insufficiency with elevated right-sided present in the first month of life, typically have ventricular pressures. There was no patent ductus arte- either a cyanotic or an acyanotic lesion that is so riosus. The child was treated for sepsis and also under- severe that they require blood shunting through went pediatric cardiology consultation. He was trans- the ductus arteriosus in order to sustain life. The ferred to a tertiary care center with pediatric cardiac lesions are varied – Tetralogy of Fallot, left surgery capabilities. The child’s septic work-up was ventricular hypoplasia, transposition, and many ultimately negative, and he underwent surgical correc- other lesions may be ductal dependent, if severe tion of his heart defects and had an uneventful post- enough. The key is that, when every other operative course. modality has failed to improve the clinical picture of a neonate in shock, prostaglandin should be References tried. A well-known serious side effect of 1. van der Linde D, Konings EE, Slager MA, et al. Birth prostaglandin is apnea, which may require prevalence of congenital heart disease worldwide: A intubation.8 If prostaglandin seems to be systematic review and meta-analysis. J Am Coll Cardiol improving the child’s clinical status, the child’s 2011; 58: 2241–7. supplemental oxygen should be decreased, as a 2. Peterson C, Ailes E, Riehle-Colarusso T, et al. Late high arterial oxygen tension promotes ductus detection of critical congenital heart disease among US closure. An oxygen saturation in the 80s is infants: Estimation of the potential impact of proposed universal screening using pulse oximetry. JAMA acceptable in these children. Diuresis with Pediatr 2014; 168: 361–70. furosemide can be given to help improve 3. Kuehl KS, Loffredo CA, Ferencz C. Failure to diagnose oxygenation.6,7 Cardiac output can be improved congenital heart disease in infancy. Pediatrics 1999; with a number of inotropes.6,7 r 103: 743–7. Disposition:Patientswithnew-onsetCHDwill 4. Eckersley L, Sadler L, Parry E, et al. Timing of need admission for hemodynamic monitoring diagnosis affects mortality in critical congenital heart and treatment, depending primarily on the type of disease. Arch Dis Child 2016; 101: 516–20. lesion and severity of symptoms. Transfer of 5. Ross RD, Bollinger RO, Pinsky WW. Grading the patients to a tertiary facility with more expertise is severity of congestive heart failure in infants. Pediatr also appropriate, depending on the hospital’s Cardiol 1992; 13: 72–5. capabilities. Disposition decisions are usually 6. Rosenthal D, Chrisant MR, Edens E, et al. made in consultation with a pediatric cardiologist. International Society for Heart and Lung In patients on prostaglandin therapy, prophylactic Transplantation: Practice guidelines for management

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r of heart failure in children. JHeartLungTransplant HEENT: Bilateral eyelid swelling. No scleral 2004; 23: 1313–33. icterus. PERRL. Mouth and oropharynx without 7. Brooks PA, Penny DJ. Management of the sick neonate lesions. with suspected heart disease. Early Hum Dev 2008; 84: r Neck:Supple,withnoadenopathy. 155–9. r Cardiovascular: The patient is tachycardic, with 8. Meckler GD, Lowe C. To intubate or not to intubate? no M/R/G. Transporting infants on prostaglandin E1. Pediatrics r Lungs: Tachypneic, with increased work of 2009; 123: e25–30. breathing and mild intercostal retractions. Lungs are CTA, with no W/R/R. Case 8 r Abdomen and genitourinary: Distended but not tender to palpation. No hepatosplenomegaly or Contributing Authors: Natalie Moore and masses. The child has mild scrotal edema. Rebecca Jeanmonod r Extremities and skin:Thepatienthas1+ pitting edema of both upper and lower extremities. His History skin is warm, dry, and intact, with no petichiae, The patient is a previously healthy 17-month-old male jaundice, or bruising. who presents to the ED because his mother notes that r Neurologic: He has a non-focal neurologic he has been breathing increasingly hard over the past examination. week. The labored breathing was particularly noted r Pertinent laboratory values: WBC 11,500, Hb 7.5, when playing with his sister. Mom also notes general HCT 24.6, MCV 70, MCHC 30, Plt 499,000, Cr fatigue over the past week and some swelling around 0.2, BUN 15, ALT 13, AST 36, total bilirubin 0.1, his eyes. Over the past 3 days, he began to have swelling lipase 47, albumin 1.3, LDH 169, iron level 7, in his legs as well. On further questioning, mom states TIBC 159, iron saturation 4%, ferritin level 4. His that he had been sick with a viral URI about 10 days stool is positive for occult blood. The urine dip is ago. He also had four to five episodes of non-bloody, negativeforprotein,WBC,RBC,nitrites,or non-bilious vomiting and six to seven episodes of diar- leukocyte esterase. rhea about 1–2 weeks before these symptoms started. r Pertinent radiographs:CXRwithbilateralsmall He otherwise has had no recent travel, is not prone pleural effusions. Otherwise, clear lungs, without to bruising or frequent infections, and has not experi- consolidation or interstitial edema. enced any recent visual blood loss from stool, gums, or nose. The mother notes that he is a picky eater and has a limited solid food intake and drinks over 40 ounces Questions for Thought of cow’s milk daily. r Once you have found that a patient has decreased hemoglobin, what other diagnostic Past Medical History r tests should be sent to assess for the etiology of No significant past medical or family history. anemia? Vaccinations are UTD. r In what category of anemia would you place this child given his Hb, MCV, MCHC, and iron studies? r Medications What other types of anemia cause microcytic red r None. blood cells? r What are other causes of anemia? Allergies r NKDA. Diagnosis Physical Examination and Ancillary Studies r Iron-deficiency anemia caused by inappropriate r Vital signs: T 98.7 °F, HR 170, RR 38, BP 139/100, diet with excessive intake of cow’s milk. Also O2 sat 98% on room air. contributing to his anemia was enteropathic r General: Awake and alert in his mother’s arms. He protein loss from destruction of the epithelial appears pale and in mild respiratory distress. lining of his gut from his recent viral illness.

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Discussion non-modified cow’s milk. Cow’s milk should not r Epidemiology: Anemia is a common condition be introduced into the diet prior to 12 months of that affects approximately 20 percent of children age secondary to the decreased concentration of in the USA at some point during their iron in the milk and because protein present in childhoods.1 Globally, anemia affects cow’s milk may cause a colitis, leading to occult 3 approximately 50 percent of children.2 Anemia is intestinal blood loss. Inadequate iron absorption defined as a reduction in hemoglobin occurs when there is malabsorption in the concentration two standard deviations below the intestine secondary to chronic disease such as mean hemoglobin for age and gender.3 celiac disease, inflammatory bowel diseases, or Iron deficiency is the most common iatrogenic causes from bowel resection. nutritional deficiency in children, and Inadequate absorption can also occur acutely iron-deficiency anemia is particularly high in from GI illness causing inflammation and African American and Hispanic populations as destruction of the lining of mucosal cells. Finally, well as children who live in poverty.1–4 It affects iron-deficiency anemia can also be caused by approximately 4 percent of patients between 6 and increased blood loss. r 12 months, 12 percent over 12 months, and 7–9 Presentation:Themostcommonpresentationof percent of toddlers.1–4 anemia is an asymptomatic patient. However, r Pathophysiology: Anemia has numerous causes, other symptoms of iron-deficiency anemia are and any of them may present with shortness of fatigue, irritability, shortness of breath, not being breath. Oxygen delivery to tissues requires intact able to keep up with the other children, decreased lungs, a working pump, and blood for delivery. performance or attention in school, and cold 2 Therefore, a breakdown in any step of this process intolerance. Another presenting symptom is pica, can result in dyspnea, weakness, or syncope. which is when the patient eats non-food Ultimately, it is this failure in oxygen delivery that substances such as sand, clay, dirt, or paper, and causes dyspnea. craves ice. Physical examination findings include Iron-deficiency anemia is a specific subset of lethargy,tachypnea,tachycardia,flowmurmur, anemia.Ironisabsorbedintheintestines, pallor (which is best seen on the palms, nail beds, primarily in the duodenum and upper jejunum. and conjunctiva), glossitis (swelling and redness After absorption by the mucosal cells, iron binds of the tongue and disappearance of the papillae), to transferrin, which delivers the iron to the liver, angular stomatitis (fissures in the corner of the where it is primarily stored in a form called mouth), splenomegaly, koilonychias (concave/ ferritin.5 When erythropoietin is released from spoon-shaped nails), and impaired growth. r the kidney, iron is released to make red blood cells Diagnosis: Diagnosis of anemia requires inthebonemarrow.Anormalredbloodcell laboratory measurement of Hb and HCT. The circulates for approximately 120 days; it is then differential diagnosis for anemia is broad, and can reabsorbed by the spleen and the iron is recycled. be roughly divided into anemia from losing red Iron-deficiency anemia is caused by either blood cells, anemia from destroying red blood insufficient dietary intake of iron, inadequate iron cells, and anemia from failing to make red blood absorption, or increased intestinal blood loss. cells. Although a complete discussion of all Infants have enough iron stores for the first 6 subsetsofanemiaisbeyondthescopeofthis monthsoflifeandthentheyrequireironintheir book, there are laboratory tests that can help diet. Per AAP guidelines, infants who are determine the category into which a given breastfed should be given daily iron patient’s anemia falls. supplementation until iron-rich foods can be Patients with anemia from losing red blood introduced into their diet.3 They also recommend cells will, by definition, have a low Hb and HCT. screening for anemia at 9–12 months of age.3 They should also have an elevated reticulocyte Inadequatedietaryintakeiscommoninchildren count, which is evidence of the patient’s bone between6monthsand24monthsofage, marrow increasing red blood cell production in especially in children who are picky eaters and response to the losses. Since the body relies on those who drink excessive amounts of recycling of iron from “expired” red blood cells by

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the spleen, when blood is lost externally over blood cell. The reticulocyte count will be low time, the patient will eventually additionally because the bone marrow is lacking one of the develop iron-deficiency anemia. They will then building blocks for the production of red blood drop their reticulocyte counts as well, because of cells, iron. In patients with microcytic anemia, an inability to produce cells. Occult blood loss iron studies should also be obtained, as this is the most commonly occurs from the GI tract or from most common cause of microcytic anemia. menorrhagia in adolescent girls.2 In anemic Patients with iron-deficiency anemia will have patients, therefore, a stool guaiac and menstrual low serum iron, low ferritin level, increased total historyshouldbeobtained.Acuteblood-loss iron binding capacity, and low transferrin anemia tends to be normocytic. saturation.6 Patients with anemia from red blood cell r Treatment: Treatment for iron-deficiency anemia destruction may have an intrinsic process, such as depends on the cause and severity. If it is caused an inherited problem with making red blood cell by inadequate intake of iron, treatment is to walls (for instance, spherocytosis) or problems increase dietary iron and take an iron supplement. that interfere with glycolysis (such as G6PD Iron-rich foods include meat (especially beef and deficiency), both of which will cause a shortened liver), eggs, lentils, dark-green leafy vegetables, red blood cell lifespan.2 They may also have an andiron-fortifiedcereals.Ferroussulfate extrinsic process, such as autoimmune hemolytic supplement is recommended. Enteral iron side anemia or hemolytic uremic syndrome.2 In effects include GI symptoms such as abdominal addition to anemia, these patients will have an pain,nausea,diarrhea,constipation,andblack elevated reticulocyte count as well as elevated stool. Parenteral iron may also be a good option levels of the products of hemolysis, including for iron-deficiency anemia in children who indirect bilirubin, increased lactate cannot absorb iron or have undergone surgery dehydrogenase, and decreased haptoglobin.2 which has limited their ability to absorb iron. These anemias tend to be normocytic. There are no guidelines for an absolute Patients with anemia from failure to make red hemoglobin threshold for transfusion of packed blood cells are the largest group of pediatric red blood cells for patients with iron-deficiency anemic patients. These patients have an anemia, thus the decision to transfuse would be inappropriately low reticulocyte count for their dependent on the child’s clinical picture. anemia. Their bone marrow cannot respond to the r Disposition: Most children with iron-deficiency low HCT with increased red blood cell anemia can be discharged home, with follow-up production. This can occur from primary with their pediatricians for a recheck of bone-marrow failure or malignancy, from viral hemoglobin or potentially for further testing and infections (such as parvovirus B19 or hepatitis), referral to hematology. Children with severe or, most commonly, from iron-deficiency anemia. symptomatic anemia should be transfused and These anemias tend to be macrocytic or admitted to the hospital. microcytic. In diagnosis of iron-deficiency anemia, a CBC will reveal decreased Hb and HCT. These patients Historical clues Physical findings Ancillary studies also tend to have an elevation in platelet count r r r Recent viral r Pallor Decreased Hb from increased erythropoietin release, which illness, which Tachycardia and HCT likely caused r Tachypnea r Low MCV and cross reacts with thrombopoietin receptors destruction of r Fatigue MCHC 6 leading to an elevation in platelet count. When the intestinal r Low serum iron evaluating red blood cell indices, a patient with mucosal lining and serum ferritin r Excessive cow’s r Elevated total iron-deficiency anemia will have a low MCV, milk intake iron binding which is a measure of average volume of red blood r Increased r capacity cells in a specimen. They will also have a fatigue Low transferrin r Increased work saturation decreased MCHC, which is the measure of the of breathing concentration of hemoglobin in a given red

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Follow-Up 2. Recht M. Thrombocytopenia and anemia in infants Due to his abnormal vital signs and anasarca, the child and children. Emerg Med Clin N Am 2009; 27: 505–23. was admitted to the PICU for his symptoms. While 3. Baker RD, Greer FR, and the Committee on Nutrition. inpatient, he began having desaturations to 92 percent Clinical report: Diagnosis and prevention of and was placed on oxygen. He was also treated with iron-deficiency anemia in infants and young children (0–3 years of age). Pediatrics 2010; 126: 1040–50. furosemide and albumin, and was transfused for his anemia. His clinical picture eventually improved, and 4. Short MW, Domagalski JE. Iron deficiency anemia: Evaluation and management. Am Fam Phys 2013; 87: he was discharged home 6 days later, with parental 98–104. counseling regarding excessive milk intake. 5. Waldvogel-Abramowski S, Waeber G, Gassner C, et al. Physiology of iron metabolism. Transfus Med References Hemother 2014; 41: 213–21. 1. Centers for Disease Control and Prevention. Iron 6. Walters MC, Abelson HT. Interpretation of the Deficiency – United States, 1999–2000. See www.cdc complete blood count. Pediatr Clin North Am 1996; 43: .gov/mmwr/preview/mmwrhtml/mm5140a1.htm. 599–622.

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Case 1 developmentally normal, just beginning to walk. Contributing Author: Rebecca Jeanmonod History Medications A 14-month-old girl is brought into the ED by her r Acetaminophen. grandmotherforfeverandabnormalmovement.The child has had a runny nose, dry cough, and low-grade fever for the last 2 days. Grandma has been giving Allergies her acetaminophen intermittently and suctioning her r Penicillin – gets rash. nose before bed. The child has continued to be active and playful, and Grandma reports that the child has been making a usual number of wet and dirty diapers, Physical Examination and Ancillary Studies although she has a slightly decreased oral intake, par- r Vital signs: T 103.5 °F, HR 170, RR 38, BP 93/62, ticularly for solids. She has not been vomiting or had O2 sat 99% on room air. any diarrhea. This afternoon, the child became pale r General: The child is somnolent but rouseable. She and listless. Grandma took her temperature rectally is irritable. and noted that it was 103.7 °F. The child started to have r HEENT:Therearenosignsofheadtrauma. twitching in her left face, which progressed to involve PERRL. The child has moderate nasal discharge. the whole left side of her body. The child did not She has mild bilateral tonsillar hypertrophy and respond to Grandma during the episode, which lasted erythema, without exudate. Her tympanic for about 3–4 minutes. Grandma lives two blocks from membranes are normal. the hospital, and ran with the child down the street to r Neck: Supple, with bilateral shotty adenopathy. the ED, thinking the child was dying, and not willing to r Cardiovascular: Regular tachycardia, with no wait for an ambulance. Grandma reports that the child M/R/G. Normal capillary refill. hasbeensomnolentandirritablesincetheevent,but r Lungs: CTA bilaterally, with good air movement. has been breathing the whole time. Grandma reports She has an intermittent dry cough. that nothing like this has ever happened to the child r Abdomen and genitourinary:Softand before. non-tender/non-distended, with no masses or organomegaly. Normal genitalia. r Skin and extremities: Hot to touch. No rashes or Past Medical History vesicles. No signs of trauma. r r Term neonate, mom with narcotic addiction. Neurologic: The child is fussy and sleepy. She Child underwent inpatient detoxification after moves all four extremities spontaneously and is birth and has been in Grandma’s custody since purposeful. She has normal reflexes. She responds then, although she has regular contact with to her grandmother’s voice. mom. She is UTD on immunizations and r Pertinent laboratory values: Fingerstick glucose 87.

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Questions for Thought symptoms, abnormalities in behavior, staring r spells, syncope, thought disturbances, visual In this clinical scenario, when does the child symptoms, or prominent autonomic symptoms. require extensive testing to determine the source Simple febrile seizures marginally increase the of fever? risk of adult epilepsy (2 percent, compared to r Do children with this diagnosis require LP? r When is it necessary to perform neuroimaging of background risk of 1 percent in the general children with this diagnosis? population), while complex seizures increase risk 4 r What counseling can you provide the caregivers to 4–6 percent. r regarding prevention of further episodes? Presentation: Most children will present after their seizure is over. Seizures in general typically last about 3 minutes, so most patients will have stopped seizing in the time it takes to travel to the Diagnosis ED. Most children will present in a post-ictal r Complex febrile seizure. state, which should resolve within the hour. Some children may have a prolonged post-ictal period, Discussion or Todd’s paralysis, but this is atypical. Since r Epidemiology: Seizure disorders are common in children who are post-ictal are usually somnolent children. 0.05–1 percent of children will have a or irritable, it can be difficult to determine which seizure from a metabolic or neurologic process, children with seizure are “sick” versus “not sick.” 0.1 percent will develop repetitive seizure In the child with febrile seizure who is no longer episodes, and 2–4 percent will have at least one post-ictal, presentation is largely dependent upon febrile seizure.1,2 Febrile seizures are defined as a the underlying process that is causing the fever. seizure that occurs in the setting of fever in the MostfebrileseizureshaveURIastheunderlying absence of intracranial infection, metabolic cause, source of fever, and human herpes virus 6 has an or prior afebrile seizure history.3 First febrile association with febrile seizure,3,4 but the seizure typically occurs between age 6 months and clinician should consider the possibility of other 5 years, with peak onset at 18 months of age.3 serious bacterial infection (UTI, meningitis, About 30 percent of children have a family bacteremia, soft-tissue infection) as well as toxins history of febrile seizures, suggesting a and environmental sources of fever. genetic component to its etiology.3 Children r Diagnosis: The diagnosis of febrile seizure is with developmental delay are most clinical. In well-appearing children with an susceptible.4 uncomplicated febrile seizure, there is no role for r Pathophysiology: All seizures are a result of an routine laboratory work or neuroimaging.4,6 The abnormal discharge of electrical activity in the AAP does not advocate for routine LP in cases of brain. Febrile seizures are thought to be related to simple febrile seizure.6 They do state that LP is an the increased excitability of neurons in the option in the child with febrile seizure between developing brain.5 Hyperthermia generates the ages of 6 and 12 months whose vaccination seizures in animal models, as well.5 This may status is incomplete or unknown, and in those occur secondary to disrupted function of who are taking antibiotics, which might mask temperature-sensitive ion channels or due to meningitis symptoms.4,6 Likewise, in children inflammatory mediators from underlying with complex febrile seizure, there is no evidence infection, combined with a genetic that CT should be performed,7 nor has it been predisposition.5 About two-thirds of febrile demonstrated that these children benefit from seizures are defined as simple, meaning that they routine LP.4 Performing an EEG has also been meet all of the following criteria: duration less shown to be unhelpful in the febrile seizure than 15 minutes, generalized seizure, single population.4 Instead, the clinician should focus on episodein24hours,inchildrenage6–60 the child’s overall status. An ill-appearing child or months.4,6 All others are characterized as a child with altered mental status requires a full complex. Although the majority of febrile seizures evaluation, including LP. A young child with a are generalized, they may present with focal fever of no apparent source also requires some

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evaluation, in keeping with standard guidelines, seizures can recur in 30 percent of children, and most commonly CBC, blood culture, and urine that there are no preventative measures that have culture. The ED provider should perform a been identified. thorough history, including family history, feeding/formula history, and a complete examination in all these children, and order Historical clues Physical findings Ancillary studies r r r ancillary studies as indicated by the history and History of r Post-ictal state Normal glucose physical examination. In any child with altered febrile illness Examination r Focal seizure consistent with sensorium and abnormal vital signs, the provider witnessed by r URI should consider the dangerous differential r caregiver Fever diagnosis, THE MISFITS (Trauma, Altered mental status Hypovolemia/heart, Endocrine, Metabolic, Intestinal disasters, Seizures, Formula misadventures, Inborn errors of metabolism, Toxicologic, and Sepsis). In this case, the child Follow-Up remains post-ictal with altered mental status, and The provider ordered CT scanning, blood work, and it is appropriate to initiate neuroimaging urine studies and planned to perform LP.The child was (especially given the focality of the seizure), blood given rectal acetaminophen for her fever. While the work, cultures, and metabolic studies. The child was waiting for her CT, she rapidly returned to provider for the child in this particular case her normal self, awake, and interacting with Grandma. should consider traumatic injury, CNS infection On reassessment, she had an entirely non-focal exam- or masses, hypoglycemia, or toxins as possible ination, with the exception of her runny nose and seizure causes. The child should only be dry cough. All diagnostic studies were cancelled, and diagnosed with a complex febrile seizure after the child was discharged home with her grandmother these other possibilities are eliminated. On the to follow up with her pediatrician in the next 24–48 other hand, if the child returns to her normal hours. functioning and is well-appearing in the ED, with a benign examination and reassuring history, no References further studies are necessary, as the child has a 1. Panayiotopoulos CP. Benign childhood epilepsy with source for her fever. occipital paroxysms: A 15-year prospective study. Ann r Treatment: Treatment of ongoing seizure activity Neurol 1989; 26: 51–6. in the ED is usually accomplished with 2. Hauser WA. The prevalence and incidence of benzodiazepines as a first-line agent, and any convulsive disorders in children. Epilepsia 1994; 35 patient in status epilepticus should receive Suppl 2: S1–6. benzodiazepines. Status epilepticus is rare in 3. Sharawat IK, Singh J, Dawman L, et al. Evaluation of febrile seizures, and most children require only risk factors associated with first episode febrile seizure. supportive care. Acetaminophen or other JClinDiagnRes2016; 10: SC10–13. antipyretics may be given for the child’s comfort, 4. Graves RC, Oehler K, Tingle LE. Febrile seizures: risks, but these do not reduce recurrence or incidence of evaluation, and prognosis. Am Fam Phys 2012; 85: febrile seizure.8 Although some providers 149–53. prescribe intermittent benzodiazepines or 5. Dube CM, Brewster AL, Baram TZ. Febrile seizures: phenobarbitaltochildrenwithrecurrentfebrile Mechanisms and relationship to epilepsy. Brain Dev 2009; 31: 366–71. seizures, there are no data that this has any clinical benefits to the child.8 6. Subcommittee on febrile seizures. Febrile seizures: r Guideline for the neurodiagnostic evaluation of the Disposition: The majority of children with febrile childwithasimplefebrileseizure.Pediatrics 2011; 127: seizures have a benign course, and most are 389–94. discharged home with reassurance and 7. DiMario FJ. Children presenting with complex febrile instructions to family regarding safe positioning seizures do not routinely need computed tomography of the child during seizure, and other supportive scanning in the emergency department. Pediatrics measures. Parents should know that febrile 2006; 117: 528–30.

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r 8. Offringa M, Newton R. Prophylactic drug Abdomen and urogenital: Soft, non-distended, management for febrile seizures in children normoactive bowel sounds. No masses or (review). Evid Based Child Health 2013; 8: organomegaly. Normal genitalia with no rash. 1376–485. r Skin and extremities:Skinwarmtotouch.No rashes appreciated. Case 2 r Neurologic: Moves all extremities. Fussy but consolable. Normal neonatal reflexes. Contributing Author: Shellie Asher r Pertinent laboratory values: r U/A: 2+ leukocytes, moderate bacteria; History r CBC: WBC 15,000, remainder within normal The patient is a 3-week-old female brought to the ED limits; byhermotherafterthepatient’srectaltemperaturewas r ° Electrolytes, renal function, and glucose: found to be 100.8 F. The patient’s mother states that normal; she took the baby’s temperature because she seemed r Blood culture: pending; morefussythanusual,butwasconsolable.Therehas r CSF: 0 WBC, 1 RBC per high-powered field. been no vomiting or diarrhea, no rashes, and no cough Gram’s stain negative. or other symptoms of URI. She has been breastfeeding r well with normal urinary and stool output. She is an Pertinent radiologic studies:CXRwithno only child and there are no known sick contacts. The cardiomegaly, effusions, consolidations, or patient’s mother reports that the infant was born via infiltrates. spontaneous vaginal delivery at 39 weeks’ gestation, and that she had a normal, healthy pregnancy. Mother had normal prenatal care without any concerns for Questions for Thought maternal infection. r What are the primary sources of infection to be concerned about in this patient? r Past Medical History What maternal factors should be considered in r the evaluation of a neonate with a fever? None. r What type of laboratory testing/imaging should be performed in this type of patient? r Medications How is a deﬁnitive diagnosis made in the ED, and what treatment is necessary? r None.

Allergies Diagnosis r NKDA. r Neonatal fever secondary to UTI.

Physical Examination and Ancillary Studies Discussion r ° Vital signs: T 101 F, HR 167, RR 32, O2 sat 99% r Epidemiology:Theevaluationandmanagementof on room air. Ͻ r neonates (age 28 days) and young infants (age General: Resting comfortably in mom’s arms, no 28–60 days) with fever (defined in this age group acute distress. as a temperature Ͼ 100.4 °F) is focused on serious r HEENT: Anterior fontanelle is open and flat. Neck bacterial infections. Up to 3 percent of neonates is supple. Oropharynx is moist and pink, no presenting with fever have a serious bacterial evidence of thrush. infection, including UTI, meningitis, pneumonia, r Cardiovascular:Regularrhythm,withnoM/R/G. and bacteremia.1 Infections in the first 7 days of Capillary refill Ͻ 2 seconds life are typically associated with vertical r Lungs: Equal expansion, without retractions. transmission, or infection that is transmitted from Equal breath sounds, without crackles or the mother to the infant.1 After the first 7 days of wheezing. life, infections are typically acquired from sick

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contacts in the home, community, or hospital general appearance, including activity level, tone, environment. The rate of serious bacterial presence of cyanosis or jaundice, and irritability infection in infants 28–60 days of age may be as or lethargy; signs of focal infection including skin, high as 6–10 percent, with the most common HEENT including fontanelles, lungs, abdomen etiology being UTI.1 including the umbilical stump, and GU, noting r Pathophysiology: Bacterial and viral infections in circumcision status if pertinent. the neonatal and young infant period may result Allneonateswithadocumentedrectal from vertical (maternal to fetal) transmission or temperature greater than 100.4 °Fshouldhavea community exposure (household, child care, full sepsis evaluation including CXR, peripheral hospital, etc.). While the prenatal environment is WBC, blood cultures, U/A, urine culture, and CSF ideally sterile, infection may be introduced studies including cell count, Gram’s stain, glucose, through amniotic membrane disturbance prior to protein, enterovirus/herpes PCR, and culture. labor, resulting in clinical presentations that range Stool culture is indicated if there are any changes from occult infection to chorioamnionitis. Risk to the infant’s usual stooling habits or if there is factors for early-onset neonatal sepsis include blood or mucous in the stool. preterm birth, group B streptococci positivity in In the 29–60 day age group, there is more of a mother, prolonged rupture of membranes, and role for clinical evaluation in the decision-making maternal fever and tachycardia.1 Immature process regarding fever evaluation. The immune systems and a less-developed ill-appearing child (lethargic, irritable, poor blood–brain barrier in the neonate and infant perfusion, or clinical impression) should have a result in increased susceptibility to bacterial full sepsis work-up as previously described. The infections. Serious etiologies of bacterial infection well-appearing child without clinical evidence of include meningitis, pneumonia, UTI, and acute viral bronchiolitis (tachypnea, hypoxia, bacteremia. Significant viral infections may also wheezing in the setting of fever) should have occur, with serious sequelae. laboratory tests, including CBC and blood r Presentation: Although there are no historical cultures drawn, as well as U/A and urine factors that rule out serious infection in neonates culture.1,2 CXR and stool studies may be and young infants, there are several that increase performed per clinical indications. “Low-risk” the likelihood that fever is associated with a infants (previously healthy, full-term, serious bacterial infection, including cough, poor well-appearing, WBC 5,000–15,000 without feeding, irritability, lethargy, diarrhea, and bandemia, negative urine and no clinical signs of seizures.1 That said, many children present with focal infection) may have LP and CSF studies isolated fever. performed depending on the clinician’s 1,2 r Diagnosis: The critical evaluation of the neonate assessment. r or young infant with fever starts with a careful Treatment: Management of the neonate and young history and physical examination. This evaluation infant with a fever depends on the patient’s age maybechallengingduetolackofclinicalsignsor group, risk factors, and clinical presentation. Any symptoms of focal infection in this age group. diagnosed focal infection such as pneumonia or Historical elements should include thorough UTI should be treated according to clinical prenatal and maternal history, birth history, guidelines, with patterns of local bacterial presence of underlying diseases or conditions, antibiotic resistance taken into account. All medications used (including herbal or neonates with a documented rectal temperature over-the-counter), presence of sick contacts, diet greater than 100.4 °Fshouldbeadmittedtothe (breast- or bottle-fed and how feedings are hospital and empiric antibiotic/antiviral treatment prepared), signs or symptoms of focal bacterial should be started while sepsis work-up results are infection as described above, previously pending. Empiric antibiotic treatment in neonates diagnosed infections, and antibiotic use, presently includes coverage for group B streptococci, or in the recent past. Escherichia coli, Haemophilus influenzae, Pertinent physical examination elements Moraxella catarrhalis, Neisseria meningitidis, include vital signs with rectal temperature; Staphylococcus aureus,andListeria monocytogenes

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with ampicillin and an aminoglycoside such as Case 3 gentamycin, or ampicillin and cefotaxime.1,2 In addition, empiric treatment with acyclovir Contributing Authors: David H. Long and should be administered for possible HSV infection, especially if there is any positive Janet Young history of maternal herpes, prolonged vaginal History delivery, or vesicular rash in the 1,2 The patient is a 7-year-old female brought to the ED infant. by her mother after the patient’s oral temperature was Older infants (age 29–60 days) who are found to be 101.8 °F. Her fever was preceded by four well-appearing may be treated empirically with 1,2 bouts of vomiting that started earlier in the day while ceftriaxone while cultures are pending. If sepsis she was at school. The patient was diagnosed with ALL is suspected in this age group, empiric therapy for 9monthsago;otherwiseshehadbeenahealthychild the organisms listed above includes ampicillin, prior to her leukemia diagnosis. She is on chemother- cefotaxime, and vancomycin. r apy managed by her oncologist, and her last mainte- Disposition:Allneonateswithfevershouldbe nancedosewas6daysago.Priortotodaythepatient admitted to the hospital for empiric therapy as had been in good spirits, eating and drinking well, described while cultures are pending. Infants 28 and tolerating her chemotherapy regimen with mini- days and greater, who look well and are classified mal side effects. The mother states that the oncologist as low risk for bacterial infection, may be admitted provided strict precautions to go immediately to the to the hospital or discharged home depending on EDforevaluationifthepatienteverdevelopsafever. clinical evaluation, social factors, including ability The patient has had one episode of non-bloody, non- to return to the hospital, and the established local bilious vomiting upon arrival to the ED, but otherwise standard of care for these patients. has had no associated symptoms.

Past Medical History Historical clues Physical findings Ancillary studies r ALL, diagnosed 9 months ago. r Neonate Ͻ 28 r Fever r U/A positive for days old r Otherwise normal WBC and bacteria r Ͼ ° r Medications r T 100.4 F examination Other studies Fussy unremarkable for r infectious source Methotrexate. r 6-Mercaptopurine. r Prednisone. Follow-Up r Ondansetron (as needed for nausea). Clinical evaluation of the infant did not reveal any evidence of focal bacterial infection, and U/A was positive Allergies r for leukocytes. The patient was admitted to the hospital NKDA. and started empirically on ampicillin and gentamycin. Urine culture grew out E. coli. Blood and CSF cultures Physical Examination and Ancillary Studies were negative. The patient completed her course of r Vital signs: T 102.1 °F, HR 167, BP 90/50, RR 24, antibiotics and was discharged home after an unevent- O2 sat 97% on room air. ful hospital course. r General: Female child lying supine, tearful. She withdraws to her mother several times during examination as she appears fearful and states she References wants to go home. 1. Hamilton J, John S. Evaluation of fever in infants r HEENT: Normocephalic, atraumatic. PERRL. No and young children. Am Fam Phys 2013; 87: 254–60. conjunctival pallor. Tympanic membranes clear, nares clear. No pharyngeal erythema or oral 2. Polin R. Management of neonates with suspected or lesions. proven early-onset bacterial sepsis. Pediatrics 2012; r 129: 1006–15. Neck:Supple,withnoadenopathy.

16:13:00 3 05 Chapter 4: Fever r Cardiovascular: Tachycardic, otherwise regular febrile patient is approximately 10–40 percent.1 rhythm, with no M/R/G. Ͻ 2secondcapillary Gram-positive and Gram-negative organisms refill. account for 85–90 percent of documented r Lungs: Mild expiratory coarse breath sounds infections.1,2 Common sites of infection include bilateral upper and lower lung fields; otherwise the respiratory tract, urinary tract, skin, GI/GU good air movement. tract, and oral cavity.1–3 Bacteremia is the most r Abdomen and genitourinary: Soft, non-distended, common infection. Viral infections must also be normoactive bowel sounds. No rectal or vaginal considered in the neutropenic patient, with bleeding, no fissures or abscesses. Varicella zoster virus and HSV being the most 1 r Skin and extremities:Skinwarmtotouch. common viral etiologies. Patients are also Well-appearing nail beds upper and lower susceptible to fungal infections. These are less extremities. Tunneled IV port upper-left chest common but more likely to occur in the setting of wall with no tenderness to palpation, well-healed prolonged neutropenia (Ͼ 10 days), prolonged surgical scar. No erythema, induration, or antibiotic use, steroid use, or after bone marrow purulence around port site. transplant in the setting of chronic r immunosuppression therapy. Neurologic:Orientedtotime,person,andplace. r Cranial nerves II–XII grossly intact. Cerebellum Pathophysiology: Chemotherapy treatment places testing normal (rapid alternating movements, heel a burden on both the patient’s innate and adaptive to shin, finger to nose), negative pronator drift immune system. The innate immune system and Romberg. Reflexes +2 upper and lower provides protection through non-specific extremities. Normal gait. recognition of pathogens. Common components r Pertinent laboratory values: ANC of 234 cells/␮L. include mucosal barriers, natural killer cells, r Pertinent radiologic studies:CXRwithno phagocytic cells, macrophages, and monocytes. cardiomegaly, effusions, consolidation, or The adaptive immune system mounts an immune infiltrates. Tunneled IV catheter tip visualized in response by producing specific antibodies and superior vena cava–atrial junction. lymphocytes to target invading pathogens. Chemotherapy treatment causes bone marrow suppression, which in turn causes the immune Questions for Thought system to become weakened due to the decrease r in immune cells available to fight infection. Why is this type of patient at high risk in regards Another side effect of chemotherapy is its to infection? non-specific destruction of rapidly dividing cells, r Are there any “typical” signs and symptoms for this patient’s diagnosis? such as mucosal and epithelial cells. Breakdown of r What type of laboratory testing/imaging should oral and intestinal mucosa, as well as skin, allows be performed in this type of patient? invasion of pathogens. Many patients also are on r How is a deﬁnitive diagnosis made in the ED, and steroid treatment, which also suppresses the what treatment is necessary? immune system. All of these factors place the patient at increased risk of bacterial, viral, and fungal infections. r Presentation: Neutropenic patients have a Diagnosis r depressed immune system, so it is important to Neutropenic fever in pediatric patient with cancer remember the patient may not mount a response (chemotherapy-induced neutropenia). to an infection. Therefore, finding a source of infection may be challenging. In fact, fever may be Discussion the only sign of infection in a neutropenic patient. r Epidemiology: Neutropenic fever in cancer Due diligence in obtaining a detailed history, full patients is considered a medical emergency. set of vitals, complete review of systems, and a Infections left untreated can lead to thorough physical can all lead to finding a life-threatening complications and death. The rate primarysourceofinfection.Thenadirfor of documented infections in the neutropenic absolute neutrophil count (ANC) is typically

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5–10 days after the last chemotherapy treatment, ordered if a clean-catch sample can be collected. although neutropenic fever can occur at any time. Other laboratory studies, including peripheral r Diagnosis:Thecriticalevaluationofachildwith blood cultures, skin swabs, throat cultures, and LP febrile neutropenia is a careful history and are not routinely useful and should be ordered physical examination. Neutropenia in a febrile based on clinical indications. Imaging should also pediatric cancer patient is defined as an ANC of be ordered as clinically warranted. Ͻ 500 cells/␮L, or an ANC expected to drop r Treatment: Current evidence recommends Ͻ 500 cells/␮L in the next 48 hours. The lower the providing prompt administration of antibiotic ANC and the greater duration of neutropenia therapy within 1 hour of presentation for the (Ͼ 7 days), the greater the risk of infection.1–3 febrile, neutropenic pediatric patient.1–3 Fever is defined as a single temperature of 101 °F Administration of antibiotics greater than 60 in neutropenic patients, or a temperature minutes after presentation has been associated Ͼ 100.4 °F for longer than 1 hour, or a with increased morbidity and mortality. temperature Ͼ 100.4 °F recorded at least two Antibiotic selection will be based on regional times within a 24-hour period.1 Temperatures resistance patterns and hospital protocols. shouldbetakenorallyorintheaxilla.Rectal Recommended initial therapy for febrile temperatures are contraindicated as they can neutropenia includes monotherapy with a broad- increase the risk of mucosal damage leading to spectrum third- or fourth-generation bacteremia. As already discussed, fever is often antipseudomonal cephalosporin (ceftazidime or the only sign of infection in a neutropenic patient. cefepime), an antipseudomonal penicillin On the other hand, patients may not mount a (piperacillin/tazobactam), or a carbapenem fever (due to poor immune function and (meropenem or imipenem–cilastin).1–3 immunosuppressive medications), and their only Randomized controlled studies have shown sign of infection may be an abnormal vital sign. monotherapy to be as efficacious as combination Tachypnea, tachycardia, hypothermia, or therapy, with fewer side effects. However, hypotensionshouldalwaysbeconsideredcritical additional therapies should be added based on findings. Regardless of temperature, the risk of clinical presentation. For example, overt infection infection in a neutropenic pediatric patient should at indwelling catheter sites or skin breakdown be considered if the patient has unstable vitals or warrants adding vancomycin to the antibiotic has signs of clinical deterioration. A thorough regimen. If an intra-abdominal infection is history should include a list of chemotherapy suspected or diagnosed, metronidazole should be agents, the last treatment date, a list of all other administered. Lastly, if the patient is clinically medications prescribed to the patient, the unstable with no source of infection, a second duration and intensity of the fever, as well as any Gram-negative antibiotic (aminoglycoside) exposure to sick contacts at home or school. A should be started. Antivirals are not considered complete head-to-toe examination should be first-linetreatments,butshouldbeadministered performed to search for possible sources of if clinically warranted. Lastly, fungal therapy is infection. Symptoms or physical findings such as also not considered first-line treatment, but headache, cough, congestion, sore throat, ear should be administered for persistent fever more pain, difficulty breathing, chest pain, abdominal than 4 days after the initial antibiotic therapy.1–3 pain, dysuria, rectal pain, and skin lesions can r Disposition: Increasing evidence has shown that lead to a primary source of infection. Pay careful febrile neutropenic patients can be treated based attention to indwelling catheter sites, oral lesions, on categorization into high- and low-risk and nailbed lesions due to the risk of skin and categories using clinical decision rules.1–3 Placing mucosal breakdown in these patients. Indicated patients into these groups can assist in deciding if laboratory studies include a complete blood count a patient is a candidate for either inpatient or with differential and platelet count, complete outpatient therapy, and IV versus oral antibiotics. metabolic profile (electrolytes, Cr, BUN, liver Unfortunately, current clinical decision rules are transaminases, total bilirubin), and blood cultures only validated for adults. Although there are at from all CVC ports. Urine cultures can also be least 16 clinical decision rules proposed for

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children, none of them have met the rigorous undergoing hematopoietic stem-cell transplantation. J requirements for validation.1–3 The patient’s Clin Oncol 2012; 30: 4427–38. oncologist should always be consulted for further recommendations, modification of therapy, and Case 4 determination as to whether the patient is suitable for inpatient or outpatient therapy. Developing a Contributing Author: Shellie Asher final disposition will be dictated by the patient’s clinical presentation, the patient’s oncologist, and History local hospital protocols that are put in place for The patient is a 17-year-old male with autism spectrum pediatric patients with febrile neutropenia. disorder who presents to the ED with fever, irritability, and muscle stiffness. The patient’s parents state that he wasinhisusualstateofhealthuntilabout2daysago Historical clues Physical findings Ancillary studies when he developed low-grade fever, muscle aches, and r History of ALL r Fever r ANCϽ 500/␮L repetitive right arm movements. Today his symptoms r Last r Tachycardia worsened, he became irritable, had difficulty walking, chemotherapy and his temperature increased to 103 °F. They deny any 6daysago r Vomiting other recent illnesses, nausea/vomiting, diarrhea, rash, respiratory symptoms, or any other concerns.

Follow-Up Past Medical History r Autism spectrum disorder. Due to her temperature and absolute neutrophil count, the patient was started on broad-spectrum antibiotic Medications monotherapy with cefepime after blood cultures were r Aripiprazole (AbilifyR ). drawn. After consulting her oncologist, it was decided r to admit the patient for IV antibiotic treatment and Melatonin as needed for sleep. observation. Two days later her blood cultures came back posi- Allergies r tive for Gram-negative rods. She was kept in the hos- NKDA. pital until culture sensitivities were reported. On day three cultures grew Pseudomonas aeruginosa suscep- Physical Examination and Ancillary Studies r tible to cefepime. She was discharged by her oncolo- Vital signs: T 104.5 °F, HR 122, RR 28, O2 sat 99% gist with daily IV antibiotic administration through a on room air. home health provider. Antibiotics were continued for r General:Agitated,restless. a total of 14 days. Blood cultures were redrawn after r HEENT: Drooling, slurred speech. Tympanic finishing her antibiotic regimen, and the results came membranes normal, pharyngeal structures back negative. midline. PERRL. r Neck: No adenopathy. Patient resists ranging, but References does not seem tender. r 1. Villafuerte-Gutierrez P, Villalon L, Losa JE, et al. Cardiovascular: Tachycardic, regular, with no Treatment of febrile neutropenia and prophylaxis in M/R/G. Ͻ 2secondcapillaryrefill. hematologic malignancies: A critical review and r Lungs: Equal expansion, without retractions. update. Adv Hematol 2014; 2014: 986938. doi: Equal breath sounds, without W/R/R. 10.1155/2014/986938. r Abdomen: Firm, no apparent tenderness. 2. Dubos F, Delebarre M, Martinot A. Predicting the risk r Skin and extremities: Skin warm to touch and of severe infection in children with diaphoretic. chemotherapy-induced febrile neutropenia. Curr Opin r Hematol 2012; 19: 39–43. Neurologic:Confusedandagitated.Unableto 3. Lehrnbecher T, Phillips R, Alexander S, et al. assess orientation. Increased muscle tone Guideline for the management of fever and throughout. Unable to assess sensory examination neutropenia in children with cancer and/or or gait. Diminished reflexes.

16:13:00 05 Chapter 4: Fever r Pertinent laboratory values: dopaminergic effects. Risk factors for NMS r WBC 16,000; include use of high-potency agents, high doses, a r CPK 898 U/L (normal range 22–198); rapid increase in dose, long-acting depot agents, prior episodes of NMS, and a recent history of r AST 92 U/L, ALT 85 U/L; catatonia. Illness, dehydration, concurrent r LDH 440 U/L. medication use (especially lithium), and genetic factors may also play a role in the development of NMS.2 Questions for Thought r Presentation: NMS occurs in the setting of r What is the diﬀerential diagnosis for this patient’s neuroleptic medication use and is characterized presentation? by hyperpyrexia (temperature Ͼ 100.4 °F), muscle r What type of laboratory tests/imaging should be rigidity, altered mental status, and autonomic performed in this type of patient? r dysfunction (sialorrhea, diaphoresis, How is a deﬁnitive diagnosis made in the ED, and incontinence, tachycardia, labile blood pressure).2 what are the priorities in management? Children with NMS tend to present with dystonia, as opposed to the prominent tremor typically seen in adults.2 Symptoms tend to develop over 2 Diagnosis approximately 24–72 hours. Signs and symptoms r of a dopaminergic blockade include muscle Neuroleptic malignant syndrome (NMS). rigidity, dysphagia, shuffling gait, tremor, dystonia, and dyskinesia.2 Psychomotor agitation Discussion is evidenced by excessive or purposeless motor r Epidemiology: NMS may develop in 0.07–2.2 activity and/or tremor. Mental status alteration percent of patients taking neuroleptic may progress from agitation to delirium to medications.1,2 Meanonsetis10daysafter coma.2 initiation of therapy, but may occur much later, r Diagnosis: The diagnosis of NMS depends ona even years, into treatment.1,2 NMS is more careful and accurate history (particularly common in males, with a male:female ratio of 2:1, medication history) and physical examination. andmayoccuratanyagewiththemeanagebeing Diagnostic criteria include recent treatment with 40 years.1 In pediatric cases, 9 percent result in neuroleptics, hyperthermia Ͼ 100.4 °F, and death, with 20 percent of survivors going on to muscle rigidity in addition to at least five of the have significant sequelae.1,2 following: altered mental status, tachycardia, r Pathophysiology: The generally accepted hyper- or hypotension, diaphoresis or sialorrhea, mechanism for NMS is dopamine receptor tremor, incontinence, increased CPK or urinary antagonism in the hypothalamus, nigrostriatal myoglobin, leukocytosis, metabolic acidosis, or pathways, and spinal cord.2 This blockade results other evidence of autonomic instability. In in extrapyramidal symptoms such as muscle addition, alternate diagnoses must be excluded. rigidity and tremor. Dopamine receptor blockade Differential diagnoses to consider include, but are also results in a dysfunction of temperature not limited to, withdrawal of dopaminergic autoregulation and a blockade of cooling medications (such as those used for Parkinson mechanisms such as vasodilation and sweating.2 disease), acute dystonia, acute akathisia, tardive Increased calcium release from the sarcoplasmic dyskinesia, Parkinsonism, pseudoparkinsonism, reticulum may result in increased contractility, catatonia, serotonin syndrome, CNS infections, hyperthermia, rigidity, and muscle cell status epilepticus, tetanus, thyroid storm, heat breakdown.2 “Traditional” neuroleptic drugs, stroke, sepsis, and toxic exposures.2–4 such as haloperidol, act directly through the The distinction between serotonin syndrome inhibition of dopamine receptors, while “atypical” and NMS can be difficult, especially in patients agents, such as olanzapine, risperidone, and in taking both serotonergic and neuroleptic this case aripiprazole, primarily cause a blockade medications. Some helpful differentiating features of serotonin receptors but may have secondary include:

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r Serotonin syndrome is characterized by altered JAmAcadChildAdolescPsychiatry1999; 38: mental status, autonomic nervous system 187–94. disturbances, neurologic dysfunction, clonus, 2. Neuhut R, Lindenmayer J-P, Silva R. Neuroleptic and hyperthermia in the setting of serotonergic malignant syndrome in children and adolescents on medication use.3,4 atypical antipsychotic medication: A review. JChild Adolesc Psychopharmacol 2009; 19: 415–22. r NMS is characterized by muscle rigidity, hyperpyrexia, altered mental status, and 3. Katus LE, Frucht SJ. Management of serotonin autonomic instability in the setting of syndrome and neuroleptic malignant syndrome. Curr Treat Options Neurol 2016; 18: 39. neuroleptic medication use.3,4 4. Perry PJ, Wilborn CA. Serotonin syndrome vs r In patients taking both serotonergic and neuroleptic malignant syndrome: A contrast of causes, neuroleptic medications, laboratory findings of diagnoses, and management. AnnClinPsychiatry elevated CPK, abnormal liver function tests, 2012; 24: 155–62. low serum iron and leukocytosis favor a diagnosis of NMS over serotonin syndrome.3,4 r Treatment:Neurolepticmedicationsmustbe Case 5 stopped immediately as soon as the diagnosis of NMS is considered.2–4 Most patients with NMS Contributing Authors: Kristine Marie J. Casal respond well to supportive management including and Melanie K. Prusakowski IV fluid resuscitation, benzodiazepines for rigidity History and agitation, cooling measures, and respiratory support as needed.3,4 Rarely, paralysis and The patient is a 15-month-old African American intubation as well as dantrolene may be used in male with a history of wheezing in the past who refractory cases.3,4 presents with increased work of breathing, rhinor- r Disposition: Patients with NMS should be rhea, cough, and wheezing for one day. Mother gave admitted to an intensive care setting for close albuterol at home; however, the patient did not appear respiratory and cardiovascular monitoring. Most to respond to treatments. The patient was seen by patientswithNMSwillbeabletotoleratea his primary physician where he had tachypnea of 56 different antipsychotic medication after a washout breaths per minute, O2 sat 96% on room air and HR period of at least 2 weeks. 194. He received oral steroids, an albuterol nebulizer treatment, and supplemental oxygen, with only mild improvement. Due to the severity of his illness he was Historical clues Physical findings Ancillary studies referred to the ED where he was found to have a fever r r r History of Fever Elevated CPK of 101.2 °F. autism r Agitation r No infectious r Atypical r Muscle rigidity source antipsychotic Past Medical History use r Sickle cell disease, type SC. r Mild intermittent asthma. Follow-Up The patient’s aripiprazole was stopped immediately. He Medications was actively cooled with a cooling blanket. Benzodi- r Penicillin daily. azepines were administered for agitation and muscle r Albuterol nebulized as needed. rigidity, and fluid resuscitation was started. The patient was admitted to the ICU and improved over 48 hours. Allergies He was discharged home to follow up with his outpa- r tient provider. NKDA. References Physical Examination and Ancillary Studies r ° 1. Silva RR, Munoz DM, Alpert M, et al. Neuroleptic Vital signs: T 101.2 F, HR 178, RR 44, BP 129/69, malignant syndrome in children and adolescents. O2 sat 96% on room air.

16:13:00 05 Chapter 4: Fever r General: Very playful, well-developed, and amino acid valine is substituted for glutamic acid, non-toxic toddler, who appears to be in mild causing a mutation in the beta-globulin structure respiratory distress. of hemoglobin. This defect causes hemoglobin to r HEENT: Moist mucous membranes, normal have reduced plasticity and to polymerize and tympanic membranes, PERRL, no mucosal sickle when deoxygenated.1 This abnormal shape lesions. results in more rapid filtering and destruction in r Neck: Supple, with no tenderness or adenopathy. the spleen, leading to anemia. The shape of sickled r Cardiovascular: Tachycardia, normal S1, S2, no hemoglobin causes it to adhere to the audible M/R/G. endothelium, leading to chronic inflammation r Lungs: Tachypnea, with fair air entry on lung and reperfusion injury. When this damage occurs fields bilaterally, prolonged expiratory phase with in the spleen, it results in autoinfarction of the wheezing and mild subcostal retractions. No nasal small vessels, decreased splenic function, and an flaring or supraclavicular retractions. increased risk of infections due to encapsulated r bacterial organisms.1 Abdomen: Normal scaphoid appearance, soft, r non-tender, without hepatomegaly. Presentation: Acute illness in children with sickle r Skin and extremities: No rashes, jaundice, or cell disease may have a similar presentation to pallor. No signs of trauma. No joint pain. typical childhood ailments, such as fever, common cold, and pneumonia. However, r Neurologic: Awake, interactive, and appropriate, bacterial infections can rapidly progress to with normal tone and reflexes. fulminant sepsis; thus, timely recognition and r Pertinent laboratory values: WBC 8,500, Hb 10.4. management of these children is important.2–5 r Pertinent radiographs: CXR with no infiltrates, Fever may be the first sign of sepsis. effusions, or consolidations. Other presentations of illness in sickle cell disease can vary from generalized fatigue and Questions for Thought pallor during episodes of acute anemia or splenic r sequestration to severe pain. Pain crises can occur What other laboratory tests are necessary at this in the digits (dactyitis), skeleton, chest, and time? abdomen. Children often have a typical site of r What complications are associated with this pain for their crises, but pain crisis should be condition? r What treatments need to be initiated in the ED? considered in pain of any location in a child with r What is the management of this condition? sickle cell disease, especially in the absence of a known injury. Fever can be the presenting symptomofeachoftheseserioussequelaeof sickle cell disease in the absence of infection, as well. Diagnosis Infants with sickle cell disease may also r Fever in a patient with sickle cell disease. present with jaundice, splenomegaly, and increased irritability. In some patients who have Discussion not been diagnosed with sickle cell disease on r Epidemiology: Sickle cell disease is an autosomal newborn screening, first presentation may be with recessive disorder that affects about 250,000 disseminated encapsulated infection (such as children worldwide and occurs in approximately pneumococcus) or sepsis. one out of every 500 black or African American r Diagnosis: Fever may be the initial presentation births.1 One in 12 blacks or African Americans for acute chest syndrome or sepsis. Patients older carries sickle cell trait. It affects up to 2,000 US than 2 months with a known history of sickle cell born infants annually and it is the most common disease, who present with a temperature of disease detected by routine newborn Ͼ 101.3 °F (38.5 °C), should be promptly screening.1 evaluated by performing a history and physical r Pathophysiology: Sickle cell disease is an examination, and laboratory studies including a autosomal recessive genetic disorder where the CBC with differential, reticulocyte count, and

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bloodcultureshouldbeperformed.6 Urine the risk for developing sepsis has dramatically cultureshouldbestronglyconsideredinpatients decreased; however, patients with sickle cell with past history of UTI, current symptoms of disease are immunocompromised, and dysuria, or young age at risk for pyelonephritis.6 maintaining a high index of suspicion for sepsis is Fever in infants less than 2 months requires a full an important step in preventing morbidity and sepsis work-up and empiric antibiotics.6 mortality. Children with sickle cell disease who have fever and dyspnea, tachypnea, cough, or rales require CXR immediately to evaluate for acute Historical clues Physical findings Ancillary studies 6 chest syndrome. Similarly, bone pain in an r Fever r Fever r Negative CXR atypical location or pain associated with local r r History of sickle r Tachycardia swelling or erythema may indicate osteomyelitis. cell disease Tachypnea r Cough and r Abnormal lung In these cases, radiographs may determine the respiratory examination etiology of the pain, although bony changes on difficulty plain film in osteomyelitis tend to be a late finding. With a high index of suspicion, consideration should be given to MRI. Follow-Up r Treatment: Fever in a patient with sickle cell diseaseisanemergencybecausethesechildrenare The patient was admitted to the hospital and started on at an increased risk for severe bacterial infection empiric antibiotics even though his CXR and symp- due to reduced splenic function.1–5 Empiric toms suggested a viral source. Blood cultures drawn antibiotics with appropriate coverage for prior to antibiotic administration were negative, and Streptococcus pneumoniae and Gram-negative a respiratory swab was positive for human metapneu- enteric organisms (ceftriaxone or cefotaxime, for movirus. The patient recovered well with appropriate example) should be utilized while cultures are treatment for bronchospasm, which was likely due to pending.3–7 Parenteral antibiotics are his viral infection, and was discharged home on hospi- recommended even if the presenting illness tal day 4. appears to have a focal source (for example, viral URI). Supplemental oxygen should be provided to References patients who present with hypoxia. If acute chest 1. Centers for Disease Control and Prevention. Sickle cell syndrome is suspected, CXR and pulse oximetry disease: Data and statistics. See https://www.cdc.gov/ should be obtained for further evaluation. ncbddd/sicklecell/data.html (accessed December 2016). Immediate IV fluid resuscitation should be initiated in cases of hypovolemia or hypotension. 2. Bansil NH et al. Incidence of serious bacterial Pain control in patients with sickle cell disease is infections in febrile children with sickle cell disease. Clin Pediatr 2013; 52: 661–6. important in treating an acute vaso-occlusive crisis. Mild to moderate pain may be controlled 3. Morrissey BJ et al. Incidence and predictors of bacterial infection in febrile children with sickle cell with NSAIDs such as parenteral ketorolac, while disease. Hemoglobin 2015; 39: 316–19. opioids may be added for severe pain. r 4. Narang S et al. Bacteremia in children with sickle Disposition: Patients with a history of sickle cell hemoglobinopathies. JPediatrHematolOncol2012; disease who present with fevers should be 34: 13–16. promptly evaluated for sepsis, started on IV 5. Savlov D et al. Predictors of bacteremia among antibiotics, and admitted for further management. children with sickle cell disease presenting with fever. J In addition, other acute complications of sickle Pediatr Hematol Oncol 2014; 36: 384–8. cell disease including acute chest syndrome, 6. Schultz CL et al. Adherence to prompt fever evaluation splenic sequestration, and aplastic crisis should be in children with sickle cell disease and the health belief considered during febrile illnesses. Infection is the model. Pediatr Blood Cancer 2015; 62: 1968–73. major cause of death in children with sickle cell 7. Shihabuddin BS, Scarfi CA. Fever in children with disease. With the introduction of Haemophilus sickle cell disease: Are all fevers equal? JEmergMed influenzae type B and pneumococcal vaccinations, 2014; 47: 395–400.

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Case 6 organomegaly. No tenderness overlying the kidney transplant site. Contributing Author: Taylor R. Spencer r Skin and extremities:Somewhatwarmtothe touch but dry without rashes. No cellulitic History changes. A well-healed surgical scar is noted on The patient is a 12-year-old female with a history of the abdomen, without any acute findings. a renal transplant, who presents for fever. Her family r Neurologic: Cranial nerves intact, no focal reports that she has had increased fatigue over the past neurologic deficits, normal alertness. ° 2 days. She has had fever measured orally to 101.8 F r Pertinent laboratory values: at home. This is associated with weight loss, myalgias, r WBC 14,300, including absolute neutrophil fatigue, and nausea without vomiting. She notes a mild count of 3,400; diffuse abdominal discomfort without exacerbating or r alleviatingfactors.Therehavebeenmultipleepisodes Cr 1.3, consistent with baseline laboratory of non-bloody diarrhea. She has no head or neck pain. values; r She has no congestion, cough, sore throat, or chest U/A with trace protein, but no evidence of pain. She has no dysuria or pelvic pain, and reports leukocytes, nitrites, or bacteria; no rash. The patient denies prior similar episodes. She r Lactate is within normal limits; has no sick contacts or recent travel. After calling her r Stool has no fecal leukocytes, and negative for transplantteam,thefamilywasinstructedtogotothe Clostridium difficile and for ova and parasites; ED for further evaluation. r Cytomegalovirus (CMV) serology is positive. r Pertinent radiographs: CXR with no infiltrates or Past Medical History other acute pathology. Non-contrasted CT of the r Renal transplant 2 years previous, without abdomen and pelvis with non-specific small complications. Transplant was the result of focal bowelwallthickening. segmental glomerulosclerosis leading to chronic renal failure. Questions for Thought Medications r What sources of fever are unique to patients with r Mycophenolate mofetil. r transplant? Tacrolimus. r What non-infectious causes of fever must be r Prednisone. considered after transplant? r How do anti-rejection drugs inﬂuence the Allergies presentation of infectious processes? r r Penicillin, which causes a rash. What ﬁndings on history or examination are suggestive of CMV infection? r Physical Examination and Ancillary Studies When may it be appropriate to decrease r immunosuppressant therapy in transplant Vital signs: T 100.5 °F, HR 108, RR 14, BP 138/82. patients with fever? r General:Awakeandalert,innoacutedistress. r HEENT: No tympanic membrane erythema, no sinus tenderness, no rhinorrhea, and no pharyngeal injection or exudates. Diagnosis r r Neck: Moderate shotty cervical lymphadenopathy Transplant-associated CMV infection. is seen. r Cardiovascular:Regular,withnoM/R/G. Discussion r Lungs: Normal work of breathing, lungs clear and r Epidemiology: In the USA, nearly 30,000 organ equal, with no W/R/R. transplantations are performed annually. Renal r Abdomen: Vague diffuse discomfort on palpation, transplants are most common, followed by liver, without Murphy’s sign, Rovsing’s sign, or heart, and lung. While only a small proportion of McBurney’s point tenderness. Soft without these are pediatric cases, fever is not an

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uncommon complication in the pediatric Consideration must be given for common transplant population. community-acquired infections in the pediatric Infection is the most common cause of fever transplant patient with fever. Pneumonia may be after pediatric transplant.1–3 Epidemiologically, community- or healthcare-acquired, and accounts these may be divided into patient-derived for a large portion of infections seen. The infections, host-derived infections, incidence varies based upon the type of healthcare-acquired infections, and transplant. For example, UTI is the most common community-acquired infections. Certain patient bacterial infection in kidney transplant characteristics are associated with increased risk recipients.1–3 Antimicrobial resistance must be forinfection,includingblackorHispanicrace,the considered due to the possibility for prior nature of the transplant and pre-transplant health antibiotic exposures and recurrent infections in status, and age.1,2 For example, RSV and influenza this group. Other community bacterial or viral may present with more severe infection in infectious may also be seen in patients who are younger transplant recipients compared with immunosuppressed due to transplantation and older children. However, younger patients are also anti-rejection medications. Vaccine-preventable less likely to have acquired pathogens that induce infections are in the differential diagnosis, lifelong latent infection.2 particularly with an incomplete vaccination The time since transplantation also influences record or without previously developed immunity. infectious risk.1–3 In the first month, bacterial Non-infectious etiologies may cause fever in post-operative infections are most likely. the pediatric transplant recipient, with estimates Opportunistic infections and latent pathogens ranging from one in four to one in eight of from the recipient or donor are more prevalent in transplant patients presenting with fever.1,2 the next 6 months. After 6 months, Rejection, malignancy, adrenal insufficiency, and community-acquired infections and those drug fever are common non-infectious causes.1–3 associated with chronic graft dysfunction Rejection accounts for around 4 percent of predominate. episodes.1 Especially of concern among Of significant concern is the subset of malignancy is PTLD as a complication of EBV in infections particularly associated with transplant patients, and 80 percent of these cases transplantation and immunosuppression. CMV is initially present with fever.1,2 one of the most common and important viral All of the relevant exposures and risk factors pathogens. Infection can be asymptomatic or must be considered in the evaluation of fever in symptomatic. It can be due to primary infection, the pediatric transplant recipient. reactivation, or superinfection.2 CMV is one of r Pathophysiology: The pathophysiology of fever is the most common infectious diarrheas in this influenced by a variety of factors, including population, although Clostridium difficile must aspects related to host, donor, infection, and the also be considered. EBV is also important to type of transplantation. consider in transplant recipients. Presentations Many infections in transplant recipients may range from a non-specific viral illness to be a reactivation of a latent infection to which the post-transplant lymphoproliferative disease patient has been previously exposed. CMV and (PTLD), including lymphoma.2 BK viral infection EBV are associated with such reactivation. This is an important cause of nephropathy and renal occurs in the transplant patient because dysfunction in pediatric renal transplant with a 5 anti-rejection medications blunt the immune percent incidence.4 response that would normally keep such r Pneumocystis jirovecii (formerly Pneumocystis infections dormant. Therapeutic carinii or PCP) is a fungal pneumonia with an immunosuppression can also decrease the incidence of roughly 5–15 percent after immunogenicity of vaccines, increasing transplantation. Like the aforementioned viral susceptibility to these infections. Neutropenia infections, this is of particular concern in patients may be seen in transplant recipients and can who are immunosuppressed, and fungal infections directly increase the risk for infection in patients show increased prevalence in this group.4 with organ transplantation. Management of

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febrile neutropenia is discussed in this chapter, regimens. With newer regimens, acute rejection Case 3. episodes may only be detected by laboratory Alternatively, the transplanted organ may testing. contribute to fever in the pediatric transplant r Diagnosis: Physical examination is crucial in population. Donor infections have a high risk of identifying subtle sources for infection. In the transmission to the recipient.1–4 Organ mismatch absence of localizing findings, consideration can be another source for fever, mostly as human should be given for the following:

leukocyte antigen mismatch can precipitate organ r 1 CBCwithdifferential,particularlyfor rejection. Rejection can be acute or chronic, and identification of neutropenia; mediated by cellular, antibody, and humoral r U/A and urine culture, including pyuria that mechanisms. Fevers result from the immunologic may suggest renal rejection; and inflammatory response in these cases. r CXR; The nature of the transplantation itself can r Blood cultures; also contribute to pathophysiologic processes in r some cases. Pediatric transplant recipients often CMV PCR; r receive organs from adult donors, with a resultant Purified protein derivative or QuantiFERON discrepancyinorgansize,whichcanleadtoan testing; increased risk for anastomotic complications such r Antigen detection tests available for as leakage, thrombosis, or necrosis.1 adenovirus, influenza A, RSV, and rotavirus; r Presentation: In transplant recipients, fever is PCR may also be available. defined as a temperature of at least 101 ºFatleast r U/S or CT imaging may help to diagnose twice in a 24-hour period.4 However, the rejection or deep-tissue infection. antimetabolite immunosuppressive drugs While all of these tests need not be pursued in mycophenolate mofetil and azathioprine are all patients, they should be considered as a means associated with lower maximum temperatures to identify common triggers and causes of subtle and leukocyte counts. One of the great challenges presentations following pediatric transplants. with fever in the transplant patient is the broad While a broad evaluation can be considered array of potential etiologies and degrees of for fever in the child with a transplantation, severity, which leads to a wide range of associated work-ups should focus on likely sources of presentations. The clinician must be vigilant to infection. When pulmonary symptoms subtle and atypical presentations, particularly predominate, this could include sputum cultures, given the potential for immunosuppression to Legionella antigen, sputum acid-fast bacillus blunt the infectious and inflammatory response. testing, or direct fluorescent antibody for P. Clinical presentation can suggest the jirovecii.2,4 In contrast, LP and CSF analysis can underlying source of infection, yet the severity of evaluate fever with neurologic symptoms.4 Up to these symptoms is hard to predict. For example, 20 percent of these patients will also require an most pediatric organ recipients experience typical MRI for abscesses, non-focal lesion, and other childhood respiratory and GI illnesses without pathology. Diarrhea can suggest initial evaluation significant issues.3 In contrast, some viral with fecal leukocytes and cultures, C. difficile infections, such as RSV, influenza virus, or testing, and ova and parasites.4 Endoscopy may parainfluenza, can cause severe disease, especially ultimately be needed, with mucosal biopsy and if they occur soon after transplant and during immunohistochemical stains for CMV. In the maximal immunosuppression. interim, blood tests for CMV PCR can help to Malignancy such as PTLD, thromboembolic diagnose. When lymphadenopathy is noted in the disease including pulmonary embolism, drug febrile transplant patient, serum EBV and CMV fever, and acute allograft rejection must also be are particularly warranted. Serologic evaluation considered in the setting of transplant-associated for EBV antibodies is unreliable in the transplant fever.1 The classic presentation of acute rejection patient, and PCR testing of viremia may be with fever and graft tenderness is observed less preferred when a clinical concern exists. In commonly with current immunosuppressive addition, Bartonella (catscratch disease) and

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Toxoplasmosis gondii may be assessed. r Disposition:Mostpatientswithfeverand Lymph-node biopsy is often diagnostic for EBV immunocompromise related to transplantation and PTLD, augmented by using the Epstein–Barr require hospitalization. In some cases, children encoded RNA probe. CT scanning of the neck, with a low-risk fever may be considered for initial chest, abdomen, and pelvis in these patients can or step-down outpatient care, with oral antibiotics characterize the extent of nodal involvement. as needed. This determination should be based on r Treatment: With regard to management of fever a clinical risk stratification strategy. Given the after a transplant, properly targeting the source is complexity of pediatric transplantation, close crucial. However, the etiology is often unknown collaboration with the patient’s primary care and in the early stages and empiric therapy may be specialist providers is essential for all necessary. For example, unless another source of management and disposition planning. fever is apparent, a febrile kidney transplant patient who demonstrates acute renal injury Physical should be treated with empiric antibiotics, Historical clues findings Ancillary studies including Gram-negative coverage, particularly r Immunosuppression r Fever r Renal function Pseudomonas. When prescribing such empiric due to anti-rejection r Non-specific with no findings antibiotics, the provider should consider the most r medications physical of acute kidney likely site of infection, the possibility of Fever with examination injury abdominal pain and findings r No neutropenia antimicrobial resistance, and prior antibiotic use. diarrhea r CMV serology If broad-spectrum antibiotics are used, the positive spectrum should be narrowed as soon as is feasible, to target the specific identified Follow-Up organism. In the hospital, the patient’s transplant surgeon and A low threshold for antiviral therapy is nephrologist were consulted. Infectious disease was appropriate in the transplant patient. Initial consulted, too. The patient was initially placed on treatment of CMV includes IV ganciclovir with broad-spectrum antibiotics with meropenem and concomitant reduction of immunosuppression admitted for further care. Blood cultures and stool (unless there is evidence of rejection).1–4 The use cultures ultimately returned negative. Antibiotics were of effective antiviral therapy has improved discontinued based upon this further evaluation. Due outcomes in this population. For EBV, a stepwise to the positive CMV serology, IV ganciclovir was approach to therapy is recommended, starting administered with concomitant reduction of immuno- with reduced immunosuppression. Similarly, the suppression. Her renal function remained unaffected, consensus supports reducing immunosuppression and her symptoms resolved with treatment. She to treat polyomavirus-associated nephropathy due was discharged following the course of IV antiviral to BK viral infection. therapy. Empiric antifungal treatment can be considered, particularly if the immune suppression is associated with neutropenia.2,4 References When diagnosed, fungal pneumonia from P. 1. Bouza E, Loeches B, Munoz˜ P. Fever of unknown jirovecii can be managed with origin in solid organ transplant recipients. Infect Dis Clin North Am 2007; 21: 1033–54, ix-x. trimethoprim–sulfamethoxazole.2,4 With the potential for non-infectious causes, 2. Green M, Michaels MG. Infections in pediatric solid organ transplant recipients. J Pediatric Infect Dis Soc treatment should address these alternative 2012; 1: 144–51. etiologies if they are identified (for example, treating acute rejection or a pulmonary 3. Lau KK, Giglia L, Chan H, et al. Management of children after renal transplantation: Highlights for embolism). general pediatricians. Transl Pediatr 2012; 1: 35–46. Antipyretics can be considered but are not 4. Munoz˜ P, Singh N, Bouza E. Fever in organ transplant necessarily routinely recommended due to recipients. Antimicrobe: Infect Dis Antimicrob Agents. potential for masking of symptoms and drug Available online at http://www.antimicrobe.org/e54 interactions. .asp (accessed December 2016).

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Case 7 rhinorrhea. Tympanic membranes normal. Tacky mucous membranes, no pharyngeal erythema, no Contributing Author: Sarah Hudgins tonsillar edema/exudates. r Neck: Supple, with no lymphadenopathy. History r Cardiovascular: Heart rate is tachycardic, with a A 20-month-old female presents to the ED with her regular rhythm, no audible M/R/G. Peripheral motherforanevaluationoffever.Themotherstates pulses are thready. Capillary refill Ͼ 3 seconds. that the child is not acting normally and has had sev- r Lungs: Tachypneic, with equal but diminished eral episodes of vomiting as well as difficulty breath- breath sounds bilaterally. Scattered rales, no ing (she described this as “breathing fast as if she wheezing or rhonchi. cannot catch her breath”). The mother first noticed r Abdomen: Soft, non-distended, diffusely tender these symptoms after waking the child for daycare this abdomen, with decreased bowel sounds. No morning. The mother states the child is healthy at base- hepatosplenomegaly. No palpable masses. One line and had no symptoms when she went to bed last episode of hematemesis shortly after arrival. night. The child has had no cough or cold symptoms, r Skin and extremities: Skin is intact and dry, no wheezing or stridor, diarrhea, blood in her vomit or signs of trauma. No edema. stool, dysuria, or rash. She has had no known sick con- r Neurologic: Child moves all four extremities tactsatschoolorhome,hasaPCP,andisUTDonvac- symmetrically, but does not follow commands. cinations. She lives with her mother and father. She is She is lethargic. the middle child of three children with the youngest sibling being less than a month old. Upon further questioning, mom conveys that the Questions for Thought child was found yesterday rifling through one of the r medicine cabinets. The mother states that although her Based on this child’s history and physical childwastryingtodrinkfromasmallbottleinthecab- examination, what tests should be considered? r Knowing the potential time of ingestion, would inet she was stopped just as she was placing it to her lavage be indicated? How about activated lips so “she couldn’t have drank very much.” The child’s charcoal? father has left work to go home in order to determine r What other toxins can present in this way? What the name of the liquid to which the child was exposed. non-toxicologic etiologies are there? The child has had no resolution of dyspnea using her r What tests would help you exclude older sibling’s albuterol nebulizer prior to arrival. non-toxicologic causes for this presentation? Past Medical History r None. Vaccinations are UTD. Diagnosis Medications r Acute salicylate toxicity secondary to methyl r No routine medications. salicylate overdose.

Allergies Discussion r NKDA. r Epidemiology: The unintentional ingestion of pharmaceutical agents is a leading cause of Physical Examination and Ancillary Studies morbidity and mortality in children. Children less r Vital signs: T 103.8 °F, HR 156, RR 60, BP 100/60, than 3 years old account for greater than 35 O2 sat 100% on room air. percent of toxic ingestions, with almost half of all r General:Thechildappearstobeinmoderateto unintentional ingestions occurring in children severe distress, she is tachypneic and lethargic, she less than 6 years of age.1 Annually, approximately will open her eyes on occasion but is not tracking 20,000 of those unintentional ingestions are from or following commands. salicylate products.1 Fatal poisonings from r HEENT: Her head is normocephalic and salicylates have been reported in 5percentof atraumatic. PERRL. No nasal congestion or ingestions secondary to pulmonary and cerebral

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edema, renal failure, and severe acid–base in a downward spiral of complications, in which imbalances.2,3 Delay in diagnosis is a large acidosis leads to excretion issues, which again contributing factor in fatal outcomes. leads to worsening acidosis.2,3 r The number of salicylate-related fatalities has Acid–base imbalances are not the only decreased since the 1980s as a result of aspirin no concerning outcomes of salicylate toxicity. GI longer being a prevalent treatment for children toxicity can result from either the direct due to its association with Reye’s syndrome, more interaction of salicylate with the gastric mucosa or child-resistant packaging methods, and secondarily from neurotoxic effects.2,3 manufacturing limits on the quantities per bottle Dehydration is a common complication of distributed.3 Aspirin and its derivatives are found salicylate toxicity. Up to 10 percent of total body in many formulations and are also a component of water can be lost as a result of vomiting, several well-known over-the-counter products hyperpnea, and fever.2,3 such as Excedrin, Percodan, Bengay creams, and r Presentation: Patient presentation varies greatly Pepto-Bismol. Methyl salicylate (oil of based on the quantity and timing of toxic wintergreen) remains the most potent form of ingestion. The classic triad of salicylism is tinnitus, salicylate available. As little as 5 mL equates to hyperventilation, and GI irritation.3,4 Early 7,000 mg of aspirin, over 85 baby aspirin tablets. manifestations are a combination of potentially Lethaldoseshavebeenreportedinyoung reversible respiratory, GI, and neurologic children with exposure to as little as one teaspoon complications.3,5 Symptoms early in the overdose of methyl salicylate. include: nausea and vomiting, tinnitus and/or r Pathophysiology:Onceconsumed,aspirin vertigo, and anorexia. On presentation, patients products are quickly converted to salicylic acid, can appear well although they will often appear ill. where they are primarily absorbed in the small Patients can be diaphoretic and tachycardic, with intestine. Salicylic acid is metabolized by the liver hyperventilation that can appear as respiratory and excreted in small quantities in the urine, but distress. Later symptoms of salicylism are the inlargedoses,thelivercannotadequately result of severe acid–base abnormalities as well as metabolize the drug load, and urinary excretion pulmonary and cerebral edema.3,5 These becomes increasingly important.3 symptoms can include: fever, lethargy, altered Salicylates typically cause a respiratory mental status, agitation, seizures, hallucinations, alkalosis followed by an anion gap metabolic and renal and respiratory failure. A high index of acidosis.2,3 The first phase of salicylate toxicity is suspicion should be maintained in children and the direct stimulation of the respiratory center of adolescents presenting with these features as a the brain that causes tachypnea, hyperventilation, toxic ingestion history is not always easily and respiratory alkalosis.2,3 Salicylic acid then divulged and delayed treatment can cause causes a metabolic acidosis through the significant morbidity or even mortality. uncoupling of oxidative phosphorylation in r Diagnosis: Although the patient history often mitochondria and the inhibition of the Krebs leads the clinician to consider a toxic ingestion, cycle. This increase in metabolic demand the diagnosis of salicylate toxicity is obtained with combines with the inability to utilize aerobic serum salicylate levels. Based solely on reported metabolism to shift the cells to anaerobic and lipid ingestion, a mild toxicity is defined as consuming metabolism, producing large quantities of lactic between 150 and 300 mg/kg of salicylate.5 A acid and ketone bodies.2,3 moderate to severe toxicity will range from 300 to As only non-ionized salicylic acid is able to 500 mg/kg and a severe toxicity can be found with cross cell membranes, serum and urine pH are any ingestion greater than 500 mg/kg.5 For serum major contributors of salicylic acid distribution salicylate levels, a toxic ingestion is any level and elimination. As non-ionized salicylic acid greater than 30 mg/dL.5 Lethal toxicity can occur more readily crosses the blood–brain barrier, with an acute ingestion level of greater than 100 worsening metabolic acidosis can cause a greater mg/dL or a chronic ingestion level of 60 mg/dL. degree of neurotoxicity.2,3 The non-ionized Additional laboratory studies that should be salicylic acid decreases renal excretion, resulting obtained with salicylate toxicity include: ABG,

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electrolytes, glucose, BUN/Cr, LFTs, coagulation dialysis or filtration system is initiated, it should studies, CBC, serum calcium, U/A, and urine pH. be continued until serum salicylate levels are less These laboratory studies guide treatment by than 20 mg/dL.3 determining the extent of acid–base disorders, Intubation may be required for patients who severity of dehydration, metabolic abnormalities, present with severe toxicity, signs of and underlying organ damage.3 cerebral/pulmonary edema or refractory shock. EKG, CXR, and abdominal X-ray are the The underlying severe metabolic acidosis in standard diagnostic studies used to evaluate for combination with the increased metabolic complications of overdose. Additional tests are demand of salicylate overdose raises specific often used to exclude other diagnoses when the intubation concerns.3 Ventilator settings such as historydoesnotdefinitivelyleadtosalicylate PEEP and respiratory rate will have to be overdose. Differential diagnoses that can mimic secondarily adjusted based on ABG analyses, and salicylate poisoning include diabetic ketoacidosis, it is challenging to meet the patient’s ventilatory sepsis,andotheringestionssuchasironortoxic requirements to allow adequate compensation for alcohols. metabolic acidosis.3 Patients will often require an r Treatment: Treatment for salicylate toxicity will additional bicarbonate bolus as a buffer for the depend on the time elapsed between the patient’s transition, and providers should be prepared to ingestion and presentation to the hospital as well provide emergent hemodialysis upon intubation asthesalicylatelevelandsymptom as ventilator settings are incapable of adequately manifestations.3,5 Patients with known or compensating for the effects of salicylate suspected salicylate ingestion should be poisoning.3 immediately stabilized.3 Patients with toxic r Disposition: If the provider is sure of the dose, the salicylate levels (greater than 30 mg/dL) should be dose is less than 125 mg/kg, and the patient is treated quickly and monitored closely for acute asymptomatic, he or she may be discharged changes. If the patient has presented within 1 hour home.5 The remainder should be observed with of ingestion, gastric lavage is a reasonable repeat aspirin levels, as levels may not peak for 12 decontamination strategy.5 Activated charcoal hours.5 Obviously, any symptomatic patient or should be given at a 1–2 g/kg dose, and repeated any patient requiring intubation or dialysis should every 3 hours during management while be admitted to an ICU. repeating salicylate levels to determine the peak.3,5 The provider should gain IV access, pursue aggressive fluid resuscitation, and correct Historical clues Physical findings any metabolic derangements.3,5 Patients with r r History of witnessed r Fever salicylate toxicity can be severely dehydrated upon accidental ingestion Tachypnea r Altered mental status r Signs of cerebral edema (lethargy) presentation, often losing several liters of fluid r Vomiting r Signs of GI toxicity (hematemesis) prior to arrival. Bicarbonate drips should be r Tachypnea by report r Signs of pulmonary edema (rales) adjusted to maximize urine output and urine pH (goal of at least 7.5).3,5 Patients will require repeat laboratory tests (ABG, electrolytes, and salicylate Follow-Up levels) every 1–2 hours as well as close monitoring Father called the hospital 20 minutes later stating of blood glucose levels.3 that he found a partially empty bottle of wintergreen Hemodialysis will be necessary for patients oil in the medicine cabinet. He was asked to mea- who have salicylate toxicity levels greater than 100 sure the remaining liquid from the 100 mL bottle mg/dL, critical symptoms (defined as signs of which revealed 12 mL, a little over two teaspoons, was either pulmonary or cerebral edema or a severe missing. acid–base imbalance), or those patients not After arriving to the hospital, the child rapidly responding to conservative treatment.3,5 deteriorated and required intubation. Her salicylate Exchange transfusions can be considered for levels returned at 110 mg/dL. The child was treated young infants when there is significant with IV fluids as well as bicarbonate infusions and hemodynamic instability. Once a method of immediately transitioned to hemodialysis. She was

16:13:00 7 05 Chapter 4: Fever senttothePICUwhereshecontinuedtohavehourly Jersey.Thecarwasnotleftintheshade.Thechildhas laboratory tests (ABG, electrolytes, salicylate levels). not had any recent illnesses, and was in her usual state Despite the provider’s exhaustion of all available treat- of health this morning. ment options, the child continued to clinically deteriorate, progressed to a coma, and died later that after- Past Medical History noon. Based on the missing amount of liquid from the r Inguinal hernia with repair shortly after birth. bottle of wintergreen oil, the maximum amount the Immunizations are UTD. child could have consumed would have been the equivalent of 16,000 mg of aspirin – over twice the lethal Medications dose for her age. r None. Allergies References r 1. Poison Control: National Capital Poison Center. Peanuts and red dye. Poison statistics: National data 2014. Poison Statistics National Data 2014. See www.poison.org/ Physical Examination and Ancillary Studies poison-statistics-national (accessed December 2016). r Vital signs: 103.7 °F, HR 171, RR 36, BP 108/67, 2. Defendi GL. Acute salicylate toxicity in children: O2 sat 100% on room air. Diagnosis and treatment of over ingestion. CPF 2013; r General:Thechildisirritableandawake, 12: 547–52. consolable, and calling for her mother. 3. O’Malley GF. Emergency department management of r HEENT: PERRL. Oropharynx with tacky mucous the salicylate-poisoned patient. Emerg Med Clin N Am membranes. No tears. 2007; 25: 333–46. r Neck: Supple and non-tender, with no adenopathy. 4. Frithsen IL, Simson WM. Recognition and r Cardiovascular: Tachycardic and regular, no management of acute medication poisoning. Am Fam Phys 2010; 81: 316–23. M/R/G. r Lungs: Clear and equal, with no W/R/R. 5. Dargan PI, Wallace CI, Jones AL. An evidence-based r flowchart to guide the management of acute salicylate Abdomen: Soft and non-tender. No masses or (aspirin) overdose. Emerg Med J 2002; 19: 206–9. guarding. r Skin and extremities:Skinisclammyand diaphoretic. The child has gooseflesh. Case 8 r Neurologic: Irritable. Moves all four extremities Contributing Author: Rebecca Jeanmonod symmetrically.

History Questions for Thought A 20-month-old girl is brought to the ED by a panicked r Whatareappropriatewaystocoolthechild? father with concern for her temperature. Dad was sup- Does the child need to be cooled? posed to drop the child at daycare this morning, which r How do you determine which children require is a break in his usual routine. Typically, the child is extensive laboratory evaluation and which can brought by her mother, but her mother is out of town be observed and treated with supportive care? r on a business trip. Dad put the child in the car, but in Do you need to contact CPS? r the course of his drive, the child fell asleep, and he for- How do you clinically distinguish among got she was there. He went to work and left her in the diﬀerent kinds of heat illness? car. His wife called his office about 2 hours into his workday to ask how he was doing as a “single dad,” and he immediately realized his mistake. He ran out to Diagnosis the car to find his daughter still buckled into her front- r Heat exhaustion. facing car seat. The child was upset and crying. She had vomitonhershirtandcarseat.Shefeltverywarmto Discussion touch, so he brought her in for evaluation. The car has r Epidemiology: Although death from heat stroke is dark upholstery. It is July and the family lives in New relatively rare, heat illness is common, accounting

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for approximately 325,000 ED visits each summer Exertional heat stroke is most common in in the USA.1 When heat stroke occurs, the case school-aged athletes who exercise excessively in fatality rate is about 50 percent, but most patients warm environments, such as football practice with heat-related illness are discharged home during the summer months.2,3 Regardless of the from the ED.1 The overall incidence of type of heat stroke, the end result is the same. As heat-related illness is likely much higher than body temperature continues to rise and these numbers indicate, as it is probable that dehydration decreases sweat production, the child many cases of more mild heat illness are treated in develops SIRS.2 Heat-sensitive organs, such as the the field. brain and the liver, become affected, and the child r Pathophysiology: The body produces heat may develop cardiomyopathy and disseminated continuously, and maintains a constant intravascular coagulopathy.2 In fatal cases, diffuse temperature gradient to allow for dissipation of serosal petechiae and pulmonary edema are that heat from the core to the periphery.2 Sweating common.2,6 At temperatures above 107 °F, also allows for cooling through evaporation. proteins denature and cell death occurs. Children have less efficient sweating and therefore r Presentation: Heat illness includes prickly heat (a have less ability to cool by this mechanism, benign rash that is typically pruritic, which is although their larger surface areas allow for more secondary to keratin plugs blocking sweat ducts), heat dissipation through convection.2,3 However, heat-related edema (dependent edema from since sweating is the body’s predominant cooling vasodilation), and heat-related syncope mechanism, children have less ability to cool. (orthostatic syncope related to vasodilation). Additionally, children’s large surface area allows These are not associated with elevated core them to increase their temperature more quickly temperature and are benign. More severe forms of than adults by the mechanism of convective heat illness include heat cramps, heat exhaustion, warming when in a warm environment.2 This or heat stroke.Heatstrokecanbefurtherdivided combination of decreased ability to dissipate heat into classic heat stroke and exertional heat stroke. with an increased ability to absorb heat makes r children more prone to heat-related illness. Heat Heat cramps are severe, typically lower 2,3 illness occurs when the body’s ability to cool is extremity cramps that occur after exertion. inadequate to match the environmental or They are often attributed to hyponatremia endogenous heat burden and is overwhelmed.2–4 secondary to sodium losses during sweating, Classicheatstroke(heatstrokefromincreased and although they are painful, they typically do ambient temperature in a patient with normal not occur in conjunction with elevated core 2,3 endogenous heat production) and exertional heat temperature. stroke (heat stroke from increased production of r Heat exhaustion is characterized by an inability heat secondary to activity, in addition to increased to continue activities secondary to heat, often Ͻ ° 2,4 ambient temperatures) affect different pediatric with increased temperature to 104 F. populations. Classic heat stroke is more common Common presenting symptoms include in small children who cannot remove themselves increased thirst, irritability, nausea, vomiting, from the hot environment and cannot access diarrhea, headache, tachycardia, weakness, and 2,4 fluids on their own, such as our patient.2,3 heavy sweating. Patients may have Children entrapped in cars are subjected to piloerection from sympathetic stimulation. temperatures much higher than the outside r Heat stroke isthemostsevereformof temperature. As the sun warms the interior heat-related illness. It is characterized by a surfaces within the car, and subsequently the air temperature Ͼ 104 °Fandalteredmental in the car, the hot air cannot escape. The surfaces status.2,4 Patients may lack sweating, but this is within the car can reach temperatures in excess of not a prerequisite to make the diagnosis. Since 180 °F, and the air temperature in the car can heat exhaustion and heat stroke exist on a reach 150 °F within 15 minutes.5 Leaving a continuum, patients may have some elements car window open does not significantly alter of heat exhaustion and some features of heat this. stroke. In these cases, the provider should err

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on the side of treating the patient for heat neck, and groin to assist in cooling.2 Although it is stroke, as heat stroke has a high mortality and impractical in most institutions to submerge heat requires aggressive intervention. These patients stroke patients in cold water, this is probably the maybeobtundedorseizing,ormayhavesubtle best way to cool a patient.2,4 Arealisticoptionis alterations in mental status. It is important to to spray the patient down with water from a spray get a core body temperature on all patients bottle and use a large fan to assist in evaporative with symptoms consistent with heat stroke, as cooling. Patients who have cooling measures other forms of temperature assessment have provided within 30 minutes of recognition of heat been found to be unreliable. stroke have lower mortality than those with a r Diagnosis: Diagnosis is clinical, based on history, delay to cooling, and therefore EMS providers core temperature, and presenting symptoms. It is should be educated and should begin cooling 2 not necessary to get further ancillary testing in measures in the field when possible. Patients with patients with heat cramps or in patients with mild heat stroke who develop multi-system organ heat exhaustion. These patients generally have failure may require intubation and more normal or near-normal laboratory findings, and aggressive supportive measures. there is no role for imaging. In patients with In patients with a disease that is unclear in severe heat exhaustion in whom heat stroke is a severity, attempts may be made at oral rehydration diagnostic consideration and in those with heat and supportive care. If the patient’s symptoms are stroke, extensive laboratory testing is indicated. notimprovedat30minutes,moreaggressive evaluation and treatment should be undertaken. These patients can develop rhabdomyolysis, renal r failure, and disseminated intravascular Disposition:Patientswithmildillness(heat coagulopathy. Therefore, they should have CBC, cramps or heat exhaustion with elevated core electrolytes, coagulation studies, calcium, temperature but no altered mental status) may be magnesium, phosphorus, creatine kinase, and treated and observed in the ED for symptom lactate levels checked. In patients in whom the resolution, and discharged home. Most patients diagnosis is not clear, toxic causes (for example, with heat stroke require admission to the hospital, sympathomimetics, anticholinergics, aspirin, and those with laboratory derangements will often psychiatric medications, serotonergic require ICU-level care. For children who are left medications), infectious causes, endocrine causes in vehicles or who are playing unattended and (such as thyroid), drug withdrawal, and become entrapped in vehicles, CPS should be neurologic causes should be considered.2 These consulted for concern of neglect. patients may require further ED testing such as neuroimaging, toxicologic screening, and LP to Historical clues Physical findings define the source of the symptoms. r r r Left in vehicle Fever Treatment: Mild disease requires little more than r Vomiting r Tachycardia supportive care and provision of oral rehydration r r Irritability fluids. This will typically improve symptoms from Clammy skin with gooseflesh heat-related syncope as well as heat cramps. The major goals of treatment for patients with more severe disease are to rapidly cool the patient Follow-Up and to restore circulating volume, as most of these IV access was established and the child received a total patients are hypovolemic. Initial resuscitative of 30 cc/kg normal saline. Her clothing was removed, measures should begin with the ABC algorithm, she was sprayed with water, and a fan was brought as in any sick patient. IV access should be into the room to aid with cooling. She received IV established, and the patient should be volume ondansetron for her nausea. Because the child was resuscitated with room-temperature normal irritable and it was unclear if she had altered mental saline. This by itself will assist in cooling the status, she had laboratory testing performed includ- patient’s core. Excess clothing should be removed. ing CBC, electrolytes and renal function, glucose, cre- Ice packs may be placed at the patient’s axillae, atine kinase, calcium, magnesium, and phosphorus.

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The child had mild hyponatremia and a slightly low Medications bicarbonate, but the remainder of her laboratory val- r None. ues were unremarkable. Her symptoms improved over thecourseof2hoursintheED.CPSwerecontacted because of the nature of the child’s presentation, and Allergies r they planned to follow up with the family within 24 Seasonal allergies. hours. The child was discharged home with her father r Sulfonamide antibiotics – nausea only. after her ED stay. Physical Examination and Ancillary Studies References r Vital signs: T 100.5 °F, HR 99, RR 20, BP 124/79, 1. Hess JJ, Saha S, Luber G. Summertime acute heat O2 sat 98% on room air. illness in U.S. emergency departments from 2006 r General: Well-developed and well-nourished. No through 2010: Analysis of a nationally representative obvious distress. sample. Environ Health Perspect 2014; 122: 1209–15. r HEENT: PERRL. No signs of trauma. Moist 2. Atha WF. Heat-related illness. Emerg Med Clin N Am mucous membranes. Clear oropharynx. 2013; 31: 1097–108. r Neck: Supple neck, with no Brudzinski’s sign. No 3. Bytomski JR, Squire DL. Heat illness in children. Curr nuchal rigidity. He has tenderness to the posterior Sports Med Rep 2003; 2(6): 320–4. c-spine with bilateral paraspinal tenderness and 4. Becker JA, Stewart LK. Heat-related illness. Am Fam pain with range of motion. Phys 2011; 83: 1325–30. r Cardiovascular: Regular tachycardia. No M/R/G. 5. FerraraP,VenaF,CaporaleO,etal.Childrenleft r Lungs: Normal work of breathing, lungs are clear, unattended in parked vehicles: A focus on recent with normal breath sounds. Italian cases and a review of literature. Ital J Pediatr r 2013; 39: 71. Abdomen:Soft,withnormalbowelsounds.No tenderness, distension, guarding, or rebound. 6. AdatoB,Dubnov-RazG,GipsH,etal.Fatalheat r stroke in children found in parked cars: Autopsy Extremities and skin: Normal range of motion, findings. Eur J Pediatr 2016; 175: 1249–52. with warm and perfused extremities. Normal capillary refill. r Neurologic: Cranial nerves intact, alert and Case 9 oriented, non-focal examination. r Pertinent laboratory values: WBC 7,700, Hb 13.6, Contributing Authors: Keel Coleman and rapid strep positive, monospot positive. Khalief Hamden Electrolytes and LFTs normal. r Pertinent imaging: EKG shown in Figure 4.1. History The patient is a 17-year-old male who presents with a complaint of headache. The patient reports a fever Questions for Thought (103 °F) at home, starting yesterday, that improved r How do patients typically present with this with acetaminophen. The onset of the headache was illness? 3 days ago, and is associated with blurred vision, vom- r What laboratory ﬁndings would support this iting (one episode this morning), sore throat, and neck diagnosis? pain. He also complains of back pain after hitting a r What EKG changes are typically found in patients deer in his vehicle last week. The patient denies diar- with this disease? rhea, difficulty breathing, abdominal pain, ear pain, r What treatments should be initiated in the ED? r sinus symptoms, or chest pain. The patient reports a What is the deﬁnitive treatment of this condition? history of recurrent migraines in the past.

Past Medical History Diagnosis r Migraine headaches. r Acute viral perimyocarditis.

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Figure 4.1 EKG demonstrating normal sinus rhythm with J-point elevation in leads I, II, aVL, aVF, V2, and V3.

Discussion malignancy-related diseases, metabolic and r Epidemiology: Pericarditis is responsible for up to endocrine disease, trauma, and iatrogenic 1,2 5 percent of all non-ischemic chest pain causes. Malignancy-related pericardial disease presenting to EDs in developed countries.1,2 In isthemostfrequentcausativefactorof 5 patients with ST elevation, pericarditis is tamponade from effusion in developed countries. identified as the etiology of the EKG findings in1 Uremia accounts for up to 10 percent of cases percent of cases.3 The actual incidence of reported in patients with advanced renal failure pericarditis is likely much higher, but is difficult to prior to initiation of dialysis. Although rare in diagnose. Subacute cases may go unrecognized North America, in developing countries due to the lack of clinical significance, and acute tuberculosis-induced pericarditis is a significant 1,2 cases may present non-specifically.1,2,4 The source of mortality and morbidity. Pericarditis majority of recorded cases in developed countries is more common in men than women, and is (40–90 percent) are idiopathic; however, it is predominantly an adult disease. However, in postulated that many idiopathic cases actually children, there is a bimodal age distribution have a viral etiology.1,2 When an infectious agent affecting primarily young children under 2 years 4 isidentified,viralismorecommonthanbacterial. of age and adolescents (14–18 years). r Non-infectious causes of pericarditis include Pathophysiology: Inflammatory cell infiltration of autoimmune diseases (3–5 percent), the pericardium is the primary mechanism of

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injury in pericarditis. There are three r Suggestive changes on electrocardiography inflammatory subtypes found along the spectrum (widespread ST-segment elevation or PR of disease: (1) dry, (2) serous, and (3) fibrinous. depression); Dry pericarditis involves inflammation of r New or worsening pericardial effusion. pericardial tissue that does not include epicardial Additional supportive criteria may include: vessel permeability. In contrast, serous r pericarditis results when a protein-rich exudate is Elevation of markers of inflammation (e.g. deposited along the pericardial wall, with ESR, CRP, or WBC); r resultant effusion. Fibrinous pericarditis follows Evidence of pericardial inflammation by an serous pericarditis as the fibrinogen in the imaging technique (CT or MRI). exudate is converted to fibrin, resulting in Perimyocarditis may be discernible by the deposits along the normally smooth elevation of injury markers (e.g. troponin or visceral–parietal interface. creatine kinase). r Presentation:Chestpainisthemostcommonly r Treatment: The complaint of chest pain or identified complaint in the patient suffering with diagnostic tests revealing potential cardiac pericarditis.1,2,4 The pain is often pleuritic, but instability warrants a thorough evaluation for may be described as pressure, aching, sharp, or life-threatening causes. When there is diagnostic dull. Radiation is not common but referred pain certainty that the entity being evaluated is in fact to the trapezius, arm, or jaw may be present. The pericarditis, the mainstay of treatment remains pain may be worsened by reclined positioning or NSAIDs.1,2,4,6 Ibuprofen is considered first-line swallowing. Improvement is often noted when the therapy and a weight-based dose should be given patientispositionedtoleanforward.Inthe every 6 hours (up to 3,200 mg/d). Acetylsalicylic setting of effusion, dyspnea is frequently acid (2–4 g/d) and indomethacin (75–150 mg/d) reported.1–4 Cough, dysphagia, and low-grade are considered second-line. Indomethacin has fever frequently accompany the complaint of chest specific drawbacks of reducing coronary flow and pain.1,2 Night sweats and weight loss may be a poor side-effect profile. Colchicine (0.5 mg/d) reported by those afflicted by malignancy or hasalsobeenusedinadditiontoNSAIDsin tuberculosis. On physical examination, children children, but support for doing so is limited to are often ill-appearing and tachycardic.1,2,4 A several case series and expert opinion.4 In adults, careful examination to evaluate for signs of heart thereisconvincingevidencethattheuseof failureisimperativeasthismayindicate colchicine can prevent recurrent pericarditis.1,2 constrictive pericarditis or pump failure from Low-dose corticosteroids (0.25–0.5 mg/kg per perimyocarditis. The astute physician should also day) are recommended only for cases that are keep in mind that the presence of a friction rub refractory to NSAIDs.1,2 may indicate the presence of a pericardial effusion r Disposition:Clinicaldecisiontoolstogradethe while muffled heart sounds associated with degree of illness may be of assistance in treatment jugular venous distention and hypotension and disposition. Absence of all of the following increases the likelihood of a large effusion and complicating factors increases the likelihood that pericardial tamponade. a patient is safe for outpatient treatment and r Diagnosis: The European Society of Cardiology discharge: fever greater than 100.4 °F, subacute guidelines are the only international guidelines onset, immunosuppression, trauma, oral assembled for the diagnosis of pericarditis.1 anticoagulation therapy, NSAID treatment failure, The criteria for the diagnosis of acute perimyocarditis, and severe effusion or pericarditis include at least two of the tamponade.1,6 following:1 Physical r Chest pain (sharp and or pleuritic, worsened Historical clues findings Ancillary studies by supine position improved by sitting up and r Fever r Tachycardia r Abnormal EKG leaning forward); r Non-specific symptoms r Fever r Positive troponin r r Pericardial friction rub; Recent viral illness

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Follow-Up References The child had a troponin drawn, which showed an ele- 1. Adler Y, Charron P, Imazio M, et al. 2015 ESC vated level of 0.25 (reference range Ͻ0.08). A repeat guidelines for the diagnosis and management of level was 0.41. Because this patient had the combi- pericardial diseases: The Task Force for the Diagnosis nation of an abnormal EKG and elevated troponins and Management of Pericardial Diseases of the and the diagnosis was uncertain, he was given a single European Society of Cardiology (ESC) endorsed by The European Association for Cardio-Thoracic dose of acetylsalicylic acid (325 mg) as thrombosis pre- Surgery (EACTS). Eur Heart J 2015; 36: 2921–64. vention for the concern of myocardial infarction. The patient was transferred to a tertiary care facility, where 2. Imazio M, Gaita F, LeWinter M. Evaluation and treatment of pericarditis: A systematic review. JAMA he was admitted to the PICU. The patient was started 2015; 314: 1498–506. on IV fluid therapy, antipyretics for fever and antibi- 3. Brady WJ, Perron AD, Martin ML, et al. Cause of ST otics for streptococcal pharyngitis. His troponins were segment abnormality in ED chest pain patients. Am J trended every 6 hours and peaked at 1.88 ng/mL after Emerg Med 2001; 19: 25–8. about 24 hours. He had an echocardiogram which was 4. Bergmann KR, Kharbanda A, Haveman L. Myocarditis foundtobenormal.Thepatientwasevaluatedbypedi- and pericarditis in the pediatric patient: Validated atric cardiology who felt the diagnosis was a mild case management strategies. Pediatr Emerg Med Pract 2015; of perimyocarditis due to the lack of chest pain and 12: 1–22. characteristic changes on the EKG. The patient was dis- 5. MerceJ,Sagrist´ a` Sauleda J, Permanyer Miralda G, chargedhometofollowupwithpediatriccardiology et al. Pericardial effusion in the elderly: A different to ensure the return to baseline of his troponins and to disease? Rev Esp Cardiol 2000; 53: 1432–6. clear him to resume physical activity. On follow-up, the 6. Imazio M, Demichelis B, Parrini I, et al. Day-hospital patient continued to improve and his EKG returned to treatment of acute pericarditis: A management normal. program for outpatient therapy. JAmCollCardiol 2004; 43: 1042–6.

16:13:00 05 Chapter5 Eye, Ear, Nose, and Throat Complaints

Case 1 membrane and no foreign body. Hearing is symmetric. Contributing Authors: Jason Schwaber, r Neck: Supple, with no lymphadenopathy. r Cardiovascular:Regular,withnoM/R/G.Good Taylor R. Spencer, and Rebecca Jeanmonod perfusion and normal capillary refill. History r Lungs: Normal work of breathing, CTA bilaterally, The patient is a 6-year-old boy who is brought in by with no W/R/R. r his mother, stating: “I put a pencil in my ear,” while Abdomen:Soft,withouttenderness.Nomasses. at school. He denies any headache, dizziness, bleeding, Normal bowel sounds. r hearing changes, discharge, or vomiting. His mother Skin and extremities: No rashes, full range of reports that he had tympanostomy tubes at age 2, but motion, warm, and well-perfused. “they fell out years ago.” r Neurologic: Alert and interactive. Cranial nerves II–XII intact. Normal for age. Past Medical History r Seasonal allergies. Questions for Thought r What dictates the urgency of foreign-body Medications removal? r r Fluticasone 50 mcg intranasal. What other structures can be damaged during foreign-body placement and removal? r When should ENT be consulted or the patient Allergies referred? r r NKDA, has tree pollen allergies. What other body areas should be examined for foreign bodies? Physical Examination and Ancillary Studies r Vital signs: T 98.4 °F, HR 98, BP 104/74, RR 22, O2 sat 98% on room air. Diagnosis r r General: Well-developed, well nourished Foreign body in external auditory canal. school-aged child sitting in bed. He is anxious but consolable. Discussion r HEENT: PERRL. Nares are clear bilaterally, r Epidemiology: Children presenting with foreign oropharynx with moist mucous membranes. bodies in the ear have a median age of 8, slightly Teeth O and P are missing. Tonsils have no older than those with nasal foreign bodies.1 Older exudate. Right ear with pencil core in external children and adults will sometimes present with canal 2 mm from tympanic membrane. Mild objects in their ears, as well. They are more often superficial laceration of canal. Tympanic foundintherightear,perhapsbecauseof membrane is translucent with an area of handedness.1 Multiple objects have been found in tympanosclerosis. Left ear with normal tympanic ear canals, including insects, beads, paper,

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pebbles, organic material, small batteries, and bodies pass without incident into the stomach, hearing aids.1 Nasalforeignbodiesarealso sharp objects, long objects, and large objects may commonly seen in children. Common items all get stuck. include food, beads, buttons, paper, cloth, and r Presentation: In the majority of cases, the child is candle wax.1 Esophageal foreign bodies are broughtinbyacaregiverwhowitnessedthechild commonly coins, but batteries, sharp objects, and place the foreign body. For ear foreign bodies, food objects can be seen. children may also report pain, bleeding, hearing r Pathophysiology: The extent of harm depends on loss, or ear discharge.1 Less commonly, the child the object involved, its location, and its duration. may present with cellulitis or other evidence of In the ear, sharp materials can lacerate the fragile infection. Some foreign bodies are found during skin of the external auditory canal or tympanic routine medical care for another issue. membrane.1 Drainage of cerumen from the ear Nasal foreign bodies are also commonly can be blocked by organic materials that swell witnessed. Children may also present with pain or with moisture.1 Insects cause irritation and local bleeding. They may also present with a voice tissue reaction as well as vertigo.1 Button batteries change (a nasal voice), unilateral nasal drainage, a that leak contents cause necrosis of the foul odor from the child’s nose, or evidence of surrounding tissues and can be very destructive.1 infection.1 Up to 25 percent of nasal foreign Any foreign body that is present for a long period bodies present greater than 24 hours after of time can cause infection and tympanic placement and are unsuspected by the caregiver. membrane perforation. In these cases, if the foreign body is not visualized, The nose consists of two nasal fossae separated the diagnosis is often made by ENT when the by a vertical septum and subdivided into three child is referred for examination to rule out passages by the nasal turbinates. Nasal foreign tumor, mass, or anatomic abnormality causing bodies are usually lodged below the inferior chronic nasal drainage. turbinate, or anterior to the middle turbinate. In Esophageal foreign bodies may be the nose, foreign bodies may cause similar asymptomatic or may cause respiratory complications to those in the ear. Sharp objects compromise or drooling and pain. They are may cause direct trauma, and large objects, those sometimes diagnosed incidentally during which have expanded from absorbing moisture, evaluation for cough or pneumonia. In children can prevent sinus drainage and lead to secondary with lodged button batteries, the presentation may sinus infection.1 Button batteries may cause septal be dramatic and rapidly progressive, with erosion and subsequent saddle nose deformity or esophageal perforation and fulminant collapse. mayleadtonecrosisofotherfacialstructures.1 r Diagnosis: The diagnosis of ear or nasal foreign They can produce nasal or choanal stenosis. body is made by history and physical Obstruction of the sinuses by swelling can lead to examination. The provider should use an otoscope secondary rhinosinusitis. Other infectious to detect ear foreign body or a nasal speculum to complications reported from nasal foreign bodies assess for nasal foreign body. Children should have been reported including otitis media, have both ears and nose evaluated, since some periorbital cellulitis, and meningitis. Nasal foreign children may have several foreign bodies. The bodies also pose the risk of object aspiration into provider should assess for presence of infection as the pulmonary tree. For further discussion of well as complications of foreign body, such as foreign-body aspiration, please see Chapter 3, tympanic membrane perforation. The provider Case 1. should also test and document cranial nerves as In the esophagus, foreign objects may be well as conductive vs. sensorineural hearing with lodged at any of the three narrowings within the the Rinne test with a 512 hertz tuning fork. esophagus: proximal esophagus at the thoracic Esophageal foreign bodies are also typically inlet, mid esophagus at the carina and aortic arch, diagnosed by history. In the case of swallowed or distal esophagus at the gastroesophageal metallic objects, radiography is quite helpful. junction. Although most esophageal foreign Coins in the esophagus will appear en fasse on

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mineral oil or lidocaine.1 Theinsectcanthenbe irrigated out of the ear.1 Although forceps can be used to pull out beetles, for insects such as spiders forceps may simply serve to dismember the insect, resulting in multiple foreign bodies. For inorganic firm smooth objects in ears, suction or irrigation may be successful. Occasionally, a right-angle hook can be advanced just distal to the object and used to dislodge the object from the canal. In the nose, a small catheter with a balloon may be advanced past the object, the balloon inflated, and the object pulled out.1 A single positive pressure breath through the mouth with occlusion of the unaffected nostril or positive pressure oxygen directly into the unaffected nostril can also dislodge the object, particularly if the object is filling much of the nasal canal, such as in cases of crayon foreign body.1 Round smooth objects in ears have a high rate of removal failure in the ED, and are more likely to require specialist care or sedation.2 Organic foreign bodies, such as popcorn in either the nose or the ear, may be removed with forceps. These should not be irrigated, as irrigation may cause them to swell and become Figure 5.1 Anterior–posterior CXR demonstrating a penny stuck more difficult to remove.1 in the esophagus at the level of the thoracic inlet. Batteries pose a true emergency. They can cause low-voltage electrical currents and anterior–posterior film, whereas those in the destruction of tissue. They can leak at any time trachea will appear edge-on (Figure 5.1). Button after placement, causing irreversible tissue batteries can be identified by their size and often destruction from sodium hydroxide and chlorine by their rounded edge, which distinguishes them gas, or they can cause liquefactive necrosis from from coins. Food boluses which are impacted are their alkaline contents. Therefore, although it is typically diagnosed by history, followed by reasonable for the provider to attempt to remove endoscopy. them (taking great care not to crush the battery), r Treatment: For any foreign-body removal, the goal the child should be seen by ENT for immediate is to remove the foreign body with minimal risk to removal if the provider fails. Batteries should the patient while maximizing patient comfort. It is NOT be irrigated out of ears. important that you make your first attempt at Magnetic foreign bodies in the nose create a foreign-body removal your best attempt, as risk for pressure necrosis and septal perforation, success in foreign-body removal decreases with and also require prompt removal. subsequent attempts. Emergency medicine Esophageal foreign bodies are usually providers are commonly successful at removed by a gastroenterologist by endoscopy if foreign-body removal, but round ungraspable the foreign body is in the lower portion of the objects increase the rate of failure.2 The method of esophagus, but are sometimes removed by ENT or retrieval depends on both the object location and pulmonologyiftheyarehighup.Youshould the physical characteristics of the object.1,2 become familiar with the regional differences or For live insects in the ear, the provider should particular practices of your hospital. For rounded begin by killing or immobilizing the insect with items that are not batteries, it is within the

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standard of care to allow the item 24 hours to pass with alligator forceps under direct visualization and spontaneously so long as the child has reliable retrieved in a single attempt. Examination after follow-up and can handle his or her secretions. removal demonstrated a small laceration to the exter- These children may be admitted for observation nal auditory canal. The patient was prescribed otic ormaybedischargedtoreturninadayfora ciprofloxacin–dexamethasone solution twice a day and repeat CXR to track progress. Once the object referred to his PCP for follow-up in the next 5–7 days. passes the pylorus, it is likely to continue on through the GI tract. Batteries and long, sharp References objects should be removed emergently. Since 1. Heim SW, Maughan KL. Foreign bodies in the ear, some parents lack the means to bring their child nose and throat. Am Fam Phys 2007; 76: 1185–9. back to the hospital promptly, it is appropriate to 2. Thompson SK, Wein RO, Dutcher PO. External remove objects that are lodged at the time of auditory canal foreign body removal: Management presentation where services are immediately practices and outcomes. Laryngoscope, 2003; 113: available, even if the object is rounded and lower 1912–15. risk,asmanywillstillremainlodged. The Academic Life in Emergency Medicine blog has After removal, the child should be examined multiple articles on particular techniques for particular again to ascertain any injury that was masked by types of foreign objects. See www.aliem.com. the foreign-body presence, or that occurred secondary to its removal. Potential complications of ear foreign-body removal include laceration of Case 2 thethinskinoftheexternalauditorycanal, formation of a hematoma, facial nerve palsy, Contributing Author: Edwin Layng perforation of the tympanic membrane, History disruption of the ossicular chain, and movement An 8-year-old girl presents to the fast track area of your of the foreign body proximally. For noses, ED with a complaint of bleeding from her right nos- complications include bleeding, pushing the tril for the past 3 hours. Her mother tells you that she object deeper, or inadvertent dislodgement into has recently recovered from a URI, in which she had the airway. r a low-grade fever as well as coryza for the past week. Disposition: Patients with ear foreign bodies that Upon questioning, the patient admits to picking her are successfully removed without complications nose earlier in the day and that the bleeding began can be discharged home. Patients with laceration shortly after that. The mother has tried putting tissue to the canal or tympanic membrane perforation paper under the bleeding nostril as well as instructing require otic antibiotics such as ciprofloxacin– the child to “tilt her head back,” but neither of those 1 dexamethasone and outpatient follow-up. Those techniques were able to stop the bleeding. The child with objects that cannot be removed require ENT has no complaints of dyspnea, swallowing blood, nau- consultation or referral for removal with sea, vomiting, diarrhea, fever, or chills. She denies any microscopy or in the OR. Button batteries need recent trauma. This is the child’s first nosebleed and emergency removal. Esophageal foreign bodies there is no family history of bleeding diathesis. may be removed endoscopically, after which the child may be discharged home. Past Medical History r Asthma. Historical clues Physical findings r Eczema. r Report of child placing object r External auditory canal in ear r foreign body Laceration Medications r Albuterol inhaler. Follow-Up After discussion of the risks and benefits with the Allergies r parent and the patient, the pencil core was grasped Pollen, dust, and mold.

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Physical Examination and Ancillary Studies and should prompt consideration of trauma or r 4 Vital signs: T 99.2 °F, HR 95, BP 100/60, RR 20, O2 serious illness. Resolved nosebleeds in infants sat 99% on room air. may be secondary to attempted smothering or r General:Uncomfortable-appearingchild,awake suffocation. Roughly 10 percent of epistaxis in and alert, leaning forward in bed. children is caused by bleeding diatheses, including r HEENT: There is a moderate amount of blood blood-clotting disorders, telangiectasis, juvenile flowing from the right nostril. Upon examination angiofibroma, von Willebrand’s disease, and with a nasal speculum, bleeding is seen in the idiopathic thrombocytopenia purpura. Children antero-inferior part of the right nasal septum. with systemic predisposing factors rarely present with self-limited bleeds. There is no bleeding from the left side. No septal r hematoma. No blood in the oropharynx. Mucous Pathophysiology: The nose functions to humidify membranes are moist. and warm air as it passes through to the lungs as r Neck: Supple, with a midline trachea and no well as to filter allergens, irritants, and pathogens. adenopathy. As such, it has a large surface area with a thin, r Cardiovascular: Regular rate and rhythm, with no highly vascular mucosa that provides little M/R/G. Good capillary refill. support or protection to the underlying blood vessels. These characteristics predispose the nasal r Lungs:CTAbilaterally,withnoW/R/R. mucosa to bleeding. The major source of bleeding r Abdomen: Soft with no tenderness, no masses, no in most patients is Kesselbach’s plexus, a highly distension. r vascular area in the anterior nasal septum formed Skin and extremities:Noedema,clubbing,or by the anastamosis of the anterior ethmoidal cyanosis. No bruising or petechiae. artery, the lateral nasal branch of the sphenopalatine artery, and the superior labial Questions for Thought artery. Posterior bleeds arise from branches of the sphenopalatine or posterior ethmoidal arteries r What is the most common location of bleeding in pediatric epistaxis? that supply the posterolateral wall and the r posterior choanae. What is the treatment algorithm for pediatric r epistaxis? Presentation: The majority of children present r Are prophylactic antibiotics indicated, and if so, with self-limited bleeding from one or both nares. which? Anterior bleeds are more commonly unilateral, r What are other diagnoses that should be although it is possible to have bilateral anterior considered in young infants and neonates with bleeding or reflux of blood from an anterior bleed epistaxis? into the nasopharynx with subsequent leakage out the other side. Digital trauma from nose-picking is by far the most common cause of anterior nosebleeds in children. Other types of trauma to Diagnosis r the face are also commonly encountered. If there Anterior epistaxis. is purulent discharge associated with the nasal bleeding, one should consider a nasal foreign Discussion body. r Epidemiology: Epistaxis is very common in Posterior nosebleeds are more often bilateral, children and the vast majority of cases are heavier, and associated with back-bleeding (blood self-limited.1–3 The lifetime incidence of epistaxis leaking down the pharynx and into the esophagus is 60 percent, with most first occurrences in or even into the airway). Rarely, posterior bleeding childhood or adolescence.1,2 The incidence of may present with catastrophic exsanguination pediatric epistaxis is highest during the winter, from an arterial aneurysmal source. andthisisthoughttobesecondarytoincreased r Diagnosis:TheEMprovidershouldseekhistorical frequencyofURIsaswellasdryingofthenares clues that might point to any condition that might due to low ambient humidity from indoor heating. predispose the child to bleeding. Family and Epistaxis is rare in patients less than 2 years old, personal history of coagulopathy or bleeding

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disorder should be sought. The provider should For the initial tamponade, the patient is query the family regarding night sweats, easy instructed to blow out blood and clots. bruising, bleeding on toothbrushing, Application of a topical vasoconstrictor/anesthetic hemarthroses, fevers, weight loss, or any historical such as oxymetazoline and 1% lidocaine into the or physical examination elements that suggest nares, either using a spray bottle, atomizer, or underlying malignancy or medical disorder. applying cotton-soaked pleats, will aid in Recent trauma, surgery, and anticoagulant use examination.1 Cocaine can also be used. Next, use should be reviewed. Over-the-counter and a nasal speculum to find the source of bleeding by prescription medications such as intranasal first inspecting Kesselbach’s plexus. It is important decongestants could be a possible cause. Cocaine also to assess for the presence of a septal and other inhaled illicit substances can also cause hematoma. Next, inspect the oropharynx for epistaxis. The provider should make certain to bleeding. Have the patient pinch the alae together ascertain that the bleeding is in fact nasal, and not andholdforroughly10minutes.Ifthepatientis hematemesis or hemoptysis. The provider should too young to reliably pinch his/her nose closed, do a careful head and neck examination using a the parents or clinical personnel can perform the nasal speculum and a good light source to attempt compression maneuver. During the initial to determine the source of bleeding.1 Anterior compression, the child should be sitting up and epistaxis is diagnosed on examination, with either bent forward at the waist to minimize bleeding a fresh clot or active bleeding indicating the into the oral cavity and hypopharynx, as this location of hemorrhage. If bleeding is determined predisposes to vomiting. to be nasal in origin and an anterior site cannot be If the bleeding is able to be stopped after direct visualized, posterior bleeding should be presumed pressure and/or chemical cautery, the patient to be present. should be prescribed a topical antibiotic ointment, In well children over the age of 2 without a such as bacitracin.5 This may be applied three concerning history or examination, laboratory or times per day. Patients should also be educated imaging evaluation is generally not indicated for a about the use of humidifiers to help keep the nasal single episode of anterior epistaxis.3,5 Coagulation mucosa moist and the importance of not picking studies should be ordered for patients with a thenosetopreventagainstfuturebleeds.For known or suspected coagulopathy or bleeding chronic or recurrent epistaxis, one can use diathesis. In children with recurrent unilateral hydrocortisone ointment 1%, applied topically to epistaxis, referral to ENT for assessment for a the anterior septal mucosa (twice per day for mass is appropriate.3,5 In very young children 10 days, limited to no longer than 2 weeks to with nosebleeds, consideration should be given prevent thinning of the mucosa). for non-accidental trauma as well as for If the nasal bleeding is refractory to direct hematologic malignancy, and work-up for these pressure, but slows or stops temporarily and an entities is appropriate.4 ENT should be anterior source is clearly visualized, proceed to consulted for all cases of posterior nosebleeds in chemical cautery with 75% silver nitrate.1,3 Dab children. the applicator gently around the suspected source r Treatment:Whentreatingepistaxis,itisimportant of bleeding. Avoid prolonged cautery and bilateral to use personal protective equipment, including a cautery to prevent septal perforation.1 Do not face mask, gloves, and a gown, as the patient attempt to cauterize an actively bleeding vessel. sneezing or coughing can lead to an exposure risk. If the bleeding is swift after direct pressure or Since some nosebleeds may interfere with airway attempts at cautery are unsuccessful, topical and breathing, initial assessment of airway prothrombotic agents such as topical thrombin or patency and vital signs is necessary. If the patient gelatin-impregnated products can be attempted. If is hemodynamically unstable or unable to protect this fails or is unavailable, the provider should his or her airway, proceed to resuscitation proceed to nasal packing. Nasal packing may be algorithms. Severe bleeding, signs of anemia, or achieved using strips of petroleum-impregnated hemodynamic instability require IV access, a stat gauze, applied in layers to fill the entire nasal Hb/HCT test, and blood crossmatching. cavity, or with a commercial nasal tampon

16:18:46 06 Chapter 5: Eye, Ear, Nose, and Throat Complaints designedforthispurpose.Coatthenasaltampon r Disposition: Patients with resolved or treated with bacitracin ointment, then insert it directly anterior nosebleeds may be discharged home. back into the nasal cavity with constant pressure. Those with packing in place should have it It is important to apply constant pressure and not removed in 2–5 days. Patients with posterior delay advancing the nasal tampon, as it begins to nosebleeds or concerns for underlying serious expand once exposed to the moist environment of pathology should be admitted to the hospital for the nare. Expand the tampon with the remaining observation. oxymetazoline and 1% lidocaine or a normal saline flush. Non-absorbable packs are typically Historical clues Physical findings leftinplacefor1to5daysandthenremovedby r Recent URI r Bleeding from left nare from ENT as an outpatient. While the pack is in place, r r History of epistaxis r Kesselbach’s plexus and even after its removal, there may be a History of No other abnormalities on potential risk of staphylococcal toxic shock nose-picking examination to suggest underlying pathology syndrome. Neither prophylactic systemic antibiotics nor impregnation of nasal packing with antibiotic ointment eradicate nasal carriage Follow-Up of staphylococcus or reliably prevents against toxic shock syndrome.2,6 Thus, antibiotics are not This patient had anterior epistaxis caused by digital routinely recommended. However, antibiotics trauma. Her recent URI and being in a low-humidity may be prescribed if there is evidence of an environment during the winter put her at a greater risk underlying sinus infection or if follow-up is of developing epistaxis. After compressing the nares anticipatedtobemorethan48hours.Commonly for roughly 15 minutes, the bleeding stopped. Chemi- used antibiotics include amoxicillin–clavulanate cal cautery was applied with 75% silver nitrate and the or clarithromycin. patient was prescribed a topical antibiotic ointment to One should suspect a posterior bleed if the apply three times each day. She was educated about the patient reports swallowing blood after anterior use of humidifiers to help keep the nasal mucosa moist nasal packing or if bleeding is refractory to and the importance of not picking the nose to prevent anterior packing. Posterior bleeds are much more against future bleeds. serious as they tend to bleed more, their location makes them more difficult to tamponade, and the References risk of airway compromise from bleeding into the 1. American College of Emergency Physicians. Focus on: posterior oropharynx is increased. Posterior Treatment of epistaxis. See www.acep.org/Clinical— bleeds require an ENT consultation and inpatient Practice-Management/Focus-On–Treatment-of- admission. These are treated with the insertion of Epistaxis/ (accessed August 23, 2016). a balloon catheter. A 10 or 14 French Foley 2. Cohn B. Are prophylactic antibiotics necessary for catheter can be used if a standard balloon catheter anterior nasal packing in epistaxis? Ann Emerg Med designed for nasal packing is unavailable. The tip 2014; 65: 109–11. of the Foley catheter is cut off and advanced until 3. Qureishi A, Burton MJ. Interventions for recurrent itcanbeseenintheposteriororopharynx.The idiopathic epistaxis (nosebleeds) in children. Cochrane Database Syst Rev 2012; 9: CD004461. balloonistheninflatedandtuggedbackuntilitis seated just above the soft palate. It is further 4. McIntoshN,MokJYQ,MargerisonA.Epidemiology of oronasal hemorrhage in the first 2 years of life: inflated until the soft palate begins to bulge or the Implications for child protection. Pediatrics 2007; patient complains of pain. It is then fixed in place 120:1074–8. with a Kelly clamp and tape, taking care not to 5. Patel N, Maddalozzo J, Billings KR. An update on apply pressure to the alar rim. This can be an management of pediatric epistaxis. Int J Pediatr uncomfortable procedure. As a last resort, Otorhinolaryngol 2014; 78: 1400–4. operative management or endovascular treatment 6. Biggs TC, Nightingale K, Patel NN, et al. Should of refractory bleeds can be considered if a patient prophylactic antibiotics be used routinely in epistaxis is critically ill or if the bleeding cannot be patients with nasal packs? Ann R Coll Surg Engl 2013; stopped. 95: 40–2.

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Case 3 Contributing Author: Shellie Asher History The patient is a 12-year-old boy who was playing with a stretchy rubber action figure when it snapped back, striking him in the left eye. He complained of eye pain and presented to the school nurse who examined his eye and referred him to the ED for further evaluation. The patient currently complains of 8/10 left eye pain, tearing, and blurry vision. He has no other complaints or injuries. Past Medical History r None. Figure 5.2 Photograph of patient’s left eye, demonstrating an irregular pupil and extruded iris. For the color version, please refer to Medications the plate section. r None. Diagnosis Allergies r Globe rupture due to penetrating trauma. r No known food or drug allergies. Discussion Physical Examination and Ancillary Studies r Epidemiology:Globeinjuriesarecommonly r Vital signs: T 98.6 °F, HR 82, RR 16, BP 98/52, O2 encountered in EDs, and may result from blunt or sat 100% on room air. penetrating trauma. The annual incidence of r General: Appears well-developed and globe rupture or laceration is approximately 3.5 1 well-nourished, resting on the stretcher, in no per 100,000 worldwide. In the USA, 2.4 million acute distress. eye injuries occur annually, with over a third of 2 r HEENT:Therightpupilisroundandreactiveto these occurring in children. The majority of light. The globe appears normal, the anterior patients presenting with globe injury are young chamber and cornea are clear. Right eye visual and male. In younger children, injuries tend to be acuity is 20/20. The left pupil is irregularly shaped related to running or walking with sharp objects and minimally reactive to light. The anterior such as scissors or pens, whereas older patients chamber and cornea are clear. Visual acuity is tend to have work-related injuries or injuries 1–3 20/200. Visual fields are full to confrontation, and sustained in motor vehicle crashes. Intraocular extraocular movements are intact. The foreign bodies are common in patients with globe 1–4 conjunctivae are diffusely injected, with no limbic rupture. Children also commonly present with sparing. In the two o’clock position there is noted other ocular traumatic injuries, such as corneal an extruded portion of iris through a foreign body, hyphema, corneal or scleral full-thickness corneal laceration (Figure 5.2). laceration, corneal abrasion, corneal ulcer, traumatic iritis, traumatic glaucoma, vitreous Questions for Thought hemorrhage, retinal trauma, optic nerve injury, r lens dislocation, or injuries to the lids or What historical elements are important in the surrounding bony structures. assessment of eye trauma? r Pathophysiology:Openglobeinjuriesare r What physical examination elements are important in the assessment of eye trauma? characterized as globe rupture (caused by blunt r What are other traumatic eye injuries? injury) or globe laceration (caused by penetrating r What is the appropriate evaluation and injury). The globe is relatively protected from management for this condition? blunt injury by the surrounding bony structures. High-impact blunt trauma with enough force to

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injure the bony structures may also result in globe should be assessed in each eye independently. injury. In blunt trauma, globe rupture typically Structures surrounding the eye should be occurs behind the insertion of the rectus muscle, carefully assessed for associated injury. where the sclera is weakest. Penetrating injury is r Fluorescein staining may reveal Seidel’s sign, more common in children.2 In the setting of which is a streaming away of fluorescein from penetrating injury, lacerations typically occur in the site of a corneal puncture from leaking the cornea, followed by scleral or limbal aqueous humor. This is pathognomonic for lacerations. Intraocular foreign bodies should be globe rupture. Fluorescein uptake may be seen considered and may be found in any chamber of in corneal abrasions or ulcers, and may help the eye. Extrusion of intraocular contents may delineate a corneal foreign body. Vertical occur secondary to penetrating trauma or due to abrasions may be evidence of a foreign body increased intraocular pressure after blunt trauma. under the eyelid. r Presentation: Patients may present with an r Slit-lamp examination may demonstrate isolated globe injury or with a globe injury in the inflammation in the anterior chamber (cell and setting of a multi-system trauma. In the setting of flare) from traumatic iritis. Photophobia is also multi-system trauma, life-threatening injuries common in iritis due to pupillary spasm. must be addressed prior to the globe injury. In any r U/S is a helpful adjunct and may demonstrate patient with head or facial trauma, the globe vitreous hemorrhage, traumatic retinal should be inspected carefully. High-risk detachment (which is rare), or traumatic lens mechanisms of injury include high-velocity dislocation. projectiles, injuries from sharp objects, and r CT imaging of the globe may be used as an high-force blunt trauma. Patients may present adjunct to a thorough history and physical with eye pain, blurry vision, tearing, or a paucity examination when globe rupture is suspected, of symptoms, particularly in penetrating, small, and may be useful when intraocular foreign high-velocity injuries. The clinician should have a bodyissuspected.However,thesensitivityofa high index of suspicion and perform a complete CT scan for globe rupture is 56–75 percent and eye examination in any patient with a concerning thus should not be considered definitive when history (for example, hammering metal on metal pre-test probability is high.4 without eye protection). r r Diagnosis:Diagnosisofgloberuptureand Treatment: Management of globe injury should differentiation of this entity from other ocular occur in the setting of standard trauma emergencies is made with a careful history and management for other associated injuries. If globe physical examination. injury is highly likely, the clinician should take care to avoid maneuvers that may increase r Important elements of history include time and intraocular pressure and therefore exacerbate the mechanism of injury, complaints of pain, visual globeinjury.Theeyeshouldbeshielded,andthe disturbances, and associated injuries. patient should be encouraged to rest quietly.1,2 r Physical examination should include a Associated vomiting should be treated, and the complete slit-lamp examination as well as patient’s pain should be managed appropriately. visual acuity. In globe rupture, findings may An ophthalmologist should be consulted include decreased visual acuity, an irregularly emergently when globe rupture is diagnosed or shaped pupil, hyphema, visible laceration of highly suspected. Patients should be kept NPO the cornea and/or sclera, extrusion of ocular and receive empiric antibiotic therapy and tetanus contents, and gross deformity of the globe. If prophylaxis.1,2 Definitive management of globe the provider is concerned globe rupture exists, rupture is surgical intervention. Vision may be he or she should avoid any maneuvers which preserved in more than half of pediatric patients may increase intraocular pressure, such as with appropriate, rapid evaluation and direct pressure on the globe, tonometry, or management.2 r eyelid retraction, as these may result in further Disposition:Patientswithdiagnosedorhighly extrusion of ocular contents. Visual acuity suspected globe injuries should be evaluated by an

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ophthalmologist or transferred to a facility where reportsshehasbeenfallingovermorefrequentlyand consultation is available. If examination is not responding to her name as she normally would. difficult, the patient should go to the OR for She has been tolerating PO without difficulty although examination under anesthesia. she is drinking less than usual. She is wetting diapers and passing stool normally. There are no rashes. Her Historical clues Physical findings mother called her pediatrician to ask for a prescription r History of eye trauma r Irregular pupil for amoxicillin, which typically works for her, but the r Eye pain r Decreased acuity pediatrician referred her to the ED for evaluation. r Blurry vision r Visualized laceration with extrusion of iris Past Medical History r Recurrent episodes of otitis media. r Follow-Up Immunizations are UTD. The patient was taken emergently to the OR by oph- Medications thalmology for surgical repair of his corneal laceration r None. and reduction of extruded ocular contents. He did well post-operatively, with preserved vision in the affected Allergies eye. r NKDA. References Physical Examination and Ancillary Studies r ° 1. Gelston CD. Common eye emergencies. Am Fam Phys Vital signs: T 102.2 F, HR 132, RR 26, BP 90/50, 2013; 88: 515–19. O2 sat 99% on room air. r 2. Li X, Zarbin MA, Bhagat N. Pediatric open globe General: Well-developed child, fussy and crying injury: A review of the literature. J Emerg Trauma throughout examination. Shock 2015; 8: 216–23. r HEENT: PERRL, extraocular movements intact. 3. May DR, Kuhn FP, Morris RE, et al. The epidemiology Left ear appears to be “bulging” forward and is of serious eye injuries from the United States Eye asymmetric compared to the right ear. The left Injury Registry. Graefes Arch Clin Exp Ophthalmol external ear canal is erythematous and swollen, 2000; 238: 153–7. with mucopurulent drainage, the tympanic 4. Yuan WH, Hsu HC, Cheng HC, et al. CT of globe membrane is difficult to visualize but appears rupture: Analysis and frequency of findings. AJR Am J erythematous with bulging and appears opaque Roentgenol 2014; 20: 1100–7. with no bones visible. Posterior to the auricle there is swelling, redness, induration, and Case 4 tenderness over the mastoid process. No lymphadenopathy present. No depressions or Contributing Author: Tom Dittrich elevationsintheskull.Thelefteyeappearsgrossly History unremarkable and the orbit is without swelling or erythema. The neck has no decreased range of The patient is a 2-year-old girl with history of recur- motion nor tenderness on examination. rent otitis media, who presents with left-ear pain and r Cardiovascular: Tachycardic and regular, without yellow drainage from the ear canal for the past 3 days. M/R/G, S1 and S2 appeciated. Ͻ 2second Thechildhasbeenfussierthanusualandispullingat capillary refill. the left ear, which is when mom “knows there’sgoing to r Lungs:CTAbilaterally,withnoW/R/R. be another ear infection.” She noticed yellow drainage r from the ear canal today and was referred to the ED. Abdomen: Soft and non-tender throughout, Mom notes she has had fever of 102.2 °Fbyrectal normal bowel sounds. r + thermometer for the past 2 days. She has been using Extremities and skin: Warm and well perfused, 2 radial and dorsalis pedis pulses. ibuprofen and acetaminophen appropriately. Mom is r more concerned about this episode because she feels Neurologic: Awake, symmetric face, normal level that her daughter’s ear is bulging forward and doesn’t of alertness, moves all four extremities match the opposite side, which is new for her. She also spontaneously.

16:18:46 06 Chapter 5: Eye, Ear, Nose, and Throat Complaints r Pertinent laboratory values: WBC 17,600, all other laboratory tests are unremarkable. r Pertinent radiologic studies:HeadCT demonstrates fluid-filled mastoid air cells, with destruction of the bony septae normally found there.

Questions for Thought r What is the diﬀerential diagnosis for this child’s symptoms? r What are the indications for obtaining an imaging study for this patient? r How should treatment be approached? r What should this patient’s disposition be from the ED?

Diagnosis r Acute mastoiditis. Discussion r Epidemiology: The vast majority of cases of mastoiditis occur in the same age group as cases Figure 5.3 Erythema and swelling behind the pinna. For the color of acute otitis media, usually 6 months to 2 years version, please refer to the plate section. of age.1 The disease process does occur in older children but the incidence drops off as the child infection encompasses the facial nerve, than a gets older. This is thought to be secondary to the facial nerve palsy can be the result. Extension into anatomy of the eustachian tube and an immature the inner cortical bone yields bacteria in the immune system.1 Generally, risk factors for acute cranialfault,whichcanleadtomeningitis,sinus mastoiditis parallel those for acute otitis media, venous thrombosis, or intracranial abscess. The which include age, tobacco-smoke exposure, bacteria most commonly implicated are non-breast-fed infants, daycare, and family Streptococcus pneumoniae, S. pyogenes,or history of acute otitis media.1 Staphylococcus aureus.3–5 r r Pathophysiology:Acutemastoiditisisa Presentation: Children may present with a range complication and an extension of otitis media.2 of complaints depending on the progression of the The mucosa that lines the inner ear extends tothe disease and the direction of bacterial extension. lining of the mastoid air cells. When bacteria The child may complain of otalgia, otorrhea, fever, induce inflammation in this lining, the bacteria headache, malaise, or vertigo. Examination cantakeholdwithinthemastoidaircells.Ifthe findings may include mastoid tenderness, inflammation destroys the thin walls of bone erythema, and swelling (see Figure 5.3), between air cells, called coalescent mastoiditis, protrusion of the auricle, meningeal findings, then tiny pockets of abscess may form and may abnormal tympanic membrane, obtundation, or spread to nearby areas.2 The direction of the sepsis. bacterial extension will determine the patient’s r Diagnosis:Thediagnosiscanbemadeclinicallyby symptoms. If the bacteria travel to the outer historical and physical examination features. CT cortex of the bone, then an abscess may form imaging of the head is not always indicated. CT there, called a sub-periosteal abscess, marked by imaging can be helpful to investigate cases without induration and fluctuance. If there is extension classic findings, evaluate for complications such as into the round window, leading to the vestibular an abscess, which will require further intervention labyrinths, then suppurative labyrinthitis develops beyond antibiotics, or to determine the extent and giving vertigo, hearing loss, and tinnitus. If the severity of the disease. CT findings include fluid

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in the middle ear and air cells of the mastoid Historical clues Physical findings Ancillary studies bone, abnormal densities of the mastoid bone, r r r History of otitis r Protruding pinna r Leukocytosis thickening of the periosteum, or findings of r media Tender, red CT with fluid complications such as extra-axial fluid collections. Fever postauricular coalescing within r Complaints of space mastoid air cells MRI with gadolinium is an alternative option to r ear pain and r Otorrhea CT but is generally more difficult to obtain. drainage Fever r Treatment: Broad-spectrum antibiotic treatment should be initiated for all pediatric patients Follow-Up suspected to have acute mastoiditis. Generally, The patient’s head CT demonstrated signs consistent coverage for Gram-positive organisms, including with acute mastoiditis with periosteitis. A myringot- MRSA, are of greatest importance as these omy was performed, yielding white purulent fluid organisms are the most common.3–5 For those which was sent for Gram’s stain and culture. Blood with recurrent acute otitis media, which is a cultures were obtained. The patient was started on common occurrence, coverage for Gram-negative vancomycin and piperacillin–tazobactam per recom- organisms, including Pseudomonas aeruginosa mendation from ENT. She was admitted to the hospi- coverage, should be provided.3–5 Generally, tal and demonstrated improvement. Cultures returned vancomycin and piperacillin–tazobactam is positive for S. pyogenes sensitive to amoxicillin– typically the first-line recommended antibiotic clavulanate. The patient was transitioned to oral antibi- therapy. For penicillin-allergic patients, otics to complete a 4-week course and had a full aztreonam or cefepime are reasonable alternatives recovery. to piperacillin–tazobactam. Obtaining cultures fromthemiddleear,anabscess,blood,orCSF(if clinically indicated) can help identify the References pathologic organism. Broad-spectrum IV 1. Uhari M, Mantysaari K, Niemela M. A meta-analytic antibiotics should be given for a minimum of review of the risk factors for acute otitis media. Clin Infect Dis 1996; 22: 1079–83. 7 days or until clinical improvement. Coverage may continue as an outpatient with oral 2. Lin HW, Shargorodsky J, Gopen Q. Clinical strategies antibiotics to complete a 4-week course. for the management of acute mastoiditis in the pediatric population. Clin Pediatr (Phila) 2010; 49: As mastoiditis represents an abscess, drainage 110–15. is an integral aspect to the treatment. 3. Bilavsky E, Yarden-Bilavsky H, Samra Z, et al. Clinical, Myringotomy, with or without tympanostomy laboratory, and microbiological differences between tube placement, should occur in all patients children with simple or complicated mastoiditis. Int J suspected of mastoiditis, to allow for drainage of Pediatr Otorhinolaryngol 2009; 73: 1270–3. the infection and for collection of culture 4. LuntzM,BrodskyA,NusemS,etal.Acute 4 specimens. Patients with infections refractory to mastoiditis – the antibiotic era: A multicenter study. treatment with IV antibiotics and tympanostomy Int J Pediatr Otorhinolaryngol 2001; 57: 1–9. tube placement may require resection of the 5. Nussinovitch M, Yoeli R, Elishkevitz K, et al. Acute mastoid bone (mastoidectomy) in order to help mastoiditis in children: epidemiologic, clinical, eradicate the infection. All patients with microbiologic, and therapeutic aspects over past years. mastoiditis should be referred for consultation by Clin Pediatr (Phila) 2004; 43: 261–7. ENT for further evaluation. r Disposition: Patients with mastoiditis will require broad-spectrum IV antibiotic therapy and Case 5 therefore will universally require admission to the hospital. If there are symptoms of meningeal Contributing Authors: Jonathan R. Morgan involvement or intracranial extension, then and Melanie K. Prusakowski childrenmayrequireICUlevelofcarefor monitoring of neurologic examinations. Once History clinical improvement has occurred, patients The patient is a 13-year-old boy who was hit in the left should be discharged to follow up with ENT. eye with a baseball. He reportedly lost consciousness

16:18:46 06 Chapter 5: Eye, Ear, Nose, and Throat Complaints for a few seconds, which prompted transport to the r What signs and symptoms on this child’s ED. Per EMS, he had one bout of vomiting en route. examination give away the diagnosis? He presents with eye pain, blurred vision, nausea, and r What are common associated complications? vomiting. He has severe pain with eye movement and r What is the management of this condition? throbbing pain when not moving the eye. Upon questioning, he also complains of numbness under the left eye. There is no headache or neck pain. Diagnosis r Past Medical History Fracture of the left orbital floor with inferior r Eczema. rectus entrapment. Discussion Medications r Epidemiology: Facial fractures have an incidence r No medications. of 5–15 percent in the pediatric population. Nasal Allergies fractures are the most common, and are generally r handled in a conservative fashion. Orbital NKDA. fractures represent the third most common type of pediatric facial fracture.1 The orbital floor and Physical Examination and Ancillary Studies medial wall are the most common sites for orbital r 2–4 Vital signs: T 98.6 °F, HR 44, RR 16, BP 120/70, O2 fractures. The primary mechanism of injury is sat 99% on room air. blunt trauma, often with a direct blow to the r General: Well-developed, well-nourished teenager, periorbital region, and is most frequently related who is alert and oriented, in moderate distress to sports activity or motor vehicle collisions.2–4 secondary to pain. r Pathophysiology: Controversy surrounds the r HEENT: PERRL. Decreased visual acuity in left causative mechanism of fractures to the orbital eye (20/30); diplopia and limited upward gaze in floor and/or medial wall, commonly referred to as the left eye. Appreciable orbital dystopia and blow-out fractures. There are three current hyphemainthelefteye.Noperiorbital theories: the bone conduction theory, the globe to ecchymosis. Palpable tenderness and crepitus of wall theory, and the hydraulic theory. The bone the left zygomatic arch. conduction theory states that the transmission of r Neck: Supple and non-tender, with full range of force from the strong orbital rim causes the thin motion. internal orbital bones to buckle.2 The globe to wall r Cardiovascular: Bradycardia, normal S1, S2, no theory proposes that, under a force, the globe audible M/R/G. contacts the floor and results in an orbital floor 2 r Lungs: Clear and equal, with no W/R/R. fracture. The hydraulic theory attributes the r Abdomen: Soft and non-tender, with no signs of fracture to an increase in indirect pressure from 2 trauma. the globe. There is evidence to support each r Extremities and skin: Warm and well-perfused, theory, and the actual cause is likely to be a with no signs of trauma and good pulses. combination or interaction of all three theories. r Neurologic: GCS 15. Speech fluent. Strength is 5/5 Although blow-out fractures are the most in all extremities. Sensation is intact. Deep tendon common orbital fracture, children can suffer other reflexes are 2+ and symmetric. forms of orbital and facial fracture. Nasoethmoid fractures result from the collapse of the nasal bones into the skull base and accompanying Questions for Thought fractures that displace paired nasal, lacrimal, and ethmoid bones. Orbital roof fractures in children r What is the diﬀerential diagnosis for this child’s commonly have a fracture pattern that extends symptoms? r What other injuries are potentially associated from the orbital roof through the supraorbital 4 with this condition? foramen and along the frontal bone. An orbital blow-in fracture refers to the collapsing of the

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orbital roof from an inferior supraorbital impact. r Diagnosis: Patients with a history of blunt orbital The zygomatic complex is a quadripod structure trauma should be promptly evaluated for consisting of the lateral orbital wall, the lateral traumatic injuries to the eye. The physical orbital rim, the inferior orbital rim, the examination should include assessment of the zygomatic-maxillary buttress, and the zygomatic facial bones, surrounding soft tissues, and the eye arch. Orbital zygomatic fractures commonly itself. A complete ophthalmologic examination occur along the three buttress-related sutures. should occur quickly as periorbital swelling may Orbital fractures can result in entrapment of progress. The child may need help retracting a orbital tissues, especially fat or extraocular swollen lid so that visual acuity, pupillary muscles.2,5,6 Children, whose bones are less function, and extraocular motility can be calcified and therefore more pliable with external assessed. Eyelid retractors (Desmarres) may be force, can develop a trapdoor variant of a needed. When feasible, a slit-light lamp blow-out fracture that results in extreme external examination should be completed. ophthalmoplegia.5,6 Another pediatric-specific A thin-cut coronal CT scan of the orbit should variant is the “white-eyed blow-out,” where a lack be performed in patients with a history of orbital of typical signs of surrounding periorbital trauma trauma combined with any of the following belies underlying significant bony trauma. findings: palpable crepitus or step-off, severe pain, The oculocardiac reflex may be seen in limited extraocular motility, decreased visual patients with orbital bone injuries. This reflex acuity, enophthalmos, proptosis, widened occurs when eye pain/pressure causes a drop in intercanthal distance, activation of the blood pressure or heart rate. Activation of the oculocardiac reflex, or extrusion of intraocular oculocardiac reflex is associated with nausea, contents. CT imaging can also provide necessary bradycardia, and, potentially, syncope.5,6 The information when the child cannot cooperate ophthalmic division of the fifth cranial nerve with a full examination due to pain. controls the afferent limb of the oculocardiac As with any trauma to the head, a complete reflex. Impulses pass to the vagus nerve, then neurologic examination and c-spine assessment travel through the spinal cord to vagal nerves that should be performed. Pediatric facial injuries deliver the signal to the heart and stomach. commonly occur with concomitant injury to the Orbital fractures present a sufficient opportunity skull and brain, and therefore a high index of for activation of the oculocardiac reflex, which suspicion for associated injuries should be results in physiologic responses. maintained.1 r Presentation: Orbital fractures in children have r Treatment: A conservative treatment plan is varying presentations. Typical signs of an orbital recommended for orbital fractures in children to fracture include pain, periorbital swelling, and prevent disruptions in growth and the formation periorbital ecchymosis.1,2 Numbness, decreased of periosteal bone. Patients with associated globe visual acuity, diplopia, limited extraocular injuries, severe vagal symptoms, or visual motility, orbital dystopia, and enophthalmos may impairment require immediate ophthalmologist also be seen.1–6 Children may experience evaluation.2 Muscle entrapment, enophthalmos, vomiting, bradycardia, and syncope with orbital orbital dystopia or injury to the lacrimal fractures, due to entrapment of extraocular apparatus, and/or medial canthal ligament also muscles.5,6 Entrapment most commonly results in need emergent consultation with an double vision on directed gaze. Palpable ophthalmologist.2 Nausea, vomiting, and pain tenderness, crepitus, and/or step-off of the facial may also need to be controlled. There is limited bones suggest an underlying fracture. Signs of a evidence to support or refute the use of possible displaced fracture include proptosis, prophylactic antibiotics covering sinus pathogens widened intercanthal distance, subconjunctival for patients with fractures into a sinus. An effort emphysema, and CSF leak.1,2 Children may also should be made to reduce local swelling with cold present with signs of globe rupture (irregular packs. pupil), corneal abrasions, lens dislocation, r Disposition: Patients with an orbital wall fracture hyphema, lacrimal injuries, or retinal detachment. not associated with decreased vision, globe

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References 1. Chao MT, Losee JE. Complications in pediatric facial fractures. Craniomaxillofac Trauma Reconstr 2009; 2: 103–12. 2. Bord SP, Linden J. Trauma to the globe and orbit. Emerg Med Clin N Am 2008; 26: 97–123. 3. Gerber B, Kiwanuka P, Dhariwal D. Orbital fractures in children: A review of outcomes. Br J Oral Maxillofac Surg 2013; 51: 789–93. 4. Hatton MP, Watkins LM, Rubin PA, et al. Orbital fractures in children. Ophthal Plast Reconstr Surg 2001; 17: 174–9. 5. Wei LA, Durairaj VD. Pediatric orbital floor fractures. J AAPOS 2011; 15: 173–80. 6. Cohen SM, Garrett CG. Pediatric orbital floor fractures: Nausea/vomiting as signs of entrapment. OtolaryngolHeadNeckSurg2003; 129: 43–7.

Case 6 Figure 5.4 Coronal section of CT face demonstrating an inferior orbital wall fracture with herniation of orbital contents into the left maxillary sinus. Contributing Authors: Denis R. Pauzeand´ Daniel K. Pauze´ trauma, or extraocular muscle entrapment may be History suitable for discharge. Such children should be The patient is a 14-year-old male who presents to fast instructed to use cold compress for 48 hours, keep track with a sore throat. Ten days prior to arrival he the head elevated during sleep, use nasal developed a sore throat with fever. He was seen by his decongestants (if age appropriate), and avoid nose PCP and had a negative rapid strep test. His symptoms blowing. Follow up can be arranged with persisted, and 5 days prior to arrival he again saw his ophthalmology or oromaxillofacial surgery, PCP,this time with swelling of the left side of the neck. depending on regional practices. He was diagnosed with lymphadenitis and started on amoxicillin–clavulanate. The pain and swelling in the Historical clues Physical findings neck persisted, and he again saw his PCP. Blood work r r r History of eye trauma r Decreased visual acuity was checked, and he was found to have WBC of 25,000. Blurry vision Limited extraocular motility HewastoldtogototheED. r Numbness to cheek r Orbital dystopia r r His family decided to “wait it out” for 2 more days Pain with eye movement r Hyphema Zygoma tenderness and crepitus and show up to the ED today. The child arrives with persistent sore throat, neck pain, and neck swelling. On review of systems, there is no trauma, recent dental Follow-Up work,chestpain,orshortnessofbreath.Hedoeshave The child underwent CT scanning of his facial bones, an occasional cough. The triage nurse states that “it is which revealed a left orbital blow-out fracture with just a fast-track sore throat patient.” entrapment (Figure 5.4). He was admitted to the pediatric service due to intermittent bradycardia. He Past Medical History received surgical reduction of the left orbital wall frac- r None. ture and the entrapment of his inferior rectus muscle. He remained in the hospital one night for control Medications of pain and swelling. At discharge he had no residual r Amoxicillin–clavulanate; acetaminophen as vision deficits. needed for pain or fever.

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Allergies the onset of a sore throat of severe pyrexial attacks r NKDA. withaninitialrigor,...theoccurrenceof pulmonary infarcts and arthritic manifestations, Physical Examination and Ancillary Studies constitute a syndrome so characteristic that mistake r Vital signs: T 101.3 °F, HR 97, BP 157/68, RR 16, is almost impossible ...”1 O2 sat 97% on room air. Sore throat is a commonly encountered r General: Awake and non-toxic in appearance, in complaint, with at least 10 million annual no acute distress. healthcare encounters. Pharyngitis is the most r HEENT: PERRL. Extraocular movements intact. common cause of sore throat, and is usually found Oropharynx clear, posterior pharynx, with mild to be viral or bacterial in nature. Group A erythema. No exudates, lesions, petechiae, or beta-hemolytic Streptococcus is the most common masses. bacterial etiology (see Chapter 7, Case 9 for a r Neck: Decreased range of motion. Left side of detailed discussion of this entity). Although neck is tender and warm. There is anterior usually self-limiting, life-threatening causes of cervical adenopathy. Non-erythematous, no sore throat and pharyngitis do exist, and include crepitus. deep space infections such as parapharyngeal r Cardiovascular: Normal S1, S2. No M/R/G. Brisk abscess or retropharyngeal abscesses (discussed in capillary refill. detail later in this chapter). Unvaccinated children areatadditionalriskforlife-threateningcausesof r Lungs:CTAbilaterally,withnoW/R/R. sore throat, as they are at higher risk for r Abdomen: Non-tender. No splenomegaly. r diphtheria or Haemophilus influenzae infections, Extremities and skin: No rashes or joint swelling. such as epiglottitis. Warm and well-perfused. r Lemierre syndrome is another rare cause of Neurologic:Awake,alert,andageappropriate, life-threatening pharyngitis. Fortunately, this with no focal deficits. r entity is rare. There is an estimated annual Pertinent laboratory values: WBC 23,000; incidence of approximately five cases per million HCT 37, Plt normal. CRP 11, ESR 59. Na 129, people.2,3 K 3.3, Cl 88, bicarbonate 31. BUN, Cr, and LFTs r Pathophysiology:Lemierresyndromeisclassically normal. caused by normal oropharyngeal bacteria, most commonly Fusobacterium necrophorum.4–6 Questions for Thought Fusobacterium are Gram-negative anaerobes and r Should you have any concerns for airway are part of the normal mucosal flora. As an involvement or compromise? anaerobe, they can invade tissue and act as a r Does the child’s vaccination status matter? pathogen. They produce an endotoxin that r What are common complications of this entity? destroys cells and causes platelet aggregation. r What imaging study, if any, is warranted? Other causative organisms may include Eikenella, Bacteroides, Peptostreptococcus,and Streptococcus.4,5 These organisms migrate from Diagnosis the oropharynx into the adjacent parapharyngeal r space, where they subsequently infiltrate the Lemierre syndrome (septic thrombophlebitis of nearby carotid sheath. From there, they infiltrate the internal jugular vein). the internal jugular vein and gain access to the vascular system. Once in the vascular system, Discussion infection can spread to the lungs, brain, joints, r Epidemiology: The first case description of sore liver, or heart valves.2–6 Local infectious spread throat and jugular vein thrombosis came in 1900 canresultinanexpandingneckabscess, by Courmont and Cade. In 1936, Dr. Lemierre compromising the upper airway. r reported a case series of 20 patients with similar Presentation:Patientsareusuallyteenagersor findings. In this article, Dr. Lemierre stated: young adults, although cases in toddlers and “...the appearance and repetition several days after young children have been described.6 Sore throat

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and pharyngitis are common initial Surgical intervention may be needed for complaints.1,2–5 Patients may be on antibiotics drainage of abscesses. Surgical intervention on the and complain of “not getting better.” Commonly, jugularveinalsoremainsdebatable,andmaybe the pain expressed by the child seems in excess of utilized when the patient does not respond to IV the physical findings on oropharyngeal antibiotic therapy. examination. Vital signs may reveal fever, r Disposition: All patients with a diagnosis of tachycardia, and, with advanced illness, Lemierre syndrome should be admitted to the hypotension. Examination may (but will not hospital. Patients with hemodynamic compromise always) show abnormalities of the oropharynx, or airway involvement should be admitted to the such as erythema, fluctuance, and/or petechiae.2,3 ICU. Tenderness overlying the jugular vein/sternocleiodomastoid muscle may be Historical clues Physical findings Ancillary studies observed. This tenderness is sometimes r Sore throat r Pain out of r Elevated WBC impressive and prominent, and is often with no proportion to r Elevated ESR accompanied by a palpable mass. Children may improvement r examination also present with late complications, such as septic on antibiotics Neck mass r Unilateral neck r Fever emboli to the lung, septic joint, or a brain r r swelling Tachycardia abscess.2,3 Children who are on antibiotics Ongoing fever may have attenuated symptoms, but many children with Lemierre syndrome are toxic-appearing. Follow-Up r Diagnosis: Blood cultures usually reveal normal The patient was diagnosed with Lemierre syndrome. oropharyngeal flora pathogens, with the most He was evaluated by vascular surgery, hematology, and common being F. necrophorum. F. necrophorum is infectious disease specialists and was started on IV afastidiousorganismandculturescanbefalsely ampicillin–sulbactam. After a week of hospitalization, negative. F. necrophorum is also rarely cultured with significant clinical improvement, he was transi- from the oropharynx, as it requires a special tioned to a PICC line and completed a 6-week course medium that is not routinely used.4 ACTscanof of IV antibiotics with no significant sequelae. theneckwithIVcontrastrevealsathrombusin the internal jugular vein, and an extension of the References CT into the lungs commonly demonstrates septic 1. Lemierre A. On certain septicemias due to anaerobic pulmonary emboli. U/S can also evaluate for organisms. Lancet 1936; 227: 701–3. thrombosis of the internal jugular vein. 2. Phua CK, Chadachan VM, Acharya R. Lemierre r Treatment: Treatment regimens start with prompt syndrome: Should we anticoagulate? A case report antibiotic use. Antibiotic therapy should include a and review of the literature. Int J Angiol 2013; 22: beta-lactamase-resistant beta-lactam antibiotic.4,5 137–42. Options include ampicillin–sulbactam or 3. Tromop-van Dalen C, Mekhail A-M. Lemierre piperacillin–tazobactam. Carbapenems such as syndrome: Early recognition and management. CMAJ. imipenem or meropenem may also be used. 2015; 187: 1229–31. Metronidazole is an option, as it also has 4. Goldenberg NA, Knapp-Clevenger R, Hays T, et al. bacteriocidal activity against F. necrophorum. Lemierre’s and Lemierre’s-like syndromes in children: Survival and thromboembolic outcomes. Pediatrics Antibiotic treatment is indicated for several 2005; 116: e543. weeks. 5. RamirezS,HildTG,RudolphCN,etal.Increased Anticoagulation therapy for jugular vein diagnosis of Lemierre syndrome and other thrombosis is debated and remains somewhat Fusobacterium necrophorum infections at a children’s 2 controversial. Currently, there is not enough hospital. Pediatrics 2003; 112: e380. evidence to support the use of anticoagulation for 6. Garcia-Salido A, Unzueta-Roch JL, Garcia-Teresa MA, isolated thrombosis. Some clinicians advocate for et al. Pediatric disseminated Lemierre syndrome in 2 anticoagulation when there is extension of the infants: Not too young for an ancient disease. Pediatr thrombus. Emerg Care 2017; 33: 490–3.

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Case 7 r Extremities and skin: No rashes or petechiae. Ruddy cheeks. No joint swelling or deformity. Contributing Authors: Dorota Pazdrowska r Neurologic: Normal mental status, fussy but consolable. and Melanie K. Prusakowski r Pertinent laboratory values: WBC 29,000, Plt History 596,000, HCT normal. r The patient is a 30-month-old female who presents Pertinent radiographs:Soft-tissuelateralneck withdroolingforoneday.Oneweekagoshedevel- radiograph shows moderately prominent oped a URI, which subsequently resolved. Four days adenoidal soft tissues and prominent prevertebral prior to arrival she developed fevers, with a maximum soft tissues, which may be positional in nature. temperature of 102.6 °F yesterday. During the previous 24 hours, she refused all oral intake. When mom Questions for Thought noticed that she had difficulty moving her neck, she r was taken to the pediatrician, who diagnosed her with What is the differential diagnosis for decreased viral meningitis. She was prescribed hydroxyzine to neck movement in a toddler? r What is the utility of radiographic studies in help with sleep. There was no travel history or sick confirming or ruling out the diagnosis? contacts. The patient has had multiple mosquito bites r What are definitive treatments? throughout the summer and the family dog had a tick removed 2 weeks ago.

Past Medical History Diagnosis r Concussion at 27 months. r Left peritonsillar abscess. r Eczema. Discussion Medications r Epidemiology: Peritonsillar abscess is the most r Hydroxyzine for the last 2 days. common head and neck abscess in children, with an incidence of about 30 in 100,000 cases per Allergies year.1,2 The disease coincides with periods of highest incidence of streptococcal pharyngitis.1,2 r NKDA. Although it is most commonly seen in teenagers and young adults, it has been reported in infants Physical Examination and Ancillary Studies and toddlers, as well.2,3 r ° Vital signs: T 100.2 F, HR 150, RR 48, BP 132/72, r Pathophysiology: Peritonsillar abscess is a O2 sat 97% on room air. r collection of purulent fluid in the soft tissues General: Awake and alert. Child appears fussy and surrounding the palatine tonsil. Most commonly, intermittently irritable. r it develops between the tonsillar capsule and the HEENT: PERRL. No injection. Atraumatic head, pharyngeal muscles (superior constrictor and tympanic membranes clear bilaterally. palatopharyngeus muscles).1–4 It can be Erythematous oropharynx, without exudates. Left associated with cellulitis of the palatal tissues.4 tonsil enlarged, no petechiae. The infection tends to be polymicrobial, including r Neck:Noadenopathy,midlinetrachea,child group A streptococci, Staphylococcus aureus,and resists movement. respiratory anaerobes.1–5 These organisms can r Cardiovascular: Regular tachycardia, normal S1, spread to the masseter and other nearby S2, no murmurs, femoral pulses 2+ bilaterally. musculature, subsequently with infiltration of the r Lungs: Breathing non-labored, CTA bilaterally, no carotid sheath. This can result in bacteremia, W/R/R. sepsis, and airway compromise. r Abdomen and genitourinary: Soft, non-tender, no r Presentation: Children with peritonsillar abscess organomegaly, bowel sounds present, normal may have a preceding diagnosis of exudative female genitalia. tonsillitis, or they may have their first presentation

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of their illness with the abscess already present. peritonsillar space. CT provides highly specific Aboutone-fifthhavepriordiagnosisofURIatthe characterization of pediatric deep neck infections time of the diagnosis of peritonsillar abscess.3 The and masses.4,5 MRI provides better soft-tissue time from the onset of symptoms to abscess definition than CT scan, without exposure to formation ranges from 2 to 8 days. The most radiation, which may improve detection. In common initial complaint is a sore throat in the straightforward cases, diagnosis can be confirmed majority of children, which is typically unilateral, upon abscess drainage with no imaging at all. followed by fever.3 They may complain of neck r Treatment: Management of peritonsillar abscess pain and neck stiffness, or the caregiver may have begins with an airway evaluation and noted a neck mass. Although older children management of acute obstruction when present. characteristically have a sore throat, about a third IV fluid therapy may be required for patients with of children under the age of 12 will not have this poor oral intake. In some instances, IV antibiotics complaint, and therefore a careful physical may be the only treatment necessary.4,5 More examination is always warranted.3 Patients may commonly, the definitive treatment is drainage of have dysphagia and/or odynophagia. Trismus may the abscess by needle aspiration, or incision and be seen and is also a hallmark feature of drainage.4,5 Use of U/S to guide drainage peritonsillar abscess.3 It results from irritation improves diagnostic accuracy and outcomes.4 and reflex spasm of the internal pterygoid muscle. Antibiotics are recommended following surgical They may have a muffled voice, known as “hot intervention, to clear remaining and disseminated potato” voice, or may report referred ear pain. infection. Common antibiotic options for r Diagnosis: The diagnosis of peritonsillar abscess children are clindamycin (30 mg/kg per day, must be considered in patients with severe sore divided every 8 hours) and cefotaxime (150 mg/kg throat, especially when accompanied by per day, divided every 8 hours). Routine culturing odynophagia, dysphagia, fever, and trismus. of the abscess is reported to be unnecessary, Severe sore throats can also be caused by although some practitioners still adhere to this. retropharyngeal abscess, tracheitis, epiglottitis, Corticosteroids may hasten recovery by reducing pharyngitis, parapharyngeal abscess, uvulitis, or edema and inflammation. A single dose of tonsillitis. These entities can be distinguished dexamethasone at 0.6 mg/kg, with a maximum from one another by direct visualization (in the dose of 10 mg, IV may improve pain.5 case of uvulitis, tonsillitis, and pharyngitis), r Disposition: Outpatient treatment may be indirect visualization (in the case of epiglottitis), appropriate in children without airway or diagnostic imaging (in the case of abscesses). compromise, who are not clinically dehydrated In physical examination of peritonsillar and can tolerate oral antimicrobials. Those abscess in patients who can comply, there is requiring immediate surgical intervention benefit edema and erythema of the affected tonsil and the from consultation with ENT and admission for IV overlying soft palate, uvular deviation to the antibiotics. Patients who complete a course of contralateral side, trismus, and lymphadenopathy. antibiotics after drainage have good outcomes, Other etiologies of unilateral tonsillar andrecurrenceinchildrenisrare.Late enlargement, such as tumor infiltration or benign recognition and inadequate treatment can result hypertrophy, and coexistent pathology, such as in complications such as jugular vein thrombosis, mononucleosis, palatal cellulitis, or local adenitis, extension of infection into tissues of the deep should be considered. neck, posterior mediastinum, or lung, and In small patients without a complaint of sore hemorrhage from erosion into the carotid sheath. throatandinwhomadetailedphysical examination is challenging, diagnosis is often made with imaging.3 Peritonsillar abscess can be Follow-Up confirmed with intraoral or transcutaneous U/S.4 ThechildwasgivenIVantibioticsandadmittedto A CT scan or MRI of oropharyngeal and neck the hospital. Her blood and urine cultures were neg- tissues is usually reserved for patients with ative, and she underwent LP, which was also nega- suspected spread of infection outside of the tive. An inpatient MRI was performed which revealed

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Historical clues Physical findings Ancillary studies at preschool. He has a history of snoring, and has a r Recent URI r Unilateral tonsillar r Elevated WBC sleep study scheduled in a month. r Decreased PO hypertrophy r Elevated Plt r Neck stiffness r Neck stiffness (acute phase Past Medical History r r Tachycardia r reactant) Two prior episodes of acute otitis media. X-ray with large r adenoids and Immunizations are UTD. generous prevertebral Medications space r None. a 3.4-cm peritonsillar abscess. The child underwent Allergies drainage of the abscess in the OR by ENT. She com- r NKDA. pleted her antibiotic course and had resolution of her symptoms. Physical Examination and Ancillary Studies r Vital signs: T 100.4 °F, HR 115, RR 20, BP 98/60, O2 sat 98% on room air. References r 1. Cirilli AR. Emergency evaluation and management of General: Well-developed and well-nourished, thesorethroat.Emerg Med Clin N Am 2013; 31: normal appearance, perfusion, and work of 501–15. breathing. r 2. Stoner MJ, Dulaurier M. Pediatric ENT emergencies. HEENT: PERRL, oropharynx with enlarged Emerg Med Clin N Am 2013; 31: 795–808. tonsils, and child with nasal voice. No trismus. 3. Hsiao H-J, Huang Y-C, Hsia S-H, et al. Clinical Righttympanicmembrane,withmildbulgingand features of peritonsillar abscess in children. Pediatr clouding. Left tympanic membrane normal. No Neonat 2012; 53: 366–70. mastoid tenderness or erythema. Moderate 4. Costantino T, Satz W, Dehnkamp W, et al. rhinorrhea. Randomized trial comparing intraoral ultrasound to r Neck: Supple, with shotty adenopathy. No masses. landmark-based needle aspiration in patients with r Cardiovascular: Regular rate and rhythm, with no suspected peritonsillar abscess. Acad Emerg Med 2012; 19: 626–31. M/R/G. r Lungs:CTAbilaterally,withnoW/R/R.No 5. Powel J, Wilson JA. An evidence-based review of retractions, grunting, or flaring. peritonsillar abscess. Clin Otolaryngol 2012; 37: r 136–45. Abdomen: Soft and non-tender, with no masses or organomegaly. r Skin and extremities: Warm and well-perfused, Case 8 good capillary refill, no rashes. r Neurologic: Normal mental status, follows Contributing Author: Rebecca Jeanmonod commands. History Questions for Thought A 4-year-old boy presents to the ED with his father r with a chief complaint of right ear pain. The child has Does this child have acute otitis media? Is his had a coarse cough and runny nose for the past 5 days, disease severe? r Does this child require antibiotics? but has otherwise “been fine.” Dad didn’t check his r temperature, but didn’t think he felt particularly warm. Which children with this disease entity require antibiotics? The child had been eating and drinking well, but vom- r What role does pain management play in ited one time yesterday. There has been no diarrhea. treatment of this disease? This morning, he began crying and complaining of right ear pain. Dad denies any trauma to the ear. The child has a history of two prior ear infections, the last one about 18 months ago. He has been meeting his Diagnosis developmental milestones and passed a hearing screen r Acute otitis media.

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Discussion often have fever, malaise, vomiting, and diarrhea, r or may present with otorrhea from tympanic Epidemiology: Acute otitis media is exceedingly membrane perforation.2 Older children often common in children, affecting 80 percent of 1 complain of headache and disrupted hearing, as children prior to entering school. Most children well.2 have their first episode prior to age 3.2 Many r Diagnosis:Earpaincanbeprimary or secondary children have recurrent episodes during their in etiology, and it is important for the medical childhoods. Risk factors for developing recurrent provider to determine which. Primary ear pain, or otitis media include allergy, craniofacial pain arising from the ear itself, can be caused by abnormalities, GERD, large adenoids, exposure acute otitis media, chronic otitis with effusion, to smoke, daycare attendance (or multiple otitis externa, bullous myringitis, trauma, or siblings), lack of breastfeeding, and pacifier foreign body. Innervation to the ear arises from use.3 r cranial nerves V, VII, IX, and X, as well as cervical Pathophysiology: Acute otitis media generally nerves 1–3. Therefore, referred pain to the ear can occurs secondary to eustachian tube dysfunction 1,4 be related to any structures innervated by these coincident with an acute URI. It is defined by nerves, including the temporomandibular joint, the presence of fluid in the middle ear with acute the teeth, the brain or cranium, the thyroid, or the local or systemic illness, and is distinct from otitis c-spine. media with effusion, which also consists of fluid in To make the diagnosis of otitis media, then, the middle ear but is in the absence of acute local the provider must take a history that helps to or systemic illness. Otitis media with effusion is exclude other sources of ear pain. The history not a medical emergency, and children should be should not only include items related to the ear, referred back to their pediatricians for monitoring but also to the neurologic and musculoskeletal for resolution of effusion or referral to ENT as system.Theprovidershouldaskabouttongue necessary. In acute otitis media, the middle ear function, including chewing and swallowing as fluid may contain a variety of bacterial pathogens, well as speech, should inquire about dental with Streptococcus pneumoniae and Haemophilus 2,5 symptoms or problems, and should consider influenzae historically the most common. Since trauma. Smoke exposure and alcohol use should introduction of the S. pneumoniae vaccine in the also be reviewed. USA, the relative proportion of cases of acute A complete examination for ear pain should otitis media secondary to S. pneumoniae has include inspection of the external ear, speculum decreased, and the relative proportion of those 1,2 examination of the internal ear, assessment of the secondary to H. influenzae has increased. Otitis sinuses and nose, oropharyngeal examination, media with effusion is more commonly associated 4 neurologic examination, neck examination, and with H. influenzae. skin examination. This will minimize the From the middle ear, acute otitis media can likelihood of the EM provider erroneously spread to involve other local structures, resulting attributing ear pain to the wrong source. in mastoiditis, meningitis, brain abscess, venous Per the AAP, the diagnosis of acute otitis sinus thrombosis, labyrinthitis, osteomyelitis, or mediashouldonlybemadeinchildrenwith facial nerve paralysis. Otitis media with effusion moderate to severe bulging of the tympanic does not have local or systemic inflammatory membrane or new otorrhea in the absence of otitis findings by definition, and therefore does not lead externa, or in children with mild bulging and to the same complications as acute otitis media. recent onset of significant ear pain or intense The primary morbidity of otitis media with erythema of the tympanic membrane.6 Acloudy effusion is chronic effusion with hearing loss, color to the tympanic membrane is common in which can disrupt speech development in young acute otitis media and impaired mobility of the children.4 r tympanic membrane also increases the predictive Presentation: Most children present with ear pain value of physical examination.4 The most accurate and many have ear tugging, although neither of way to assess tympanic membrane mobility is 2 these complaints is very specific. Small children with pneumatic otoscopy or tympanometry, but

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these techniques are not always feasible in agitated r Disposition: Non-toxic-appearing children can be small children, and tympanometry is not available discharged home with careful return precautions in most EDs. to follow up with their PCP within 48–72 hours. r Treatment:Acuteotitismediamaybeviralin origin, and antibiotics do not benefit every case. The AAP recommends that children be assessed Historical clues Physical findings r r and treated for pain, as this is the most common r Recent viral illness Tympanic membrane reason for their presentation to the ED.6 They History of snoring (suggesting clouding and mild enlarged adenoids and possible bulging recommend initiation of antibiotic therapy for all eustachian tube dysfunction) r Low-grade fever children6monthsofageorolderwithacuteotitis r Ear pain r Enlarged tonsils media with severe signs or symptoms (severe or moderatepainforatleast2daysanda temperature ࣙ 102.2 °F).6 In children without severe signs or symptoms, antibiotics should be Follow-Up initiated in those less than 2 years of age with 6 Dad was advised to give the child ibuprofen for ear bilateral acute otitis media. For unilateral pain, and was given a prescription for amoxicillin to non-severe disease in children less than 2, or be filled if the child was still complaining of pain unilateral or bilateral disease in children older at 48 hours after his index visit. The child was low than 2, the clinician can use deferred antibiotics risk, and deferred antibiotics are acceptable for this (“watchful waiting”) and close follow-up, or may 6 age group with non-severe disease. The child had prescribe antibiotic therapy. Children with no improved symptoms when following up with his pedi- improvement at 48–72 hours follow-up should atrician 2 days later, and was referred to ENT. The receive antibiotics. The antibiotic of choice is child’s sleep study was positive for apnea, and the child currently high-dose amoxicillin (90mg/kg per went on to have his tonsils and adenoids removed, day) in children without allergies who have not with improved snoring and no further episodes of received a beta-lactam antibiotic in the prior otitis. 30 days.6 In children whose disease is accompanied by purulent conjunctivitis, the pathogen is likely to be H. influenzae,andshould References be treated with amoxicillin–clavulanate, as it is 1. Harmes KM, Blackwod RA, Cook JM, et al. Otitis media: Diagnosis and treatment. Am Fam Phys 2013; resistant to amoxicillin alone.4 Even with 88: 435–40. antibiotics, not every child shows improvement or a shortened course. For every 20 children 2. Thomas JP, Berner R, Zahnert T, et al. Acute otitis media: A structured approach. Dtsch Arztebl Int 2014; prescribed antibiotics for acute otitis media, one 111: 151–60. will have decreased pain at day 3 of illness, and 3. LubiancaNetoJF,HembL,SilvaDB.Systematic one will get a rash, diarrhea, or vomiting from the 7 literature review of modifiable risk factors for antibiotics. Thirty-three children need to be recurrent acute otitis media in childhood. JPediatr treated to prevent a single tympanic membrane (Rio J) 2006; 82: 87–96. 7 rupture. 4. Conover K. Earache. Emerg Med Clin N Am 2013; 31: Duration of therapy is a subject of debate in 413–42. the literature, with the initial recommendation of 5. Ngo CC, Massa HM, Thornton RB, et al. Predominant 10 days of therapy stemming from literature for bacteria detected from the middle ear fluid of children treatment of other Streptococcus infections. experiencing otitis media: A systematic review. PLoS Longer courses appear more effective in younger One 2016; 11: e0150949. children,sochildrenlessthan2yearsofage 6. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The should receive a 10-day course.6 In children age diagnosis and management of acute otitis media. 2–5, 7 days of therapy appear as effective as 10, Pediatrics 2013; 131: e964–99. andsoitisreasonabletogivethesechildrena 7. Venekamp RP, Sanders SL, Glasziou PP, et al. 7-day course of antibiotics.6 In children older Antibiotics for acute otitis media in children. Cochrane than 5, 5–7 days of antibiotics are sufficient.6 Database Syst Rev 2015; 6: CD000219.

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Case 9 She resists side-to-side movement of the head. There is mild cervical adenopathy. Contributing Author: Khalief Hamden r Cardiovascular: Regular rate and rhythm, with no M/R/G. Peripheral pulses are palpable and History symmetric. The patient is a 3-year-old girl brought to the ED r Lungs: Breath sounds are normal. No evidence of because she “will not turn her head.” Mom reports labored breathing. No W/R/R. that the child’s symptoms started 3 days ago with a r Abdomen: Soft and non-tender with normal bowel high fever, cough, and nasal congestion. The next day, sounds. No distension or tenderness. No mom took the patient to her pediatrician, where she organomegaly or palpable masses. was evaluated and diagnosed with a routine URI. She r Skin and extremities:Thereisamaculopapular, was started on azithromycin. That evening the patient patchy, erythematous but blanching rash on the started complaining of pain in the back of her neck trunk. and a sore throat. Mom noted that the fever had con- r Neurologic: She is awake and alert. Face is tinued, and this morning the patient was unwilling to symmetric. Speech and gait are normal. 5/5 upper turn her head at all. Mom states that she only turns her extremity and lower extremity strength. shoulders in order to look to the side. This prompted r Pertinent laboratory values: WBC 18,300, Hb, a visit to an urgent care center where the patient was HCT, and Plt normal. ANC 12,900. advisedtocometotheEDforevaluationofpossible Comprehensive metabolic panel with bicarbonate meningitis. 18, anion gap of 20. U/A shows small amount of The patient has been tolerating fluids by mouth blood with occasional renal epithelial cells on buthasnotbeeneatingwell.Shehasbeenmaking microscopy but no other abnormalities. LP was wet diapers. Her fevers have been well controlled with performed and CSF is clear and colorless, WBC 2 antipyretics, allowing her to play and interact at her andRBC2oncellcount. baseline until today. There are no known sick contacts. r Pertinent radiographic findings:Soft-tissueneck Past Medical History X-ray and soft-tissue neck CT were performed and are shown in Figures 5.5 and 5.6. r Full term, UTD on immunizations.

Medications Questions for Thought r Azithromycin. r How do patients typically present with this illness? Allergies r What laboratory findings would support this r NKDA. diagnosis? r What is the role of imaging studies in making the Physical Examination and Ancillary Studies diagnosis? r r Vital signs: T 98.3 °F, HR 129, RR 25, BP 137/75, What findings on X-ray are considered abnormal? r What treatments should be initiated in the ED? O2 sat 98% on room air. r What is definitive treatment of this condition? r General: The patient is non-toxic-appearing. There is no respiratory distress. She is interactive. r HEENT: Normocephalic and atraumatic. Extraocular movements are normal. PERRL. Diagnosis Tympanicmembranesnormalbilaterally.Oral r Acute retropharyngeal abscess. mucosa is moist with mildly enlarged tonsils, withoutsignificanterythemaorexudate.Nasal Discussion congestion is present with some cobblestoning of r Epidemiology: The incidence of retropharyngeal the nasal mucosa. abscess in the USA has increased over the last r Neck: The patient has decreased mobility of her decade. Using the Kid’s Inpatient Database, neck. She will not turn her head when tracking Woods et al. report that the incidence of side to side, instead turning only her shoulders. retropharyngeal abscess from 2003 to 2012 has

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Figure 5.5 Lateral view of the c-spine. The film demonstrates prevertebral edema of 1.5 cm concerning for a retropharyngeal abscess.

Figure 5.6 CT cervical soft tissue with IV contrast. These images demonstrate a fluid collection measuring approximately 9 x 8 x 11 mm at the level of C3 with prevertebral soft-tissue swelling from the skull base to approximately C6, consistent with a retropharyngeal abscess.

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increased dramatically from 2.98 to 4.10 per Lateralneckradiographsareareasonable 100,000 children.1 The disease is more common in screening test but may appear normal as often as younger children under the age of 6 but can also 12 percent of the time.2,4 Prevertebral edema is afflict older children and even adults. Males are suggested when the distance from the anterior affected more commonly than females. The surface of the vertebrae to the posterior border of disease is also more commonly diagnosed in the the airway exceeds 7 mm at the level of C2 or winter and spring months. 14 mm at the level of C6 in a child. r Pathophysiology: Retropharyngeal abscesses are an When there is a high degree of suspicion, a infrequent complication of URIs and ear contrast-enhanced CT of the soft tissue of the infections. There are many potential bacterial neck is the diagnostic study of choice. Sedation culprits, including Gram-positive organisms, may be needed to obtain a contrast-enhanced CT Gram-negative organisms, and species from the scan. MRI is probably superior for the evaluation respiratory tract, particularly anaerobes. Thus, of soft-tissue infection but availability and the polymicrobial treatment is indicated. necessity for sedation limit its utility in the ED. The lymphatic drainage of these tissues Since these children may have airway proceeds through the retropharyngeal space into a compromise, sedation should be done for CT pair of paramedian lymph node chains between scanning cautiously. Prudence may warrant ENT the base of the skull and the level of T1.2 consultation with examination under anesthesia Suppuration of these lymph nodes may result in in the OR for particularly ill children. abscess formation, which subsequently allows for r Treatment: The mainstay of treatment is antibiotic the spread of infection to adjacent structures such therapy. Clindamycin or ampicillin–sulbactam are as the jugular vein, carotid artery, or distally into considered first-line treatment options. They will the mediastinum. In younger children, the not, however, provide the ideal and perfect retropharyngeal lymph nodes are quite prominent coverage for Gram-positive organisms. Therefore, but usually regress and involute by early vancomycin or linezolid may be added to combat adolescence. This is a potential explanation for the MRSA or group A streptococci. decreased incidence in children over the age of 6. Several recent studies have demonstrated that r Presentation: The presentation of retropharyngeal many children do well without surgical abscess is completely variable. The age of the child, intervention.5–9 A rational protocol for surgical as well as abscess size and location, determines the intervention was suggested by Hoffman et al., presentation. The disease is usually preceded bya which suggests drainage only for abscesses greater URI and therefore symptoms of fever, cough, than 20 mm in diameter or in the case of sepsis, congestion, rhinorrhea, and sore throat are airway obstruction, or vascular compromise.5 If common.3 Antibiotics may have been prescribed not responding to antibiotics within 24–48 hours, without improvement (or even worsening of repeat imaging and consideration of surgery or symptoms). Older children may complain of pain CT-guided needle aspiration may be with swallowing whereas children too young to warranted.5–9 verbalize complaints may simply have poor oral r Disposition: Children with retropharyngeal intake. More suggestive of the diagnosis is neck abscess should be admitted to the hospital for IV stiffness or torticollis. Trismus, neck swelling, or antibiotics. ENT consultation for management adenopathy may also be present. In the case of decisionsisappropriate. severe disease, symptoms of airway obstruction, such as respiratory distress or stridor, may be present. Children may also present with sepsis. Historical Physical r Diagnosis: Physical examination findings of clues findings Ancillary studies r r r nuchal rigidity or neck stiffness in a child with the r Fever r Fever r Elevated WBC aforementioned presentation should prompt Recent URI Torticollis Negative LP (reducing r Worsening on likelihood of meningitis) further investigation. Leukocytosis and elevated r r antibiotics Neck X-ray with widened inflammatory markers such as sedimentation rate Neck stiffness r prevertebral space and/or CRP may also raise clinical suspicion. CT with abscess

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Follow-Up 4. Craig FW, Schunk JE. Retropharyngeal abscess in This patient was found to have a small retropharyngeal children: Clinical presentation, utility of imaging, abscessonCTscanoftheneckatacommunityhospi- and current management. Pediatrics 2003; 111: 1394–8. tal ED. The case was discussed with a pediatrician ata nearby tertiary care facility and the patient was trans- 5. Hoffman C, Pierrot S, Contencin P, et al. Retropharyngeal infections in children. Treatment ferred by ambulance and admitted to the pediatric strategies and outcomes. Int J Pediatr Otorhinolaryngol floor. The following day she was evaluated by ENT who 2011; 75: 1099–103. decided against draining the abscess due to the small 6. GeorgetE,GauthierA,BrugelL,etal.Acutecervical size and positive response to IV antibiotics. She had lymphadenitis and infections of the retropharyngeal an uneventful hospital course. She was noted to have and parapharyngeal spaces in children. BMC Ear Nose some improvement in rotating her head on hospital Throat Disord 2014; 14: 8. day 3. On hospital day 4 she had resolution of her fever 7. Martin CA, Gabrillargues J, Louvrier C, et al. and was able to tolerate food by mouth. She was subse- Contribution of CT scan and CT-guided aspiration quently discharged on hospital day 4 with instructions in the management of retropharyngeal abscess in tofinisha10-daycourseoforalclindamycin. children based on a series of 18 cases. Eur Ann Otorhinolaryngol Head Neck Dis 2014; 131: References 277–82. 8. Grisaru-Soen G, Komisar O, Aizenstein O, et al. 1. Woods CR, Cash AM, Smith MJ, et al. Retropharyngeal and parapharyngeal abscess in Retropharyngeal and parapharyngeal abscesses among children: Clinical presentation, utility of imaging, and children and adolescents in the United States: current management. Int J Pediatr Otorhinolaryngol Epidemiology and management trends, 2003–2012. 2010; 74: 1016–20. JPediatrInfectDisSoc2016; 5: 259–68. 9. Cramer JD, Purkey MR, Smith SS, et al. The impact of 2. Coulthard M, Isaacs D. Retropharyngeal abscess. Arch delayed surgical drainage of deep neck abscesses in Dis Child 1991; 66: 1227–30. adult and pediatric populations. Laryngoscope 2016; 3. Stoner MJ, Dulaurier M. Pediatric ENT emergencies. 126: 1753–60. Emerg Med Clin N Am 2013; 31: 795–808.

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Case 1 r HEENT:Noevidenceofheadtrauma.Neckis supple. Contributing Author: Rebecca Jeanmonod r Cardiovascular:Normalheartrate,without murmur or arrhythmia. Normal capillary refill. History r Lungs: Clear and equal, with good air entry. An 18-month-old girl presents to the ED with mom r Abdomen: Soft and non-tender, with no rebound, complaining of arm pain. Mom states the child was guarding, or masses. playing unsupervised with a 4-year-old sibling in their r Skin and extremities:Radialandfemoralpulses shared bedroom when she heard crying. When she are 2+, and skin is warm and well-perfused. Child went in the room, the 18-month old indicated she is holding her right arm semi-flexed and had pain in her right arm. The 4-year-old was unable pronated. There is no swelling or deformity, no to tell mom what happened. Mom did not see any bruising or rashes. signs of trauma to the child, so she did not bring r Neurologic: Normal sensation in affected limb, her in immediately. However, after 3 hours, the child otherwise normal examination. wasstillnotusingherarm,somombroughther in for further evaluation. The child has been consolable since the event, but periodically cries when Questions for Thought sheattemptstomovethearm.Shehasnothadcon- r Do you need to get a radiograph on this child’s fusion, vomiting, difficulty breathing, or any other arm? complaints. r What is the best way to reduce this injury? r What are the items on the diﬀerential diagnosis Past Medical History that are important to not miss? r The child was a term neonate born by NSVD. She has had all her immunizations and has not had any other health problems. Diagnosis r Radial head subluxation, or nursemaid’s elbow. Medications r None. Discussion r Epidemiology: Nursemaid’s elbow is a common Allergies injury of childhood. Most cases occur in children r under the age of 5, with the majority under 2 years NKDA. of age.1,2 It is slightly more common in female children and more commonly involves the left Physical Examination and Ancillary Studies arm.1,2 It can recur in up to 25 percent of r 1,2 Vital signs: T 98.6 °F, HR 110, RR 25, BP 90/40, O2 susceptible individuals. It is rarely bilateral, and sat 100% on room air. seldom occurs in adults. r General:Awake,alert,interactive,withnormal r Pathophysiology: Nursemaid’s elbow occurs when work of breathing, mental status, and perfusion. the annular ligament that attaches the proximal Child is not in distress. end of the radius to the ulna becomes displaced

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and entrapped at the radiocapitellar joint. This is manner, but the affected arm is fully pronated and generally precipitated by tractional force applied straightened while pressure is applied to the radial to the pronated arm, although it has also been head. Both methods are similar in ease of reported with falls and even with rolling over.1,2 performanceaswellasintermsofpainforthe The force required to cause the injury is minor, child, but the hyperpronation technique has a and the elbow typically shows no evidence of higher first-attempt success rate, and should be swelling, ecchymosis, or deformity. attempted first.4,5 r Presentation: The patient usually presents with the r Disposition: Most children with a reduced history of tractional force applied to the arm, nursemaid’s elbow will move their arm within although the event may have been unwitnessed or minutes after reduction. Some may be delayed for unclear. The child will not use the arm, and often hours, however. If a child continues not to use the holds it semi-flexed and pronated, while arm, the provider can consider performing a supporting it with the unaffected arm. radiograph to rule out occult fracture or may r Diagnosis: It is important to consider the attempt repeat reduction. With negative films and possibility of occult supracondylar fracture or ongoing pain, the child can be placed in a splint child abuse in children with elbow pain. Arthritis, and reassessed at 24 hours. Parents should be whetherinfectious(forexample,Lymediseaseor educated as to the etiology of this disease process, Staphylococcus aureus)orimmune-mediated,may and may be taught reduction techniques to apply also present with elbow pain. One of the at home prior to deciding whether they need to important distinguishing factors is that children visit the ED. with nursemaid’s elbow have a normal examination, without systemic findings, skin Historical clues Physical findings findings, or musculoskeletal abnormalities. Their r Child in appropriate r No musculoskeletal abnormality radiographs, if performed, are also typically age group r Held in “nursemaid’s position” normal.3 r Isolated elbow pain The critical evaluation of a child with nursemaid’s elbow is a thorough history and a Follow-Up carefulexamination.Thereisnorolefor radiography in the diagnosis of nursemaid’s The baby’s elbow was reduced with hyperpronation elbow, although imaging may rule out other and extension and she was pain free and using the arm pathologic entities. Certainly, in the child with a prior to discharge. typical history, nursemaid’s elbow can be treated presumptively. There is some evidence that, in References children without the typical history but 1. Vitello S, Dvorkin R, Sattler S, et al. Epidemiology of presenting with a benign examination and nursemaid’s elbow. West J Emerg Med 2014; 14: holding their arms in the typical position, 554–7. reduction may be attempted without prior 2. Irie T, Sono T, Hayama Y, et al. Investigation on 2331 radiography. If reduction is not able to be cases of pulled elbow over the last 10 years. Pediatr Rep performed empirically, radiography should be 2014; 6: 5090. considered to rule out occult fracture. 3. GuzelM,SaltO,DemirMT,etal.Comparisonof r Treatment: Treatment of nursemaid’s elbow hyperpronation and supination–flexion techniques in children presented to emergency department with involves manipulation of the elbow to reduce the painful pronation. Niger J Clin Pract 2014; 17: 201–4. interposed annular ligament. There are two 4. Eismann EA, Cosco ED, Wall EJ. Absence of commonly employed reduction techniques. In the radiographic abnormalities in nursemaid’s elbows. J first, the child is held firmly on the caregiver’s lap Pediatr Orthop 2014; 34: 426–31. and the affected arm is completely supinated and 5. Gunaydin YK, Katirci Y, Duymaz H, et al. Comparison then fully flexed while pressure is placed on the of success and pain levels of supination–flexion and child’sradialheadwiththeoperator’sthumb.In hyperpronation maneuvers in childhood nursemaid’s the second method, the child is held in the same elbow cases. Am J Emerg Med 2013; 31: 1078–81.

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Case 2 right medial malleolus, heel, mid foot, or right lower leg. There is mild swelling of the lateral Contributing Author: Lauren Snyder right ankle without ecchymosis, with mild pain on palpation of the area anterior and inferior to the History lateral malleolus, but non-tender over the bony The patient is a 17-year-old male who presents to the malleolus itself. He has pain with talar tilt testing ED following an ankle injury at school. The patient with varus stress. The patient has intact sensation reports that he was playing catch and tripped as he was andisabletomovealltoesoftherightfoot. running for the football. The patient states he “rolled” Peripheral pulses are intact with 2+ dorsalis pedis his ankle, motioning to demonstrate ankle inversion. pulse palpable on examination bilaterally. The There was a hole in the grass that caught his right foot, patient is able to bear weight and take four steps which twisted his ankle. After the injury, he began to with a slight limp while in the ED. The skin is have pain and difficulty walking, prompting the school warm and well-perfused. nursing staff to send him to the ED for evaluation. He r Neurologic: The patient is alert and is able to state reports right lateral ankle pain and swelling, but denies his name, current location, and the date. No focal numbness or tingling. The patient notes he still has dif- neurologic deficits are observed during ficulty walking in the ED. examination. r Pertinent imaging: Radiographic series of the right Past Medical History ankleisnegativeforfractureordislocation,but r The patient denies any previous medical history does identify mild soft-tissue swelling and is UTD on his vaccinations. He lives with surrounding the lateral ankle. both parents and attends high school.

Medications Questions for Thought r None. r What is the utility of obtaining X-rays in this patient? r Allergies Which patients need X-rays with the complaint of r NKDA. ankle pain? r Which ligaments are involved in the injury? How do you examine for these ligaments? Physical Examination and Ancillary Studies r How is the mechanism of injury helpful in r Vital signs: T 97.9 °F, HR 62, RR 16, BP 129/70, O2 determining the structures involved in the injury? sat 100% on room air. r General: The patient is alert and with occasional facial grimaces secondary to ankle pain. Diagnosis r HEENT: PERRL, intact extraocular movements. r Grade I sprain of right anterior talofibular Oropharynx is clear. ligament. r Neck: Supple, with no midline tenderness or step-offs. Discussion r Cardiovascular: Regular rate and rhythm, no r Epidemiology: Ankle sprains, defined as a M/R/G, normal peripheral perfusion. stretching, partial tear, or complete tear of at least r Lungs: CTA bilaterally, respirations are one ligament, are one of the most common non-labored, breath sounds are equal. complaints in EDs. According to the CDC, in r Abdomen: The abdomen is soft and non-tender to 2011 the USA had 1.6 million ED visits for palpation, non-distended, and with normal active injuries of the lower leg and ankle, with ankle bowel sounds. sprains accounting for an estimated 85 percent of r Skin and extremities:Therightanklehaslimited all ankle injuries.1 active and passive range of motion secondary to r Pathophysiology: The pathophysiology of all pain. There is no tenderness to palpation of the sprains is related to injury to ligaments, in

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distinction from strains, which are related to Table 6.1 Grading of ankle sprains injuries of tendon–muscle complexes. Any joint Physical canbestrainedorspraineddependingonthe Ligamentous signs and individual ligaments or tendons involved. As a injury symptoms Ambulation general principle, joints with a greater degree of Grade I Ligament Mild swelling and Minimal pain mobility (such as the shoulder) undergo strain stretched tenderness with more frequently, and those with less mobility beyond normal weight-bearing range of motion and (such as the knee) undergo sprain more resulting in ambulation frequently. Any joint that is completely disrupted microscopic by sprain or strain warrants urgent orthopedic tears consultation. Fortunately, it is relatively Grade II Incomplete Moderate pain, Weight- uncommon for a patient to have complete ligament tear swelling, bearing and ecchymosis, and ambulating are disruption of any joint, and most patients present tenderness. May painful with some combination of pain, swelling, and have joint dysfunction that can be managed with instability and restricted range immobilization, symptom management, and of motion outpatient referral to sports medicine or Grade III Complete Severe pain, Unable to bear orthopedics. ligament tear swelling, weight or Ankles are the most common joint to suffer tenderness, and ambulate 1–4 ecchymosis. sprain injury. The pathophysiology of ankle Significant joint sprains is related to the mechanism of injury and instability with the ligaments involved. The lateral ankle loss of function ligaments are most frequently injured, with and motion medial ankle ligaments and ligaments between the tibia and fibula (including the IO membrane) less commonly involved.2 strength of the deltoid ligament and thus is A grading system is traditionally used to uncommon.2–4 classify ankle sprains, with grades I, II, and III A syndesmotic sprain, sometimes referred to describing the severity of ligamentous tear that as a “high ankle sprain,” involves injuries to the occurred (Table 6.1). Based on the physical ligaments connecting the tibia and fibula, which examination findings, clinicians can use the are also essential for ankle stability. Dorsiflexion grading system to classify the degree of ankle and/or eversion of the ankle can cause injury to sprain.2–4 the anterior tibiofibular, posterior tibiofibular, Lateral ankle sprains are the result of foot transverse tibiofibular ligaments, or the IO inversion, often with the foot in plantar flexion. membrane. A syndesmotic ankle sprain is more This mechanism causes damage to the lateral likely to occur in an individual with recurrent ankle ligaments in a predictable fashion as the ankle sprains and chronic ankle instability. forces of the injury increase. The lateral ankle r Presentation: In the majority of cases, patients will ligaments include the anterior talofibular be able to identify the exact time of onset of their ligament, the calcaneofibular ligament, and the pain, as ankle sprains are an acute injury that most posterior talofibular ligament. Generally, the often result from stress to the ankle joint due to a ligaments are injured in that order as the forces of traumatic event. Patients’ major complaints will the injury increase. In the majority of all ankle include pain, swelling, tenderness, and difficulty injuries, the anterior talofibular ligament is the with ambulation and movement. Depending on only ligament that is injured.2–4 the grade of the ankle sprain, the patient will have The ligament of the medial ankle, the deltoid varying degrees of pain, swelling, ecchymosis, and ligament, is infrequently injured, as the inability to bear weight or ambulate. In patients mechanism of injury is forced eversion of the foot. who suffer major trauma, other injuries take This requires a larger amount of force due to the priority and ankle sprains may go undiagnosed.

16:14:23 07 Chapter 6: Extremity Complaints r Diagnosis: The diagnosis of ankle sprain is made that while the Ottawa Ankle Rules have been clinically, based on the history and mechanism of tested and validated in adult patients, they can the injury along with findings on physical still be helpful when applied to pediatric patients.7 examination.2–4 Radiographs are not helpful in If the following criteria are met, radiographs of identifying sprains, although they are often thefootorankleshouldbeobtained: obtained to identify associated fractures that may have resulted from the injury.5 In pediatric Ankle series radiographs are indicated in patients, ankle injuries may also cause fractures patients with pain in the malleolar zone AND: through the growth plate (Salter–Harris r bony tenderness at the posterior edge of fractures). The growth plate is a relatively weak distal 6 cm or tip of the lateral malleolus OR; structure and can fracture even without severe r bony tenderness at the posterior edge of the ligamentous injury. It is often difficult to distal 6 cm or tip of medial malleolus OR; distinguish Salter–Harris type I fractures from r inability to bear weight both immediately sprains, and so traditionally these injuries are after the injury and for four steps in the ED. treated as fractures with splinting of the ankle. There is some debate regarding how much Foot series radiographs are indicated in patients immobilization should occur with possible with pain in the midfoot zone AND: Salter–Harris type I fractures of the distal r bony tenderness at the base of the fifth 5,6 fibula. metatarsal OR; When evaluating a patient with ankle trauma, r bony tenderness at the navicular OR; it is important to gather the following pieces of r inability to bear weight both immediately information: after the injury and for four steps in the ED. r the mechanism of injury; r Treatment: For ankle sprains, initial treatment is r thepatient’sabilitytobearweightorambulate conservative irrespective of the grade of the following the injury; sprain. RICE (rest, ice, compression, elevation) is r prior injury to the ankle. the treatment of choice for initial management, r A thorough physical examination in addition to encouraging the patient to limit weight-bearing the history and mechanism of injury will aid in with use of crutches until their normal gait forming the diagnosis of ankle sprain. In addition returns, applying ice or cold-water immersion to examining the ankle itself, the fibula, distal every few hours initially, compression with soft tibia,foot,knee,andAchillestendonshouldalso elastic bandage to minimize swelling, and be assessed for tenderness or injury, and a elevation above the level of the heart whenever complete neurovascular examination should be possible, to minimize swelling. Additionally, performed.2–4 Clinicians should assess the ankle’s NSAID medications can be used for pain control passive range of motion, checking for pain with as needed. gentle eversion and inversion, which can assist in Once the pain and swelling abate, patients localizing the area of injury. The clinician should should be encouraged to gently exercise the ankle also test for ligamentous instability with anterior joint with gradual increase in range of motion. drawertestingaswellastalartilttesting, Ankle splints or braces can assist in limiting the comparing the affected to the unaffected side for extremes of joint motion and allow weight- firmness of endpoint and laxity. bearing while protecting against re-injury. r The Ottawa Ankle Rules were developed in an Grade1anklesprainsdonotrequire effort to reduce the number of plain films obtained immobilization, and a soft elastic bandage for in those acute ankle injuries in which fracture is swelling can be applied for a few days following less likely. The set of rules has been extensively the injury. Grade II and III sprains will require tested and validated for ED adult patients with additional support, including an aircast or similar acute ankle injuries, and is very sensitive for splint in addition to the elastic bandage, for up to excluding ankle fracture.7,8 It should be noted afewweeksfollowingtheinjury.2–4

16:14:23 5 07 Chapter 6: Extremity Complaints r Disposition: Most patients with ankle sprain injury 6. Boutis K. Common pediatric fractures treated with will be able to return home for the duration of minimal intervention. Pediatr Emerg Care 2010; 26: their recovery without requiring a hospital stay. 152–7. However, in a few cases that have additional 7. Plint AC, Bulloch B, Osmond MH, et al. Validation of injuries, complications, or other reasons for the Ottawa Ankle Rules in children with ankle injuries. admission, the patient may require inpatient Acad Emerg Med 1999; 6: 1005–9. status. For cases involving fracture, dislocation or 8. StiellIG,McKnightRD,GreenbergGH,etal. subluxation, syndemosis injury (“high ankle Implementation of the Ottawa ankle rules. JAMA sprain”), tendon rupture, penetrating wound 1994; 271: 827–32. involving the joint, or a patient with neurovascular compromise (decreased sensation Case 3 or circulation distal to the injury), prompt evaluation and possible orthopedic consultation Contributing Author: Melanie K. should be completed. All ankle injuries should be Prusakowski re-evaluated in the outpatient setting, so the patient should be made aware of this and set up an History appointment with their PCP, sports medicine, or The patient is a 9-year-old boy who presents with an orthopedic office for continued management and inability to bear weight on his left leg. Five days ago he clearancetoreturntosportsandactivities. fell during a soccer game without any known resulting injury. He developed mild left knee pain the next day. For 3 days he has complained of increasing knee Historical clues Physical findings Ancillary studies r r r pain and developed a worsening limp. Yesterday he Inversion injury Swelling to lateral Negative X-ray had less appetite and felt warm. His mother provided r Pain with aspect of ankle ambulation r Pain with talar tilt a weight-appropriate dose of ibuprofen and he seemed stress on anterior to improve. This morning he woke with a fever of 101.8 talofibular ligament °Fandcannotstandonhisleftleg.Hereportsno swelling of the knee. He denies numbness or tingling Follow-Up of the leg or foot, and has no back pain. The patient Although the child did not meet criteria for imag- doesnotreportdysuriabutstatesthattryingtostand ing as per Ottawa Ankle Rules, he received an X-ray, makes his belly and knee hurt. which was ordered from triage and was negative. He Past Medical History was given an elastic wrap for his ankle and discharged r The patient had tympanostomy tubes placed when to follow up with sports medicine. hewas3yearsofage. r References Exercise-induced asthma. 1. Centers for Disease Control and Prevention. National Medications hospital ambulatory medical care survey: 2010 r Ibuprofen, last dose yesterday. Emergency department summary tables. See www.cdc r .gov/nchs/data/ahcd/nhamcs emergency/2010 ed Albuterol metered-dose inhaler, last used 5 days web tables.pdf (accessed January 2017). ago. 2. Hanlon DP. Leg, ankle, and foot injuries. Emerg Med Allergies Clin N Am 2010; 28: 885–905. r 3. Wedmore IS, Charette J. Emergency department NKDA. evaluation and treatment of ankle and foot injuries. Emerg Med Clin N Am 2000; 18: 85–113 Physical Examination and Ancillary Studies r ° 4. TiemstraJD.Updateonacuteanklesprains.Am Fam Vital signs: T 101.3 F, HR 112, RR 18, BP 98/51, Phys 2012; 85: 1170–6. O2 sat 98% on room air. r 5. Boutis K, Plint A, Stimec J, et al. Radiograph-negative General:Thepatientisamildly lateral ankle injuries in children: Occult growth plate anxious-appearing, well-developed boy, who fracture or sprain? JAMA Pediatr 2016; 170: e154114. appears somewhat uncomfortable.

16:14:23 07 Chapter 6: Extremity Complaints r HEENT: PERRL. Oropharynx clear with no r Pathophysiology:Mostcasesofpediatricseptic exudates. Mucous membranes moist. arthritis are the result of hematogenous spread of r Neck: Supple and non-tender, with no adenopathy. bacterial infection, but direct inoculation can r Cardiovascular:Mildtachycardia,withnoM/R/G. result from nearby bone and soft-tissue infection, 1 r Lungs: Lungs are symmetric and clear, with no penetrating injury, or iatrogenically. Synovial W/R/R. tissue has no basement membrane, so r Abdomen:Soft,withactivebowelsounds.Mild blood-borne organisms can pass into the joint tenderness to palpation of the left lateral pelvis. space and synovial fluid. The most common r Extremities and skin:Thereisfullpassiverangeof causative organism is Staphylococcus aureus, followed by group A streptococci and motion in the patient’s left knee, but internal 1 rotation of the left thigh results in pain. There are Enterobacter. Children with sickle cell disease are no knee joint effusions, no erythema of the knee also at risk for salmonella joint or bone infections. or thigh, no calf tenderness, and no edema or MRSA is an increasing consideration, especially clubbing bilaterally. His sensation and dorsalis in patients with a known prior history or current pedis pulses are normal. There is no pallor or signs of MRSA soft-tissue infection. Kingella rash. kingae has been increasingly implicated in osteoarticular infections of children less than 4 r Pertinent laboratory values: WBC 13,600, CRP 9.1 years old.1,3 Neisseria gonorrhoeae is a mg/dL. consideration in sexually active adolescents and r Pertinent radiographs:X-rayofthepelvisandleft young adults. Once bacteria spread to the joint hip demonstrate no fractures, dislocation, or and initiate the inflammatory cascade, masses. No evidence of osteomyelitis. U/S of the inflammatory mediators cause destruction to left hip reveals a small intra-articular effusion. articular cartilage in as little as 8 hours.1 Permanent damage to the cartilage and 1 Questions for Thought sub-chondral bone may occur within 3 days. r r Presentation: Pediatric septic arthritis occurs in What other laboratory diagnostics could help 1 make the diagnosis? the lower limbs 80 percent of the time. Patients r What are the typical laboratory ﬁndings in this often present with a limp or refusal to bear 1,2 condition? weight. Classically, patients have pain with even r What are some considerations to guide the use of very small passive movements of the affected radiographic diagnostic modalities? joint.Feveriscommon,butabsentinupto20 r What treatment should be initiated in the ED? percent of patients. For this reason, lack of fever r What is the deﬁnitive treatment of this condition? cannot rule out septic arthritis. The classic signs of warmth, erythema, and edema are less often seen in septic arthritis of the hip, but may be more Diagnosis evident in smaller joints. Neonatal patients with r Septic arthritis of the left hip. septic arthritis can be difficult to diagnose, since they may lack classic signs of joint swelling or Discussion warmth and can present with only irritability or r Epidemiology: Septic arthritis is a joint-space and limited motion of a limb. It is not uncommon for synovial-fluid infection, most commonly affecting the joint pain to be attributed to an incidental largejointssuchasthehip(20percent)orknee trauma that is unrelated. r (40 percent). The incidence is about 10 cases in Diagnosis:Achildpresentingwithanisolated 100,000 children, with most cases occurring in limp or refusal to bear weight is a diagnostic children less than 3 years of age.1 Boys are affected challenge. The provider must determine if the more commonly than girls.1,2 At-risk populations abnormalgaitisrelatedtopain,weakness(aswith include patients who are less than 3 years of age, neuromuscular disorders), or anatomic processes immunocompromised hosts, or children lacking a (for instance, dysplasia). Once the provider functional spleen (i.e. splenectomy, sickle cell determines that the gait problem is secondary to disease).1,2 pain, he or she must carefully consider other more

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common etiologies of pediatric joint pain, such as arthritis in the study population; three of the transient synovitis, trauma, and juvenile criteria is 93 percent specific.5 Similarly, having idiopathic arthritis, as well as other infectious only one of the four criteria reduces the risk of a etiologies, such as osteomyelitis, Lyme disease, septic hip to only 3 percent.5 Other studies have cellulitis, and psoas muscle abscess.2 History can failed to reproduce this positive predictive help in narrowing down these possibilities. Pain value.8 that was acute in onset and is associated with an Assessment of synovial fluid obtained by activity is more likely to be traumatic. Pain that is arthrocentesis is the standard diagnostic modality. worse at night suggests malignancy. Pain that is Typically, the synovial fluid WBC will be Ͼ 50,000 better with activity suggests rheumatologic in a septic joint.9 Gram’s stain is positive in only disease, while that which is worse with activity 30 percent of pediatric patients, but blood culture suggests an overuse injury. Pain with systemic can identify the organism in some instances of symptoms is concerning for an infectious process, hematogenous dissemination.9 Molecular be it arthritis, osteomyelitis, or abscess, or diagnostic studies, such as PCR, enhance potentially a malignancy. discovery of infectious organisms such as N. Examination is also helpful to rule out other gonorrhoeae, Borrelia burgdorferi,andK. kingae.9 processes. It is important to examine the child Although joint aspiration is the current gold thoroughly, assessing for rashes (that might standardfordiagnosis,itisnotperfectly suggest endocarditis or gonococcal infection or reliable.9 erythema migrans), abdominal pain (suggesting r Treatment: Bacterial septic arthritis is a medical psoas abscess or acute abdomen with referred hip emergency. Treatment requires drainage and pain), strength and sensation (to assess for antibiotic therapy.1,9 Drainage of the affected joint neuromuscular processes), and a thorough is traditionally done as an open procedure, but assessment of the limb itself, palpating for masses, aspiration or serial aspirations can be part of the effusion, tenderness, and deformity. management of smaller joints, as well as part of Radiographs can be helpful in the work-up of the diagnosis.9 Ideally, samples are obtained pediatric joint pain, as they are a reasonable initial before beginning antimicrobial therapy unless screen for cancers, malformations, and abuse.2 patient acuity (i.e. sepsis) prohibits it. Because the However, small effusions may be missed by plain causative pathogen in most pediatric septic film. MRI is sensitive and specific for detecting arthritis is a Gram-positive microorganism, osteomyelitis or septic arthritis of the pediatric beta-lactam antibiotics are typical first-line hip,buthasnotbeentestedinotherjoints.2 U/S is treatment. Broader-spectrum antimicrobials are a sensitive, non-invasive modality for hip effusion appropriate in children who present with signs of that can usually be performed without sedation in sepsis or underlying immune compromise. Gram’s pediatric patients.2 It can also aid arthrocentesis stain of the joint aspirate can direct treatment and for diagnosis or treatment. However, an effusion coverage can be narrowed pending cultures. seen on U/S cannot differentiate the more The duration of IV antibiotic treatment for prevalent transient synovitis from bacterial septic pediatric septic arthritis can be 1 to 7 weeks. arthritis, and it may not demonstrate an effusion Transition to oral antimicrobials is typically in septic arthritis if it is performed very early in dictated by a combination of defervescence, thecourseofillness.4 return of joint mobility, and normalization of Elevated WBC, CRP, and ESR values suggest inflammatory markers like CRP.10 A brief course infection, but are non-specific for septic of low-dose steroids may ameliorate some of the arthritis.5–8 The Kocher criteria can be used as a joint dysfunction after septic arthritis and may clinical decision tool to differentiate septic improve symptoms if started early in the disease arthritis from other painful hip etiologies. The course.11 four criteria are: refusal to bear weight on the Complications of late or inadequate treatment affected side, an ESR Ͼ 40 mm/hr, WBC Ͼ of pediatric septic arthritis include joint capsule 12,000, and presence of fever.5 The presence of all damage, chronic arthritis, growth disturbances, four criteria has a 99 percent specificity for septic osteomyelitis, joint subluxation, and sepsis.

16:14:23 07 Chapter 6: Extremity Complaints r Disposition: Pediatric patients with septic arthritis of the hip in children. A prospective study. J Bone Joint should be admitted for joint drainage and IV Surg Am 2006; 88: 1251–7. antibiotics. Patients are at risk for sepsis and 7. Levine MJ, McGuire KJ, McGowan KL, et al. readmission for under-recognized associated Assessment of the test characteristics of C-reactive osteomyelitis. Factors associated with poorer protein for septic arthritis in children. JPediatrOrthop prognosis include delay in treatment (especially 2003; 23: 373–7. more than 4 days of symptoms), younger age, and 8. Luhmann SJ, Jones A, Schootman M, et al. S. aureus infection. Differentiation between septic arthritis and transient synovitis of the hip in children with clinical prediction algorithms. J Bone Joint Surg Am 2004; 86-A: 956–62. Historical clues Physical findings Ancillary studies 9. Kang SN, Sanghera T, Mangwani J, et al. The r r r management of septic arthritis in children: Systematic Complaint of r Fever r Elevated WBC knee pain (hip Pain with internal r Elevated CRP review of the English language literature. J Bone Joint often refers to rotation of left hip Negative X-ray Surg Br 2009; 91: 1127–33. knee) r Tenderness in left r U/S with hip r Fever pelvis effusion 10. Arnold JC, Cannavino CR, Ross MK, et al. Acute r Inability to bear bacterial osteoarticular infections: Eight-year analysis weight of C-reactive protein for oral step-down therapy. Pediatrics 2012; 130: e821. Follow-Up 11. Odio CM, Ramirez T, Arias G, et al. Double blind, randomized, placebo-controlled study of The child received a left hip U/S-guided arthrocente- dexamethasone therapy for hematogenous septic sis. The joint aspirate had elevated WBC of 89,000. He arthritis in children. Pediatr Infect Dis J 2003; 22: 883. was admitted for an operative joint drainage and 4 days of IV cefazolin. The child was intermittently febrile for the first 48 hours of admission. The joint aspirate Case 4 culture grew S. aureus sensitive to cephalosporins. On the third day he had increased range of motion of the Contributing Author: Dorka M. hip and was willing to bear weight. When he tolerated Jimenez´ Almonte oral intake, the patient was discharged on 10 days of cephalexin. History An 8-year-old boy presents with left knee pain and References bleeding after he suffered an injury while running at theschoolgymjustpriortoarrivaltotheED.The 1. Ceroni D, Kampouroglou G, Anderson della Llana R, et al. Osteoarticular infections in young children: patient was playing at the gym when a friend acciden- What has changed over the last years? Swiss Med Wkly tally pushed him. The patient fell and his left lower 2014; 144: w13971. extremity slipped under a metal frame. The patient had 2. NaranjeS,KellyDM,SawyerJR.Asystematic immediatepaintohisleftkneearea.Hewasableto approach to the evaluation of a limping child. Am Fam standandwalk,butthennoticedacutonhisknee. Phys 2015; 92: 908–18. Moving the knee aggravates the pain, but the child 3. Yagupsky P, Porsch E, St Geme JW 3rd. Kingella denies any difficulty moving the knee otherwise. The kingae: An emerging pathogen in young children. patient denies any associated symptoms such as tin- Pediatrics 2011; 127: 557–65. gling or numbness. He also denies any other injuries. 4. Gordon JE, Huang M, Dobbs M, et al. Causes of The patient’s parents report his immunizations are cur- false-negative ultrasound scans in the diagnosis of rent,hereceivedthefifthdoseoftetanusimmuniza- septic arthritis of the hip in children. JPediatrOrthop tion at the age of 5. 2002; 22: 312–16. 5. KocherMS,ZurakowskiD,KasserJR.Differentiating Past Medical History between septic arthritis and transient synovitis of the r hip in children: An evidence-based clinical prediction Mild intermittent asthma. algorithm. J Bone Joint Surg Am 1999; 81: 1662–70. 6. Caird MS, Flynn JM, Leung YL, et al. Factors Medications r distinguishing septic arthritis from transient synovitis Albuterol as needed.

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Allergies common problem faced by the ED provider. One r NKDA. out of three injuries in children involve a laceration, with boys injured more commonly Physical Examination and Ancillary Studies than girls. In younger children, the most common r Vital signs: T 98.9 °F, HR 105, RR 14, BP 105/65, mechanism of injury is falling, whereas violent O2 sat 100% on room air. encounters are more likely in older children. r General: Well-appearing young male, in no acute Laceration repair accounts for approximately distress. 50 percent of all the procedures performed in the r ED. HEENT:Therearenosignsofheadtrauma. r PERRL. Oropharynx clear, with moist mucous Pathophysiology: The skin is the largest organ of membranes. the body, and provides the critical service of a r Neck: Supple, with no tenderness and normal barrier to infection. Skin integrity is critical to this range of motion. function. Breaks in integrity can occur from shear forces, tension, and compressive forces, with r Cardiovascular: Regular rate and rhythm, with no resulting lacerations, abrasions, avulsions, or M/R/G. Intact and equal distal pulses. pressure ulceration. Thermal injury can also r Lungs: Normal work of breathing, with clear and disrupt skin integrity, and is discussed in equal breath sounds. Chapter2,Case5.Thepathophysiologyof r Abdomen: Non-distended, soft and depressible, wounds are dependent upon the type of wound, with no tenderness to palpation. r the location of the wound, the circumstances Musculoskeletal and skin: There is a flap laceration under which the wound was received, and the measuring approximately 5 cm at the left anterior underlying comorbidities of the patient with the knee, just superior to the patella. There is no injury.1–3 The skin is under constant tension due active bleeding. The subcutaneous adipose tissue to high collagen content, and is increased in areas is exposed, there are no visible tendons or deep overlying dynamic structures such as tendons and structures. The range of motion is intact. The muscles. Lacerations overlying joints or running patient is able to extend the knee against gravity perpendicular to skin tension lines are higher risk and against resistance without problems. for poor cosmetic outcome. Dirty wounds (for Capillary refill Ͻ 2 seconds r example, those incurred in farming accidents or Neurologic: The left lower extremity strength is 5/5 from bites), crush wounds (as opposed to wounds and equal compared to the right lower extremity. from a sharp object), wounds in areas of relatively The sensation to light touch is intact. Awake and decreasedbloodflow(forinstance,theshin),and alert. wounds in immunocompromised patients are higher risk for poor healing and infection.1–3 Questions for Thought The wound healing process begins with hemostasis via the coagulation cascade and r Is there any diagnostic testing (laboratory or imaging) indicated? platelet activation as well as an inflammatory 4 r Would you give a tetanus booster to this patient? response, which protects against infection. Next, r Does this child require antibiotics? theproliferativephaseischaracterizedby r Would you close this wound primarily? granulation, epithelialization, and contraction of r Does the patient require referral to an orthopedic the wound.4 Wound edges should be slightly surgeon? everted during wound closure in order for the skin to become flat after contraction occurs. Complete maturation and remodeling of the Diagnosis wound may continue for up to 2 years. Tensile r Knee laceration. strength is regained very slowly; with only 5 percent of the previous strength by 2 weeks, 30 Discussion percentat2monthsand80percentby1year.Scar r Epidemiology: Lacerations and other forms of formation ultimately results from the body’s wounds (such as abrasions) are an exceedingly repair of injured tissue, as opposed to regenerative

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healing (for instance, with mild abrasions) that radiopaque foreign bodies such as glass, stones, or resultsinnoscar.4 metallic objects. U/S can locate radiolucent r Presentation: It is extremely important to obtain a objects such as wood and plastic, and can be used detailed history of the time and mechanism of real-time during wound exploration.1–3 CT and injury as it has a direct impact on management. MRI can be used, if necessary, to localize a foreign Patients may present with an isolated soft-tissue body if plain radiographs or U/S fail.1–3 MRI injury,asinthispatient,ormaypresentwith should not be used for metal objects. major trauma. A clear understanding of the r Treatment:The“goldenperiod”forwoundclosure mechanism of injury allows for thorough was classically taught to be within 6 hours of investigation of the possible magnitude of the injury; however, non-contaminated wounds can injury such as an underlying fracture, violation of be closed successfully up to 12 hours after the a joint space, or the possibility of a severe crush injury, and in highly vascular areas like the face injury. Wounds caused by animal bites have a very and scalp, 24 hours may be acceptable, as the risk high risk of infection, as do those caused by of infection is lower.1–3,5 There are no good data human bites, and patients may not readily admit toestablishanydefinitivetimelimitforwound that a hand injury was suffered as a consequence closure.5 In general, closure of animal and human ofpunchinganotherpersoninthemouth.The bites is avoided and healing by secondary possibility of a retained foreign body in the wound intention is preferred due to the high rate of also needs to be considered and explored, for infection, unless the wound is in a highly vascular instance from window glass in an auto accident or area or is deforming.1–3 in a kitchen-related accident. Patients may present Abrasions require local care only, with with loss of sensation or severe pain from irrigationandanocclusivedressingtooptimize underlying nerve injury, fracture, or compartment healing conditions.2 syndrome.1–3 Preexisting or acute medical Pain management is a crucial aspect when problems may impact presentation, such as a providing care for the injured child. Whenever seizure or syncopal event that led to the injury. possible, the use of a topical anesthetic agent such r Diagnosis:Thewoundneedstobecarefully as compounded lidocaine, epinephrine, tetracaine examined, documenting the location, size, depth, is preferred. Blanching of the site after application presence of foreign matter, and any associated indicates effective anesthesia. A local anesthetic tissue injury.1–3 Adequate illumination and can also be applied using a small gauge needle to hemostasis are imperative for an evaluation of the avoidpainassociatedtotheinjection,butthis laceration. The vascular, neurologic, and tendon method usually causes significant anxiety in function need to be carefully assessed. A detailed children. Benzodiazepines such as midazolam via vascular examination should include observation an oral or intranasal route can help reduce patient for the presence of pallor or cyanosis, capillary anxiety. Procedural sedation and regional nerve refill, and palpation of pulses distal to the wound, blocks could be necessary for management of to assess tissue perfusion. A thorough motor complicated wounds. Distraction techniques such examination should be performed, including as listening to music, watching a video, or flexor and extensor tendons near a wound. The listening to a story are also very effective in sensation examination should include two-point reducing anxiety, especially if a child life specialist discrimination when developmentally is available. appropriate. If the laceration overlies a joint, the Although traditional dogma would joint should be meticulously examined for signs recommend sterile technique for wound repair, a of joint capsule penetration or damage to tendon large prospective randomized blinded trial found structures. If the provider is unsure of joint no difference in wound infection rate between involvement, methylene blue or saline may be wounds closed using clean technique (clean, injected into the joint to demonstrate joint non-sterilegloves)ascomparedtoasterile integrity versus extravasation into the wound. technique.6 Wound irrigation with normal saline Clinical suspicion for a retained foreign body or tap water can significantly reduce the risk of warrants imaging. Plain radiographs can detect infection by washing away foreign material and

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diluting bacterial concentration.1,3 The fluid used wound aftercare is critical to cosmetic outcome. for irrigation is less critical than the volume of Wounds should be kept clean and dry. The child irrigant used. Removal of hair around the wound may shower after 24 hours, wash the wound with is not recommended as it has been associated with soap and water, and dry the wound gently. The increased rates of wound infection.1 patient should avoid soaking the wound in water Suturing with monofilament non-absorbable (swimming, bathing) or scrubbing the wound. sutures of 4-0–5-0 thickness is commonly The patient’s caregivers can administer oral pain recommended for repair of lacerations located on medicationssuchasacetaminophenoribuprofen the extremities or trunk. Monofilament of 6-0 is as needed. Topical antibiotics may be applied to recommended for the face. Staples may be used on the wound. Detailed instructions to monitor for the scalp, and tissue adhesives provide equivalent signs of infection should be given (increased pain, repair to sutures in simple lacerations in swelling, redness, warmth, or drainage from the low-tension, low-moisture areas. 2 Absorbable wound) as well as instructions to return if wound sutures are appropriate for oral mucosa. dehiscence occurs. Sutures in the face should be Most wounds can be approximated effectively removed in 3–5 days, those in the scalp and arms with simple interrupted sutures. The needle can be removed in 7–10 days, those in the trunk, should pierce the skin at a 90-degree angle while legs, hands, or feet can be removed in 10–14 days, pronating the wrist, causing the needle tip to and sutures on the palms and soles can be penetratedeeplyintothewoundtoattain removed in 14–21 days.3 Sunscreen may be adequate wound-edge eversion. Sutures should applied to scars in areas exposed to sunlight to take equal bites from both wound edges to avoid minimize wound hyperpigmentation for up to margins from overlapping. Sutures should be 1–2 years after injury. placed close enough to approximate wound edges, but not excessively tight as to cause tissue necrosis, following the long-taught wisdom of Historical clues Physical findings r r “approximate, not strangulate.” The knots are Fall injury Flap laceration r Sharp mechanism (metal r Subcutaneous adipose with no secured using an instrument tie and then pulled frame) foreign body and no visualized to one side of the wound, to decrease wound r r Recent time interval r tendons inflammation that may occur by a knot becoming Able to bear weight range of motion and tendon r No numbness or tingling function intact incorporated into the wound. Oral antibiotic r No relevant medical or r Palpable pulses, adequate prophylaxis is only indicated for wounds with a immunization history perfusion higher risk of infection, and is most commonly used for cases of animal bites and open fractures.1–3 Contaminated wounds also require Follow-Up antibiotics. Surgical consultation should be Given there were no signs of tendon injury or viola- considered for deep wounds of the hand or foot, tion of the joint space the laceration was repaired by severe crush injuries, severely contaminated the ED provider. A corner suture (half-buried mattress wounds, wounds that raise a concern for cosmetic subcuticular suture) was used to approximate the tri- outcome, and lacerations involving nerves, angular edge of the wound. Fifteen interrupted sutures arteries, joints, or bones.1,3 were placed along the sides of the flap wound with- Tetanus prophylaxis should be provided to out complications. Lidocaine, epinephrine, and tetra- children with no history of tetanus immunization caine was used for anesthesia with excellent results. and those with an incomplete series or who have The patient watched a movie during the procedure not had a booster injection in 10 years.2 which provided distraction. Tetanus prophylaxis was Unimmunizedchildrenshouldalsoreceive not indicated given that the patient had received more tetanus immunoglobulin if they have a deep than three doses of tetanus immunizations, with the puncture or contaminated wounds.2 last dose given 3 years ago (less than 5 years prior). r Disposition:Mostpatientsaredischargedhome Detailed wound care instructions were given upon dis- after wound management. Careful wound care charge. The patient was instructed to visit his pediatri- instructions should be provided at discharge, as cian in 10 days for suture removal.

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References Allergies r 1. DeBoardRH,RondeauDF,KangCS,etal.Principles NKDA. of basic wound evaluation and management in the emergency department. Emerg Med Clin N Am 2007; Physical Examination and Ancillary Studies 25: 23–39. r ° 2. Worster B, Zawora MQ, Hsieh C. Common questions Vital signs: T 98.8 F, HR 108, RR 20, BP 108/60, O2 sat 99% on room air. about wound care. Am Fam Phys 2015; 91(2): 86–92. r 3. Forsch RT. Essentials of skin laceration repair. Am General: The patient is a well-developed child in Fam Phys 2008; 78(8): 945–51. no acute distress, playful and interactive until his 4. Walmsley GG, Maan ZN, Wong VW, et al. Scarless knee is touched or he is stood up by his parents. He then begins to grimace and cry. wound healing: Chasing the holy grail. Plast Reconstr r Surg 2015; 135: 907–17. HEENT: PERRL. No conjunctival injection or 5. Zehtabchi S, Tan A, Yadav K, et al. The impact of pallor. Oropharynx clear, with moist mucous wound age on the infection rate of simple lacerations membranes. repaired in the emergency department. Injury 2012; r Neck: Non-tender, with no adenopathy. 43: 1793–8. r Cardiovascular: Regular rate and rhythm. No 6. Perelman VS, Francis GJ, Rutledge T, et al. Sterile M/R/G. Good capillary refill. versus nonsterile gloves for repair of uncomplicated r Lungs: CTA bilaterally without W/R/R. lacerations in the emergency department: A r randomized controlled trial. Ann Emerg Med 2004; 43: Abdomen: The abdomen is soft, with bowel 362–70. sounds present and no rebound or guarding. r Extremities and skin:Thepatient’sleftkneeis moderately swollen, mildly tender, and warm to Case 5 palpation but without erythema or induration. He complains of pain when his knee is touched, Contributing Author: Rachel A. Patterson extended, or flexed. He is otherwise able to move History his bilateral hips, ankles, and arms without The patient is a 4-year old male who presents to the difficulty. There is no evidence of swelling tohis ED with his mother, complaining of left knee pain and extremities otherwise. He has no petechiae or rash. swelling for 1 day. The patient’s mother first noticed r a limp the day prior to presentation while watching Neurologic: Appropriate for age, normal extremity strength and reflexes. a parade outside. She noted continued worsening of r his gait and swelling of the left knee over the next 24 Pertinent laboratory values: WBC 11,640, ESR 38, hours to the point that the patient completely refused CRP 8.8. r to stand or walk. He also complained of pain when the Pertinent radiographs:KneeX-rayandU/Swith knee was touched or moved. The family does recall an joint effusion. erythematous rash on his arm during the summer but it resolved quickly so no further evaluation was performed at that time. The patient has otherwise been in Questions for Thought his normal state of health and family denies any recent r traumas, falls, or illnesses. What are the important historical clues that should be obtained when evaluating this patient? r Past Medical History What are the key physical examination ﬁndings? r What is the typical diagnostic testing performed The patient has a history of conductive hearing loss for this condition? with developmental speech delay. He has had bilat- r What treatment should be initiated in the ED? eral myringotomy tube placement and is UTD on his immunizations.

Medications Diagnosis r r None. Lyme arthritis.

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Discussion r Diagnosis: The diagnosis of Lyme arthritis is r Epidemiology: Lyme disease was first identified in initially based on clinical history and physical the 1970s in the Connecticut town of Lyme, when examination. This is especially true if the patient a cluster of children were being evaluated and livesinanareaorhastraveledtoanareathatis treated for oligoarthritis.1 Lyme disease is endemic for Lyme disease and has the currently the most common vector-borne disease characteristic rash of erythema migrans. Most in the USA.2 It is a tick-borne illness that is patients with Lyme arthritis have involvement of primarily caused by the spirochete Borrelia the knee or hip and also are less likely to have a burgdorferi and according to the CDC, there are fever or other systemic symptoms of illness at 5 currently over 30,000 new cases of Lyme disease presentation. each year in the USA.2 When presenting with later stages of Lyme r Pathophysiology:ThespirocheteofB. burgdorferi disease, additional testing in conjunction with a attaches to the skin and if not overwhelmed by clinical examination and history is used to make host defenses it may cause the rash of erythema the diagnosis. Unlike in early Lyme disease, migrans. The spirochete can disseminate patients with Lyme arthritis should have positive 7 throughout the body with predilection for the serologic antibodies to B. burgdorferi. Serologic skin, heart, joints, CNS, and eyes. Further testing should be completed with a two-tier discussion of this can be found in Chapter 10, approach of ELISA followed by Western blot Case 7. testing. It can take days, however, for these results r Presentation:Lymediseasecanbedividedinto to return, and a diagnosis often needs to be made early localized, early disseminated, and late urgently to differentiate Lyme arthritis from other disease. Lyme arthritis is the most common late septic and non-septic causes of monoarticular manifestation of the disease and occurs in arthritis. Arthrocentesis of a joint for synovial approximately 50 to 60 percent of patients who go fluid analysis should be performed. The synovial untreated for early Lyme disease.3 Patients fluid can have varying WBC as high as 100,000, presenting with Lyme arthritis may have an but often the WBC will be between 10,000 and antecedent history of erythema migrans, 25,000 with polymorphonuclear leukocyte 8 intermittent arthralgias, and myalgias; however, predominance. Therefore, cell counts alone these are not necessary for the diagnosis.4 The cannot be used to exclude or make a diagnosis of symptoms of arthritis generally occur within Lyme or septic arthritis, as there is considerable weekstomonthsofinitialinfectionandtendtobe overlap between threshold values. A key characterized by either an acute onset of joint laboratory criteria to differentiate Lyme from swelling that may persist, or recurrent episodes of bacterial arthritis is a culture negative for a self-resolving migratory monoarthritis of various bacterial pathogen. Synovial-fluid PCR for B. large joints.4–6 If untreated, approximately 10 burgdorferi DNA can also help make the diagnosis percent of these patients will develop chronic of Lyme arthritis. monoarthritis.5 Although it can be either mono- Laboratory evidence of inflammation includes or oligoarticular, the knee is the most commonly elevated ESR levels, CRP levels, and peripheral affectedjointandisinvolvedinover90percentof WBC; however, these are not specific to Lyme patients presenting with Lyme arthritis.5 Other arthritis and additional testing should be used to commonly affected joints include the ankle, hip, support the diagnosis. Markedly elevated and elbow.5,6 On presentation, the affected joint is peripheral WBC and ESR levels are more swollen and with limited range of motion to common in septic arthritis than Lyme arthritis, varying degrees. Although some patients are but lack sufficient specificity and sensitivity to be used to rule out the diagnosis.9 unable to bear weight, others are able to ambulate r without significant difficulty. Fever, erythema, and Treatment: Successful treatment of Lyme arthritis warmth are variably present with Lyme arthritis can be achieved in over 90 percent of patients but are much less common than with septic following a 28-day course of antibiotics. For arthritis.5,6 pediatric patients who are less than 8 years old,

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amoxicillin is the initial recommended treatment References regiment.10 For children 8 years of age or older, 10 1. SteereAC,MalawistaSE,SnydmanDR,etal.Lyme doxycycline is first-line therapy. Patients may arthritis: An epidemic of oligoarticular arthritis in have residual symptoms of mild joint swelling and children and adults in three Connecticut communities. pain after the initial course of antibiotics that Arthritis Rheumatol 1977; 20: 7–17. continues to resolve slowly over weeks. 2. Centers for Disease Control and Prevention. Lyme Anti-inflammatories are key for adjunctive disease: Data and statistics. See www.cdc.gov/lyme/ symptomatic control for these patients. stats/index.html (accessed January 2017). Re-treatment with a 4-week course of oral 3. Warde N. Treating pediatric Lyme arthritis. Nat Rev antibiotics or IV antibiotics should also be Rheumatol 2010; 6: 312. considered in patients with only moderate 4. Rose CD, Fawcett PT, Eppes SC. Pediatric Lyme or mild improvement of symptoms, arthritis: Clinical spectrum and outcome. JPediatr respectively.10 Orthop 1994; 14: 238–41. r Disposition: When treated with antibiotics, Lyme 5. Thompson A, Mannix R, Bachur R. Acute pediatric arthritis has an excellent prognosis. If the patient monoarticular arthritis: Distinguishing Lyme arthritis has no systemic symptoms, can ambulate without from other etiologies. Pediatrics 2009; 123: 959–65. difficulty, and has a physical examination/joint 6. Wright WF, Riedel DJ, Talwani R, et al. Diagnosis and aspiration negative for septic arthritis, he or she management of Lyme disease. Am Fam Phys 2012; 85: can safely be discharged to home with initiation of 1086–93. oral antibiotics and follow-up with his or her PCP. 7. Puius YA, Kalish RA. Lyme arthritis: Pathogenesis, clinical presentation, and management. Infect Dis Clin North Am 2008; 22: 289–300. Historical clues Physical findings Ancillary studies 8. Deanehan JK, Nigrovic PA, Milewski MD. Synovial r r r fluid findings in children with knee monoarthritis in Knee pain Joint pain and Negative X-ray Lyme disease endemic areas. Pediatr Emerg Care 2014; r Rash over the effusion (excluding occult r 30: 16–19. summer r Absence of fever trauma) Absence of 9. Deanehan JK, Kimia AA, Tan Tanny SP, et al. warmth and Distinguishing Lyme from septic knee monoarthritis erythema in Lyme disease-endemic areas. Pediatrics 2013; 131: e695–701. 10. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The Follow-Up clinical assessment, treatment, and prevention of Lyme The patient’s clinical examination as well as history was disease, human granulocytic anaplasmosis, and concerning for Lyme arthritis. He had an U/S of his babesiosis: Clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis left knee that showed a moderately sized joint effusion, 2006; 43: 1089–134. and an arthrocentesis was performed under U/S guidance, revealing cloudy, yellow joint fluid. The synovial fluid was sent for a Gram’s stain, aerobic and anaerobic Case 6 cultures as well as cell count, crystals, glucose, protein, and Lyme PCR. His synovial fluid was significant for Contributing Author: Benjamin Kitt over 60,000 WBC; however, the Gram’s stain was negative. The joint fluid otherwise revealed normal glu- History cose and protein and was negative for crystals. Because The patient is a 17-year-old male who presents to thepatientwasunabletoambulate,hewasadmitted the ED for 2 weeks of steadily increasing left upper to the hospital and started on anti-inflammatories for arm pain. The pain was initially mild and sporadic in pain and oral antibiotics for presumptive Lyme disease nature. The pain is described as sharp and occurs both while awaiting more definitive negative cultures. His at rest and with movement. There is no known trauma Lyme titer was ultimately positive, as was his synovial or repetitive motion activity. The patient reports he fluid Lyme PCR. He was eventually discharged with an was recently evaluated at another ED, where he was uneventful post-hospitalization course. diagnosed with a muscle strain. Over the next 2 days,

16:14:23 5 07 Chapter 6: Extremity Complaints the pain increased substantially, which prompted this r Pertinent radiographs:Lefthumerusradiograph second ED visit. His pain has now increased to 10/10, reveals a humeral midshaft lesion and a CT is which prevents him from sleeping at night. He also has recommended. CT demonstrates a 9-mm lucent developed numbness and throbbing in his forearm. He lesion at the midshaft of the left humerus. denies fever, rash, chest pain, shortness of breath, nausea, vomiting, abdominal pain, weakness, fatigue, or Questions for Thought malaise. There hasn’t been any recent travel or known r sick contacts. The patient denies illicit drug use. What is the diﬀerential diagnosis of this lesion? r Are there additional studies you would like to obtain? Past Medical History r What are the next steps in the management of r Mild intermittent asthma. this patient? r r UTD on immunizations. Who would you consult for further management?

Medications Diagnosis r Albuterol inhaler as needed. r Osteomyelitisofthehumeruswithabscess formation. Allergies r NKDA. Discussion r Epidemiology: Osteomyelitis is an infection of the Physical Examination and Ancillary Studies bone resulting in inflammation of the surrounding tissues. It is a rare disease in r Vital signs: T 99.7 °F, HR 88, RR 18, BP 109/61, O 2 pediatric populations, with an estimated annual sat 98% on room air. incidence rate of 13 per 100,000 in patients under r General: Lying in bed, clutching his arm, in the age of 18.1,2 The highest incidence occurs in moderate distress from pain. children under the age of 3.1–3 For unknown r HEENT: PERRL. Mucous membranes are moist. reasons, osteomyelitis tends to affect males more No signs of trauma. r than females, in a ratio of 2:1. Osteomyelitis of Neck: Supple, with a midline trachea and no hematogenous origin is more common in children adenopathy. 2–4 r than in adults. Risk factors for osteomyelitis in Cardiovascular: Regular rate and rhythm, with no infants less than 30 days of age include urinary Ͻ M/R/G. Capillary refill 2 seconds. No tract anomalies, prematurity, CVC placement, appreciable cyanosis. 4 r complicated delivery, or overlying skin infection. Lungs: CTA bilaterally with no W/R/R. In older children, hematogenous risk factors for r Abdomen: Soft and non-tender to palpation, with osteomyelitis include: sepsis, indwelling catheters, normal bowel sounds. bacteremia secondary to trauma, sickle cell r Extremities and skin: There is tenderness to disease, and immunodeficiency disorders.2–4 palpation along the left shoulder laterally and the Osteomyelitis may be acute (less than 2 weeks of left upper arm. There are no palpable masses and symptoms), subacute (symptoms for 2 weeks to 3 there is no obvious deformity or edema. The left months), or chronic (symptoms for greater than 3 shoulder has limited range of motion secondary months).2 Chronic osteomyelitis is rare in to pain but is without swelling. Muscular children.3 compartments are all soft. The right upper and r Pathophysiology:Therearevariousetiologiesand both lower extremities are without swelling or sources of infection for osteomyelitis. One of the tenderness. The skin is warm and dry with no most common causes of pediatric osteomyelitis is erythema or rashes. via hematogenous seeding;1–4 these are typically r Neurologic: Intact cranial nerves. Normal monomicrobial infections. Osteomyelitis can also sensation, tone, and strength in the extremities. occur secondary to a localized infection, such as a r Pertinent laboratory values: WBC 13,500, Hb 11.6, soft-tissue or joint infection, or through direct ESR 91, CRP 25. inoculation of infection to the bone from trauma

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r or surgery;3 these are often polymicrobial Diagnosis: The diagnosis of osteomyelitis is often infections. The development of osteomyelitis difficult due to the non-specific presentation and depends largely on the pathogen that infects the nature of the disease. The provider must consider bone and the virulence of that organism. These alternative possibilities, such as malignancy, septic factors can include the organism’s ability to enter arthritis, autoimmune disease, Lyme arthritis, and adhere to the cells, as well as the immune occult or non-accidental trauma, and referred status of the patient. For instance, patients with pain, and an evaluation must be undertaken to sickle cell disease lack functional spleens, which exclude these other diagnoses. makes them more prone to bacteremia and r In patients where osteomyelitis is suspected, a therefore more likely to develop osteomyelitis. CBCwithdifferential,CRP,ESR,andtwoblood As discussed above, hematogenous seeding is cultures are generally recommended. Although the most common cause of osteomyelitis in not specific, elevations in acute phase reactants children, and the infection usually seeds to support the diagnosis. Radiographs are long-bone metaphysis. The exact mechanism for inexpensive and widely available, which make this process is unknown, but it is likely due to the themareasonablefirstchoiceforimaging.Itis large volume of blood that passes through the important to note that the sensitivity and metaphysis as well as an increased permeability of specificity of plain films in the diagnosis of the capillaries.3 Once bacteria begin to proliferate osteomyelitisispoor.Theplainfilmscanhave within the area, they cause inflammation, with suggestive features of osteomyelitis, such as resulting destruction of trabecular bone and its soft-tissue swelling or cortical erosion. Although vascular channels.2 This destruction may make more difficult to obtain emergently, MRI is highly antibiotics ineffective, as they may not be able to sensitive in detecting osteomyelitis.1–3 It also has reach the site of the infection due to the disrupted the added benefit of avoiding radiation in blood flow.2 children. Although CT imaging is not as good as The most common organisms isolated in MRI in delineating osteomyelitis, it is a reasonable osteomyelitis are Gram-positive bacteria and, in alternative. particular, MRSA. Other notable organisms r Treatment: The treatment of osteomyelitis is often include, but are not limited to: group A and B an extended course of antibiotics. Due to this fact, streptococci, Streptococcus pneumoniae, it is important to obtain cultures with sensitivity Escherichia coli,andKingella kingae.2 While less testing to ensure the correct antibiotic is used as common than bacterial infections, fungal species therapy.1,2 Though blood cultures can be positive have been known to cause osteomyelitis.1 and aid in the diagnosis of the organism, a biopsy r Presentation: Osteomyelitis often presents and culture of the lesion is ideal.2 However, the insidiouslyandcanbemissedoninitial condition of the patient must take priority, and if evaluation.3 The symptoms are non-specific in the patient is manifesting signs of serious nature and include decreased range of infection, broad-spectrum antibiotics should be motion/weight-bearing on the affected bone, initiated. Consultation with orthopedics and fever, malaise, pain, local swelling, tenderness, or infectious disease for assistance in starting warmth. Presentation also varies depending on appropriate therapy is recommended. the age of the child. Older children are often able r Disposition: Patients with osteomyelitis require to localize the pain and provide historical events hospital admission for IV antibiotics and for of the progression of the pain. In young children surgical debridement and washout if they do not who are unable to localize pain or communicate, have a prompt clinical response. the diagnosis can be even more difficult to make. The child may refuse to use the affected extremity, Physical Ancillary such as preferentially using the unaffected arm or, Historical clues findings studies with lower extremity, refusing to weight-bear on r r r r Gradually increasing pain Tenderness r Elevated CRP the affected side. Infants may present by crying No improvement with r over humerus r Elevated ESR during diaper changing, crying when the affected conservative treatment No signs of Abnormal r Pain with activity or rest trauma X-ray and CT extremity is touched, and refusing to crawl or sit.

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Follow-Up right elbow. The parents note elbow swelling and said An MRI of the left humerus was obtained and demon- that he doesn’t want to move it. He has some pain strated a 1-cm cortical lesion within the anterior cortex in his hands but denies any numbness or tingling. of the mid-humeral shaft suspicious for osteomyelitis. He denies difficulty breathing, headache, pain in his Orthopedics surgery and pediatric infectious disease chest or belly, and is acting normally according to his services were consulted. The patient underwent biopsy parents. and drainage of the bone abscess. He was initially started on IV vancomycin but did not achieve thera- Past Medical History peutic levels, and was subsequently switched to dapto- r Prior tonsillectomy. mycin. Culture results from the abscess demonstrated r UTD on immunizations. MRSA. The patient then underwent another surgical drainage a week later due to persistent fevers, swelling Medications of his arm, and drainage from wound. Vancomycin- r None. impregnated beads were placed during the operation. The patient completed a 14-day course of daptomycin and was discharged on clindamycin for an antici- Allergies r pated 3-month course with orthopedic and infectious NKDA. disease follow-up. Physical Examination and Ancillary Studies References r Vital signs: T 98.9 °F, HR 104, RR 22, BP 112/76, 1. Riise, ØR, Kirkhus E, Handeland KS, et al. Childhood O2 sat 99% on room air. osteomyelitis: Incidence and differentiation from other r General: Patient is tearful but awake and alert, acute onset musculoskeletal features in a population- looking around the room. He is well-nourished, based study. BMC Pediatr 2008; 8: 45. appears mildly anxious, and has a normal body 2. Ceroni D, Kampouroglou G, Anderson della Llana R, habitus for his age. et al. Osteoarticular infections in young children: r HEENT: The head is atraumatic. There is no What has changed over the last years? Swiss Med Wkly 2014; 144: w13971. tenderness or swelling noted on palpation of the scalp. PERRL. Extraocular muscles intact. 3. Hatzenbuehler J, Pulling TJ. Diagnosis and r Neck: No midline tenderness, no step-offs. management of osteomyelitis. Am Fam Phys 2011; 84: r 1027–33. Cardiovascular: Regular tachycardia, with no + 4. Dartnell J, Ramachandran M, Katchburian M. M/R/G. Radial pulses are 2 bilaterally and Haematogenous acute and subacute paediatric capillary refill is brisk in both hands. osteomyelitis: a systematic review of the literature. J r Lungs: The lung sounds are clear, with good air Bone Joint Surg Br 2012; 94: 584–95. movement bilaterally. r Abdomen: Soft and non-distended, with no signs of trauma. No tenderness or masses. Case 7 r Extremities and skin:Therightarmisheldin flexion with moderate swelling of the right elbow. Contributing Author: M. Bryan Dalla Betta The patient cries and withdraws at any attempt to manipulate the elbow. There is no deformity or History tenderness to the right shoulder, clavicle, forearm, A3-year-oldmalepresentsbyprivatevehicletothe or wrist. There are superficial abrasions to the ED complaining of right arm pain after a fall. Accord- palmsofbothhandsbutotherwisetheskinis ing to the parents, the patient was playing basketball intact, including at the right elbow. r at the park when he tripped and fell forward onto Neurologic: The grip strength of the right hand is both hands. There was no loss of consciousness and decreased to 4/5 due to pain. When asked to make he cried immediately and clutched his right upper an “OK” sign, there is decreased flexion of the extremity. He has been in significant pain since the distal right index finger to a pincer-like fall. The patient states that his pain is worst in his configuration. Finger spread and wrist extension

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weakness. Transverse fractures through this area of the distal humerus are termed supracondylar fractures. The proximity of the brachial artery and median, ulnar, and radial nerves to the supracondylar fracture site adds to the clinical importance of the diagnosis.2–5 Because of the proximity of these neurovascular structures, angulated or displaced supracondylar fractures can cause neurovascular compromise to the distal extremity. r Presentation: The mechanism of supracondylar fractures can vary, but a history of a fall onto an Figure 6.1 Lateral view of the right elbow shows a non-displaced outstretched hand or flexed elbow is most supracondylar fracture (black arrow) with a posterior fat-pad sign common. Some patients will have only elbow pain (white arrow). and mild swelling, while others can present with gross deformity, sensory deficit, or absent distal are intact with 5/5 strength. There is no sensory pulses. Patients will typically have considerable loss in the hand, forearm, or elbow. pain and significantly impaired range of motion at r Pertinent radiographs: Elbow radiograph shown in the elbow, and may cradle the extremity in flexion Figure 6.1. close to the body. r Diagnosis: Diagnosing elbow fractures in general requires knowledge of appearance of growth Questions for Thought r plates, as growth centers can look like fractures. If What is the typical mechanism of injury for this you are unsure, you should obtain a radiograph of condition? r the other elbow for comparison. The capitellum is What vascular injury is associated with this thefirstgrowthcentertoappear(ataboutage1), condition? followed by the radial head (at about age 3), the r What radiographic views are best to evaluate for this kind of injury? medial epicondyle (at about age 5), the trochlea r What ﬁndings would mandate operative (at about age 7), the olecranon (at about age 9), intervention in this injury? and the lateral epicondyle (at about age 11). The growth centers fuse and are no longer visible sometime around age 13. The diagnosis of supracondylar fractures is Diagnosis made with anterior–posterior and lateral views of r Supracondylar fracture of the humerus. theelbow.Theanteriorhumeralline,alinedrawn down the anterior surface of the humerus, should Discussion pass through the middle third of the capitellum in r Epidemiology: Supracondylar fractures occur in a normal, true lateral film of the elbow, as it does in children primarily between the ages of 5 and 10 patients with non-displaced fractures like the one yearsold,butcanbeseenintheearlyorevenlate shown in Figure 6.1. An angulated fracture should teenage years as well. Most are caused by a fall on be suspected if this line does not pass through the an outstretched hand and they account for middle third of the capitellum (Figure 6.2). The approximately 60 percent of pediatric elbow presence of a posterior fat-pad sign or a sail sign fractures.1–3 (large anterior fat pad) should also raise suspicion r Pathophysiology:Inchildren,thehumerusjust for fracture. Radiographs of the forearm and proximal to the medial and lateral condyles is proximal humerus may also be obtained due to relatively weak. Falls on outstretched hands (or the incidence of associated fractures in these areas. rarely, onto a flexed elbow) cause forces to be Extension fractures are described using the transmitted up the arm to this area of relative Gartland classification system, where fracture

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metacarpals, with the elbow in less than 90 degrees of flexion to prevent additional swelling. Displaced or angulated fractures, as well as any open fracture or fracture with neurovascular compromise or concern for compartment syndrome, require emergent orthopedic consultation in the ED. Displaced or considerably angulated fractures may require surgical pinning, open reduction, or exploration in the OR.4 r Disposition: Children with non-angulated and non-displaced fractures can be discharged home with long arm splint and sling. Consultation with orthopedics is recommended to determine a preferred time frame for follow-up, but generally Figure 6.2 Radiograph demonstrating the anterior humeral line this should occur within 2–3 days and no longer (black dotted line) that does not pass through the capitellum (white than 1 week. It is important to give parents good arrow), indicating a displaced fracture. instructions regarding neurovascular compromise, and many physicians advocate either type ranges from I to III depending primarily on an observation admission or a return visit for an the amount of fracture angulation present. A examination for neurovascular function at supracondylar fracture without angulation or 24 hours. displacement is the least severe (type I), while Any evidence of open fracture, compartment fractures with angulation or displacement usually syndrome, neurovascular compromise, or any require surgical evaluation, reduction, and/or displaced or angulated fractures requires pinning (types II and III).1,3,4 Type II fractures orthopedic consultation in the ED. These patients involve extension of the humerus with the are often admitted to the hospital, and therefore posterior cortex still touching or even intact decisions for these patients should be made in (angulated without complete translation), while conjunction with the orthopedic surgeon. type III involve a fully circumferential cortical break, with complete displacement of the distal fragment posteriorly.1,3,4 Historical clues Physical findings Ancillary studies r r r r Treatment: Treatment of supracondylar fractures Fall on Elbow X-ray with outstretched swelling/deformity fracture and begins on initial patient presentation with r r arm Restricted range posterior fat-pad appropriate analgesia and temporary splinting for Child 5–10 r of motion and sail sign comfort. Any evidence of vascular compromise years Signs of r Elbow pain neurovascular warrants immediate orthopedic consultation even injury ifthereisevidenceofdistalperfusion.The integrity of the brachial artery as well as the median, ulnar, and radial nerves should be Follow-Up assessed rapidly after initial presentation. A cold, An orthopedic consultation was requested for this pulseless, or pale distal extremity mandates patient and after adequate pain control and re- emergent orthopedic involvement, and closed examination it was determined that no reduction or reduction should be attempted in the ED to operative intervention was emergently required. The restore distal perfusion and avoid ischemia. patient was placed in a long arm splint with sling for Supracondylar fractures without immobilization and comfort, and arrangements were displacement, angulation, or other complicating made for follow-up with the orthopedic department factors can be managed with application of a long in the next several days. He was placed in a cast for 6 arm posterior splint in the ED. The splint should weeks but regained full function and range of motion extend from the proximal humerus to the of the affected arm.

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References Allergies r 1. Thornton MD, Della-Giustina K, Aronson PL. Peanuts and sulfa drugs. Emergency department evaluation and treatment of pediatric orthopedic injuries. Emerg Med Clin N Am Physical Examination and Ancillary Studies 2015; 33: 423–49. r Vital signs: T 99.2 °F, HR 82, RR 15, BP 118/65, O 2. Lins RE, Simovitch RW, Waters PM. Pediatric elbow 2 sat 100% on room air. trauma. Orthop Clin North Am 1999; 30: 119–32. r General: Well-developed and well-nourished, 3. Allen SR, Hang JR, Hau RC. Review article: Paediatric supracondylar humeral fractures: Emergency sitting upright in stretcher with left arm held assessment and management. Emerg Med Australas slightly abducted, internally rotated, with elbow 2010; 22: 418–26. flexed. She appears uncomfortable. r 4. Abzug JM, Herman MJ. Management of supracondylar HEENT: PERRL. No signs of trauma. No humerus fractures in children: Current concepts. JAm malocclusion. Oropharynx clear. Acad Orthop Surg 2012; 20: 69–77. r Neck: No midline tenderness or step-offs. Trachea 5. Wu J, Perron AD, Miller MD, et al. Orthopedic pitfalls is midline. No adenopathy. in the ED: Pediatric supracondylar fractures. Am J r Cardiovascular: Regular rate and rhythm. No Emerg Med 2002; 20: 544–50. M/R/G. 2+ radial pulses in both arms. r Lungs:CTAbilaterally,withnoW/R/R.No chest-wall tenderness or deformity. Case 8 r Abdomen:Soft,withnotendernessormasses. Pelvis stable. Contributing Author: Rebecca Jeanmonod r Extremities and skin: Extremities are warm and History well-perfused. She has a small abrasion to her left A 14-year-old girl presents to the ED with a chief com- palm. She has no edema and normal capillary plaint of left shoulder pain. The girl had been at rugby refill. She has flattening beneath her left acromion, practice and was tackled from behind. She put her and her humeral head is palpable anterior to the hands up to protect herself during the fall, and denies glenoid. She has no arm or clavicular tenderness. strikingherhead,butcomplainsofleftshoulderpain. Sheisunabletorangetheshoulder,buthasintact Since the event, the child has been unable to move the rangeofmotionofelbow,wrist,contralateralarm, shoulder. She denies neck pain, chest pain, or difficulty and bilateral lower extremities. r breathing. She has an area of tingling on the lateral Neurologic: Her cranial nerves are intact. She has aspect of her left shoulder, but otherwise denies numb- intact strength and sensation in her lower ness or sensory symptoms. She states she does not feel extremities. She has decreased sensation over her weak, but can’t move the arm secondary to pain, which left lateral deltoid, but her radial, median, and she localizes entirely to the shoulder. She denies elbow, ulnarnerveshaveintactfunction.Shecannot wrist, or hand pain. She is right hand dominant. Her participate in strength testing at the shoulder coach brought her to the ED, and her parents are on secondary to pain. their way in to the ED, but have given verbal permission to treat the child by phone. Questions for Thought r Past Medical History What is the patient’s diagnosis? r Does the patient require imaging? r Prior open surgical repair of right-sided Colles r What is the best way to treat this injury? fracture 1 year ago. r r What is the appropriate deﬁnitive treatment for Seasonal allergies. this condition? r Immunizations UTD.

Medications Diagnosis r Loratadine. r Anterior shoulder dislocation.

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Discussion and reduced range of motion after a mechanism r Epidemiology: Shoulders are the most commonly of direct shoulder trauma or fall on outstretched dislocated joint in the body, accounting for 50 hand. Rarely, patients will present in a delayed percent of all dislocations.1,2 Finger dislocations fashion, particularly if the dislocation occurred are also fairly common. Isolated patella and elbow during intoxication or seizure. The patient with an dislocations occur less frequently, and hip inferior dislocation presents with an inability to dislocations typically only occur in the setting of adduct the arm, and it is easy to spot because the high-energy trauma, such as dashboard injury in arm is extended over the head. The patient with a motor vehicle accidents. Ankle dislocations are posterior dislocation presents with an internally rare in the absence of coincident fracture. The rotated and adducted arm. He or she has shoulder shoulder’s high rate of dislocation is explained by pain and reduced range of motion, but it is often its high degree of mobility. Although dislocations missed because radiographs may be misleading can occur at any age, the natural history of the and the examination is subtle. Anterior disease differs by age. Younger patients have a dislocationsmaypresentacutelyorinarecurrent much higher incidence of recurrence than older fashion. Recurrent dislocations tend to occur people,andagelessthan20atfirstdislocation while the patient is extending and externally confers a greater than 12× risk of recurrence, with rotating the shoulder during regular activities, mean time to recurrence less than one year.3 such as hair brushing or bench pressing. These r Pathophysiology:Shoulderdislocations patients typically have a history of prior traumatic are classified by location of the humeral head dislocation. r (anterior, posterior, or inferior) and by recurrence Diagnosis: Diagnosis of dislocation is based on (acute traumatic versus recurrent). Ninety percent history and physical examination. A history of the of shoulder dislocations are anterior, and are most mechanism of the injury and prior dislocations commonly incurred by sporting injuries or direct should be elicited, as well as a neurovascular shoulder trauma in teenagers.2 The shoulder tends review of systems. The patient with an anterior to dislocate anteriorly because of the relatively dislocation may have paresthesias or numbness in thinner joint capsule there. Inferior shoulder the distribution of the axillary nerve or in the dislocations may be secondary to seizures or major entire arm from traction on the brachial trauma. Posterior dislocations are rare and are plexus.The patient will typically have a sulcus just often missed on initial presentation, as the humeral inferior to the acromion, which is easily palpable. head may be difficult to palpate in the posterior Further palpation will often reveal the humeral deltoid musculature and because the force head anteromedial to the glenoid. In posterior necessary to cause a posterior dislocation often dislocations, palpation will reveal the humeral causes other more pressing and obvious injuries. head in the posterior deltoid muscle. When the shoulder dislocates, it can injure the Radiographs are helpful in making the anterior glenoid rim and avulse the labrum diagnosis of anterior shoulder dislocation, but are (Bankart lesion), leading to a predisposition to not necessary if the provider is clinically certain of 2 future anterior dislocations.1–3 It can also cause the patient’s pathology. Particularly in the cases rotator cuff tears or injure nerves in the brachial of dislocation at sporting events or ski slopes, if plexus.Themostcommonlyinjurednerveisthe the provider has no immediate access to axillary nerve, which runs inferiorly to the radiography, the better course of action is to shoulder joint capsule, and may be stretched or reduce the injury, as delay to reduction prolongs damaged during dislocation.1 The axillary nerve is patient discomfort and results in increasing responsible for sensation over the lateral aspect of difficulty in reduction over time. Although the thedeltoid.Itisalsoresponsibleforarm presence of a fracture may have implications on abduction, which cannot be assessed until the long-term treatment and rehabilitation, it does shoulder is reduced. not impact emergency management, and prompt r Presentation: Patients typically present reduction with referral for outpatient radiography immediately following trauma with shoulder pain is reasonable. The outpatient radiograph is

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important for assessment for occult physeal injury extremely likely to have recurrent dislocations, at the humeral head, which can have an impact surgical intervention is often indicated, and on limb length in growing children. This child, therefore referral to a surgeon is appropriate.3,8 who is 14, has likely reached her full growth potential. Historical clues Physical findings When radiographs are obtained, the scapular r r Y view is the most important in determining Fall on outstretched Sulcus beneath acromion arm r Humeral head palpable anteriorly humeral head location relative to the anatomic r r r Shoulder pain Decreased sensation over lateral position. In this view, the X-ray beam passes Lateral shoulder deltoid (indicating axillary nerve through the axilla, projecting the appropriately tingling traction) placed humeral head at the center of a Y shape that is formed by the scapular body, the acromion, Follow-Up and the coracoid process. If the humeral head is Radiology was delayed for this child due to a multi- anterior to this Y, the dislocation is anterior, and if ple trauma activation. The provider injected 20 cc of itisposteriortothisY,itisaposteriordislocation. 1% lidocaine into her left shoulder joint via a posterior r Treatment: The ED management of a shoulder approach and let it dwell for 20 minutes. The child then dislocation is to reduce it. The first step is to underwent shoulder reduction with external rotation. provide adequate analgesia. For the calm and She was placed in a sling and discharged home with her cooperative patient, several self-reduction parentstofollowupwithorthopedicsurgery. methods are described.4 Most patients require manual reduction by a healthcare provider. There are over 20 described reduction methods for References shoulder dislocations, some of which rely on 1. Bonz J, Tinloy B. Emergency department evaluation traction/countertraction, some of which rely on and treatment of the shoulder and humerus. Emerg MedClinNAm2015; 33: 297–310. leverage, and some of which rely on manipulation.4 Any one of these techniques is 2. Quillen DM, Wuchner M, Hatch RL. Acute shoulder injuries. Am Fam Phys 2004; 70: 1947–54. acceptable, and is largely a matter of provider preference. 3. Wasserstein DN, Sheth U, Colbenson K, et al. The true Options for pain control range from oral recurrence rate and factors predicting recurrent instability after nonsurgical management of traumatic anti-inflammatory medications to procedural primary anterior shoulder dislocation: A systematic sedation in intra-articular anesthesia. review. Arthroscopy 2016; 32: 2616–25. Intra-articular anesthesia with lidocaine or 4. Alkaduhimi H, van der Linde JA, Flipsen M, et al. A bupivacaine has been demonstrated to be as systematic and technical guide on how to reduce a comfortable for patients as procedural sedation, shoulder dislocation. Turk J Emerg Med 2016; 16: with fewer complications and shorter ED stays, 155–68. and is therefore a reasonable first-line choice for 5. Kashani P, Zarchi FA, Hatamabadi HR, et al. pain management.5 Intra-articular lidocaine versus intravenous sedative Once reduction is complete, the patient should and analgesic for reduction of anterior shoulder beimmobilizedinasling.Thereisnodefinitive dislocation. Turk J Emerg Med 2016; 16: 60–4. evidence that external rotation immobilization 6. Whelan DB, Kletke SN, Schemitsch G, et al. provides better outcomes than a simple sling, and Immobilization in external rotation versus internal this is more difficult to apply.6 Although many rotation after primary anterior shoulder dislocation. AmJSportsMed2015; 44: 521–32. providers choose to obtain post-reduction radiographs, they do not add to the emergency 7. Hendey GW. Necessity of radiographs in the management of these patients in most emergency department management of shoulder dislocations. Ann Emerg Med 2000; 36: 108–13. circumstances and are not strictly necessary.7 8. Longo UG, Loppini M, Rizzello G, et al. Management r Disposition: Once reduction is complete, most of primary acute anterior shoulder dislocation: patientscanbedischargedhometofollowupwith Systematic review and quantitative synthesis of the orthopedic surgery. Since young patients are literature. Arthroscopy 2014; 30: 506–22.

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Case 9 the fibular head and has a normal range of motion at the hip and knee bilaterally. His lateral Contributing Author: Rebecca Jeanmonod malleolus is not tender. His skin is warm and well-perfused. The remainder of his extremities History are atraumatic and normal. A 10-year-old boy presents to the ED with right ankle r Neurologic: Normal mental status. Intact sensation pain. The child was playing soccer in gym class when to the foot. Has minimal dorsi- and plantar he tried to capture the ball from another player. His flexion of the right ankle secondary to pain. right foot became entrapped between the other player’s r Pertinent radiographs: X-ray demonstrating feet. He lost his balance and fell to the ground, causing Salter–Harris II fracture of right distal tibia. his foot to be twisted laterally. Since that time, he has been unable to walk on the ankle secondary to pain. Questions for Thought Hedidnotstrikehisheadorloseconsciousness.He r denies neck pain, arm pain, chest pain, or abdominal How do children’s fractures diﬀer from adult pain. He denies numbness, tingling, or weakness in any fractures? r What is the prognostic value of the Salter–Harris of his extremities. classiﬁcation system for fractures? r What are principles of splinting for fractures? Past Medical History r Transposition of the great vessels, which was corrected during infancy. Diagnosis r Immunizations UTD. r Salter–Harris II fracture of the distal tibia.

Medications Discussion r None. r Epidemiology:Fracturesarecommoninchildren, occurring with an annual incidence of 180 per Allergies 10,000 children younger than age 16.1 Upper r None. extremities are injured far more commonly than lower extremities, with the clavicle and distal Physical Examination and Ancillary Studies radius being the most commonly fractured bones.1,2 r Vital signs: 97.9 °F, HR 110, RR 19, BP 105/70, O 2 Ankle fractures account for about 5 percent of sat 99% on room air. r all pediatric fractures, and account for about 20 General: Well-developed child, crying on the percent of pediatric physeal injuries.3 They stretcher, holding onto his ankle. r typically occur related to sporting injuries or HEENT: PERRL. Oropharynx with moist mucous motor vehicle accidents, and are more common in membranes and no lesions. Head is atraumatic. 1 r children with an elevated BMI. Neck: No midline tenderness, no step-offs or r Pathophysiology: Children’s bones are more adenopathy. r pliable and porous than adult bones, with a Cardiovascular: Regular rate and rhythm. No thicker and stronger periosteum and an increased M/R/G. Brisk capillary refill. ability to remodel.2 These properties are largely r Lungs:CTAbilaterally,withnoW/R/R.No responsible for the way in which children’s bones chest-wall tenderness. fracture. These properties are also responsible for r Abdomen:Soft,notenderness,nosignsoftrauma. why children’s fractures are less likely to displace, r Extremities and skin: Child with swelling and less likely to suffer non-union, and more likely to tenderness to right medial malleolus, with no heal quickly. obvious deformity. He has intact dorsalis pedis Because of the relative strength and flexibility and posterior tibial pulses and a normal sensory of the periosteum, children may have plastic examination of the foot. He has no tenderness at deformity, in which a force is applied to a bone

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Figure 6.3 Salter–Harris fracture classification system for physeal injuries. Arrows indicate fracture location.

that is great enough to deform the bone without remotely. It is not uncommon for a child to being so great as to break the periosteum.2 complain of wrist pain at the site of a torus Further force may break one side of the bone’s fractureforadayortwobeforethecaregiver periosteum, but may not extend completely brings the child in for medical care. Occasionally, through, causing an incomplete or a greenstick the trauma history is unwitnessed or unknown. fracture.2 Acompressiveforcemaycauseabuckle Particularly in non-verbal children, the chief or torus fracture which is identified by a loss of complaint may be vague, such as “crying” or smoothness to the cortex on radiography. Finally, “fussiness.” Children with lower-extremity children have physes, or growth plates, that are fractures will generally refuse to bear weight or madeofcartilageandarearelativelyweakareaof will limp. Those with upper-extremity fractures pediatric bone. Physeal fractures are traditionally may refuse to use the affected limb, or may simply categorized by the Salter–Harris (S–H) complain of discomfort. Children with clavicle classification system, which both describes the fractures may have pain with head movement, or injury and is prognostically important. S–H I their caregivers may attribute their pain to an arm fractures are fractures through the physis only and rather than a clavicle injury. The practitioner may not be visible on radiography. These are should always have a high index of suspicion for diagnosed based on tenderness on examination, non-accidental trauma and injuries that are and have an excellent prognosis. S–H II fractures inconsistent with the stated mechanism. extend through the metaphysis into the physis, r Diagnosis: Although most fractures are and are the most common S–H fracture. These are definitively diagnosed on radiography, the history diagnosed by radiography, and also have an and physical examination guides the provider to excellent prognosis. They often do not require determine which areas to image. The medical surgery.3,4 S–H III fractures extend from the provider should completely expose the patient physis through the epiphysis, and are therefore and assess him or her just like any other trauma intra-articular fractures. These are higher risk for patient. Every bone should be palpated, every later arthritis or dysfunction, and require joint should be ranged. It is important to do a reduction, sometimes with open technique.4 S–H thorough neurovascular examination in all IV fractures extend from the metaphysis, through extremities. Some injuries, such as elbow fractures the physis, and into the epiphysis. These injuries or dislocations, have exceedingly high rates of commonly require operative fixation, and have a arterial and nerve injury (in this case, the brachial high rate of later growth disturbance.2,4 S–H V artery and the ulnar nerve in 5–10 percent of fractures are secondary to axial load and crush the patients). Shoulder dislocations, humeral-shaft physis. These are often missed on radiographs, fractures, posterior clavicular dislocations, knee and have a high rate of later growth failure and a dislocations, and lower leg fractures all have poor prognosis.2,5 Figure 6.3 demonstrates the well-described neurovascular complications, and S–H fracture classification system. anyfracturehasthepotentialtocauseinjuryto r Presentation: Children with a fracture typically surrounding structures. present with pain and swelling at the affected site. Once the injured area has been identified, the Although most children present acutely after the provider should obtain appropriate radiographs to index trauma, sometimes children present assess the injury. Classically, the radiograph

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shouldincludeimagingofthejointaboveandthe Historical clues Physical findings Ancillary studies joint below the injury to rule out associated r Twisting injury r Tenderness and r X-ray with S–H II injuries. Since pediatric growth centers can cause r to ankle swelling over fracture of distal both false positive and false negative radiographs, Inability to bear r medial malleolus tibia if unsure, the provider should image the weight Intact neurovascular unaffected limb for comparison. If there is any examination doubt as to the presence of a fracture, the child should be splinted and referred to orthopedics. r Treatment: Fractures that are minimally angulated Follow-Up and not rotated are generally treated with casting, The child’s fracture was determined to be non- although some debate exists as to the utility displaced. He was placed in a long leg splint and pro- 6,7 of casting for torus fractures. Lower-extremity vided with crutches and teaching in crutch use. He fractures should be made non-weight-bearing, followed up with orthopedics 2 days later and was typically for 6 weeks. S–H I and non-displaced casted. He had an excellent functional recovery. S–H II fractures are usually treated with casting alone.2–5 In the ED, it is appropriate to splint these children and call orthopedics to facilitate follow- References up in the next 1–2 days for cast application after 1. Randsborg PH, Gulbrandsen P, Saltyte´ Benth J, et al. swelling has gone down. S–H III–V fractures, any Fractures in children: Epidemiology and fracture with rotational deformity, open fractures, activity-specific fracture rates. J Bone Joint Surg Am fractures with neurovascular compromise, 2013; 95: e42. and fractures associated with compartment 2. Thornton MD, Della-Giustina K, Aronson, PL. syndrome generally require emergency Emergency department evaluation and treatment of orthopedic consultation. The ED provider pediatric orthopedic injuries. Emerg Med Clin N Am should attempt to reduce any fracture with 2015; 33: 423–49. neurovascular compromise rather than wait for 3. Su AW, Larson AN. Pediatric ankle fractures: a specialist, as ischemia time worsens prognosis. Concepts and treatment principles. Foot Ankle Clin Splints should immobilize the joint above and 2015; 20: 705–19. below the injury, and should have one open side 4. Larsen MC, Bohm KC, Rizkala AR, et al. Outcomes of to allow for tissue swelling. nonoperative treatment of Salter–Harris II distal r radius fractures: A systematic review. Hand (NY) 2016; Disposition: Non-displaced fractures in patients 11: 29–35. whose pain is adequately controlled may be 5. Arora R, Fichadia U, Hartwig E, Kannikeswaran N. discharged and orthopedic follow-up should be Pediatric upper-extremity fractures. Pediatr Ann 2014; arranged. Family should be instructed regarding 43: 196–204. elevation, ice, and analgesia. Displaced, angulated, 6. Firmin F, Crouch R. Splinting versus casting of “torus” open, rotationally deformed, or complicated fractures to the distal radius in the paediatric patient fractures require ED orthopedic consultation and presenting at the ED: A literature review. Int Emerg often require admission for surgical reduction and Nurs 2009; 17: 173–8. fixation. Children with minor fractures in whom 7. YeungDE,JiaX,MillerCA,etal.Interventionsfor non-accidental trauma is suspected should also be treating ankle fractures in children. Cochrane admitted and CPS should be notified. Database Syst Rev 2016; 4: CD010836.

16:14:23 07 Chapter7 Vomiting

Case 1 Medications r Metoclopramide. Contributing Author: Rebecca Jeanmonod r Ondansetron. History A 9-month-old boy is brought in by his mother for Allergies vomiting. The child has been having vomiting chroni- r None. cally on and off since birth, and mom has had him evaluated by pediatric gastroenterology, who diagnosed Physical Examination and Ancillary Studies him with gastroparesis. The child has been receiv- r ° ing metoclopramide for this, but still has occasional Vital signs:T99 F, HR 180, RR UTO, BP UTO, O2 sat UTO. paroxysms of vomiting. Mom told the triage nurse that r the child has been having difficulty keeping anything General: The child is actively seizing. r down for the last 48 hours. He was seen by his pedia- Primary survey: The child is drooling/foaming at trician, who told her the child had gastroenteritis and the mouth. He is cyanotic. He has pulses. You do prescribed a bland diet and ondansetron. Last night, not have an IV line. the child was able to take 6 ounces of formula, but vomited during the night and then vomited again this morning. Mom states that the child has not had diar- Questions for Thought rhea, and his bowel movements have been normal. She r Before moving on with your examination, what has not noted fever or rashes. He has not had blood test must you have? in his diaper. During the triage assessment, the child r What interventions should you perform? becomes unresponsive and has generalized seizure. r What medications should you give? The nurse rushes him back to an available room, where he continues to seize.

Physical Examination and Ancillary Studies Past Medical History r Bedside testing: The child has a fingerstick glucose r Induced at 37 weeks for intrauterine growth of 32. You recognize that the nurse has been retardation, birth weight 5 pounds. The child had unable to obtain peripheral access ×2, and place a brief NICU stay for hypoglycemia and an IO line in the child’s right tibia and give the hypothermia, and had feeding difficulty, resulting child 2 cc/kg of 25% dextrose solution through the in him having a 10-day course in the neonatal line. You place the patient on 100% oxygen by nursery. facemask and place the child on the monitor. The r The child has been consistently below the 5th child stops seizing. r percentile for body weight. He has lagged in his Vital signs:T99°F, HR 150, RR 45, BP 95/60, O2 milestones and cannot sit unsupported yet. sat 100% on room air. r He is UTD on immunizations. r General: The child is lethargic and post-ictal.

16:16:45 147 08 Chapter 7: Vomiting r HEENT:Therearenosignsofheadtrauma. r Pathophysiology: Inborn errors may disrupt PERRL. The child has no oral lesions. His mucous carbohydrate metabolism, protein metabolism, membranes are somewhat dry. fatty acid oxidation, or glycogen storage. When we r Neck: His neck seems supple, and you do not eat, our bodies break down food into glucose and appreciateanyadenopathyormasses. other metabolic products that are ultimately r Cardiovascular: Regular tachycardia, with no excreted. Excess glucose is stored as glycogen in M/R/G. Ͼ 3secondcapillaryrefill. the liver and muscle for use in times of fasting. r Lungs: CTA bilaterally, with good air movement. When liver glycogen stores are depleted and the r Abdomen:Soft,withnormalbowelsounds.No plasma glucose has been used, the body will make masses. No hepatomegaly. new glucose from amino acids (gluconeogenesis) r and then, finally, will use fatty acid oxidation to Extremities and skin: Pale skin with no rashes or 3 vesicles. No signs of trauma. create substrate for the Krebs cycle. To broadly simplify, diseases that result in errors in breaking r Neurologic: The child is lethargic and has poor down foodstuffs will often cause hypoglycemia, tone. He is becoming more responsive, moves all ones that interfere with excretion of metabolites four extremities spontaneously, and is will cause intoxication (most commonly with intermittently crying. ammonia), and ones that interfere with fatty acid r Pertinent laboratory values: WBC 19,000, Hb oxidation can cause hypoglycemia and acidosis. normal. Na 141, K 5, Cl 105, bicarbonate 11, BUN Disorders of glycogen storage do not usually 11, Cr 0.3. Urine dip + ketones. LP with low present acutely and will not be further addressed glucose, no cells. here. r Pertinent radiographs: CXR and head CT negative. r Presentation: Children with profound errors in carbohydrate metabolism present catastrophically Questions for Thought in the neonatal period, and may be r When faced with the seizing hypoglycemic indistinguishable clinically from septic neonates. infant, what laboratory tests should you draw to Because these are heterogeneous diseases, though, help with later diagnosis? they can present in a variety of ways. Diseases that r If the child continues to be hypoglycemic, how result in intoxication will typically progress over would you manage him? r time with lethargy and altered mental status, If the child wakes up suﬃciently and seems diseases causing acidosis will present with hungry, what should you feed him? vomiting and tachypnea, and diseases causing hypoglycemia will present with altered mental status and seizure. However, there is much overlap Diagnosis in different syndromes, and children can present r Inborn error of metabolism. with a mixed presentation or with episodic, seemingly non-progressive symptoms. The most Discussion common presentations for inborn errors of r Epidemiology: Inborn errors of metabolism are a metabolism are neurologic (poor tone, poor suck, heterogeneous group of inherited disorders that developmental delay or loss of milestones, involve problems of protein and carbohydrate seizure) or related to the GI tract (vomiting, food metabolism and storage. Although each known intolerance, hepatomegaly, diarrhea, syndrome is rare, all errors combined occur in dehydration).3,4 Patients may also present with about 1 in 2,500 births, making them a significant psychosis, behavioral, or learning disabilities, or source of pediatric morbidity and mortality.1,2 autonomic instability.3,4 Although neonatal screening detects many Symptoms may be precipitated by an disorders, it misses others. Furthermore, inborn intercurrent illness that increases catabolism (i.e. errors of metabolism can present in any age febrile condition), fasting (whether because of group, with only half presenting in the neonatal progressive spacing of feeding during infancy or period.3 Therefore, it is important to consider this during GI illness that causes vomiting), dietary diagnosis in the appropriate clinical scenario. changes, or other stressor.3–5 Often, a precipitant

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will not be identified, but a review of the child’s this is that the provider has no way of knowing history may reveal recurrent feeding issues, failure which dietary item is responsible for the child’s to thrive, or behavioral and developmental symptoms, and therefore it is imperative to concerns. prevent ongoing metabolism.3,5 Additionally, r Diagnosis: Definitive diagnosis of a specific inborn since the provider will have no way to know if the error of metabolism is not a reasonable goal in the process involves gluconeogenesis or fatty acid ED.Thatsaid,itisimportantnottomissthese oxidation, the provider must provide enough children, as delay to diagnosis can lead to substrate (glucose) to the patient to prevent them morbidity and mortality. The first step to from becoming catabolic and potentially diagnosis is considering inborn errors of worsening their status. Therefore, these children metabolism in the differential for the child with should be provided with 10% dextrose solution in hypoglycemia, neurologic abnormalities, or GI 1/4 normal saline at 1 1/2 maintenance.3,5 If the complaints, or in any ill-appearing neonate. child develops hyperglycemia, insulin (0.2 IU/kg Although the specific diagnosis may require per hour) should be given. Nitrogen scavengers specialized testing that isn’t usually performed in (sodium phenylacetate or sodium benzoate) can the ED, such as serum and urine amino and be used for patients with elevated ammonia, but organic acids, most if not all symptomatic toxic children and those with ammonia Ͼ 600 children with inborn errors of metabolism will should be treated with dialysis.3,5 have elevated lactate levels, hypoglycemia, r Disposition: A child with a clinical and laboratory hyperammonemia, or acidosis on blood testing, or picture for inborn errors of metabolism should be ketonuria or elevated urine reducing substances admitted to a pediatric center with access to a on urine testing.3–5 Therefore, a reasonable metabolic specialist. Most children require ICU approach to the child with a possible inborn error admission. Prognosis varies widely depending on of metabolism in the ED is to use serum pH, the specific inborn error and the degree of lactate, ammonia, electrolytes, and glucose enzymatic dysfunction. testing, together with urine testing, as a screen for this group of diseases. Should the testing be Historical clues Physical findings Ancillary studies concerning for inborn errors of metabolism, r r r furthermorespecifictestingshouldbeorderedin Failure to thrive Seizure Hypoglycemia r Developmental r Vomiting r Acidosis (elevated consultation with a metabolic specialist. r r delay r Dehydration r anion gap) It is important to draw all blood for diagnostic Frequent Tachypnea Ketonuria testing at the time of the patient’s presentation. vomiting (signaling r Prior episodes of acidosis) Laboratory abnormalities in some inborn errors hypoglycemia of metabolism may be transient and only present and hypothermia when the child is symptomatic. Therefore, the only opportunity for diagnosis may be on presentation, and diagnosis may be elusive after Follow-Up treatment is begun.3–5 Because of this, even The patient remained lethargic with poor tone in the though the specific diagnostic tests are not ED. He was given broad-spectrum antibiotics and IV typical “ED” tests, the blood should be drawn in access was attempted, which failed, but blood was the ED. drawn. The patient’s IO line became dislodged. The r Treatment:Illchildrenshouldberesuscitated, patient had a second seizure after 45 minutes in the with careful attention to the ABC algorithm. ED, and repeat glucose was 23. He was given a second Seizing children with hypoglycemia should IO line in the other leg and another bolus of dextrose. receive dextrose. If seizures continue, D10 was started, and IV access was obtained. Over the benzodiazepines should be given. The treatment course of about 90 minutes, the child returned to his of a metabolic crisis in the child with inborn error baseline functioning and mental status. He was trans- of metabolism is dependent upon what is ferred to a PICU at a nearby facility where he under- discovered during evaluation. All patients, went extensive testing, but his precise diagnosis still however, should be made NPO. The reason for eludes the metabolic specialists, as the ED was unable

16:16:45 149 08 Chapter 7: Vomiting to obtain all necessary blood work prior to treating the Past Medical History child. The child’s mother carries a written order for r Delivered full-term at 39 weeks’ gestation with no specific blood tests to be sent should the child become complications, immunizations UTD. ill and present to an ED again in the hopes of establishing a definitive diagnosis and, therefore, a tailored Medications treatment plan. In the meantime, the child is on a strict r None. elemental diet with frequent feeds and blood glucose testing at home. He is enrolled in early intervention. Allergies r NKDA. References 1. Dionisi-Vici C, Rizzo C, Burlina AB, et al. Inborn Physical Examination and Ancillary Studies errors of metabolism in the Italian pediatric r Vital signs: T 99.1 °F, HR 135, BP 90/43, RR 25, O2 population: A national retrospective survey. JPediatr sat 100% on room air. 2002; 140: 321–7. r General: The patient appears sleepy, but is easily 2. Applegarth DA, Toone JR, Lowry RB. Incidence of aroused. He becomes fussy during examination inborn errors of metabolism in British Columbia, 1969–1996. Pediatrics 2000; 105: e10. and cries, but with minimal tear production. r HEENT: PERRL. Mucous membranes are tacky 3. Fletcher JM. Metabolic emergencies and the emergency physician. JPaediatrChildHealth2016; 52: and stick to the tongue depressor. Posterior 227–30. pharynx is clear. r 4. CalvoM,ArtuchR,MaciaE,etal.Diagnostic Neck: Supple, with midline trachea, and no approach to inborn errors of metabolism in an adenopathy. emergency unit. Pediatr Emerg Care 2000; 16: 405–8. r Cardiovascular: The patient is mildly tachycardic, 5. Long D, Long B, Koyfman A. Inborn errors of without M/R/G. Central pulses and peripheral metabolism: An emergency medicine approach. Am J pulses normal. Capillary refill 3 seconds. Emerg Med 2016; 34: 317–18. r Lungs: The patient’s lungs are CTA bilaterally, without W/R/R. r Abdomen: His abdomen is soft, non-tender, and non-distended, with active bowel sounds Case 2 throughout. There are no palpable masses. r Skin and extremities: There is no peripheral Contributing Author: Erica Escarcega edema.Hisskiniswarmtothetouchandthereis no tenting of the skin. History r Neurologic: Sleepy and fussy. The child has good The patient is a 2-year-old male, who has been brought tone and normal reflexes. to the ED by his mother for vomiting, which began after waking up this morning. He has had three Questions for Thought episodes of vomiting since onset 4 hours ago. He has r not been able to tolerate solid food or liquids and vom- Whenwouldlabsbeindicatedinthe management of this patient? ited several seconds after attempting to eat breakfast. r According to his mother, he has been feeling unwell Is it possible to objectively determine the hydration status in this child without an invasive and having diarrhea for the past 2 days. She states that work-up? she has changed four to five diapers with watery stools r Should you rehydrate this child using oral each day. He had been eating and drinking normally rehydration or IV? untilthismorning.Helastateat6:00pmlastnight. r What treatments can be used if the patient Sheisunsureofwhenhelasturinatedduetothewatery continues vomiting in the ED during attempts at nature of his diarrhea. She does not believe the patient rehydration? has had a fever, but did not take his temperature. The r Are antibiotics indicated in the treatment of this child states that his belly hurts, but is unable to clarify condition? further. The patient attends daycare regularly.

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Diagnosis blood pressure generally portend severe 2 r Acute gastroenteritis. dehydration and shock. Although there are many scoring systems to help the clinician identify dehydration clinically, the assessment of Discussion hydration status is overall an imprecise science.2 r Epidemiology: Acute gastroenteritis is a common r Diagnosis: Acute gastroenteritis is usually a diarrheal illness affecting children worldwide. In clinical diagnosis. Laboratory tests are not the USA alone, more than 1.5 million outpatient routinely indicated.2 However, it is important to visits and 200,000 hospitalizations can be distinguish this from dysenteric forms of 1 attributed to acute gastroenteritis. As many as diarrheal illness, which typically will require more 300 children die each year in the USA from extensive work-up and treatment. Children who dehydration due to this prevalent illness, with have blood or mucous in their stool should have approximately 1.5 billion deaths per year stool cultures performed and may require 1 worldwide. This number has been declining, antibiotics.2 Children with a prolonged course of likely due to efforts surrounding the development illness should have stool studies, and those with of oral rehydration fluids. Acute gastroenteritis is neurologic abnormalities should be tested for commonly of viral origin, with bacterial illnesses toxin-producing pathogens.2 Patients with fever being less common in the developed world. or underlying medical conditions which may Rotavirus is the most common cause of viral result in a compromised immune system will also gastroenteritis. require more extensive work-up. More severe r Pathophysiology: Typically, acute gastroenteritis is illness can typically be ruled out through the an osmotic diarrhea occurring in conjunction history and physical. In cases of severe with vomiting. Rotavirus creates an osmotic dehydration, obtaining serum electrolytes, diarrhea by both acting directly on the intestinal bicarbonate, BUN, Cr, and glucose should be villiaswellasthroughtheproductionofan considered.2 Hypernatremia may occur in more enterotoxin, which results in malabsorption.2 severe cases. Children can experience fluid loses exceeding r Treatment: Treatment for parasitic infection or 200 mL/kg body weight per day secondary to bacterial infection may require specific diarrheal illness alone, making dehydration the antimicrobial treatment, but most gastroenteritis most common cause of morbidity and mortality is viral. Therefore, the treatment for acute that is associated with acute gastroenteritis. gastroenteritis is supportive and centered around r Presentation: Patients with acute gastroenteritis rehydration and maintenance of the patient’s fluid typically present with three or more episodes of status. Cases with mild to moderate dehydration loose or watery stools per day and a variable are usually able to be managed with oral history of vomiting.2 Variations can occur, rehydration.1 The child should be given small however, and in some children, vomiting may be amounts of rehydration solution, beginning with the primary complaint. Symptoms are generally 5mLatfirstandgraduallyincreasing,astolerated. present for less than 2 weeks and high-grade More recently, ondansetron has been used in fevers are uncommon.2 If symptoms are present children with acute gastroenteritis. Patients formorethan2weeks,thepractitionershould receiving ondansetron have been shown to be less consider parasitic causes of diarrhea.2 Patients likely to require admission to the hospital for may present with varying degrees of dehydration. rehydration, and are less likely to require IV Parents may describe the child as being more rehydration, with one in five children having irritable than usual, sleepy, or difficult to arouse. complete cessation of vomiting in the ED.3 There Eyes may appear sunken and mucous membranes are concerns, however, that ondansetron may may be sticky or dry. The child may have result in cardiac arrhythmias after the finding of decreased tear production. Heart rate and prolongedQTwith32mgIVadministration.4 respiratory rates may be elevated and pulses may Despitethis,therehavebeennoreportsof be diminished.2 Capillary refill may be prolonged arrhythmias from single oral doses of and urine output may be decreased. Decreases in ondansetron, which are typically administered in

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the ED. Antimotility agents should be avoided due she was bathing her 1-month-old infant while her tod- to limited efficacy and side effects, such as ileus, dler napped on the floor in the next room. She heard increased nausea, and drowsiness. More severe him playing and went to check on him after removing dehydration may require IV resuscitation. Please the infant from the bath. She noticed he had pulled sev- see Case 7 in Chapter 2 for further discussion on eral items off her dresser including some coins, a screw, rehydration techniques. a bottle of prenatal vitamins, a bottle of ibuprofen, and r Disposition: The vast majority of patients with a bottle of acetaminophen. The pill bottles were open, gastroenteritis may be discharged home. butthechildtoldhismotherhedidnoteatanything. Admission is appropriate for those with altered Thechildseemedtobefineatfirst,butstartedvomit- mentalstatus,evidenceofshock,andthosewho ing about 30–45 minutes later. She has noted blood in require ongoing volume resuscitation. the emesis. He is now holding his abdomen and saying his tummy hurts. Historical clues Physical findings On review of systems, mom states that he is a r r Nausea Tacky mucous membranes healthy boy and denies recent illness. She denies fevers, r Vomiting r Tachycardia r Diarrhea r Minimal tear production chills, headaches, cough, rhinorrhea, sore throat, difficulty breathing, or urinary complaints. She denies Follow-Up known sick contacts. He does not attend daycare. This child had another episode of vomiting in the Past Medical History ED when his mother attempted to give him a small r amount of rehydration fluid. The patient was given No significant medical problems. He is UTD on 2 mg ondansetron, after which he was able to toler- immunizations. ate oral rehydration without further episodes of emesis. He was discharged home in the care of his mother, Medications at which point he was able to resume his normal diet. r Pediatric chewable multivitamins. The patient had an uneventful recovery and was able to return to daycare after 2 days. Allergies r References NKDA. 1. KingC,GlassR,BreseeJ,etal.Managingacute gastroenteritis among children: Oral rehydration, Physical Examination and Ancillary Studies r maintenance, and nutritional therapy. MMWR Vital signs: T 98.2 °F, HR 165, BP 75/40, RR 42, O2 Recomm Rep 2003; 52: 1–16. sat 100% on room air. 2. Churgay CA, Aftab Z. Gastroenteritis in children: Part r General: The patient is awake, but not very I. Diagnosis. Am Fam Phys 2012; 85: 1059–62. interactive. He is laying on the stretcher looking at 3. DeCamp L, Byerly J, Doshi N, et al. Use of antiemetic his mom. He is average size for a 3-year-old. agents in acute gastroenteritis: A systematic review r HEENT: PERRL. No signs of trauma. No and meta-analysis. Arch Pediatr Adolesc Med 2008; oropharyngeal erythema or foreign body. 162: 858–65. r Neck: Supple neck, with midline trachea. 4. FreedmanS,UlerykE,RumantirM,etal. r Ondansetron and the risk of cardiac arrhythmias: A Cardiovascular: Tachycardic with regular rhythm. No M/R/G. Capillary refill Ͻ 3 seconds. systematic review and postmarketing analysis. Ann r Emerg Med 2014; 64: 19–25. Lungs:Clearbilaterally.NoW/R/R. r Abdomen: The child has positive bowel sounds. Case 3 He grimaces when the abdomen is palpated diffusely. No guarding or rebound tenderness. Contributing Author: Kinsey Leonard r Extremities and skin:Extremitieshaveno deformity or signs of trauma. Skin is warm and History dry without rashes. A3-year-oldboyisbroughttotheEDbyhistearful r Neurologic: Listless, but has symmetric strength mother with a chief complaint of vomiting. Mom states and intact reflexes.

16:16:45 08 Chapter 7: Vomiting r Pertinent laboratory values: Na 144, K 4.7, Cl 103, inhibition of an enzyme needed in thrombin bicarbonate 10, glucose 160, WBC 16,000, Hb 9.3, formation. Shock results from hypotension and Plt 300,000. vasodilation. Iron deposits also accumulate in the myocardium, causing toxicity. Questions for Thought Serum iron concentrations normally peak 6 r What imaging modalities would you use, if any, to hours after an overdose. Most studies agree that make the diagnosis? elemental iron ingestion of less than 20 mg/kg r What laboratories would you order and which does not cause significant symptoms. Ingestion of would be abnormal? greater than 60 mg/kg of elemental iron can cause r What treatments would you start in the ED? serious morbidity and mortality. r What determines the disposition of the patient? r Presentation: Patient presentation depends on time since ingestion and is divided into five phases: Diagnosis r r GI irritation (first few hours after ingestion): Acute iron toxicity. SymptomsresemblingaGIillness,including Discussion abdominal pain, fatigue, nausea, vomiting, and r diarrhea. There may be blood in the emesis or Epidemiology:IntheUSA,thereare stool. Hypovolemic shock can result during approximately 16,000 cases of iron ingestions this first stage. reported annually in children under 6 years old.1 r Latent phase (Ͼ 6hoursto24hours):GI Most ingestions are accidental, owing to the fact symptoms resolve and the patient appears that iron pills and prenatal vitamins resemble better clinically. Systemically, the child may candies, even coming in gummy formulations. become more hypovolemic and acidotic. Children with a sibling’s birth in the prior 6 Laboratory tests will differentiate worsening months and those age 3 and younger are at higher serious toxicity vs. recovery from mild toxicity. risk.2 The risk of serious toxicity is greatest when Vitals signs may also be abnormal, the patient the iron formulation is marketed for adults (e.g. may be tachycardic and/or hypotensive. adult pure iron pills or prenatal vitamins).3 r Systemic toxicity (Ͼ 6hoursto3days):Patients Children’s chewable vitamins have not been found who progress will develop lactic acidosis and to cause serious harm.3 Intentional overdoses hypovolemic shock during this phase. The typically occur in adolescent females. child may also have worsening GI bleeding due r Pathophysiology:Ironisabsorbedinthe to the disruption of the coagulation pathway. duodenum as ferrous iron and oxidized in Organ failure may occur, including respiratory mucosal cells to ferric iron. Once transferrin, the distress, cardiomyopathy (with subsequent iron binding protein, and ferritin, the intracellular cardiogenic shock), and renal failure. storage protein, are overwhelmed, ferric iron r Hepatotoxicity (48 hours to 5 days): Patients causes toxic effects by forming free radicals in whocontinuetoprogresswilldevelopelevated multiple organ systems.4 LFTs and may have liver failure secondary to Free radicals cause mucosal cell damage in the lipid peroxidation. GI tract with symptoms of abdominal pain, r Ͼ vomiting, diarrhea, and GI bleeding. Once free Gastric outlet obstruction ( 2weeksafter iron enters the bloodstream, systemic toxicity can ingestion): This is a rarely seen late be widespread. Effects include: uncoupling of the complication of iron toxicity, caused by scar oxidative phosphorylation in the mitochondria, formation from damage to the mucosa at the interference in the electron transport chain, and level of the gastric outlet. r enzyme inhibition in the Krebs cycle. Acidosis Diagnosis: History is key to making the diagnosis, results from hydroxyl free radicals and lipid as patients will typically present during the initial peroxidation. Death usually results from shock or phase that resembles a GI infection.3 Careful liver failure due to iron overload in the liver. history taking from the parents should include if Coagulation abnormalities may be seen due to the the patient was left unsupervised, had access to

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any medications, and what medications are in the Children who present with severe systemic home. This should include the type of iron toxicity, shock, metabolic acidosis, or serum iron (ferrous sulfate pills vs. prenatal vitamins vs. concentrations Ͼ 500 mcg/dL should be given multivitamins) and the suspected number of deferoxamine, an iron chelating agent. It should tablets ingested. bestartedat5mg/kgperhourbecauseitcanlead Once iron ingestion is suspected, laboratory to hypotension. The rate can be slowly increased tests should include a CBC, coagulation profile, to 15 mg/kg per hour, as tolerated. The LFTs, BUN/Cr, serum iron level, electrolytes, and recommended dose in 24 hours is 36 mg/kg or glucose. If severe toxicity is suspected, a blood 6 g. If treatment is being considered past type and screen, ABG, and lactic acid level should 24 hours, dosing should be determined with the also be ordered. If the child had access to other help of a toxicologist. Simultaneous fluid medications or drugs, acetaminophen and resuscitation should continue during treatment in salicylate levels and urine toxicology may also be the second IV site. beneficial. An abdominal plain film may be The decision to stop treatment is usually based ordered to see if any radiopaque tablets are visible. on clinical recovery. Alternatively, serial urine Chewable formulations are not usually seen on samples can be used to determine therapy plain films. duration. Deferoxamine forms ferrioxamine when Serum iron levels are helpful in confirming it chelates iron, which causes a characteristic that iron was ingested, but less helpful in orange to rusty color when it is excreted in urine determining the degree of toxicity. Absorption (“vin rose”). As iron levels fall, the urine clears. time and peak levels vary depending on the iron This method is limited since the urine color formulation. The serum iron level reflects free change is not observed in all patients. iron, while intracellular iron is what causes toxic Deferoxamine treatment requires an ICU effects. Therefore, the iron level should not falsely admission, given the side effects of the treatment, reassure the clinician that the child will not have which include hypotension, renal failure, ARDS, severe toxicity. The best time to draw serum iron mucormycosis, and sepsis. levels is 4–6 hours after ingestion. Iron levels can If the patient has coagulation abnormalities, also be trended over time during treatment, as consider treatment with vitamin K or fresh frozen treatment lowers the iron level. Generally, patients plasma. If the patient has GI bleeding and is with levels Ͻ 300 mcg/dL have absent to mild anemic, transfusion should be performed. symptoms, 300–500 mcg/dL usually have GI Hemodialysis has been used in some cases toxicity and possible systemic toxicity, Ͼ 500 mcg/ after deferoxamine treatment in patients who have dL have moderate to severe symptoms, and progressed to renal failure and cannot excrete the Ͼ 1,000 mcg/dL have significant morbidity and ferrioxamine. mortality. r Disposition: If the patient is asymptomatic, has r Treatment: The child’s ABC should be addressed. normal vitals, and ingested Ͻ 20 mg/kg, he or she Two IV sites should be established and the child canbeobservedintheEDfor6hours.Mild should be given a bolus of crystalloid and placed symptoms, including abdominal pain and less on the monitor. than three episodes of emesis, can also be Charcoal is not recommended for iron toxicity observed for 6 hours. Children with mild to since there is no evidence of benefit and it may be moderate symptoms should be admitted for a detrimental if the patient requires subsequent longer observation period. If the child received airway intervention or endoscopy. Orogastric deferoxamine, admission to the PICU is lavage can be considered if the child presents warranted. within an hour of ingestion, but will not be beneficialinremovinglargepillfragmentsand Historical clues Physical findings Ancillary studies r Ͻ r r has never shown a benefit in poisonings. r Child 6years r Hypotension Anion gap Polyethylene glycol has been shown to be Access to iron Tachypnea acidosis r Abdominal pain r Tachycardia r Non-specific beneficial in cases where the child ingests several r r r GI symptoms Abdominal leukocytosis pills (dose is 250–500 mL/hr). Blood in emesis tenderness

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Follow-Up Medications The child’s serum iron level returned at 400 mcg/dL. r None. He was given deferoxamine because of the severity of his symptoms and his acidosis. He improved over Allergies 24 hours and was ultimately discharged home with no r NKDA and recent allergy testing negative. sequelae.

References Physical Examination and Ancillary Studies r 1. Bronstein AC, Spyker DA, Cantilena LR Jr, et al. 2010 Vital signs: T 98.3 °F, HR 140, RR 36, 103/43, O2 Annual report of the American Association of Poison sat 98% on room air. Control Centers’ National Poison Data System r General: On initial evaluation the patient is limp (NPDS): 28th Annual Report. Clin Toxicol (Phila) in mom’s arms and not responding to gentle 2011; 49: 910–41. stimuli of the examination. 2. Juurlink DN, Tenenbein M, Koren G, et al. Iron r HEENT: Anterior fontanelle is soft and flat, poisoning in young children: Association with the birth of a sibling. CMAJ 2003; 168: 1539–42. mucous membranes are moist. r Neck: Supple and non-tender. 3. McGregor T, Parkar M, Rau S. Evaluation and r management of common childhood poisonings. Am Cardiovascular: Regular rate and rhythm. No Fam Phys 2009; 79: 397–403. M/R/G. r 4. Tenenbein M. Toxicokinetics and toxicodynamics of Lungs: Effort normal and breath sounds normal. iron poisoning. Toxicol Lett 1998; 102–103: 653–6. No respiratory distress noted. r Abdomen:Softandmildlydistended,patient awakes during palpation and begins crying. r Case 4 Extremities and skin: Pale, warm, dry. No signs of trauma. Contributing Authors: Angela Mastantuono r Neurologic: Tired and ill-appearing but can be stimulated, strong cry and normal tone after IV and Melanie K. Prusakowski placement. r History Pertinent laboratory values: WBC 17,800, Plt 560,000, metabolic panel within normal limits. The patient is a 4-month-old infant boy, born at term r without complications, who presents to the ED with Pertinent imaging:U/Sshowsdistendedand vomiting some of his feeds. He was acting normally fluid-filled stomach. There is a 5-cm tubular last night but woke this morning unusually fussy. He structure in the midline lower pelvis (Figure 7.1). remained fussy after his morning nap. While mom Bowelandgastricgasprohibitsfullinterrogation notes he has always been a gassy baby, today’s fussiness of the mesenteric vessels for malrotation. is out of the ordinary. He is not interested in eating. Hedoesnotnormallyspitup,buttodayheseemstobe choking and has spat up several times. He appears pale Questions for Thought to his parents and has become less active. r What diagnostic test can also treat the suspected condition? r Would any other laboratory tests be valuable? Past Medical History r r Does this patient require inpatient admission? Full-term born by spontaneous vaginal delivery, r Is this a typical presentation for this condition? without complications in pregnancy or delivery. r What vaccine was previously blamed for an r Recent allergy testing for “teal green” stool was increased incidence of this condition? negative. He was switched to an elemental formula, but parents have not noticed a difference in his gassiness or stools. r He received his age-appropriate vaccines 5 days Diagnosis ago. r Intussusception (likely colocolic or colorectal).

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Figure 7.1 U/S demonstrating a cross-sectional image through a tubular structure in the pelvis.

Discussion abdominal pain. These children often vomit after r Epidemiology: Intussusception is the most the episodes of colicky pain. The pathognomonic common cause of bowel obstruction in young “currant jelly stools” can be seen as a result of children and the second most common pediatric bowel-wall ischemia and venous engorgement, surgical emergency.1 It occurs when a portion of causing passage of mucous and blood that appears 1 the bowel “telescopes” into another segment, to look like red jelly, but this is a late finding. A potentially leading to bowel ischemia and larger proportion of children will have 1 necrosis. Intussusception is most common in hemoccult-positive stools. Ideally, children less than 5 years old (approximately 1 to intussusception is diagnosed before the 4 in 2,000 infants and children), with peak development of advanced ischemia, and so the incidence less than 1 year of age.1 A viral infection classic triad of abdominal pain, vomiting, and precedes intussusception in up to 20 percent of bloody stools is present in only a small percentage cases. of presentations. The abdominal examination can r Pathophysiology: The cause of intussusception is vary from soft and non-tender to acute. Some most often idiopathic. There is a correlation with literature describes a palpable sausage-shaped viral infections and increased incidence of mass in the right lower quadrant, but this may be intussusception during viral seasons. Sometimes a difficult to appreciate in a squirming infant. mechanical lead point, such as a polyp, Meckel’s Patients may be asymptomatic between episodes diverticulum, lymph node, or tumor can be initially but, as the intussusception progresses, the identified. Bowel is thought to telescope over such infant or child can become lethargic. Lethargy a structure. A malignant lead point is more typical may be the only presenting symptom in 10 in older children and adults.2 Intussusception percent of children, and small children may seem 1 most commonly (75–95 percent of cases) occurs to have no pain at all. r at the terminal ileum, but may occur anywhere Diagnosis: History and examination are important along the bowel. This location is presumably due to diagnosis. Physician gestalt as to which patients to the large amount of lymphoid tissue in the do not have intussusception has a specificity of 85 ileocolic region. A past formulation of the percent and a negative predictive value of 94 1 rotavirus vaccine was associated with an increased percent. Laboratory testing does not add much to incidence of intussusception, but the newer the diagnosis, although it may support concern formulation is not.3 Intussusception can become a for ischemia (elevated lactate or WBC) or surgical emergency and, if left untreated, will lead dehydration. r to death. Previously, the gold standard diagnostic and r Presentation: Classic presentations of treatment modality for intussusception was an intussusception describe intermittent but severe air- or water-soluble contrast enema. More

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recently, studies warn against moving directly to admitted to the hospital for observation and was dis- enema due to the risks of the procedure charged home with no sequelae. (bowel-wall perforation, infection) and exposure to radiation.4,5 Plain radiographs can occasionally References be useful, and may provide clues such as a paucity 1. Smith J, Fox SM. Pediatric abdominal pain: An of gas in the right abdomen or findings consistent emergency medicine perspective. Emerg Med Clin N with bowel obstruction.1 The use of screening U/S Am 2016; 34: 341–61. has decreased unnecessary enemas for clinically 2. Choi SH, Han JK, Kim SH, et al. Intussusception in suspected intussusception, and has a sensitivity of adult patients: From stomach to rectum. AJR Am J 85 percent and a specificity of 97 percent.1,4,5 Roentgenol 2004; 183: 691–8. r Treatment: Initial management involves fluid 3. Tate JE, Yen C, Steiner CA, et al. Intussusception rates resuscitation, pain control, and management of before and after the introduction of rotavirus vaccine. sepsis or shock, when present. Intussusception 2016; 138: e20161082. can become a surgical emergency and lead to 4. HentiksonS,BlaneCE,KoujokK,etal.Theeffectof death if untreated. Reduction of the screening sonography on the positive rate of enemas intussusception occurs with air- or water-soluble for intussusception. Pediatr Radiol 2003; 33: 190–3. contrast enema. If there are no signs of peritonitis 5. Bartocci M, Fabrizi G, Valente I, et al. Intussusception (a contraindication to enema), enema may be in childhood: Role of sonography on diagnosis and attempted even with 24 hours of symptoms.6 If treatment. JUltrasound2015; 18: 205–11. the intussusception cannot be reduced with an 6. van den Ende ED, Allema JH, Hazebroek FWJ, et al. enema, manual reduction with laparotomy is Success with hydrostatic reduction of intussusception in relation to duration of symptoms. Arch Dis Child required. Resection of necrotic bowel may be 2005; 90: 1071–2. necessary. Surgeons may also attempt to identify the “lead point” that caused the intussusception. 7. Al-Jazaeri A, Yazbeck S, Filiatrault D, et al. Utility of hospital admission after successful enema reduction of Occasionally, complications of reduction, such as ileocolic intussusception. JPediatrSurg2006; 41(5): bowel-wall perforation, require surgical 1010–13. intervention. r Disposition: There is a 5–10 percent recurrence rate in the first couple days after the reduction of Case 5 an intussusception.7 The decision to admit depends on the ease of the reduction, the clinical Contributing Author: Rebecca Jeanmonod status at presentation, and practitioner practice. A periodofobservationintheEDfollowingthe History reduction is considered safe practice.7 Caregivers A 38-month-old girl is brought into the ED by her of patients who are discharged must be educated distraught parents for vomiting. Her parents report about signs and symptoms of recurrence, which that she was napping on the sofa when she woke sud- generally is not associated with an unfavorable denly and complained of not feeling well. She seemed outcome.7 pale and ill-appearing to them. She then began vomiting and lost consciousness, and has not woken up Historical clues Physical findings Ancillary studies since. The parents attempted to revive her by putting r Vomiting r Distended r Elevated WBC cold water on her face and shaking her gently, but r r this was not successful. Her symptoms began about r Fussiness r abdomen Elevated Plt Pallor Tender abdomen (acute phase 10 minutes ago. Her parents, who live down the street r Limp, lethargic reactant) child r U/S with from the hospital, brought her in immediately because r Pallor intussusception “theambulancetakestoolong.”Onarrivaltotriage, the parents are screaming “somebody help my baby.” The child is brought to a resuscitation bay. As you Follow-Up initiate resuscitation, the parents report that the child The baby underwent air-contrast enema reduction has been otherwise healthy recently, with no fevers, of the intussusception with no incident. He was weight loss, or difficulty breathing. They do recall that

16:16:45 157 08 Chapter 7: Vomiting twice in the past 18 months, they had gotten up in the Diagnosis morning to get the child out of bed and noted that she r Panayiotopoulos syndrome (a common seizure had vomited in the bed, but they assumed this was disorder in children characterized by autonomic likely secondary to reflux, as the child woke in good dysfunction). spirits and otherwise seemed well.

Past Medical History Discussion r r Born at 41 weeks, c-section for failure to progress, Epidemiology: Panayiotopoulos syndrome was no complications. Child is UTD on initially described in 1989, and is thought to affect immunizations and developmentally normal. She greater than 10 percent of young children (age 1 is potty-trained and attends preschool. 3–6) with non-febrile seizures. Seizure disorders in general affect children commonly: 2–4 percent Medications of children will have at least one febrile seizure, r None. 0.05–1 percent will have a seizure from a metabolicorneurologicprocess(mostcommonly Allergies inthefirstyearoflife),andabout0.1percentwill develop repetitive seizure episodes.2 r NKDA. r Pathophysiology: All seizures are a result of an Physical Examination and Ancillary Studies abnormal discharge of electrical activity in the brain. This abnormal electrical activity may be r Vital signs: T 100 °F, HR 90, RR 36, BP 90/60, O 2 present and evident on EEG all the time, or it may sat 99% on room air. only be present during provocation or actual r General: The child is pale and diaphoretic. r seizure. Seizures may be primary (genetically HEENT:Therearenosignsofheadtrauma.The determined or idiopathic) or they may be child has dilated pupils and tonic eye deviation to secondary to trauma, structural lesions/masses, the right. She is drooling. r toxins, infections, or metabolic derangements. Neck: Supple and non-tender, with no adenopathy. Depending upon the portion of the brain r Cardiovascular: Regular bradycardia, with no involved, seizures may present with focal or M/R/G. Ͼ3secondcapillaryrefill. generalized motor activity, abnormalities in r Lungs: CTA bilaterally, with good air movement. behavior, staring spells, syncope, thought There are transmitted upper-airway sounds. disturbances, visual symptoms, or prominent r Abdomen: Soft with hyperactive bowel sounds. No autonomic symptoms. Autonomic symptoms such masses. No hepatomegaly. as ictal vomiting are common in temporal lobe r Extremities and skin: Pale with no rashes or seizures in infants and children as well as in vesicles. No signs of trauma. Panayiotopoulos syndrome.3 r r Neurologic: The child is unresponsive, but Presentation: Seizure patients may present in breathing spontaneously. She occasionally dramatic and obvious ways, such as those vocalizes. She does not respond to voice but presenting in convulsive status epilepticus, or in unreliably responds to pain. more subtle ways, as in this case. The approach to r Pertinent laboratory values: Fingerstick glucose 75, treatment of convulsive status is addressed CBC and chemistries normal, blood culture sent. elsewhere in this book. It is critical that the EM provider remember that not all seizure patients move, and not all that move will do so Questions for Thought convulsively. In myoclonic seizures, there may be r What is the diﬀerential diagnosis for the vomiting a single jerking movement. In atonic seizures, the child with an abnormal mental status? patient loses muscle tone and may fall to the r Are there any medications that you should begin ground. In tonic seizures, there may be prior to deﬁnitive diagnosis? r generalized muscle stiffening. In complex partial What are your management priorities? seizures, the patient may seem confused and engage in automatic or restless behaviors, such as

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lip smacking or repetitive movements. In absence child’s seizure could be from traumatic injury, seizures, the child may stare off into space. In CNS infection or masses, hypoglycemia, or toxins. small children, there may be no, or subtle, motor Therefore, diagnostic evaluation should include abnormalities and they often have prominent laboratory chemistry studies (especially a autonomic symptoms.3,4 Because the clinician fingerstick glucose!), toxicology screens, and may not recognize this as a seizure, the child may neuroimaging. be misdiagnosed and undergo invasive evaluation The definitive diagnosis of seizure disorder and treatment for the wrong condition.5,6 relies on the clinical history, examination, and Children with Panayiotopoulos syndrome EEG. Not every patient with a seizure has an most commonly have seizures that occur during, abnormal EEG, and EEG abnormalities can be or shortly after, sleeping. The seizures transient or provoked. Furthermore, not every characteristically are long lasting, often greater person with an abnormal EEG has a seizure than 30 minutes, and may have no motor findings, disorder. Use of a video EEG may improve although some children will develop unilateral sensitivity and specificity. Although some convulsions near the end of the seizure. To make advocate for use of prolactin levels to diagnose the diagnosis of Panayiotopoulos syndrome, the seizure, this is not a sensitive test and has not been child must meet five of the following criteria: studied in all subtypes of seizure disorder.7 infrequent seizures, prolonged seizures lasting r Treatment: Treatment of ongoing seizure activity greater than 5 minutes, ictal vomiting, eye in the ED is usually accomplished with deviation, autonomic manifestations, behavioral benzodiazepines as a first-line agent, and any disturbances, and an altered level of patient in status epilepticus should receive consciousness.5 Because of how long the seizures benzodiazepines. In the subset of patients with last, children may present with ongoing refractory Panayiotopoulos syndrome, there is no evidence vomiting, abnormal vital signs, incontinence, and or even consensus regarding how to treat confusion. As the seizures often occur at night or autonomic status epilepticus.3 That said, a recent during naps, family may be unaware of the event study suggests that there may be progressive and only note vomiting, or may bring the child in cognitive dysfunction in children with during the post-ictal period because of abnormal Panayiotopoulos syndrome who present with level of consciousness. Children typically recover status epilepticus, which suggests rescue treatment completely within several hours and return to maystillbeindicated,andthisissupportedin their normal level of consciousness. several case reports as well.5,6 It is unlikely that r Diagnosis: The diagnosis of Panayiotopoulos the EM provider will unilaterally make the syndrome or any seizure relies on clinical diagnosis of this syndrome in the ED at the suspicion, a thorough history, a complete patient’s first presentation. Therefore, if the child examination, and judicious ancillary testing. In is recognized as actively seizing, the EM provider any child with altered sensorium and abnormal should treat the patient as any other seizing child. vital signs, the provider should consider the In general, outpatient antiepileptic therapy is dangerous differential diagnosis, THE MISFITS not prescribed to patients with Panayiotopoulos (Trauma, Hypovolemia/heart, Endocrine, syndrome because their seizures are very Metabolic, Intestinal disasters, Seizures, Formula infrequent and most patients will outgrow them misadventures, Inborn errors of metabolism, in about 2 years. EM providers should not begin Toxicologic, and Sepsis). Certainly in this case, any seizing patient on prophylactic anti-seizure this child is ill-appearing, and it is appropriate to medications without consulting with a pursue multiple differential items simultaneously neurologist, as these medications may have while actively treating the child. A thorough deleterious effects and also may interfere with the head-to-toe examination may demonstrate clues child’s future diagnostic testing. to seizure like eye deviation, or autonomic r Disposition:Achildwithafirst-timeseizurewho symptoms such as drooling and mydriasis, but has returned to baseline, has a negative even once seizure is diagnosed, the underlying evaluation, and has reliable parents with good cause of the seizure must be considered. The follow-up may be discharged from the ED with

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prescriptions and instructions for rescue report and literature review. Epilepsy Behav Case Rep medications. If any of these conditions are not 2015; 3: 12–14. met, the child should be admitted to the hospital 7. Sundararajan T, Tesar GE, Jimenez XF. Biomarkers in for observation and to initiate neurology the diagnosis and study of psychogenic nonepileptic consultation, neuroimaging, and an EEG. seizures: A systematic review. Seizure 2016; 35: 11–22. Historical clues Physical findings Case 6 r Prior episodes of r Pallor “isolated” vomiting r Eye deviaton r Onset during nap r Autonomic findings (low-grade Contributing Author: Jason Black r Altered mental status temperature, bradycardia, drooling, mydriasis, incontinence, History diaphoresis) A 4-year-old male presents for evaluation of vomiting this morning upon awakening. Mom states that Follow-Up the child has had vomiting upon awakening two other timesinthepastweek,butthenhadnofurther The patient was recognized to be having a seizure and episodes during the day. Today he has continued to was given a weight-based dose of IV lorazepam while vomit. The patient’s mother noticed some “twitch- being placed on the monitor. She was additionally ing” in her son’s right arm that lasted for a moment given 20 cc/kg of normal saline and broad-spectrum and stopped spontaneously 3 days ago. Mom also has antibioticsbecauseofherillappearanceandpoorper- thoughtthatthechildhasbeen“lesscoordinated” fusion. The child’s eye deviation resolved and she was the last couple days, bumping into things and less post-ictal,withlethargyforseveralhours.Duringthat steady on his feet, which she believed was secondary to time, she underwent head CT, which was unremark- him napping less now that preschool has started. She able, LP, which was normal, and was admitted to the does not recall any significant falls, although he does PICU for ongoing monitoring. While inpatient, the occasionally trip and fall when running. The patient child had a sleep EEG performed, which showed ictal hasotherwisebeeninhisnormalstateofhealth.His occipital discharge spikes. The child was discharged mother states he has had normal appetite and activity home the next day with neurology follow-up. She had level and has not complained of any headache, fever, two more episodes over the following 2 years, and has or abdominal pain. He has no history of seizure dis- since been seizure-free and developmentally normal. order; however, he does have intermittent breakouts of eczema that require application of a topical steroid References cream. The patient was evaluated by his pediatrician 1. Panayiotopoulos CP. Benign childhood epilepsy with 2 months ago for general well-child visit and is UTD occipital paroxysms: A 15-year prospective study. Ann with immunizations. Neurol 1989; 26: 51–6. 2. Hauser WA. The prevalence and incidence of Past Medical History convulsive disorders in children. Epilepsia 1994; 35 r Suppl 2: S1–6. Eczema. 3. Ferrie CD, Caraballo R, Covanis A, et al. Autonomic status epilepticus in Panayiotopoulos syndrome and Medications other childhood and adult epilepsies: A consensus r Triamcinolone 0.1%. view. Epilepsia 2007; 48: 1165–72. 4. Aksoy A, Haliloglu G, Yalnizoglu D, et al. Childhood Allergies epilepsy with occipital paroxysm: Classification, r Azithromycin. atypical evolution and long-term prognosis in 35 patients. Turk J Pediatr 2015; 57: 439–52. Physical Examination and Ancillary Studies 5. Zaki SA, Verma DK, Tayde P. Panayiotopoulos r ° syndrome in a child masquerading as septic shock. Vital signs: T 98.7 F, HR 98, BP 94/52, RR 18, O2 Indian J Crit Care Med 2016; 20: 361–3. sat 100% on room air. r 6. Dirani M, Yamak W, Beydoun A. Panayiotopoulos General: The patient is awake, alert, and in no syndrome presenting with respiratory arrest: A case acute distress.

16:16:45 08 Chapter 7: Vomiting r HEENT: The patient’s right pupil appears larger of the posterior fossa are more common in than the left and is sluggish to respond to light pre-adolescence, after which supratentorial reflex or accommodation. There is slight blurring tumors tend to be more common. Between 54 and of the optic disk bilaterally. His cranial nerves are 70 percent of all childhood brain tumors are intact. locatedintheposteriorfossa.2 Most brain tumors r Neck: His neck is supple, with a midline trachea. in children are primary, and most are gliomas.2 r Cardiovascular:Heartisregular,withnoM/R/G. Risk factors for developing a primary tumor Capillary refill Ͻ 2 seconds. include prior history of radiation or presence of r Lungs:CTAbilaterally,withnoW/R/R. congenital conditions, such as multiple endocrine r Abdomen: Non-tender and soft, with normal neoplasia type 1, retinoblastoma, tuberous sclerosis, or neurofibromatosis.2 bowel sounds. There is no rebound, rigidity, or r guarding. Pathophysiology:Braintumorscausesymptomsby r Extremities and skin: Extremities are warm and either their specific location disrupting brain well-perfused, with no rashes. function (causing seizures, weakness, sensory r Neurologic: The right upper extremity is weak, problems,orcerebellarfindings)orsecondaryto with decreased gross sensation compared to the increased intracranial pressure (vomiting, altered left upper extremity; the lower extremities are mental status). Symptoms depend on the location equal in strength with no sensory deficits. The of the lesion, the rapidity of growth, obstruction of CSF drainage, and intracranial pressure. Babinski sign is negative when tested on both r lower extremities. The child is mildly ataxic with a Presentation: Pediatric brain tumors, whether broad-based gait. primary or secondary, will generally present with r Pertinent laboratory values: Fingerstick glucose similar signs and symptoms. The onset of 102. symptoms is usually subtle, with gradual progression, but can present acutely if there is tumor compressing the ventricular system and 3,4 Questions for Thought blocking flow of CSF in the brain. This blockage r couldleadtomoreacutesymptoms,suchas What further diagnostic modality could you use vomiting, mental status change, and respiratory to evaluate this patient? collapse.4 The most commonly reported symptom r What are the various neurologic ﬁndings in this is headache, occurring in about 40 percent of condition? 3,4 r What are the typical causes? newly diagnosed pediatric brain tumors. This r What treatments should be initiated in the ED? headache is typically described as a non-specific r What is the deﬁnitive treatment for this tension type pattern with the location of the condition? headache being non-specific to the actual location of the underlying tumor.3 Although headache is a common first symptom of pediatric brain tumor, the average number of signs and symptoms at the Diagnosis 4 r time of diagnosis is six. Specific signs and Intracranial mass. symptoms are related to the tumor size and location. Diplopia (double vision) or Discussion homonymous hemianopsia (loss of half of the r Epidemiology: Brain tumors are said to be either field of view on the same side in both eyes) may primary (originating from the brain tissue itself indicate tumor compression on specific cranial from an individual cell mutation) or secondary nerves or visual field tracts.4 Anosmia (loss of (metastaticfromadistantprimarysite,with smell) is associated with frontal lobe tumors and migration to the brain through the blood ataxia is common in masses affecting the stream).1 In the pediatric population, brain brainstem or cerebellum.4 Other possible tumors are the second most common type of signs/symptoms include new-onset focal or malignancy after leukemia, with an estimated generalized seizure activity, cranial nerve palsies, 3.6 per 100,000 new cases annually.2 Tumors growth problems, head tilting, or changes in

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behavior.4 Papilledema (swelling of the optic disk) surgery can be achieved. In stable patients, the is a general sign of increased intracranial pressure, focus should be on symptom management and indicating possible swelling or edema, and reducing the amount and progression of cerebral is a serious sign that portends potential edema by use of corticosteroids, such as decompensation. dexamethasone. Ultimate care may involve r Diagnosis: Blood chemistries may be helpful to multiple specialties, including oncology, radiation establish baseline levels as pediatric brain masses therapy, neurology, and neurosurgery. Surgical can cause electrolyte disturbances, but these options may include tumor removal or placement studies are usually normal in the setting of a of a ventricular shunt and devices to measure primary intracranial mass. Diagnosis relies intracranial pressure to guide medical heavily upon good history taking to identify new management. red-flag symptoms and physical examination The prognosis for pediatric tumors is highly findings to identify evidence of new neurologic variable depending on the initial symptoms, dysfunction. These findings should prompt tumor subtype, and management. Patients who further diagnostic imaging such as CT or MRI of survive their malignancy may have long-term thebrain.AlthoughanIVcontrastCTprovides deficits in memory and attention.5 There is also better diagnostics than a non-contrasted CT, in concern of other sequelae in adolescence and the ED, non-contrasted CT is often performed adulthood, such as an increased risk of psychiatric initially. Imaging should be performed emergently illnesses, including depression and psychosis.6 r in the ED if the provider is concerned that the Disposition:Childrenwithnewdiagnosesofbrain patient may have increased intracranial pressure, tumors should be admitted to the hospital to in order to facilitate neurosurgical evaluation and facilitate coordination of care, and neurosurgery possible decompressive surgery. In stable children should be consulted. Patients with signs of in whom MRI can be performed on an urgent increased intracranial pressure should be basis, it is reasonable to admit the child without admitted to an ICU. ED imaging, to reduce the child’s overall exposure to ionizing radiation, as most children with brain tumors or focal neurologic findings from other Historical clues Physical findings Ancillary studies r r r sources will require MRI. MRI is superior to CT in Vomiting, Abnormal pupils Normal glucose particularly r Focal neurologic imaging the posterior fossa and does not expose upon waking deficit the child to radiation, although many smaller r r r Arm twitching r Ataxia children require procedural sedation to undergo Balance Papilledema problems MRI. In the ED, should a contrasted CT of the r Fussiness head be performed, primary tumors will generally r Pallor appear as a single mass lesion, with secondary (or metastatic) disease appearing as multiple lesions. LP is generally not indicated for the detection of an intracranial mass, and in cases Follow-Up of obstructive hydrocephalus is actually The child was sent for contrast-enhanced CT of his contraindicated because of the increased risk of head, which showed a single intracranial mass located brainstem herniation. in the posterior fossa, with moderate hydrocephalus. r Treatment: The management of pediatric He was given 10 mg dexamethasone, with slight intracranial tumors is dependent upon the size, improvement in his pupillary response and vomit- location, type, and acuity of the patient’s ing. Neurosurgery was consulted and the patient was condition. Children with rapidly progressive sent for a stat MRI-brain, with an anesthesiologist for symptoms require resuscitation using the ABC sedation. The patient was admitted and subsequently algorithm. If elevated intracranial pressure is underwent tumor resection and had a stable post- suspected, then osmotic agents such as mannitol operative course. Repeat MRI testing showed resolu- may be necessary as a temporizing measure to tion of the hydrocephalus and stable post-operative prevent herniation until definitive decompressive findings. The child was diagnosed with a pilocytic

16:16:45 08 Chapter 7: Vomiting astrocytoma. He receives routine surveillance, but has Past Medical History had no recurrence of his tumor. r No significant medical problems, UTD on immunizations. References Medications 1. DeAngelis LM. Brain tumors. NEnglJMed2001; 344: r 114–23. Oral contraceptive pills. 2. Johnson KJ, Cullen J, Barnholtz-Sloan JS, et al. Childhood brain tumor epidemiology: A brain tumor Allergies r epidemiology consortium review. Cancer Epidemiol Penicillin. Biomarkers Prev 2014; 23: 2716–36. 3. Purdy RA, Kirby S. Headaches and brain tumors. Physical Examination and Ancillary Studies r Neurol Clin 2004; 22: 39–53. Vital signs: T 98.2 °F, HR 72, BP 120/69, RR 16, O2 4. Wilne S, Collier J, Kennedy C, et al. Progression from sat 100%. first symptom to diagnosis in childhood brain r General: The patient is awake and alert. She is tumours. Eur J Pediatr 2012; 171: 87–93. letting her mother answer most of the questions. 5. Tonning Olsson I, Perrin S, Lundgren J, Hjorth L, She has a normal body habitus. Johanson A. Long-term cognitive sequelae after r HEENT: The patient has several filled caries. Mild pediatric brain tumor related to medical risk factors, erythema of the throat. Tonsils appear normal. age, and sex. Pediatr Neurol 2014; 51: 515–21. The patient’s parotid glands are enlarged 6. Shah SS, Dellarole A, Peterson EC, et al. Long-term bilaterally. Non-tender to palpation. psychiatric outcomes in pediatric brain tumor r survivors. Childs Nerv Syst 2015; 31: 653–63. Neck:Supple,withnoadenopathy. r Cardiovascular: Regular rate and rhythm, with no M/R/G. r Lungs:CTAbilaterally,withnoW/R/R. Case 7 r Abdomen: Soft, non-distended, positive bowel sounds. There is mild tenderness to palpation Contributing Author: Kinsey Leonard diffusely, with no guarding or rebound tenderness. r History Extremities and skin:Skiniswarmanddry. Capillary refill ˂ 3 seconds. No rash. Mild acne The patient is a healthy 16-year-old female who present on the patient’s face. Calluses on patient’s presents with vomiting episodes that have been occur- right hand over her metacarpophalangeal joints. ring over the last 3–6 months, per her mother’s report. Limbs are atraumatic. The patient denies complaints. She states she vomits r “now and again” when she’s sick, but she isn’t sick now. Neurologic: Alert and oriented, normal cranial nerves, strength, and sensation. Mom also reports that the patient has seemed to have r an increased appetite. She consumes larger than nor- Pertinent laboratory values: K 3.0, Cl 90, mal amounts of food at dinner, and mom has noted bicarbonate 32, amylase 130. missing items from the pantry. Mom also states that the child eats very rapidly and asks to be excused from Questions for Thought the table prior to the rest of the family. r How do you diﬀerentiate bulimia from anorexia? On review of systems, the patient states that her last r What are the criteria for making the diagosis of bowel movement was 3–4 days ago. She also reports bulimia or anorexia? r mild generalized abdominal pain. She denies fevers, What is the ED management of this condition? r chills, headaches, cough, rhinorrhea, sore throat, dif- What are the worrisome physical complications ficulty breathing, or urinary complaints. She denies of eating disorders that can result in immediate known sick contacts. morbidity or mortality? The patient states that she is sexually active with one partner in a monogamous relationship for over a year. She attends high school and denies any issues at Diagnosis school. She denies using drugs or alcohol. r Bulimia nervosa.

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Discussion patient may present with complications of repeated vomiting, such as Mallory–Weiss tears, r Epidemiology: Bulimia and anorexia nervosa have GERD, dysphagia, sore throat, hoarseness, a lifetime prevalence of 1 percent and under 1 pancreatitis,ordehydration.Theycouldalso percent, respectively, although there are present with vague complaints similar to anorexia, conflicting data given the propensity to hide the including weakness, fatigue, dizziness, syncope, disease.1–3 Both are more common in women. palpitations, or seizures. Generalized abdominal The peak incidence of anorexia is in the pain, constipation, or diarrhea might be the chief 14–18-year-old age range, while the median age complaint. On examination, they may have dental for bulimics is 18. r caries, large parotid glands, and erythema on their Pathophysiology: The exact pathophysiology of palate and throat. They may also have Russell’s both disorders is unknown. Eating disorders have sign, which are calluses over the been correlated with certain extracurricular metacarpophalangeal joints from inducing activities (for example, cheerleading, dancing, or vomiting. wrestling), having divorced parents, having r Diagnosis: Both diseases are diagnosed on the underlying self-esteem issues, and having a basis of the Diagnostic and Statistical Manual perfectionistic personality.2,3 Both conditions 5 criteria. For anorexia nervosa,theseare:6 are associated with abnormalities in neurotransmitters, and both increase the patient’s r Restriction of caloric intake relative to risk for depression, anxiety, and substance expenditure, leading to low body weight for abuse.2,4 age, sex, and development. r Presentation: Both diseases are usually found in r Intense fear of gaining weight or of becoming theteenagepopulation.Theadolescentmaybe fat or persistent prevention of weight gain. apprehensive to present to the hospital or talk r Disturbance in perception of body weight or about eating habits. The teenager often has a long acknowledgement of the seriousness of the low history of dieting and being preoccupied with body weight. weight and losing weight. Usually the teen For bulimia nervosa, the criteria are:6 continues to view herself as overweight, though r Recurrent binge eating – eating larger amounts she is either underweight (anorexia) or normal of food than normal in a given period of time, weight (bulimia). Parents may bring the where the patient feels out of control of eating. adolescent to the ED with a medical complication r Recurrent compensatory behavior to prevent of the disease as the chief complaint.5 weight gain. In anorectics, there are usually vague or no r Binging and compensatory behavior are at least complaints.2 Family members may bring the once a week for 3 months. patient to the ED because of weight loss, r weakness, fatigue, dizziness, or after a syncopal Body shape and weight overly influence self episode.2,5 Other complications of starvation may worth. r be the presenting complaint, including Binging and compensatory behavior are not low-impact fractures, amenorrhea, and poor solely during anorexia. growth. Patients may also present with abnormal Work-up should include electrolytes, divalents, vital signs, including hypothermia, hypotension, glucose, BUN/Cr, LFTs, CBC, and EKG. If the and bradycardia. Palpitations, chest pain, and patient has abnormal vitals, TSH and T4 should cardiac dysrhythmias can lead to serious be obtained. A U/A should also be performed to morbidity and mortality, including sudden look for ketosis. A urine pregnancy test should cardiac death.2,5 On examination, the patient will also be performed. be very thin, with BMI Ͻ 19, with little muscle or r Treatment: Life-threatening arrhythmias and subcutaneous fat. The patient may also have electrolyte abnormalities should be treated.5 lanugo, fine soft hair, and appear dehydrated. Rehydration may be needed in both anorexia and Bulimics may be more difficult to discover bulimia nervosa, and anorectic children may need since their body weight is usually normal. The to be admitted for refeeding.2,5 Overaggressive

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rehydration and refeeding may lead to 4. Philipou A, Rossell SL, Castle DJ. The neurobiology of cardiopulmonary failure, and should not be anorexia nervosa: A systematic review. Aust N Z J undertaken in the ED. Psychiatric consultation or Psychiatry 2014; 48: 128–52. referral is warranted. Anorexia is usually treated 5. MascoloM,TrentS,ColwellC,etal.Whatthe with psychotherapy. Bulimia is generally treated emergency department needs to know when caring for with cognitive behavioral therapy. your patients with eating disorders. IntJEatDisord 2012; 45: 977–81. Antidepressants and selective serotonin reuptake inhibitorsarealsoapprovedfortreatmentof 6. American Psychiatric Association. Diagnostic and bulimia nervosa. StatisticalManualofMentalDisorders, 5th edition. r Washington (DC): American Psychiatric Association, Disposition: Most patients with bulimia and 2013. anorexia are stable and safe to be discharged home 7. Golden NH, Katzman DK, Kreipe RE, et al. Eating with close follow-up with pediatrics and disorder in adolescents: Position paper of the Society psychiatry. The Society for Adolescent Medicine for Adolescent Medicine. J Adolesc Health 2003; 33: compiled a list of admission criteria for children 496–503. with eating disorders including: unstable vital signs, severe malnutrition, requiring aggressive rehydration, significant electrolyte abnormalities, Case 8 dysrhythmia, refusal to eat, uncontrollable binging and purging, suicidal ideation, or the Contributing Author: Sarah Hudgins presence of other psychiatric diagnoses that make it unsafe for the patient to go home.7 History A 4-week-old male with trisomy 21 (Down’s syn- Historical clues Physical findings Ancillary studies drome) is brought to the ED by his parents for a 3-hour r Repeated r Russell’s sign r Hypokalemia history of vomiting and irritability. The patient had vomiting r Dental caries/poor r Hypochloremia a sudden onset of green-tinged, non-bloody emesis r r Binge eating dentition Metabolic with multiple episodes of vomiting just prior to arrival. r Enlarged parotid alkalosis glands r Elevated amylase He has also had a decreased appetite accompanied r Throat erythema by excessive and inconsolable crying. Both parents noted abdominal swelling. The mother gave the child acetaminophen, which was immediately followed by Follow-Up vomiting. The patient is described as healthy at base- The patient’s potassium was replaced. She was referred line and was born full-term without any birth com- to psychiatry and ultimately spent 3 weeks in an inpa- plications. He has had no trauma/injuries, respiratory tient eating disorder unit. She was begun on a selective symptoms, diarrhea, blood in his stool or vomit, and serotonin reuptake inhibitor and is still undergoing hasremainedafebrile.Thechildisbottle-fedwithcom- cognitive behavioral therapy. She has shown improve- mercial formula that is mixed correctly, and he has ment in her behaviors. had no history of feeding issues. He is an only child and lives with his mother and father. He does not References attend daycare and has had no recent travel or sick 1. Hudson JI, Hiripi E, Pope HG Jr, et al. The prevalence contacts. and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry 2007; Past Medical History 61: 348–58. r Trisomy 21 2. Williams PM, Goodie J, Motsinger CD. Treating eating r Has not received 8-week vaccinations yet, but did disorders in primary care. Am Fam Phys 2008; 77: receive vaccines at birth. 187–95. r Child has been circumcized. 3. Kessler RC, Berglund PA, Chiu WT, et al. The prevalence and correlates of binge eating disorder in the World Health Organization World Mental Health Medications r Surveys. Biol Psychiatry 2013; 73: 904–14. Acetaminophen prior to arrival.

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Allergies r r If you were a provider in a rural hospital without a NKDA. pediatric surgeon, when would you obtain imaging and when would you consider transfer? r Physical Examination and Ancillary Studies What factors increase the child’s likelihood of r ° having a surgical disease? Vital signs:T97 F, HR 210, RR 50, BP 80/55, O2 r The child does not have a fever. Would you give sat 99% on room air. antibiotics? r General: The patient is crying during the examination, appears to be in moderate distress, parents and staff are unable to console the child. Child has flat facial features. Diagnosis r r HEENT: The head is normocephalic and Intestinal malrotation with volvulus. atraumatic, with flat fontanelles. PERRL, with intact red reflex and upward slant to the eyes. The Discussion childiscrying,withtearsnoted.Nonasal r Epidemiology: Malrotation occurs at a rate of 1 in congestion or rhinorrhea. Small, abnormally 500 live births with a male predominance of 2:1.1 shaped ears. Tympanic membranes are intact, Children born with Down’s syndrome, heterotaxy with a good cone of light and no erythema or syndrome, or duodenal atresia have an increased effusion. Mucous membranes are moist, no risk of malrotation. Malrotation is asymptomatic pharyngeal erythema, no tonsillar edema/ butwithvolvulusitbecomesasurgical exudates. The tongue appears enlarged and is emergency. In patients with malrotation, 90 partially sticking out of the mouth. percent will develop volvulus within the first year, r Neck: No cervical or occipital lymphadenopathy with 75 percent of those having developed it palpated. Neck is short and supple. within the first 4 weeks of life.1,2 Although most r Cardiovascular: Heart rate is tachycardic, with no cases occur in infancy, there have been reported audible M/R/G. Brachial and femoral pulses 2+ cases in young children, adolescents, and even bilaterally. Capillary refill Ͻ 3 seconds. adults.1,3–5 The mortality rate for volvulus ranges r Lungs: Limited auscultation secondary to patient from 3 to 15 percent depending on the timing of crying during examination; however, lungs the presentation and the extent of injury, and has 1 appeared to be clear, without W/R/R. improved dramatically over time. r r Abdomen:Soft,distended,abdomenwhich,with Pathophysiology:Startinginthefifthweekof palpation, causes increased distress in the child. embryologic development the fetal intestine, No audible bowel sounds auscultated. No which begins as a straight tube, protrudes into the umbilical hernia. No palpable masses. umbilical cord. As the GI tract returns into the ° r Extremities and skin: Child moving all extremities abdomen, the intestines make a 270 during examination, no external signs of trauma. counterclockwise turn, using the superior Single deep crease seen in the center of the palm mesenteric artery as an axis. With normal bilaterally. No peripheral edema. Skin is warm development, the intestine, after rotation, will be without any rashes. Extra space seen between first fixed in place by peritoneal bands (called Ladd’s and second toes. bands). These bands adhere the cecum in the right r Neurologic: Intact Moro and sucking reflex. lower quadrant and the duodenojejunal loop to Hypotonia (described as baseline). the left of the midline. Malrotation occurs when there is any variation in either the fixation or rotation during this embryologic process. Without adequate adherence, the cecum and Questions for Thought duodenum are left suspended by their vascular r What is your diﬀerential diagnosis for this child? attachments, which contain the superior r What tests would help guide you to this child’s mesenteric artery. This mesentery, which hangs diagnosis? loosely as a short stalk within the abdomen, can easily twist on itself causing a compression of the

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superior mesenteric artery. This compression can The test of choice in diagnosing malrotation lead to bowel ischemia and necrosis/gangrene with volvulus is the upper GI series with within as little as 1–2 hours. This obstruction of small-bowel follow-through. It has a 93–100 the bowel will clinically present as bilious emesis, percent sensitivity for ruling out malrotation with with the underlying bowel necrosis manifesting as a 100 percent specificity in diagnosing signs of shock. volvulus.1,2,6,7 It is limited by its poor sensitivity r Presentation: A neonate with a sudden onset of (54–79 percent) for ruling out volvulus when the abdominal pain with distension and bilious classic corkscrew appearance of the small bowel is vomiting, who appears ill and/or in shock, is notseen.Thistestisabletodiagnosemalrotation displaying the typical presentation of a patient by identifying an abnormal position of the suffering from malrotation with volvulus. The duodenal C-loop as well as a failure of the patient’s presentation can vary greatly based on duodenojejunal junction to cross the midline. whether the condition is acute or chronic. With The “double-bubble sign,” in which one pocket chronic volvulus, the intestines will twist and ofairisvisualizedfromthedilatedstomachand untwist, leading to intermixing symptoms of an additional pocket of air is visualized at the level abdominal pain and vomiting with periods that of the obstructed proximal duodenum, is the are asymptomatic. The patient’s presentation will hallmark abdominal X-ray finding. This test has greatlydependonthetimebetweenwhenthey been found to be neither sensitive nor specific in present to the hospital and the initiation of events. the diagnosis of malrotation as the double-bubble Children who present shortly after onset can sign is also present in other conditions, such as appear well at the time of the examination, pyloric stenosis and duodenal atresia.1,2,6,7 exhibiting only abdominal pain with non-bilious U/S is still a controversial yet increasingly vomiting. Contrastingly, those receiving popular method when evaluating children for treatment later in the course will display signs of malrotation.Ithasappealasalow-radiation, peritonitis with shock and can have GI non-invasive option that has been found to be hemorrhage, manifesting as bloody stools. accurate in studies with expertly trained Though this condition is typically a disease of ultrasonographers.1,2,6,7 Malrotation can be infancy it can present at any age. Features most evidenced via U/S by noting the abnormal commonly associated with malrotation outside of position of the third portion of the duodenum infancy include: colicky abdominal pain, outside of its normal retroperitoneal location. The intermittent vomiting, and failure to thrive. U/S diagnosis of volvulus consists of a “whirlpool GERD, pyloric stenosis, necrotizing enterocolitis, sign” in which the spiraled mesentery creates a intussusception, and sepsis are other conditions distinct echogenic twisting pattern. U/S is very that can have overlapping symptoms, usefulfordiagnosingorexcludingother complicating a timely diagnosis. pathologies, including appendicitis, pyloric r Diagnosis: Any child with vomiting warrants stenosis, and intussusception. Laboratory studies consideration for the dangerous differential for are not helpful in diagnosing malrotation or the unwell infant, discussed further in Chapter 3, volvulus but can be useful in determining the Case 7: Trauma, Hypovolemia/heart, Endocrine, severity of the patient’s condition. r Metabolic, Intestinal disasters, Seizures, Formula Treatment:Achildthatpresentswithsymptoms misadventures, Inborn errors of metabolism, that suggest possible volvulus should be treated as Toxicologic, and Sepsis (THE MISFITS)canall a surgical emergency. Emergent diagnosis and present with vomiting. If the process is believed to surgical intervention is necessary as intestinal be intra-abdominal, the provider should consider necrosis and gangrene can occur in as little as 1–2 evaluation for appendicitis, intussusception, hours. A pediatric surgeon needs to be consulted necrotizing enterocolitis, pyloric stenosis, even before imaging results are obtained. U/S volvulus, as well as medical pathologies such as imaging and/or upper GI series should be pancreatitis. Especially in bilious vomiting, the obtained to diagnose the condition. While in the childshouldbepresumedtohaveanemergency ED the patient will need a baseline laboratory surgical condition. panel that includes: fingerstick glucose, CBC,

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electrolytes, LFTs, and a type and screen. IV recovery, he was discharged home from the hospital on access should be initiated and a 20 cc/kg bolus as day 13. well as maintenance fluids should be administered. Cultures including urine and blood References should be obtained and antibiotics initiated. 1. Ford EG, Senac Jr MO, Srikanth MS, et al. Malrotation Recommended antibiotics for this condition are: of the intestine in children. Ann Surg 1992; 215: ampicillin with gentamycin and clindamycin or 172–8. metronidazole. In order to decompress the 2. Smith J, Fox SM. Pediatric abdominal pain: An stomach a nasogastric tube should also be emergency medicine perspective. Emerg Med Clin N placed. Am 2016; 34: 341–61. r Disposition: Ultimately, the child will need 3. Emanuwa OF, Ayantunde AA, Davies TW. Midgut surgical intervention. Stable patients in rural malrotation first presenting as acute bowel obstruction facilities should be transferred to a facility with a in adulthood: A case report and literature review. pediatric surgeon. Unstable patients will require World J Emerg Surg 2011; 6: 22. immediate surgical intervention and should not 4. Yanez R, Spitz L. Intestinal malrotation presenting betransferredifasurgeonispresent.Surgical outside the neonatal period. Arch Dis Child 1986; 61: intervention will consist of a Ladd’s procedure in 682–5. which the obstructing bands are removed and the 5. Sipahi M, Caglayan K, Arslan E, et al. Intestinal intestines are carefully untwisted and then malrotation: A rare cause of small intestinal obstruction. Case Rep Surg 2014; 2014: 453128. adhered to their proper anatomic location. If ischemic bowel is found it is resected and, if 6. Hamidi H, Obaidy Y, Maroof S. Intestinal malrotation and midgut volvulus. Radiol Case Rep 2016; 11: 271–4. needed, a diverting ileostomy or colostomy is made. An appendectomy is also performed as the 7. Khatami A, Mahdavi K, Karimi MA. Ultrasound as a new position of the child’s appendix will make feasible method for the assessment of malrotation. Pol JRadiol2014; 79: 112–16. future diagnosis of appendicitis difficult.

Historical clues Physical findings Case 9 r r r Sudden-onset symptoms r Ill-appearing Contributing Author: Erica Escarcega r Abdominal distension r Abnormal vital signs r Bilious vomiting r Abdominal distension History r Irritability r Abdominal tenderness Decreased appetite No bowel sounds The patient is a 9-year-old female who has been r Trisomy 21 brought to the ED for evaluation by her parents for vomiting this morning. The child had non-bloody, non-bilious vomiting after attempting to eat her break- Follow-Up fast this morning. The patient has not had any recent Upon presentation to the ED, the patient received an coughing or congestion. She denies diarrhea. She IV fluid bolus and maintenance fluids. These initial reports a sore throat that has been worsening over measures resulted in the stabilization of the child’s con- thepastday.Itisaburningpainthatismadeworse dition as well as an improvement in his vital signs. by swallowing both solids and liquids. She awoke this As this facility had no pediatric surgeons, a telephone morning with a fever and had a maximum temperature consultation was placed while diagnostic imaging was of 101.3 °F taken orally just prior to arrival. The patient being obtained. The upper GI series revealed an abnor- lives at home with her parents. She is in fourth grade mally positioned C-loop with the classic corkscrew andenjoysschool.Shestatesthattwoofherclass- appearance that indicated a volvulus. Being that the mates have been absent from school, but she is unsure child was hemodynamically stable at the time of diag- why. nosis, he was immediately transferred to a nearby pediatric center where an emergent Ladd’s procedure and appendectomy were performed. The child Past Medical History r had no surgical complications. After an uneventful Asthma, mild–intermittent, well controlled.

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Medications children ages 5–10. Atypical presentations are r Albuterol inhaler 90 mcg, two puffs every 4 hours more likely in children under 5 and are often as needed, last used 2 weeks ago. misdiagnosed as URIs. Complications of disease include peritonsillar abscess, retropharyngeal Allergies abscesses, suppurative cervical lymphadenitis, r NKDA. bacteremia, otitis media, sinusitis, mastoiditis, meningitis,pneumonia,andrheumaticfever.1,2 Physical Examination and Ancillary Studies Rheumatic fever is an exceedingly rare r Vital signs: T 100.6 °F, HR 98, BP 100/60, RR 18, complication of strep throat with an annual O sat 100% on room air. incidence of less than one case per million 2 population. This presents with fever, carditis, r General: The patient is alert and appears mildly subcutaneous nodules, chorea, and migratory distressed due to her throat pain. She is polyarthritis occurring 1–5 weeks after resolution cooperative with the examination. of strep throat. The asymptomatic carrier rate of r HEENT: PERRL. Mucous membranes are moist. group A streptococci is 5–21 percent in children Posterior pharynx is erythematous. Tonsils are aged 3–5 and is lower in younger and older age 2+, erythematous. White exudate is present on groups.2,3 tonsils bilaterally. No trismus. r Pathophysiology: Strep throat is caused by an r Neck: Bilateral anterior cervical lymphadenopathy. inflammatory response to group A beta-hemolytic Neck is supple and trachea is midline. r streptococci. Interleukins 1 and 6, tissue necrosis Cardiovascular: Regular rate and rhythm, with no factor,andprostaglandinsresultinfever. M/R/G. Peripheral pulses are normal. Capillary Ͻ Prostaglandins and bradykinin result in severe refill 3 seconds. throat pain. Erythema and swelling of the tonsils, r Lungs: CTA, with no W/R/R. r uvula, and soft palate result from the effect of Abdomen:Thepatient’sabdomenissoft, prostaglandins and nitric oxide release. Tissue non-tender, and non-distended, with normoactive damage from lysosomal enzymes and oxygen free bowel sounds throughout. There are no palpable radicals generates a creamy exudate seen on the masses. tonsillar pillars. r Extremities and skin: There is no peripheral r Presentation:Classicsymptomsonlyoccurin edema.Herskiniswarmtothetouchandthere approximately half of patients and are usually are no rashes noted on examination. described as severe sore throat of sudden onset, r Neurologic:Alert.Ageappropriate.Nofocal with difficulty swallowing. Patients will often have deficits. a moderate fever, which rarely is accompanied by chills or rigors. Malaise, headache, mild neck Questions for Thought stiffness, anorexia, nausea, vomiting, and r abdominal pain are also commonly seen in cases What items within the patient’s history and of streptococcal pharyngitis.1 GI symptoms are physical can help lead you to the diagnosis? more common in younger patients.1 On physical r What tests would you run on this patient? examination, patients will often have erythema r Are antibiotics indicated? r What complications may occur if you fail to treat and edema of the posterior pharynx and uvula, this condition? petechiae over the soft palate, and tonsillar hypertrophy often with a visible gray–white membrane or exudate over the tonsils. Frequently, acutely tender anterior cervical lymphadenopathy Diagnosis r is present, which may be more pronounced at the Streptococcal pharyngitis. angle of the jaw. Occasionally, patients may present with a scarlatiniform rash, which is Discussion characteristic of scarlet fever. This rash appears as r Epidemiology: Streptococcal pharyngitis is caused fine erythematous “sandpapery” papules, which bygroupAstreptococciandismostcommonin are initially present over the trunk and then

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spread to the extremities, sparing the palms and soles. Historical clues Physical findings r r r Diagnosis: Multiple clinical prediction rules have Vomiting Erythema of posterior pharynx r Sore throat r Tonsillar hypertrophy been developed to aid in diagnosis. The Centor r Fever r Exudates score is most widely used. It was developed for r r r Abdominal pain Anterior cervical adenopathy adults but has been validated in children. Using r Lack of cough the modified Centor criteria, patients are given a Age group point for fever, anterior cervical adenopathy, tonsillar exudate, and lack of cough.1,4,5 An additional point is given for patients age 3–14, Follow-Up and a point is subtracted for adults above 45 years 1 The patient was started on amoxicillin and discharged old. Patients with four or more points may be home with her parents. She was able to return to school empirically treated for streptococcal pharyngitis, 24 hours after starting antibiotics and had a full recov- although the positive predictive value is only a ery after 4 days. little over 50 percent.1 Newer rapid antigen testing, which boasts a sensitivity of 85 percent and specificity of 93 percent, can be used in References patients with a low or intermediate likelihood of 1. Choby BA. Diagnosis and treatment of streptococcal strep throat and should be confirmed with throat pharyngitis. Am Fam Phys 2009; 79: 383–90. culture. 2. Hersh AL, Jackson MA, Hicks LA. Principles of judicious antibiotic prescribing for upper respiratory r Treatment: Untreated streptococcal pharyngitis infections in pediatrics. Pediatrics 2013; 132: 1146–54. lasts approximately 8–10 days, with an infectious period extending 1 week after resolution of the 3. NussinovitchM,FinkelsteinY,AmirJ,etal.GroupA 5 beta-hemolytic streptococcal pharyngitis in preschool acute symptoms. Antibiotic treatment reduces children aged 3 months to 5 years. Clin Pediatr (Phila) 5 the symptom duration by a day. Antibiotics have 1999; 38: 357–60. very little net benefit in protecting patients against 4. Ebell MH, Smith MA, Barry HC, et al. The rational suppurative and non-suppurative complications clinical examination. Does this patient have strep in developed societies where rheumatic fever is throat? JAMA 2000; 284: 2912–18. essentially non-existent, which has led some 5. Sarrell EM, Giveon SM. Streptococcal pharyngitis: A providers to forgo treatment of presumed strep prospective study of compliance and complications. throat in low-risk populations.6 ISRN Pediatr 2012; 2012: 796389. If antibiotics are given, first-line treatment 6. Del Mar CB, Glasziou PP, Spinks AB. Antibiotics for consists of penicillin given either IM (benzathine sore throat. Cochrane Database Syst Rev 2004; 2: penicillin G) or orally (either penicillin V or CD000023. amoxicillin). Cephalosporins (such as cephalexin) 7. Hayward G, Thompson MJ, Perera R, et al. are recommended in patients who have an allergy Corticosteroids as standalone or add-on treatment for to penicillins without anaphylaxis. Even in those sore throat. Cochrane Database Syst Rev 2012; 10: with anaphylaxis, there is only a 10 percent risk of CD008268. cross-allergy to cephalosporins. Patients with a severe penicillin allergy may be treated with oral Case 10 clindamycin or with macrolides. Steroids and anti-inflammatory medications Contributing Author: Kinsey Leonard havebeenshowntodecreasepainandshorten disease course in adults when combined with History antibiotics, but have not been adequately studied A 2-month-old infant is brought into the ED by her in the pediatric population.7 mother for vomiting. Mom reports that the child has r Disposition: Patients with uncomplicated been vomiting within an hour of feeding, and that the streptococcal pharyngitis may be discharged child is vomiting with almost every feed. She states home to follow up with their pediatricians. that the vomiting does not appear to be everything

16:16:45 08 Chapter 7: Vomiting the child eats, and she estimates that it’s about 1–2 r Neurologic: Appropriate for age, normal Moro, ounces each time. There has been no blood or bile in grasp, and suck, symmetric face and extremities. thevomit.Thechildhasnotappearedtobeinpain. Shehasbeenmakingausualamountofwetanddirty Questions for Thought diapers. She has been acting like herself. The child r is formula-fed, and takes 6 ounces every 2–3 hours. What are some worrisome causes of vomiting in Mom follows the manufacturer guidelines for formula this age group? r How much should a typical baby be fed? preparation, and only uses sterilized water. The child r has not had fevers, diarrhea, sweating, pallor, cyanosis, What is the ED management of this condition? r What complications can result? or limp spells. The child will receive her 2-month immunizations next week. She has met all developmental milestones. She does not attend daycare. She has no sick contacts. Her review of systems is otherwise Diagnosis negative. r Overfeeding.

Past Medical History Discussion r r No significant medical problems. Epidemiology: Obesity is a problem in most r Normal pregnancy with spontaneous vaginal Western societies and has become more prevalent delivery at 41 weeks. in infants and children in recent years. In 2012, the CDC reported that close to 20 percent of childrenaged6to19yearsareobese.1 Up to 10 Medications percent of infants and toddlers are overweight in 1 r None. the USA. r Pathophysiology: Contributing factors to infant obesity include feeding infants too much, Allergies introducing solid foods too early, and having solid r NKDA. foods make up a large proportion of daily calories. Formula feeding also puts the infant at increased Physical Examination and Ancillary Studies risk of overfeeding since different formulations have different calorie densities. Occasionally, r Vital signs: T 99.0 °F, HR 120, BP 90/60, RR 30, O 2 caretakers may incorrectly mix formula, causing sat 100%, weight 7 kg. an overly concentrated bottle that results in r General: The patient is awake and alert. She is overfeeding. There are differences amongst looking around the examination room. She has a varying cultures in how overweight infants are social smile. r perceived, which has led to infants of certain HEENT: Normocephalic and atraumatic. Anterior cultures being larger.2 There are also differences in fontanelle is soft and flat. PERRL. Red reflex the feeding of infants among socioeconomic bilaterally. Moist mucous membranes. No classes, with more educated mothers tending to pharyngeal erythema. breastfeed exclusively and continue breastfeeding r Neck: Supple, with a midline trachea. r for a longer period of time. One study has Cardiovascular: Regular rate and rhythm, with no explored whether overfeeding is a consequence of M/R/G. mothers being more distracted during feedings r Lungs: Normal work of breathing, clear and equal and missing satiety signs from the infants.3 breath sounds, with no W/R/R. The problem is similar in toddlers and older r Abdomen: Soft, non-distended, no organomegaly, children. Parents feed children too much food for positive bowel sounds. their caloric expenditure, and many foods r Extremities and skin:Skiniswarmanddry. consumed by children offer little nutrients and are Capillary refill is ˂ 3 seconds. No rash. No signs of calorically dense, with high concentrations of trauma. processedsugar,fat,andsodium.Thisis

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compounded by the fact that modern children are toddlers, and children. The AAP recommends more sedentary than prior generations and as a breastfeeding exclusively for the first 6 months result require fewer calories. The differences in and continued breastfeeding to 1 year of life after obesity rates as a function of socioeconomic class the introduction of solid foods. Infants should not persists in these older children, with Hispanic and drink more than 32 ounces of formula in a black children at the highest risk.1 Having parents 24-hour period. Parents should be encouraged to who did not complete high school is feed their older children healthier foods and independently associated with an increased risk of engage in more physical activity. They should also childhood obesity. be counseled regarding the risk of childhood Overfeeding has been linked to GERD in obesity and increased risk of type 2 diabetes. infants, likely because overdistending the stomach r Disposition:Thepatientcanbedischargedhome leads to increased intra-abdominal pressure, with follow-up and further discussion with the encouraging regurgitation of the stomach family’s pediatrician. contents. Overfeeding at an early age puts infants andchildrenatincreasedriskofbecoming Historical clues Physical findings overweight or obese adults. It also puts them at r r risk for impaired glucose tolerance, diabetes, and Repeated vomiting after Overweight but otherwise eating well-appearing infant other metabolic problems. r r Emesis of milk and no bile r Presentation:Theinfantwillpresentwith Feeding practices that are above the needed caloric vomiting or spitting up after eating. The infant requirements may have been treated for GERD in the past. The infant will most likely be larger than normal for age, falling above the 95th percentile for weight. Follow-Up The child will otherwise have an entirely benign The child had improvement in vomiting with adjust- examination, with no worrisome findings. ment of volume of feeds, and had an uneventful r Diagnosis:Allcasesofvomitingininfancydeserve recovery. a careful history and physical examination, with consideration of the dangerous causes of vomiting in this age group, including trauma, cardiac References disease, endocrine disease, metabolic disorders, 1. Centers for Disease Control and Prevention. inborn errors of metabolism, seizures, formula Prevalence of childhood obesity in the United States, 2011–2014. See www.cdc.gov/obesity/data/childhood errors, intestinal disasters (such as volvulus), .html (accessed March 7, 2015). toxins, and sepsis. Overfeeding is diagnosed with careful history taking regarding the feeding 2. Cartagena D, Ameringer SW, McGrath JM, et al. Factors contributing to infant overfeeding in practices, including how often the infant is fed, low-income immigrant Latina mothers. JObstet how much per feeding, how many times per day, Gynecol Neonatal Nurs 2014; 43:139–59. and what the infant is fed. r 3. Golden RB, Ventura AK. Mindless feeding: Is maternal Treatment: Parents should be carefully counseled distraction during bottle-feeding associated with regarding the nutritional needs of their infants, overfeeding? Appetite 2015; 91: 385–92.

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Case 1 r HEENT: Mucous membranes are moist. PERRL. Bilateral conjunctival injection. Contributing Authors: Jonathan Nogueira r Neck: Supple, with no adenopathy. Midline trachea. and Janet Young r Cardiovascular:Regularrhythm.Tachycardia History present. No murmur. r The patient is an 8-year-old female presenting to Lungs: Breath sounds normal. No stridor. the ED with 4 days of generalized abdominal pain, Tachypnea noted at time of examination. No now worse in the right lower quadrant. She has had respiratory distress. No wheezes or retractions. r nausea, vomiting, fevers, chills, decreased appetite, Abdomen: No distension. Bowel sounds are and worsening severity of abdominal pain over time. increased. Generalized tenderness most The patient’s mother also states that she now prefers prominent in the right lower quadrant. There is to stay rather still, with increased pain while moving rigidity, rebound, and guarding. Heel tap elicits or walking, stating it hurts more with any movement. abdominal pain. r She denies ever having symptoms like this in the past. Extremities and skin: Warm and dry, capillary There has been no constipation, diarrhea, or bloody refill Ͻ 3 seconds. No petechiae and no purpura stool. She has no known sick contacts, no rash, joint noted. No diaphoresis. No cyanosis. swelling, diarrhea, sore throat, rhinorrhea, cough, or r Neurologic: Age appropriate, normal mental difficulty in breathing. The patient’s mother brought status, strength, sensation, and reflexes normal. her to the ED due to worries of worsening abdominal r Pertinent laboratory values: WBC 12,000. pain. Remainder of laboratory studies unremarkable. r Pertinent imaging: Bedside point-of-care U/S: Past Medical History linear, non-compressible structure in the right r Lyme disease approximately 2 years ago. lower quadrant, with associated tenderness. Hyperechoic area at the distal tip of this structure with a diameter Ͼ 6 mm, worrisome for Medications appendicitis. Small amount of complex free fluid r None. in the pelvis; see Figures 8.1 and 8.2.

Allergies r NKDA. Questions for Thought r What are the typical laboratory findings in this Physical Examination and Ancillary Studies condition? r r Vital signs: T 101.7 °F, HR 132, RR 20, BP 124/44, What is the appropriate first-line imaging study? r What are the typical U/S and CT findings? O2 sat 97% on room air. r What treatments should be initiated in the ED? r General: Appears well-developed and r What is the definitive treatment of this well-nourished, in moderate distress secondary to pathology? pain. Lying still on stretcher.

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Figure 8.1 Long-axis view of the appendix by bedside point-of-care U/S in the ED, showing dilated distal appendix.

Diagnosis considered in any patient with acute atraumatic r Acute perforated appendicitis. abdominal pain without prior appendectomy. r Pathophysiology: Appendicitis is typically caused by luminal obstruction of the vermiform appendix Discussion by fecalith, lymphatic tissue, or, less commonly, r Epidemiology: It is estimated that the lifetime risk tumor, foreign body, or parasitic infection. After of developing appendicitis in the USA is about 9 obstruction occurs, continued secretion of the percent for males and 7 percent for females, most luminal mucosa results in increased intraluminal commonly in patients aged 10–19 years old.1,2 pressure, leading to inflammation, bacterial Appendicitis is a frequent cause of atraumatic infection, and possibly necrosis or perforation due abdominal pain in children greater than 1 year old to increased intraluminal pressures. This leads to as well as the most common non-obstetrical pain, initially visceral, then progressing to emergency in pregnancy. Appendicitis should be somatic, as the peritoneum becomes inflamed.

Figure 8.2 Short-axis view of the appendix showing non-compressible structure, suspicious for appendicitis.

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Untreatedappendicitiswillleadtoperforation Perioperative antibiotics should be administered and intra-abdominal sepsis or abscess and could to cover common organisms such as cause death. Due to difficulties in obtaining Enterobacteriaceae (Escherichia coli, Klebsiella history and ambiguity of examination, 80–100 spp.,Proteusspp.) and Bacteroides. Antibiotic percent of children less than 3 years old present choices for simple pediatric appendicitis may with perforated appendicitis.1 Perforation rates in include ampicillin–sulbactam, cefoxitin, or older children are less, about 38 percent.1 metronidazole plus gentamycin. Antibiotic r Presentation: Early appendicitis may begin with choices for complicated appendicitis, such as pain referred to the periumbilical area due to gangrenous, perforated, abscess, or phlegmon, visceral innervation. Commonly associated may include imipenem–cilastatin, symptoms include nausea and vomiting, anorexia, piperacillin–tazobactam, or metronidazole plus and pain migrating to the right lower quadrant at aztreonam. McBurney’s point, one-third of the distance from r Disposition: When the diagnosis of appendicitis the anterior superior iliac spine to the umbilicus. has been made, appendectomy is the definitive Other findings may include guarding, rebound treatment of choice. Patients may be stable for tenderness, low-grade fever, obturator sign (pain discharge within 12–24 hours post appendectomy with internal rotation of the leg with the hip and if they are tolerating oral intake and their pain is knee flexed), psoas sign (pain with extending the well managed. Patients with complicated hip and the knee in full extension, or flexing the appendicitis may need further monitoring and hip against resistance), and Rovsing’s sign (pain in treatment as indicated. the right lower quadrant with palpation of the left lower quadrant). Once appendicitis has Historical clues Physical findings Ancillary studies perforated, children may present with sepsis and r r r with diffuse abdominal tenderness and guarding. Right lower r Tender abdomen r Elevated WBC r r quadrant pain Rebound and U/S with evidence Diagnosis:Thecriticalevaluationofachildwith Nausea and r guarding of appendicitis appendicitis is a careful history and physical vomiting Positive heel tap r Poor appetite (indicates examination, looking for findings listed above. peritoneal r Key diagnostic elements include right lower irritation) quadrant abdominal pain, anorexia, and fever. Many patients have an elevated peripheral Follow-Up WBC, but this is neither sensitive nor specific for appendicitis.1,3 The patient was made NPO and started on broad- spectrum antibiotics, as well as IV fluids, antiemet- r May have elevated CRP and ESR. ics, and analgesia. She was taken to the OR for urgent r U/Softherightlowerquadrantwith appendecomy and was found to have acute perfo- non-compressible tubular structure, rated appendicitis with periappendiceal abscess as well appendiceal lumen greater than 6 mm, as diffuse peritonitis and adhesions to the anterior increased color flow indicative of inflammation abdominal wall. There was turbid ascites in all four and hyperemia, and periappendiceal quadrants. Post-operatively, she was continued on IV inflammatory changes.3–5 antibiotics and slowly advanced to regular diet. She r If U/S is non-diagnostic, CT of the gradually recovered and was discharged home on hos- abdomen/pelvis showing periappendiceal fat pital day 6. stranding, appendiceal diameter greater than 6 mm, periappendiceal fluid, and possibly fecalith.3–5 References r 1. Smith J, Fox SM. Pediatric abdominal pain: An Treatment: Initially, patients should be made NPO emergency medicine perspective. Emerg Med Clin N duetothedefinitiveneedforsurgical Am 2016; 34: 341–61. appendectomy. Fluid resuscitation as needed and 2. Addiss DG, Shaffer N, Fowler BS, et al. The maintenance fluids should be administered, as epidemiology of appendicitis and appendectomy in the well as antiemetics and appropriate analgesia. United States. Am J Epidemiol 1990; 132: 910–25.

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3. Armstrong C. ACEP releases guidelines on evaluation Allergies of suspected acute appendicitis. Am Fam Phys 2010; r NKDA. 81: 1043–4. 4. Hansen LW, Dolgin SE. Trends in the diagnosis and Physical Examination and Ancillary Studies management of pediatric appendicitis. Pediatr Rev r Vital signs: T 99.1 °F, HR 70, BP 123/79, RR 18, O 2016; 37: 52–7. 2 sat 98% on room air, weight 129 kg. 5. Kosloske AM, Love CL, Rohrer JE, et al. The diagnosis r General: Awake, alert, appears uncomfortable. of appendicitis in children: Outcomes of a strategy Obese. based on ediatric surgical evaluation. Pediatrics 2004; r 113: 29–34. HEENT: PERRL. Mucous membranes moist. r Neck:Supple,withnoadenopathy. r Cardiovascular: Heart has regular rate and Case 2 rhythm. No M/R/G. r Lungs:Clearbilaterally.NoW/R/R. Contributing Author: Michelle Clinton r Abdomen: Obese and soft. Normal bowel sounds; History suprapubic tenderness to palpation without The patient is a 14-year-old female who was referred to guarding or rebound. Fullness is palpated in the the ED by her PCP for evaluation of abdominal pain. suprapubic region. There is no costovertebral She complains of lower abdominal pain and cramping angle tenderness. Normal genitalia. r over the past day, and has had decreased urine out- Extremities and skin:Noedema,noextremity putoverthelast2days.Thepatientstatesthatshe tenderness; distal pulses are intact. r was started on an oral contraceptive pill 16 days ago Neurologic: Cranial nerves intact, normal strength due to amenorrhea and her menstrual period started and sensation. No saddle anesthesia. r 2daysago.Shereportsthatshemissedafewdays Pertinent laboratory values:U/Aisnegativefor of taking the pill. She states that she had a normal nitrite, leukocyte esterase, WBC, RBC, protein, stool this morning and denies history of constipa- glucose, and ketones. Specific gravity is 1.009. tion, stating she generally has a bowel movement every WBC 10,800, Hb 12.9, HCT 38.9, and basic 1–2days.Shestatesshewasalsostartedonmetformin metabolic panel is within normal limits. 16 days ago due to insulin resistance. Patient denies r Pertinent imaging: Bedside U/S shown in history of difficulty urinating prior to this episode. She Figure 8.3. also denies fever, chills, nausea, vomiting, hematuria, urinary frequency, and dysuria. She denies episodes of Questions for Thought incontinence of urine or stool. She does have a his- r tory of hemorrhoids. The patient’s mother states that What further diagnostic modalities could you use to evaluate this patient? she has to hold her urine for long periods of time r What are the typical laboratory findings in this because she recently started high school. On further condition? questioning, the patient admits to having slightly less r What are the typical U/S findings? frequent, harder, smaller stools over the past several r What treatments should be initiated in the ED? weeks. r What underlying causes contribute to this condition? r Past Medical History What is definitive treatment of this condition? r Hyperinsulinemia. r Hyperandrogenemia. Diagnosis r Abnormal weight gain. r Bladder and bowel dysfunction with urinary retention and constipation. Medications r Norgestimate/ethinyl estradiol 0.25 mg/35 mcg Discussion daily. r Epidemiology: Constipation is generally defined as r Metformin 1,000 mg daily. two or fewer bowel movements per week with an

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Figure 8.3 U/S demonstrating 664 mL of urine in the bladder.

episode of fecal incontinence, in the setting of a neurologic disorders commonly suffer from history of excessive stool retention, painful or constipation as a result of delayed colonic transit hard bowel movements, presence of a large fecal times, abnormal innervation, and poor muscle mass in the rectum, and a history of stools that tone. Most constipation presenting after infancy is maystopupthetoilet. functional constipation and is often related to Constipation is a common condition affecting social factors. an estimated 5–10 percent of children and Dysfunctional elimination syndrome or accounting for 3–5 percent of pediatrician bladder-bowel dysfunction refers to the condition visits.1–3 ED visits for constipation are increasing in which constipation is associated with bladder steadily, with one study showing a 50.7 percent dysfunction. It is common for ano-rectal increase in constipation-related ED visits in dysfunction to be associated with urinary children of ages 1 to 17 from 2006 to 2011.4 symptoms;morethan50percentofchildren Constipation affects all ages of children, but is evaluated with lower urinary tract symptoms most prevalent in the preschool years. Functional meet the diagnostic criteria for functional constipation is the cause of about 95 percent of constipation.6,7 Bladder dysfunction associated pediatric constipation.1–3,5 Organic causes of with constipation can manifest as bladder under- constipation in children should be considered or over-activity, urgency, or frequency. when the presentation and physical examination r Pathophysiology: Painful defecation is often an are not consistent with a functional cause. underlying cause of functional constipation, Presenting factors that make an organic cause of a which is in turn frequently related to social factors child’s constipation more likely include neonatal that lead to stool retention. Toilet training, constipation, history of constipation since birth, inaccessible toileting facilities or unwillingness to delayed passage of meconium, failure to thrive, use public toilets, dehydration, viral illness, and vomiting, blood in the stool, abdominal stress often contribute to stool-holding behavior distension, anal stenosis, and an empty rectum on in children. This leads to increased colonic water physical examination.3 absorption from the feces and creates hard, large Neonatal constipation should raise concern stools that are painful to pass, perpetuating the for anatomic causes, Hirschsprung’s disease, problem when not properly treated. Dietary intestinal obstruction, or metabolic causes such as factors such as lack of fiber or water intake also hypothyroidism or cystic fibrosis.3 Children with contribute. Infant dyschezia is rather common in

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the first year of life and is caused by the face, as well as the passage of small, hard incoordination of abdominal muscle contraction stools. and anal relaxation necessary to produce a bowel r Diagnosis:Historyshouldfocusonidentifying movement, causing straining and grunting with signs and symptoms that are associated with the attempted defecation. The large majority of increased likelihood of an organic cause of constipation in children over 1 year of age is constipation, including melena, history of functional constipation; however, organic causes constipation since birth or delayed meconium must always be sought, particularly in young passage, urinary retention, vomiting, fever, failure children and infants. to thrive, severe abdominal distension, and Congenital aganglionic megacolon, or neurologic deficits. The presence of any of these Hirschsprung’s disease, is a rare condition caused symptoms or physical examination findings by an absence of ganglion cells in the rectum and should prompt more in-depth evaluation with often presents at birth with delayed passage of focused laboratory tests, imaging, and meconium. The rectum is usually empty on digital consultation as deemed appropriate by the examination in patients with this condition. emergency physician. Cerebral palsy and spina bifida are potential The absence of any of the above alarm signs neurogenic causes of constipation. Abnormal makes functional constipation the likely diagnosis findings in neurologic examination should raise in patients presenting with symptoms of concern for an underlying congenital neurologic constipation. The Rome IV criteria were problem or lesion involving the spinal cord, such established to aid in the diagnosis of functional as a neuroblastoma. Anatomic causes of constipation in children aged 4 or above and is constipation, such as imperforate anus, anterior defined as the presence of at least two of the displaced anus, fissures, or strictures, should be following criteria occurring at least once weekly assessed for on physical examination. over a period of at least 1 month: less than three Other potential contributing factors to stools per week, at least one episode of stool constipation include medications, lead toxicity, incontinence weekly, stool mass palpated on rectal endocrine disease, and metabolic conditions. or abdominal examination, history of retentive Anticholinergics, opiates, iron supplements, and posturing or stool withholding, history of painful, antidepressants are pharmacologic agents that can hard stools, and history of large-volume stools cause constipation. Endocrine conditions such as thatmayobstructthetoilet.Focusedhistoryand diabetes mellitus, hypothyroidism, or physical examination are generally sufficient for hyperparathyroidism may contribute to the diagnosis of functional constipation in constipation. Electrolyte disturbances are a children and further diagnostic studies are metabolic factor that often incites constipation, unwarranted. while cystic fibrosis, celiac disease, and milk The physical examination should include a protein intolerance are underlying conditions global assessment of development, weight gain, whose pathophysiology and effect on electrolytes hydration, and nutrition status. A detailed both contribute to constipation. abdominal examination should be performed and r Presentation:Constipationinchildrenmay the presence of bowel sounds, tenderness, present with a wide variety of subjective distension, and stool mass should be assessed. The complaints. Older children frequently present back and perianal area should be evaluated for with symptoms of crampy, intermittent, central evidence of a sacral dimple (which is associated abdominal pain. Parents may be unaware that the with spina bifida), perianal strep infection, skin child is constipated, but further questioning often tags, anal fissure, and anal wink. A detailed reveals that symptoms improve after a large stool. neurologic examination should be performed and Other symptoms that may be noted include should include an assessment of tone, deep abdominal distension, irritability, soiling, and tendon reflexes, saddle anesthesia, and gait. decreased appetite. Parents of infants with A digital rectal examination is invasive and constipation frequently describe straining, uncomfortable and is generally not necessary in grunting, and the infant turning red in the evaluating children presenting with constipation.

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Digital rectal examination should be performed in Rectally administered glycerin suppositories infants and patients with history of constipation are safe in young infants and are often effective in since early infancy to assess for anatomic treating infant dyschezia. Addition of abnormalities, and when alarm symptoms carbohydrate-containing osmotic liquids such as suggestive of an organic cause of constipation are prune juice, corn syrup, or malt syrup extract to present. It may also be considered when the breast milk or formula will help soften stools. Two degree of constipation is uncertain. A large to four ounces per day of fruit juice is the amount of hard stool is generally present in the suggested dose for children 4 months or older. rectum of patients with functional constipation, Polyethylene glycol may be given to infants 6 while children with colonic neuropathy tend to months and older with ongoing constipation after have scant stool and a narrow ampulla. above treatments. Sodium phosphate or mineral Imaging does not generally play a role in the oilenemasmaybeadministeredtochildrenage3 diagnosis of constipation. A recent study involving and above in whom oral treatment is resisted by 3,685 pediatric patients evaluated in an ED who the child or ineffective. An enema solution of were diagnosed with constipation revealed that, 15–30 mL per year of age is the recommended unless an alternative diagnosis is being dose. Maintenance treatment is recommended for considered, abdominal X-rays are not helpful and at least 6 months after an acute episode of can delay recognition of more serious diagnoses.8 constipation and is generally accomplished with a An abdominal radiograph was performed more lower dose of polyethylene glycol: one-half to one frequently in children with misdiagnosis of capful of polyethylene glycol in 8 ounces of liquid, constipation (75 percent vs. 45 percent).8 These one to two times daily. children more frequently had abdominal pain and Dietary changes should be discussed and the tenderness on examination. Nevertheless, if plain parents instructed to increase fiber by assuring the filmsaredone,theprovidermayseestoolinthe child gets at least five servings of fruits and rectalvaultaswellasformedstoolthroughoutthe vegetables per day. Fluid intake must also be colon(Figure8.4inCase4below). increased. Positive reinforcement is encouraged r Treatment: The treatment of pediatric and parents should be instructed to create constipation is multidisciplinary and close protected time for children to have a bowel follow-up with the patient’s PCP is important to movement by placing the patient on the toilet for assess response to treatment started in the ED, to 5–10 minutes two to three times daily to reinforce parental education, and to establish a encourage stooling. maintenance treatment plan. Oral, rectal, or a r Disposition:Constipationmaybetreatedasan combination of treatments is usually effective; outpatient, with close follow-up with the child’s however, it should be considered that rectal PCP. treatments might exacerbate the psychologic components contributing to constipation. An Historical clues Physical findings Ancillary studies aggressive oral disimpaction protocol is generally r r r very effective in treating functional constipation. Change in stool Suprapubic Bedside U/S with habits fullness urinary retention Forchildrenundertheageof5itisrecommended r r r Abdominal pain Essentially benign that a solution of eight capfuls of polyethylene Difficulty examination glycol electrolyte lavage solution 3350 in 64 urinating otherwise ounces of liquid be made. For children 5 years and older, 16 capfuls of polyethylene glycol is mixed in 64 ounces of liquid. Eight ounces may be Follow-Up administered every 15 minutes until This patient’s diagnosis of bladder-bowel dysfunc- finished. If results are unsatisfactory, this protocol tion was determined by a thorough history and the may be reattempted the following day. Lower absence of physical examination or laboratory findings dosesofpolyethyleneglycolormilkof concerning for acute infectious or other obstructive magnesia may be used in less severe cases of intra-abdominal or genitourinary pathology. Bladder constipation. catheterization was performed and 700 mL of urine

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drained from the patient’s bladder. She was observed Child/adolescent. Gastroenterology 2016; 150: and unable to urinate within 2 hours of initial catheter- 1456–68. ization. Repeat bladder U/S revealed 550 mL of urine 6. BurgersRE,MugieSM,ChaseJ,etal.Managementof in the bladder. Subsequently, the patient was able to functional constipation in children with lower urinary urinate spontaneously and final bedside U/S revealed tract symptoms: Report from the Standarization only 50 mL of urine in the bladder. The patient’s Committee of the International Children’s Continence Society. JUrol2013; 190: 29–36. mother expressed that the patient had to hold urine for long periods of time due to not being able to 7. Burgers R, de Jong TP, Visser M, et al. Functional use the bathroom very often after recently starting defecation disorders in children with lower urinary tract symptoms. JUrol2013; 189: 1886–91. high school. The patient was discharged home with instructions for timed voiding every 2 hours. She 8. Freedman SB, Thull-Freedman J, Manson D, et al. Pediatric abdominal radiograph use, constipation, was also prescribed 17 g of polyethylene glycol in and significant misdiagnoses. JPediatr2014; 164: 8-ounce liquid twice daily for constipation because it 83–8. was felt that her urinary retention was related to stool withholding. Unfortunately, this outpatient treatment was ini- Case 3 tially unsuccessful and the patient returned to the ED 4 days later with persistent abdominal pain. Labora- Contributing Authors: Alyssa Milano and tory tests were unremarkable on repeat ED evaluation. Sade´ McKenzie CT imaging was performed to evaluate for appendici- History tis as the patient had right-lower-quadrant tenderness and her morbid obesity precluded appendicitis eval- The patient is a 16-year-old male who presents to the uation by U/S. The CT was negative for evidence of ED with nausea for the past several days. He complains appendicitis or other acute intra-abdominal pathol- of abdominal pain and several episodes of non-bloody, ogy.AverylargestoolburdenwasnotedonCTand non-bilious vomiting earlier today. His abdominal the patient was admitted to the inpatient pediatrics pain is diffuse, constant, and described as crampy. He team and underwent fecal disimpaction with polyeth- denies associated fevers and diarrhea. He also com- ylene glycol 3350 via a nasogastric tube. The patient plains of a sore throat and sinus congestion. On fur- passed a large amount of stool, progressing to clear ther questioning, the patient reports recent weight loss diarrhea. The difficulty in urinating and abdominal and generalized fatigue. He denies having a headache, pain resolved and the patient was discharged home cough, chest pain, or shortness of breath. He denies with a continued daily regimen of oral polyethylene experiencing similar episodes in the past, sick con- glycol. tacts, or recent travel. Past Medical History References r Inguinal hernia repair. 1. van den Berg MM, Benninga MA, DiLorenzo C. r Seasonal allergies. Epidemiology of childhood constipation: A systematic r UTD on immunizations. review. Am J Gastroenterol 2006; 101: 2401–9. 2. GettoL,ZesersonE,BreyerM.Vomiting,diarrhea, Medications constipation, and gastroenteritis. Emerg Med Clin N r Am 2011; 29: 211–37. Cetirizine. 3. Nurko S, Zimmerman LA. Evaluation and treatment Allergies of constipation in children and adolescents. Am Fam r Phys 2014; 90: 82–90. Amoxicillin–clavulanate. 4. Sommers T, Corban C, Sengupta N, et al. Emergency Physical Examination and Ancillary Studies department burden of constipation in the United r States from 2006 to 2011. Am J Gastroenterol 2015; Vital signs: T 97.6 °F, HR 110, RR 25, BP 121/72, 110: 572–9. O2 sat 97% on room air. r 5. Hyams JS, DiLorenzo C, Saps M, et al. Childhood General: The patient is awake and alert, appears to functional gastrointestinal disorders: be in a moderate amount of distress.

16:17:38 09 Chapter 8: Abdominal and Chest Pain r HEENT: PERRL. Mucous membranes are dry. 1–10 per 100 patients per year.1,2 Risk factors for r Neck:Supple,withnoadenopathy. recurrent episodes of DKA include poor r Cardiovascular: Tachycardic, with no M/R/G. metabolic control, psychiatric diagnoses, difficult r Lungs: CTA bilaterally, without W/R/R. Patient is or unstable family, limited access to medical tachypneic but not dyspneic. services, and coexisting infection. DKA is the r Abdomen: Soft, non-tender, non-distended, with leading cause of mortality in diabetic patients less than 24 years old.4 normoactive bowel sounds. No guarding or r rebound tenderness. Pathophysiology: DKA is caused by the absolute r Extremities and skin: No rashes. Skin is warm and loss of insulin, which leads to upregulation of dry. No peripheral edema. Pulses are intact in all counterregulatory hormones, including glucagon, extremities. catecholamines, cortisol, and growth hormone. r Neurologic: Cranial nerves II–XII are intact. With the increase in these hormones, cells begin Motor strength and sensation are intact. to undergo lipolysis, proteolysis, glycogenolysis, r Pertinent laboratory values: Serum glucose 666 and decreased glucose utilization. After mg/dL, Na 130, K 5.1, Cl 106, bicarbonate 6, upregulation of these pathways, patients develop serum acetone 1+, urine ketones positive. ketogenesis with ketone body production and hyperglycemia. The major ketoacid produced (and subsequently measured) is Questions for Thought ␤-hydroxybutyrate. Elevated levels of r What laboratory tests would be diagnostic in this ␤-hydroxybutyrate ultimately cause the metabolic patient? acidosis associated with DKA. Hyperglycemia r What treatments would you initiate in this leads to glucosuria, osmotic diuresis, dehydration, patient? r and elevated serum osmolality. How would you monitor the response to therapy r Presentation: Patients presenting in DKA can have in this patient? a wide variety of complaints; however, most r What complication is unique to the pediatric population? complain of vague abdominal pain, nausea, and vomiting.3 Patients may complain of generalized malaise, getting progressively worse over the recent weeks. Further questioning may reveal a Diagnosis r history of polyuria, polydipsia, and recent weight Diabetic ketoacidosis in type 1 diabetes mellitus, loss. new onset. On physical examination, patients will likely appear dehydrated; vital signs may reveal Discussion tachycardia and hypotension, depending on the r Epidemiology:Diabetesmellitusisacommon severity of dehydration. The characteristic smell of endocrine disorder seen among pediatric and acetone on the breath may be appreciated. adult patients. There are two types of diabetes Patients may also have Kussmaul breathing, the mellitus, type 1 and type 2. In general, type 1 body’s compensatory response to the occurs in a younger population secondary to overwhelming acidosis. The remainder of the insulin deficiency while type 2 occurs in the physical examination may reveal findings middle-aged to older population, due to insulin associated with coexisting infection, as many resistance. Type 1 diabetes mellitus is the most patients with DKA have an infectious precipitant. common pediatric endocrine disorder. Of The abdominal examination is usually benign, children presenting in diabetic ketoacidosis and if abdominal tenderness is appreciated, (DKA), 27–40 percent of them will be diagnosed frequent re-evaluations must be done to monitor with new-onset type 1 diabetes mellitus.1–4 its resolution with DKA treatment. Neurologic Children less than 5 years old are more likely to examination may reveal an altered level of present in DKA.1–3 Children with a prior consciousness, ranging from lethargy to coma. diagnosis of diabetes mellitus are less likely to Cerebral edema occurs in 1 percent of all patients have recurrent episodes of DKA, approximately with DKA, most commonly in children less than

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5yearsold.1–6 Cerebral edema carries significant remainder of the fluid should be administered as morbidity and mortality, accounting for 57–87 0.45% saline over the next 48 hours. Potassium, percent of all pediatric DKA-associated deaths.1 If dosed 30–40 mEq/L, should be added to the cerebral edema is present, patients may have maintenance fluid to prevent and treat cranial nerve palsies, abnormal motor or verbal hypokalemia. Because of arrhythmia from very responses, and posturing. low potassium, the provider should not start r Diagnosis: The diagnosis of DKA is based on insulin until the potassium level is known.3 If the laboratory values. DKA is defined by the presence potassium is normal, potassium should be added of metabolic acidosis (pH less than 7.3 or (40mEq/L)tofluids,andifitislow,itshouldbe bicarbonate less than 15), with concomitant repleted concurrently with insulin initiation.3 hyperglycemia, ketonemia, glucosuria, and Once the patient is hemodynically stable, a ketonuria.1–4 The clinician should maintain a high continuous infusion of insulin at 0.1 unit/kg per index of suspicion for DKA in the vomiting child, hour is started. An insulin bolus is strongly particularly in the absence of diarrhea. When advised against, due to the fear of developing concern for DKA is present, the clinician should cerebral edema, with a rapid drop in serum obtain serum glucose, VBG or ABG, U/A, and an osmolality. Once serum glucose has decreased to electrolyte panel including potassium, sodium, 300, 5% glucose is added to the maintenance calcium, and phosphate. Patients are usually fluids with goal glucose levels of 150–300.1–3 If found to have hyponatremia on initial testing, the glucose cannot be maintained in that range, secondary to hyperglycemia and cellular fluid the insulin infusion can be decreased to 0.05 shift. The corrected sodium is obtained by the unit/kg per hour. Bicarbonate is contraindicated following formula: Na + [1.6 × (glucose – 100)]. inchildrenwithDKAasitisassociatedwitha Serum sodium levels should normalize with fluid fourfold increase in cerebral edema. r and insulin therapy. Patients typically also have Disposition: The vast majority of patients with abnormalities in potassium levels. Overall, DKAwillrequireadmissiontothehospital.In patients have a total body decrease in potassium patients with severe acidosis, admission to an ICU secondary to osmotic diuresis; however, at is warranted. Patients will require close presentation patients may appear hyperkalemic as monitoring with hourly glucose and vital-sign a result of an extracellular potassium shift in checks, along with a reassessment of electrolytes response to acidosis. Potassium levels will begin andacid–basestatusevery2hours.Asmallsubset to decrease with insulin treatment. Additional of patients, who are clinically stable with resolving laboratory tests to consider include serum ketone acidosis and close follow-up, may be discharged levels, LFTs, serum osmolality, and magnesium. home. Thediagnosisofcerebraledemais overwhelmingly a clinical one because CT scans are found to be normal in up to 40 percent of Historical clues Physical findings Ancillary studies r r r symptomatic children.1,3,6 Symptoms of cerebral Abdominal pain Tachycardia Hyperglycemia r Vomiting r Tachypnea r Elevated anion edema tend to occur 6–12 hours after therapy without diarrhea without increased gap onset; however, cases have been reported at the r r Recent viral r work of breathing r Ketonuria time of presentation before therapy initiation.1,3 illness Benign abdomen Ketonemia r Weight loss r Treatment:ThegoalsofDKAtreatmentareto restore circulating volume, replace water deficits, and clear serum glucose and ketones. Treatment of DKA is started with an assessment of the Follow-Up dehydration status and peripheral perfusion. If The child was admitted to the step-down unit after the patient is hemodynamically unstable or appropriate resuscitation in the ED. He was placed reveals signs of poor peripheral perfusion and on an insulin drip and his anion gap and serum glu- shock, a fluid bolus dosed 10–20 cc/kg of normal cose normalized. He required supplemental potas- saline can be given.1–4 Aboluscanberepeatedif siumduringhishospitalstay.Whileinpatient,heand shock persists. After the patient stabilizes, the his parents received diabetic education and had an

16:17:38 09 Chapter 8: Abdominal and Chest Pain endocrinology consultation. He was discharged on Past Medical History hospital day 3 on a home insulin regimen. r Trisomy 21. r Autism spectrum disorder. References r WasseenintheED3monthsagoandunderwent 1. Rosenbloom AL. The management of diabetic CT scan under sedation, which was remarkable ketoacidosis in children. Diabetes Ther 2010; 1: 103–20. for constipation and no other abnormalities. 2. Wolfsdorf J, Glaser N, Sperling MA. Diabetic r UTD on immunizations. ketoacidosis in infants, children, and adolescents. Diabetes Care 2006; 29: 1150–9. Medications 3. Olivieri L, Chasm R. Diabetic ketoacidosis in the r None. pediatric emergency department. Emerg Med Clin N Am 2013; 31: 755–73. Allergies 4. Westerberg DP. Diabetic ketoacidosis: Evaluation and r treatment. Am Fam Phys 2013; 87: 337–46. NKDA. 5. Glaser NS, Wootton-Gorges SL, Marcin JP, et al. Mechanism of cerebral edema in children with Physical Examination and Ancillary Studies diabetic ketoacidosis. 2004; 145: 164–71. r Vital signs:T97°F tympanic thermometer, HR 6. Levin DL. Cerebral edema in diabetic ketoacidosis. 115, RR 24, BP 125/80, O2 sat 98% on room air. Pediatr Crit Care Med 2008; 9: 320–9. r General: Agitated and difficult to assess, attempts to strike anyone who gets near him. Refuses to get on the bed, is sitting in a chair, making the sign Case 4 for “hungry” to his parents. r HEENT: PERRL, atraumatic, normocephalic, Contributing Authors: Holly Stankewicz and mucous membranes are moist, tympanic Rebecca Jeanmonod membranes normal. r History Neck: Child moves neck all around with no pain. No adenopathy. The patient is a 10-year-old boy brought in for what his r Cardiovascular:Regular,withoutmurmurs. parents believe is abdominal pain. The child is non- Good peripheral pulses and normal capillary verbal at baseline, related to trisomy 21 and “autism refill. spectrum.” The child knows a few signs and usu- r Lungs: Clear and equal, with no W/R/R. ally “makes himself understood.” His parents state r that, while walking, he periodically stops and crouches Abdomen:Childisnotcompliantwith down and appears uncomfortable. He has been play- examination. He kicks and claws when attempts ing and running around less than usual. They have not are made to palpate the abdomen. Child seems to noted fevers, and state that he is still eating well. He has range the hip without difficulty. Testicles are had his normal appetite, frequently putting his hand descended bilaterally. No penile lesions. Cannot up to his mouth to signify that he is hungry. There have appreciate masses. Cannot adequately assess for tenderness, guarding, or rebound. been no episodes of vomiting. He has chronic con- r stipation, but they do not believe that it is any worse Extremities and skin: Warm and well-perfused than usual. The child is toilet trained, so they do not without rashes or deformity. Moves all four know when he last defecated, but they report they have extremities spontaneously. Child can ambulate, not had to plunge the toilet in the last week or so. He but seems to be limping, favoring the right, and crouches down every 3–4 steps. has not had any incontinence. They are unaware of r any trauma. The child attends school, and his aide at Neurologic: Non-verbal, but interacts with school says he has been reluctant to participate in gym parents. No focal abnormalities. r forthelast2weeksorso.Theparentshavenotnoted Pertinent laboratory values: WBC 16,800, anycoughing,runnynose,orsneezing.Theyhavenot remainder of CBC and all chemistries normal. r noticed any rashes. They don’t think he has lost any Pertinent imaging: Abdominal series with stool weight. throughout colon (Figure 8.4).

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Figure 8.4 Abdominal series demonstrating constipation.

Questions for Thought children and adolescents, males are more likely to r ingest foreign bodies than females. What are possible sources of this child’s r symptoms that should be considered? Pathophysiology: Once a foreign body is r Does this child warrant imaging? Does he swallowed, the most common site of impaction is warrant admission? the thoracic inlet where skeletal muscle changes to r Does the ﬁnding of constipation on radiograph smooth muscle in the esophagus. The majority of adequately explain the patient’s presentation? esophageal impactions occur at this point, followed by the mid esophagus and the lower esophageal sphincter. Children with previous Diagnosis esophageal abnormalities are likely to have a r foreign body become lodged at the site of the Bowel perforation secondary to ingested foreign abnormality. Sharp objects may become impaled body. anywhere in the esophagus, or indeed anywhere in theentireGItract.Iftheforeignbodyreachesthe Discussion stomach, it is less likely to cause complications. r Epidemiology: It is difficult to determine the exact Exceptions include stomach ulceration from incidence of pediatric foreign-body ingestions but interaction of zinc (in coins) and stomach acid, it is a common pediatric ED complaint. Infants pointed objects, toxic objects, objects unable to and young children explore objects by putting pass through the pyloric sphincter due to length them in their mouths, and studies suggest that over6cmorwidthgreaterthan2cm,multiple there are more than 125,000 presentations of magnet ingestion, or problems related to previous foreign-bodyingestionsbychildrenyearly.1,2 The GI-tract abnormalities.1–6 If a foreign body does most commonly ingested foreign bodies are coins. become impacted it may cause local irritation, However, magnets and batteries are increasing in obstruction, bleeding, mucosal erosion, frequency, due to increasing numbers of perforation, pain, or no symptoms at all. Erosions electronic toys and devices and small magnets through the esophagus may cause mediastinitis or usedforplayortoimitatepiercings.Children6 even aortoenteric fistulas. years old and younger are the most likely to ingest Objects that pass the pylorus, even straight foreign bodies, and the frequency is higher in pins, are likely to pass through the GI tract underdeveloped countries.1–3 In young children, completely, without complication. However, males and females are equally affected. In older occasionally, objects will cause obstruction at the

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ileocecal valve or cause perforation at any area abdominal pain, observation and serial within the bowel. These perforations can self-seal abdominal examinations represent a reasonable with granuloma formation, abscess formation, or option. In this case, there was no diagnostic cause intra-abdominal sepsis. These can present certainty, and there was no ability to follow serial in a delayed fashion and with no apparent history examinations. The child had an X-ray that of foreign-body ingestion. demonstrated constipation, but does that r Presentation: Children may present with adequately explain the child’s symptoms? It has symptoms including (but not limited to) drooling, been shown in a large study that there is no fussiness, stridor, pain including chest or difference between the amount of stool seen on abdominal pain, refusal to eat or drink, wheezing, radiographs of children with serious pathology fevers, respiratory distress, cough, vomiting, compared to those with a final diagnosis of simple altered mental status, abdominal distension, constipation.7 In those with pain and tenderness, hematemesis, or hematochezia. Children may also constipation is a diagnosis of exclusion.7 be asymptomatic but present due to caregiver When possible, it is preferable to avoid CT in suspicion of an ingested foreign body or after children due to the radiation burden. However, passing a foreign body in their stool. this child illustrates an important point: serial r Diagnosis: A good history and physical will aid in examinations only work in children who can be the diagnosis in most cases, although not in this examined. U/S is an option to evaluate for case. Chest and/or abdominal X-rays will show appendicitis or intussusception or even torsion, ingested foreign bodies that are radiopaque. If the but is dependent upon the operator, and is best object is identified below the diaphragm, a single usedtoseekforaspecificclinicalentity.CT frontal radiograph is usually sufficient. If the scanning gives a more comprehensive assessment object is seen in the esophagus, frontal and lateral of the bowel, liver, and retroperitoneum, and is a CXRs are indicated to assess location as well as to reasonable option when the clinician frankly is determine what the object is and to make sure it is looking for something, but is not entirely sure one object and not two stuck together.3,4 what. The differential diagnosis in this child Additionally, the lateral CXR can aid in included surgical pathology such as appendicitis, confirmation that a coin, for example, is in the psoas abscess, hip pathology, renal or testicular esophagus and not the trachea, since coins in the pathology, or infectious disease. This particular esophagus typically appear in the coronal case has the added risks associated with sedation orientation as opposed to a coin in the trachea, for imaging, and is a difficult judgment call. r which is typically seen in the sagittal orientation. Treatment: If there is concern that the child is If a radiolucent object is suspected, diagnosis may unable to protect their airway, intubation may be beaidedbyhavingthechilddrinkasmallamount necessary. Most children who swallow a foreign of dilute contrast and repeating the study, or one body do not require any intervention at all. If the can proceed directly to endoscopy. Similarly, if child is symptomatic (cough, stridor, drooling, foreign-body ingestion is strongly suspected on pain, etc.) and there is a foreign body impacted in clinical examination and history, direct the esophagus, endoscopy is recommended. If the visualization may be the most efficient method to child is asymptomatic and there is a blunt foreign both diagnose and remove the object. Another body in the esophagus, especially if located at the possible diagnostic strategy is to use a metal lower esophageal sphincter, these children may be detector to identify the location of a metallic observed for 12–24 hours with hope of object such as a coin. CT imaging may be of spontaneous passage. If smooth objects have benefit in the assessment of foreign-body passed the duodenal sweep, they can be managed ingestion where bowel perforation or obstruction conservatively with stool inspection and possibly is suspected. Further information on this can be X-ray surveillance. If the object fails to pass found in Chapter 5, Case 1. through the GI tract or if the patient becomes Although observation is a strategy for foreign symptomatic, endoscopic or surgical intervention body, it is predicated upon the diagnosis being may be needed. Alternatives to endoscopy for made. Likewise, in cases of non-specific esophageal foreign bodies include the foley

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catheter method and the bougienage method to ingestion of multiple magnets should be remove esophageal foreign bodies.1–6 Blunt observed carefully with a low threshold for foreign bodies may be removed by passing an endoscopic or surgical removal of the magnets. uninflated Foley catheter distal to the object in a r Children with perforation or abscesses may patient who is positioned head-down on the table. need laparotomy or interventional radiology The catheter is then inflated and gently drainage as well as IV antibiotics. withdrawn, potentially bringing the foreign body r Disposition:Afteruncomplicatedremovalofan with it. The object may also be dislodged and esophageal foreign body, a healthy child may be passed into the stomach during this technique. safely discharged. Further evaluation for This technique is often performed under underlying esophageal problems should be done fluoroscopy and should be carried out by in a child with repeated foreign-body impaction experienced clinicians only. It should also only be or impaction at an unusual location. If the child done in cases where there was a witnessed has a foreign body in the stomach or lower GI ingestion of a blunt object less than 24 hours tract without symptoms or obvious complications, before the procedure, in a healthy child. The he or she may be discharged with instructions to bougienage method involves passing a bougie return if any symptoms develop, such as pain, down the esophagus in an attempt to dislodge and vomiting, constipation, or fever. Children with push the object into the stomach. It should be GI-tract abnormalities, unusual foreign bodies, or performed with the patient sitting upright. This frequent foreign-body ingestion may require technique should only be performed in a healthy additional evaluation and management. While child who had a witnessed foreign-body ingestion most foreign bodies pass without complication, less than 24 hours prior to procedure. The follow-up imaging should be performed for sharp bougienage method has been shown to be safe foreign bodies or button batteries which did not andhighlyeffectiveaswellasmoretime-and require urgent retrieval from the esophagus. cost-efficient than other treatment options. Surgery may be indicated if there are suspected complications, such as bowel perforation or Historical clues Physical findings Ancillary studies r r r obstruction. Abdominal r Tachycardia Plain film with r pain Difficult constipation r Button batteries: Patients with button batteries Crouching examination when walking lodgedintheesophagusareathighriskfor perforation due to the caustic nature of the battery. If there is concern that the foreign Follow-Up body lodged in the esophagus is a button Although the child had had a prior CT with no signif- battery, then endoscopy should be performed. icant diagosis, the parents’ concern and the provider’s If a button battery has passed into the stomach inability to assess the child led to the child undergoing it does not need to be removed immediately, as procedural sedation and CT scanning (Figure 8.5). The it will likely pass through the lower GI tract child’s CT demonstrated a needle-like foreign body without complication. Parents should be that had perforated the child’s intestine near the ileo- instructed to observe the stool for 2–3 days and cecal valve. The child was admitted for IV antibiotics if the battery has not passed, they must return and underwent interventional radiologic drainage of for repeat X-rays. If the button battery remains the abscess and a prolonged course of antibiotics via a in the stomach or is at a fixed spot in the PICC line. intestines, it should be removed. r Magnets: Patients with ingestion of one magnet References do not carry any additional risk of bowel injury. 1. Hesham A-Kader H. Foreign body ingestion: Children In the setting of ingestion of multiple magnets, like to put objects in their mouth. World J Pediatr thereisanincreasedriskofbowelinjurydueto 2010; 6: 301–10. magnetic attraction across the bowel wall and 2. Kay M, Wyllie R. Pediatric foreign bodies and their resulting pressure necrosis. Patients with management. Curr Gastroenterol Rep 2005; 7: 212–18.

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nausea and feeling bloated. She denies vomiting, vaginal bleeding or abnormal discharge, changes in bowel habits, dysuria, fever, chills or diaphoresis, chest pain, shortness of breath, or any correlation with meals. She has a history of chronic constipation, with her last bowel movement the day prior to presentation; she denies the presence of blood in the stool. She does have unprotected sexual intercourse with one male partner, with no history of sexually transmitted infections (STIs).

Past Medical History r Spontaneous abortion.

Medications r Oral contraceptives.

Figure 8.5 CT scan demonstrating needle-like foreign body in the right lower quadrant with a related abscess. Allergies r Peanuts.

3. Uyemura MC. Foreign body ingestion in children. Am Fam Phys 2005; 72: 287–91. Physical Examination and Ancillary Studies r 4. Kramer RE, Lerner DG, Lin T, et al. Management of Vital signs: 98.5 °F, HR 114, RR 20, BP 128/76, O2 ingested foreign bodies in children: A clinical report of sat 100% on room air. the NASPHAN Endoscopy Committee. JPediatr r General: Well-appearing young female; does not Gastroenterol Nutr 2015; 60: 562–74. appear to be in acute distress. 5. S¸ahin A, Meteroglu˘ F, Erbey A, et al. Insidious threat r HEENT:PERRL,mucousmembranesmoist,no of children: Esophageal foreign body ingestion. JAEM 2014; 13: 159–61. signs of trauma. r Neck: Supple and non-tender, with no adenopathy 6. CevikM,Gokdemir´ MT, Boleken ME, et al. The and midline trachea. characteristics and outcomes of foreign body ingestion r and aspiration in children due to lodged foreign body Cardiovascular: Regular tachycardia, with no in the aerodigestive tract. Pediatr Emerg Care 2013; 29: M/R/G. 53–7. r Lungs: Normal work of breathing, with clear lungs. 7. Freedma SB, Thull-Freedman J, Manson D, et al. r Abdomen: Soft and flat abdomen, normal bowel Pediatric abdominal radiograph use, constipation, and sounds, moderate tenderness at right lower significant misdiagnoses. JPediatr2014; 164: 83–8. quadrant and suprapubic area, no rebound or guarding. Case 5 r Pelvic examination: No lesions to external genitalia; age-appropriate development of external Contributing Author: Sade´ McKenzie labia; vaginal mucosa pink, with no lesions; mucopurulent discharge within vaginal vault, no History foul odor; mucopurulent discharge from cervical The patient is a 17-year-old healthy female who os with associated generalized erythema of cervix; presents with bilateral lower quadrant abdominal pain. no cervical motion tenderness, uterine fundal The pain started 5 days prior to presentation, with tenderness, no adnexal tenderness or masses. r a severity of 7 out of 10. The pain is equally severe Extremities and skin: Warm and well-perfused, on either side. She cannot describe any alleviating with normal capillary refill and no rashes. or aggravating factors. Associated symptoms include r Neurologic:Alert,withnofocalabnormalities.

16:17:38 187 09 Chapter 8: Abdominal and Chest Pain r Pertinent laboratory values: vaginalis (bacterial vaginosis). The former group r Urine pregnancy test: negative; of organisms cause inflammation of the cervix, r CBC: WBC 11,000, Hb 13.4, HCT 39.6, Plt uterus, and fallopian tubes. These may progress to 381,000; frank peritonitis and abscess of the fallopian r U/A: 1+ leukocyte esterase, 2+ hemoglobin, tubes. The latter group of organisms primarily WBC 5–10, RBC 5–10, slight epithelial cells, cause irritation of the vagina and vulva and are discussed in detail in Chapter 11, Case 7. slight bacteria; r r Neisseria gonorrhoeae and Chlamydia Presentation: Both men and women with STIs are trachomatis probes sent. Wet mount with no commonly asymptomatic. C. trachomatis and N. clue cells, budding yeast, or trichomonads. gonorrhoeae can cause urethritis, epididymitis, orchitis, proctitis, or Reiter syndrome in men; in r Pertinent imaging: Pelvic U/S reveals a small women, they cause urethritis, cervicitis, pelvic amount of fluid in the pelvis, otherwise inflammatory disease, and infertility. Urethritis unremarkable. may present with urethral discharge, dysuria, or Questions for Thought meatal pruritis in men. Epididymitis may present r with unilateral scrotal swelling and tenderness. What genitourinary pathologies can present with Pelvic inflammatory disease is defined asa abdominal pain? spectrum of inflammatory disorders of the female r What are the complications of this diagnosis? upper genital tract, including endometritis, r What practices can be employed to better ensure gathering of a complete sexual history when salpingitis, tubo-ovarian abscess, and pelvic treating adolescents and young adults? peritonitis. It is the sequela of an untreated STI. r What treatments can be initiated in the ED? Although pelvic inflammatory disease is predominantly caused by N. gonorrhoeae and C. trachomatis,itshouldbeconsidereda Diagnosis multiorganism process. The presence of abnormal r Chlamydial infection. cervical or vaginal mucopurulent discharge, cervical motion tenderness, uterine tenderness, or Discussion adnexal tenderness should raise the suspicion of r Epidemiology: The prevalence of STIs is dependent pelvic inflammatory disease. upon age, gender, and race/ethnicity. In the USA, Vaginitis, by comparison, refers to the adolescents and young adults aged 15–24 years superficial infection of the vaginal mucosa; itis old account for almost 50 percent of all cases of commonly associated with vaginal discharge and STIs each year.1 Females are generally infected at a may involve the vulva. Vaginitis can coexist with higher rate than males, with females of African STIs but is not itself classically considered an STI, American, Native American/Alaska Native, and and is discussed in more detail in Chapter 11, Hispanic ethnicities disproportionately affected.1 Case 7. Trichomoniasis classically presents with Social factors, such as poverty, limited access to malodorous, yellow-green vaginal discharge, and healthcare services, homelessness, and sexual may be associated with vulvar irritation. In men, abuse and violence, are additional factors that urethritis may develop, but they are often increase adolescents’ susceptibility to contracting asymptomatic. STIs.1 Last year, there were over 1,500,000 STIs Patients may also present with comorbid reported to the CDC.1 disease related to unprotected sex, such as r Pathophysiology: Chlamydia trachomatis is an primary HIV infection, HSV infection, syphilis, obligate intracellular bacterium responsible for or pregnancy-related complications. r chlamydial infections. Other organisms Diagnosis: Nucleic acid amplification tests allow responsible for bacterial STIs include Neisseria for very sensitive and non-invasive testing for gonorrhoeae and Trichomonas vaginalis.Although chlamydial and gonorrheal infections. Nucleic not considered STIs, women may present with acid amplification tests are licensed for use with co-infections due to Candida albicans urine, urethral, vagina,1 and cervical specimens. (vulvovaginal/vaginal candidiasis) or Gardnerella When collecting specimens, male first-void urine

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and female vaginal or cervical specimens are Historical clues Physical findings Ancillary studies considered optimal. Nucleic acid amplification r Abdominal r Tachycardia r Negative tests work well in the diagnosis of oropharyngeal r r pain Abdominal r pregnancy test or rectal gonorrheal or chlamydial infections. The Indolent course tenderness Negative wet r Sexually active r Erythema of mount turn-around time on these tests can be longer adolescent cervix than the time a patient typically remains in the r Mucopurulent ED, so high-risk patients should undergo empiric cervical discharge treatment. r Treatment: When treating an STI empirically, both gonorrheal and chlamydial infections should be Follow-Up covered, as concomitant infections are common; The patient was treated empirically for cervicitis in the treat with single-dose regimens when possible, to EDbutfailedtokeepafollow-upappointmentwith ensure compliance. the local health department clinic. She re-presented to r C. trachomatis: azithromycin 1 g orally, single the ED several months later with recurrent infection, dose, or doxycycline 100 mg orally, twice a day which had now progressed to pelvic inflammatory dis- for 7 days. ease with tubo-ovarian abscess, and was admitted for r Alternatives: erythromycin base 500 mg surgical management and parenteral antibiotics. orally,fourtimesadayfor7days; oxofloxacin 300 mg orally, twice a day for Reference 7 days; levofloxacin 500 mg orally, once a 1. Centers for Disease Control and Prevention. Sexually day for 7 days. transmitted diseases (STDs). https://www.cdc.gov/std/ r Pregnant patient: azithromycin 1 g orally, stats/ (accessed January 2017). single dose; amoxicillin 500 mg orally, three times a day for 7 days; erythromycin base Case 6 500 mg orally, four times a day for 7 days. r N. gonorrhoeae: ceftriaxone 250 mg IM, single Contributing Author: Brian Kelly dose. History r Alternatives: cefixime 400 mg orally, single A5-year-oldmalepresentstotheEDwithhisparents dose; cefotaxime 500 mg IM, single dose. for abdominal pain. The onset of the pain was yes- r Disposition: Patients should be screened for other terday while the patient was at school. He was sub- STIs (HIV, syphilis, other viral infections) and be sequently sent home due to concerns that he had the provided counseling for STI/HIV prevention and “stomach flu.” His parents were concerned that his contraception. The local health department pain was not going away and that he developed a fever ° should be notified per protocol. Patients should this afternoon of 100.7 F. They brought him for eval- establish follow-up with a PCP or local clinic, and uation because the mother remembers having similar partner(s) should be advised to seek treatment. symptoms when she had appendicitis as a child. He Patients should be advised to abstain from sexual describes the pain as cramping in nature. When asked activityforatleast7daysaftertreatment.Ifsexual to point to where his pain is, he points to his umbilicus. abuse is suspected, the incident should be The patient also admits to having a cough over the past reported to CPS, and the collection of forensic 2 days that has been intermittently productive. He has evidence may be indicated. Prepubertal girls who some nausea but denies vomiting, diarrhea, or dysuria. are the victims of sexual assault should be tested He is able to tolerate fluids but has not had an appetite for STIs, and adolescent victims of sexual assault over the past day. Neither the patient nor his family should be treated prophylactically, regardless of have been out of the country recently and he has not whether STI testing occurs. Patients who are ill had any sick contacts. with pelvic inflammatory disease should be admitted for IV antibiotics and gynecology Past Medical History consultation. r Seasonal allergies.

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Medications majority of patients presenting with acute r Cetirizine 5 mg daily. abdominal pain are diagnosed with “acute non-specific abdominal pain,” with acute Allergies appendicitis and UTI as the next two most 1 r NKDA. common entities. Approximately 2–5 percent of children with pneumonia present with abdominal Physical Examination and Ancillary Studies pain; some with abdominal pain as the only 1–3 r Vital signs: T 101.2 °F, HR 94, BP 110/68, RR 30, presenting symptom. Viral and bacterial O sat 96% on room air. pneumonia can both present as abdominal pain. 2 r r General: The patient is alert but appears to have Pathophysiology: Pneumonia results from slightly increased work of breathing. He is infection of the lung parenchyma and interactive and cooperative but appears listless. consolidation of that part of the lung and a r HEENT: PERRL. Moist mucous membranes. subsequent inflammatory cascade from the body’s Posterior pharynx is erythematous. No exudate is immune system. Basilar pneumonia may present noted on tonsils. Tympanic membranes normal with abdominal pain from diaphragmatic bilaterally. irritation or through referred pain via a shared r Neck: There is no anterior or posterior cervical dermatome. Additionally, patients with lymphadenopathy. Neck is supple and trachea is pneumonia may have inflamed abdominal lymph nodes, causing their pain.2 midline. r r Cardiovascular: The patient’s heart rate is regular, Presentation: Given that pneumonia is an with normal rhythm and no M/R/G. Peripheral infection primarily affecting the respiratory pulses are normal. Capillary refill Ͻ 3 seconds. system, the classic symptoms include cough, fever, r Lungs: Increased work of breathing. Rhonchi at dyspnea, tachypnea, generalized malaise, as well the right lung base. Otherwise there are no as a constellation of other symptoms. However, wheezesorralesinotherlungfields. referred abdominal pain may be the only presenting symptom. It is important for clinicians r Abdomen: The patient’s abdomen is diffusely to be cognizant that abdominal pain can tender in all quadrants but is soft, without commonly stem from extra-abdominal disease rebound or guarding. There is no splenomegaly or processes.1 Abdominal pain without vomiting or hepatomegaly. diarrhea should prompt the clinician to evaluate r Extremities and skin:Skiniswarmtothetouch the patient for pneumonia as well as other intra- but there are no rashes or mottling. r and extra-abdominal causes, such as pneumonia, Neurologic: Grossly intact with no focal deficits. acidosis, or tonsillitis.1 According to one retrospective study, fever was the most common Questions for Thought symptom prevalent in cases of pneumonia r presenting as abdominal pain, followed by cough What diseases, common and life-threatening, and signs of upper-respiratory-tract infection.3 should be on your diﬀerential diagnosis? Although rare, pneumonia and other r What imaging studies should this patient undergo? extra-abdominal causes of abdominal pain can be r What is the disposition for this patient? life-threatening and should not be missed, as diagnostic delay worsens outcomes. These include, but are not limited to, diabetic ketoacidosis, meningitis, Henoch–Schonlein¨ Diagnosis purpura, hemolytic uremic syndrome, leukemia, r Community-acquired pneumonia. sickle cell crisis, and streptococcal pharyngitis.1 r Diagnosis: As with any presentation, a thorough Discussion r physical examination can aid in avoiding Epidemiology: Acute abdominal pain is one of the misdiagnosis of pneumonia causing abdominal most common chief complaints in the ED. pain (i.e. rhonchi on lung auscultation). The gold According to retrospective analyses, a large standard for diagnosing pneumonia is chest

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Figure 8.6 Typical pediatric radiograph demonstrating right lower lobe infiltrate.

radiography (Figure 8.6). Chest radiography does partly on the patient’s age, risk factors, geography, sometimes lag behind the clinical presentation and clinical presentation. There does not appear and may miss diagnosing early pneumonia, and it to be an association with a specific organism in is not unreasonable to treat a patient for patients presenting primarily with abdominal pneumonia based on clinical presentation in the pain. For newborns and young infants, empiric absence of radiographic findings. In children with treatment is with ampicillin and cefotaxime or viral syndromes, who are well-appearing, with gentamycin.5 Outpatient management for infants non-focal examinations, CXR is not necessary or and toddlers is appropriate with beta-lactam indicated. Generally, viral and bacterial antibiotics. School-aged children have a higher pneumonias appear as interstitial infiltrates on incidence of atypical pneumonia (i.e. Mycoplasma CXR.4 Alveolar pneumonia and especially lobar pneumoniae) and therefore macrolides are the infiltrates tend to be indicative of a bacterial agent of choice, as pneumococcus is susceptible as pathogen.4 In terms of the presenting symptom of well.5 abdominal pain, some studies suggest that any r Disposition: The majority of children, other than child who also has a cough, fever, or dyspnea newborns and infants, can be managed on an should receive a CXR before any abdominal outpatient basis, depending on the clinical imaging.2 U/S is being studied as a potential scenario and patient comorbidities. diagnostic alternative to chest radiography for pneumonia, although currently its use is limited. Historical clues Physical findings CT has very high sensitivity and specificity but is r r generally only indicated when there are Cough Rhonchi r Fever r Lack of focal abdominal complications of pneumonia, such as concerns for r Lack of vomiting/diarrhea tenderness empyema or abscess. r Tachypnea r Treatment: As with any patient, the first priority in treatment is appropriate respiratory and hemodynamic support, if necessary. Supplemental Follow-Up oxygen or IV fluid resuscitation may be required Given the fever and the abdominal pain, U/S was in severe cases of pneumonia. The variance of ordered to evaluate for acute appendicitis. The causative organisms for pneumonia depends appendix was not visualized, however, and the patient

16:17:38 191 09 Chapter 8: Abdominal and Chest Pain had undergone laboratory work, and a CT of the mother present and he reports that he has never been abdomen and pelvis with oral and IV contrast. This sexually active. showed a normal appendix but also a right-lower-lobe infiltrate as the scan extended into the thorax. The Past Medical History patient was placed on antibiotics and discharged after r Attention deficit–hyperactivity disorder. being observed tolerating oral intake and followed up with his pediatrician as an outpatient. Medications References r Methylphenidate, extended release, daily. 1. TtsalkidisA,GardikisS,CassimosD,etal.Acute abdomen in children due to extra-abdominal causes. Allergies Pediatr Int 2008; 50: 315–18. r NKDA. 2. Moustaki M, Zeis PM, Katsikari M, et al. Mesenteric lymphadenopathy as a cause of abdominal pain in children with lobar or segmental pneumonia. Pediatr Physical Examination and Ancillary Studies Pulmonol. 2003; 35: 269–73. r Vital signs: T 99.5 °F, HR 112, RR 12, BP 128/75, 3. Homier V, Bellavance C, Xhignesse M. Prevalence of O2 sat 98% on room air. pneumonia in children under 12 years of age who r General: Patient is alert, oriented, well-developed, undergo abdominal radiography in the emergency and appears very uncomfortable. He is grimacing department. CJEM 2007; 9: 347–51. and holding his lower abdomen. 4. VirkkiR,JuvenT,RikalainenH,etal.Differentiation r of bacterial and viral pneumonia in children. Thorax HEENT: No signs of trauma. PERRL. Mucous membranes moist. Oropharynx clear. 2002; 57: 438–41. r 5. Bradley JS, Byington CL, Shah SS, et al. The Neck: Supple, with midline trachea and no management of community-acquired pneumonia in adenopathy. r infants and children older than 3 months of age: Cardiovascular: Tachycardic; regular rhythm, no Clinical practice guidelines by the Pediatric Infectious M/R/G; bilateral radial pulses equal and 2+. Diseases Society and the Infectious Diseases Society of r Lungs:Clear,equalairentrybilaterally;noW/R/R. America. Clin Infect Dis 2011; 53: 617–30. r Abdomen: Normoactive bowel sounds; tender to palpation on bilateral lower quadrants, worse on the left, no masses, negative Rovsing’s sign, negative obturator sign, negative psoas sign. Case 7 r Genitourinary examination:Thelefttesticleis high-riding with some mild erythema and edema. Contributing Authors: Cara V. Tillotson, The patient is unable to tolerate palpation of the Melanie K. Prusakowski, and Rebecca testicle due to pain. There is no movement of the testicle upon stroking of the medial inner thigh. Jeanmonod Inguinal canals are normal bilaterally. The right History testicle is non-tender to palpation. r The patient is a 13-year-old male who presents to the Extremities and skin: No rashes, purpura, petechiae, or pallor. No signs of trauma. ED with sudden-onset abdominal pain for the last r hour. His mother states that he woke up this morning Neurologic:Alertandage-appropriate,withno complaining of extreme pain and has not been able to focal deficits. r getoutofbedexcepttoridetothehospital.Thepainis Pertinent laboratory values: WBC 7,000, CRP Ͻ 3, located in his lower abdomen bilaterally, but is worse U/A normal. r on the left. He rates the pain 9 out of 10. He has vom- Pertinent imaging: Pertinent radiologic studies: ited once since the onset of symptoms. The vomit was U/S with color Doppler: left testicle mildly non-bilious and non-bloody. He denies any recent ill- enlarged with homogeneous echotexture; twisting ness or injury. He has had no fever, diarrhea, dysuria, of the spermatic cord, and absent blood flow to or hematuria. You interview the patient without the the left testis and epididymis.

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Questions for Thought position of the testicle and allows the testicle more mobility around the spermatic cord. This type of r What is the typical presentation for this torsion is termed intravaginal torsion and occurs condition? 2–4 r Which patients are at highest risk for this at any age after the neonatal period. problem? Extravaginal torsion (occurring prenatally and in r When is imaging recommended? neonates) is caused by twisting around the r Which imaging modality is preferred? spermatic cord proximal to the tunica vaginalis. r What is the treatment for this condition? This occurs during the descent of the testicles r What is the indication for surgical consultation? from the abdomen into the scrotal sac, where the testicleshavemoremobilityandarethusmore predisposed to torsion.2–4 Ovarian torsion similarly occurs when the Diagnosis r ovary twists on its pedicle, leading to obstructed Torsion of the left testicle. lymphatic and venous drainage.1 This eventually leadstoedemaandobstructedarterialflow.This Discussion may involve the ovary, the fallopian tube, or both. r Epidemiology: Testicular torsion is the twisting of Most torsed ovaries are abnormally enlarged, the spermatic cord and has an annual incidence of manygreaterthan5cm,buttherehavebeencases about 1 in 4,000 males who are less than 25 years of prepubertal girls presenting with torsion.1 old.1 It is the most common cause of testicle loss r Presentation: The classic presentation of testicular in the USA. The peak incidence occurs in ages torsion is acute, severe, unilateral scrotal pain and 12–18 years and the neonatal period, although it swelling, with nausea and/or vomiting. Children can occur at any age. Adolescents and neonates may present with abdominal pain and vomiting are more likely to have torsion of the spermatic rather than scrotal pain; it is important to keep cord (true testicular torsion), while prepubertal testicular torsion on the differential for acute boys are more likely to have torsion of the lower abdominal pain in pediatric patients.1,3,5,6 appendix testes or epididymis.2,3 Neonatal torsion The pain may be unrelenting. Physical can occur prenatally (70 percent) or postnatally examination will vary based on the time of initial (30 percent).2,3 Torsion more commonly occurs presentation. Scrotal erythema and edema are on the left side. common, and in late presentations may be severe Young females may also present with acute enough to obscure landmarks.1,3,5,6 Loss of the abdominal pain related to gonadal torsion. cremasteric reflex is classically present and is the Gonadal torsion in females is less common in the most reliable finding, but the presence of the pediatric age group, especially prior to puberty, reflex does not entirely exclude testicular torsion but has been described.1 When it occurs, it is in the setting of high suspicion.5 There is usually commonly associated with ovarian pathology (i.e. tenderness to palpation of the testicle (in massesorcysts),althoughitcanoccurinan spermatic cord torsion) or focal tenderness on the otherwise normal ovary.1 superior testis (torsed appendix testis). The torsed r Pathophysiology: Testicular torsion occurs when testicle may be high-riding and horizontally the testicle twists around the spermatic cord, oriented. compressing the vasculature and causing The presentation for ovarian torsion is also ischemia. The two types of testicular torsion are typically one of acute pain, which is usually intravaginal and extravaginal.2–4 Testicles are unilateral although it can be visceral and poorly normally covered by the tunica vaginalis, which is localized. Pain can be colicky and intermittent, attached to the posterior surface of the testicle. andisoftenassociatedwithvomiting,nausea, This prevents the testicle from excessive fever, and dysuria.1 The presentation in girls is movement. However, about 12 percent of the male often misleading, and diagnosis requires ahigh population has the “bell clapper” variation, where index of suspicion. the tunica vaginalis attaches in a higher position r Diagnosis:Thecriticalevaluationofachildwith on the testicle.1 This results in a more horizontal testicular torsion is a careful history and physical

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Figure 8.7 U/S of torsed ovary demonstrating decreased internal blood flow, but some evidence of peripheral flow. It is important to image both the affected and the unaffected side for comparison. For the color version, please refer to the plate section.

examination. Key diagnostic elements include r Treatment: Gonadal torsion is a surgical acute onset of testicular or abdominal pain and an emergency. Significant ischemia can occur as early abnormal testicular/scrotal examination. U/S with as 4 hours after onset of torsion (with 4–8 hours color Doppler may show decreased blood flow and considered the “golden” window for salvage). coiling of the spermatic cord, but is not sensitive Testicular torsion can impair sperm formation enough to exclude this diagnosis in small infants later in life even if the testicle is not removed. The in whom your index of suspicion is high (lower likelihood of viability of the gonad is inversely limit of sensitivity 88 percent).1,7 In these infants, relatedtotheamountoftimesincetheonsetof urology should be consulted, as truly, surgical pain. Those undergoing surgical correction within exploration is the gold standard for diagnosis. 6 hours have close to 100 percent salvage rate, Radionucelotide imaging was once the diagnostic while those waiting more than 24 hours have study of choice, but is rarely used since the advent virtually no chance of salvage. Surgery should not of diagnostic U/S. U/A is recommended in order be delayed in order to complete imaging in a to evaluate for other causes of acute testicular patient with a high suspicion of testicular torsion. pain, such as epididymitis or orchitis. Bacterial Manual detorsion of the testicle may be attempted infections may produce pyuria or bacteriuria. in the ED, though patients may not be able to In girls, diagnosis is more challenging and is tolerate this due to pain. Even if the testicle can be often delayed, with many girls having detorsed manually, surgical exploration is still misdiagnoses.1 U/S is the diagnostic test of choice, indicated to ensure complete resolution. Surgical and is typically performed transabdominally in correction usually includes detorsion of the young girls.1 Colorflow Doppler alone is not testicle and exploration of the contralateral adequate, as the ovary has a dual blood supply hemiscrotum. Frequently, surgeons will fix the (both ovarian and uterine artery) and up to contralateral testis to the scrotal wall in order to two-thirds of cases of torsion will have evidence of prevent recurrent torsion. If the affected testicle is blood flow (Figure 8.7).1 CT scanning may show unlikely to be viable, it is removed. If it is viable, it an enlarged ovary, but cannot rule out torsion. is fixed in a similar fashion to the scrotal wall.

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Ovarian torsion obviously cannot be manually Case 8 detorsed, and requires surgical correction or oophorectomy if the ovary is no longer viable. Contributing Author: Donald Jeanmonod r Disposition: When the diagnosis of testicular torsion has been made or is highly suspected, an History emergent urologic consult should be obtained, or A 15-year-old female presents to the ED with her the patient should be transferred emergently to a motherforevaluationofabruptonsetofabdominal center where urologic consultation is immediately pain. The patient relates that she has been feeling inter- available. mittently unwell over the past 2 weeks, with several episodes of vomiting occurring over that time period. On the day of presentation, the patient was in school Historical clues Physical findings Ancillary studies r r r in her normal state of health and without complaint Severe sudden Tender, swollen Negative U/A when she developed abrupt onset of abdominal pain. abdominal pain testicle r U/S with evidence r Vomiting r Abnormal of torsion The pain is generalized, but seems to be more severe r testicular lie in the lower abdomen. Initially, the patient reported Absent that the pain was sharp, but has now become more cremasteric reflex achy in nature. The patient reports that the pain seems Follow-Up worse when she is moving around, and is improved with lying still. Additionally, she reports that she has ThepatientwastakentotheORforemergentexplo- started to feel nauseated and slightly light-headed ration. The left testicle was detorsed, and it regained since the onset of the pain. The patient denies any blood flow and appeared viable. The contralateral headache, chest pain, cough, diarrhea, dysuria, urinary hemiscrotum was also explored and both testicles were frequency, vaginal bleeding, and vaginal discharge. She affixed to the scrotal wall to prevent future torsion. The reports some mild shortness of breath on review of patient recovered overnight on the pediatric surgery systems.Sheisunsureastowhenherlastmenstrual service. Edema and pain resolved within 24 hours, and period was. the patient was sent home with pain control. Past Medical History References r None. 1. Smith J, Fox SM. Pediatric abdominal pain: An emergency medicine perspective. Emerg Med Clin N Medications Am 2016; 34: 341–61. r None. 2. Gatti JM, Murphy JP. Acute testicular disorders. Pediatr Rev 2008; 29: 235–41. Allergies r 3. Goel A, Gaillard F. Testicular torsion. See http:// NKDA. radiopaedia.org/articles/testicular-torsion. ´ Physical Examination and Ancillary Studies 4. Bombinski P, Warchoł S, Brzewski M, et al. r Ultrasonography of extravaginal testicular torsion in Vital signs: T 99.1 °F, HR 115, RR 24, BP 88/62, O2 neonates. Pol J Radiol 2016; 81: 469–72. sat 98% on room air. r 5. Kadish HA, Bolte RG. A retrospective review of General: Appropriately developed Caucasian pediatric patients with epididymitis, testicular torsion, female adolescent, lying recumbent on the and torsion of testicular appendages. Pediatrics 1998; stretcher. The patient appears slightly pale and 102: 73–6. appears uncomfortable. 6. PogorelicZ,Mrkli´ c´ I, Juric´ I. Do not forget to include r HEENT: Head is normocephalic and atraumatic. testicular torsion in differential diagnosis of lower Eyes appear normal. Mucous membranes moist, acute abdominal pain in young males. JPediatrUrol 2013; 9: 1161–5. without pharyngeal erythema. r Neck: Unremarkable in external appearance, with 7. Baker LA, Sigman D, Mathews RI, et al. An analysis of full range of motion. clinical outcomes using color Doppler testicular r ultrasound for testicular torsion. Pediatrics 2000; 105: Cardiovascular: Tachycardic and regular, without 604–7. any M/R/G. Capillary refill 3 seconds.

16:17:38 195 09 Chapter 8: Abdominal and Chest Pain r Lungs: Slightly tachypneic, without accessory pregnancy are at significantly higher risk for muscle use. Lungs are CTA bilaterally. Normal complications. A retrospective study of 2,721 work of breathing. women, including 649 adolescents, presenting to r Abdomen: Non-distended. The patient has an ED for evaluation during the first trimester of generalized tenderness to percussion and pregnancy found the incidence of ectopic palpation. She is most tender in the lower pregnancy to be 21.7 percent in adults and 9.7 abdomen and suprapubic region. percent in adolescents.4 r Extremities and skin: No obvious abnormalities. Risk factors for ectopic pregnancy include a Full range of motion. number of conditions which result in tubal r Neurologic: GCS 15. Motor intact throughout. No scarring, including a history of infection, prior obvious deficits. surgery, or prior ectopic pregnancy. Additional risk factors include intrauterine device use and Questions for Thought cigarette smoking. When compared to the adult r cohort, adolescents are less likely to have had What elements of the history and examination prior ectopic pregnancy or surgery as a risk factor are missing on this patient? for current ectopic pregnancy and are more likely r What is the best way to approach data gathering in this patient? to have had a history of sexually transmitted r Along the spectrum of disease, is this patient sick infection or active infection at the time of their 4 or not sick? diagnosis. Patient risk factors, a history of present r What are your initial management steps? illness, and symptoms are poorly predictive of the r Given your formulated diﬀerential diagnosis, possibility of ectopic pregnancy, with reported what two tests are essential for making a likelihood ratios that are less than 1.5.5 diagnosis? r Pathophysiology: Ectopic pregnancy occurs when a fertilized egg implants somewhere other than the uterine fundus. This implanted embryo, as it Diagnosis grows, can cause tube rupture, hemorrhagic r Ruptured ectopic pregnancy. shock, abdominal pain, vaginal bleeding, or even death. Discussion r Presentation: Ectopic pregnancies can present in a r Epidemiology: Teenage pregnancy (age 15–19) variety of ways, from asymptomatic to back pain rates have declined by 64 percent since 1991 in the to abdominal pain to shock. In cornual ectopic USA, possibly through better education, more pregnancy, the pregnacy can proceed for a long abstinence, and improved access to forms of time without problems, often well into the second contraception.1 Despite falling rates of teenage trimester. The clinician needs to maintain a high pregnancy, there are still 22.3 live births per 1,000 index of suspicion for ectopic pregnancy in all females in this age group. Since the Pregnancy reproductive-aged girls. Mortality Surveillance System was implemented r Diagnosis: In 2013, individuals aged 15–24 years in 1987, pregnancy-related deaths have risen from represented 15 percent of all ED visits, with 62 7.2 deaths per 100,000 live births to 17.8 deaths percent of these being visits by adolescent and 2 per 100,000 live births between 2009 and 2011. young adult females.6 Abdominal pain Ectopicpregnancyisthoughttocomplicate represented the most common reason for ED visit 1–2 percent of all pregnancies in the USA and (8.5 percent of visits) and vaginal bleeding continues to be an important cause of represented 2 percent of visits in adolescent and first-trimester morbidity and mortality in the young females.7 In a nationwide sample of ED pregnant patient. Because of the decreased visits between 2005 and 2009, only 20.9 percent of incidence of risk factors for ectopic pregnancy in those visits included pregnancy testing.8 In this adolescents, the incidence of ectopic pregnancy in sample, patients presenting to a pediatric ED were adolescents is less than adults and reported to be even less likely to receive testing. A retrospective 3 0.3 percent. That said, patients presenting to an study of female adolescents presenting to an ED ED for evaluation during the first trimester of found that only 10 percent of patients who were

16:17:38 09 Chapter 8: Abdominal and Chest Pain eventually diagnosed as being pregnant be ectopic, until proven otherwise. mentioned the possibility of pregnancy in triage, Transabdominal and transvaginal U/S remain the and 10.5 percent denied being sexually active.9 primary methods to determine the location of Obviously, having a high index of suspicion of pregnancy in the first trimester. Previously pregnancy in any post-menarcheal female reported ␤-hCG discriminatory thresholds presenting with nausea, vomiting, abdominal or should not be used to determine U/S utility in pelvic pain, or vaginal bleeding or discharge is an evaluation of the location of a pregnancy. In a important first step to making the diagnosis. retrospective study of 693 patients presenting with The initial assessment of any patient a ruptured ectopic pregnancy, 11 percent were presenting to the ED should include careful foundtohave␤-hCG levels Ͻ 100 IU/L.13 attention to vital signs. A shock index (ratio of ED-performedU/Scanbeusedtoaccurately heart rate to systolic blood pressure) of Ͼ 0.85 in exclude ectopic pregnancy by demonstrating an pregnant patients presenting with vaginal intrauterine pregnancy with a negative predictive bleeding or abdominal pain in the first trimester value of 99.96% (95% CI of 99.6–100%) in a hasbeendemonstratedtomakethelikelihoodof pooled meta-analysis.14 U/S findings that have a ruptured ectopic pregnancy 15 times more been associated with the presence of an ectopic likely.10 After addressing instabilities in the pregnancy include an empty uterus (LR+ 3.95, primary survey, urine testing for pregnancy 95% CI of 2.70–5.77%), adnexal mass (LR+ 7.39, remains the first step in patient evaluation. 95% CI 3.63–15.05%), pelvic free fluid (LR+ Although urine pregnancy tests have been touted 6.12, 95% CI of 3.08–12.18%), and obviously a live as being very sensitive in detecting pregnancy, extrauterine gestation.15 very low concentrations (Ͻ45 IU/L) of ␤-hCG can r Treatment: Management of the patient with a result in false negative testing,11 which might pregnancy of unknown location with no definitive prompt serum ␤-hCG testing if you have a high intrauterine pregnancy and no adnexal pregnancy index of suspicion. orsuggestiveadnexalmassremainsapredicament Although ectopic pregnancy has been with frequently changing guidelines. Studies reported to be the most common cause of demonstrate that 5–40 percent of women first-trimester maternal mortality, an increased presenting with complaints in the first trimester awareness, better diagnostic modalities, improved will ultimately be diagnosed with a pregnancy of therapeutics, and better resuscitation science have unknown location. Of these patients, between 6 led to a steady decline in mortality rates from 1.15 and 20 percent will have an ectopic pregnancy. deaths per 100,000 live births between 1980 and The majority (50–70 percent) will eventually be 1984 to 0.5 deaths per 100,000 live births between diagnosed with failed pregnancies, with falling 2003 and 2007.12 Because the incidence of ectopic ␤-hCG levels, and the remainder (30–47 percent) pregnancy increases with age, mortality has been will be diagnosed with ongoing intrauterine demonstrated to increase with age as well, with pregnancy.16 Typically, management includes women aged 35–39 being 2.5 times more likely to follow-up with serial ␤-hCG levels being checked have pregnancy-related mortality, and women every 48 hours until the location of the pregnancy aged 40 years and older being 5.3 times more is confirmed. The minimal rise in ␤-hCG has likely to have pregnancy-related mortality, when consistently fallen over time, with more recent compared to women in their 20s with ectopic studies suggesting that a rise of at least 35 percent pregnancy. In addition, there are significant racial in 48 hours considered the minimal rise disparities with African Americans being 6.8 consistent with a possible intrauterine times more likely to die of ectopic-related pregnancy.16 complications when compared to Caucasians.12 After addressing the primary survey and Because the incidence of ectopic pregnancy is aggressively managing hemodynamic instability, higher in ED patients presenting with if present, management of a patient with an abdominal/pelvic pain or vaginal bleeding than ectopic pregnancy should involve consultation the group of pregnant patients at large, a diagnosis with an obstetrician/gynecologist. IV access of first-trimester pregnancy should be assumed to should be established and laboratory studies

16:17:38 197 09 Chapter 8: Abdominal and Chest Pain

Figure 8.8 U/S demonstrating empty uterus with complex free fluid.

should include a baseline CBC, renal tests and management may be used as a treatment option LFTs, a type and screen with crossmatch if for patients who are asymptomatic, have low unstable, and baseline quantitative ␤-hCG. ␤-hCG levels (Ͻ 200 IU/L), and are good Treatment options for the ectopic pregnancy candidates for compliance with every-48-hour include expectant management, medical abortive laboratory draws. therapy, or surgical treatment. The final method of managing ectopic If the patient has signs or symptoms of tubal pregnancy is with medical therapy. Methotrexate rupture, immediate surgical intervention is is an antimetabolite that binds to the catalytic site warranted. In general, surgery is the preferred on dihydrofolate reductase, leading to inhibition modality in definitive rupture, suspected rupture, of DNA synthesis and cell replication. and in the presence of a heterotopic pregnancy Observational studies have reported successful (concomitant intrauterine and extrauterine treatment rates of between 71.2 and 94.2 pregnancies). Patients who have contraindications percent,17 with higher success rates in those with to medical therapy, who are suspected of having lower ␤-hCG levels and smaller ectopic mass. issues with compliance and follow-up, who have Contraindications to methotrexate include failed medical therapy to terminate the ectopic immunosuppression, liver disease (including pregnancy, or have U/S evidence (ectopic mass Ͼ alcohol-induced liver disease), blood dyscrasias, 3.5 cm or presence of fetal heart rate) that makes renal disease, pulmonary disease, and peptic ulcer medical therapy unlikely to succeed are also disease. Methotrexate is administered as an IM candidates for surgical therapy.17 Surgical injection of 50 mg/m2, with a second dose therapies include salpingostomy, where the administered if ␤-hCG has not declined by 15 fallopian tube is incised and the fetal tissue percent on repeat testing by day 4 to 7. Fifteen to removed, and salpingectomy, where the affected twenty percent of patients will require a second portion of the tube is removed. Both procedures dose. Because methotrexate affects rapidly can be performed by either laparoscopy or dividing tissue, common side effects include laparotomy; however, laparotomy is preferred if nausea, vomiting, diarrhea, and stomatitis. the patient has ruptured. r Disposition: Disposition depends on treatment With the knowledge that many ectopic course and patient presentation. Patients with pregnancies would spontaneously abort or operative intervention require admission. Those reabsorb if allowed to run their course, expectant who are hemodynamically stable with reliable

16:17:38 09 Chapter 8: Abdominal and Chest Pain

Figure 8.9 Right-upper-quadrant view of Morrison’s pouch, demonstrating free fluid.

follow-up, and who are undergoing medical was seen in the left adnexa (Figure 8.10). An emergent management or observation, may be discharged obstetrics and gynecology consultation was placed and home with careful return precautions. the patient was taken to the OR where a diagnosis of a ruptured left adnexal ectopic pregnancy was confirmed and managed surgically. Historical clues Physical findings r r Subacute nausea Tachycardic References r Acute lower abdominal pain r Tachypneic r Light-headed r Pale 1. Hamilton BE, Mathews TJ. Continued declines in teen r Unknown last period r Hypotensive births in the United States, 2015. NCHS data Brief, no. 259. Hyattsville, MD: National Center for Health Statistics, 2016. Follow-Up 2. Centers for Disease Control. Reproductive Health: The patient’s mother was asked to step out of the Pregnancy Mortality Surveillance System. https://www room and a sexual and substance abuse history were .cdc.gov/reproductivehealth/MaternalInfantHealth/ obtained from the patient. The patient stated that she PMSS.html (accessed February 13, 2017). had had consensual vaginal intercourse on several 3. Hoover KW, Tao G, Kent CK. Trends in the diagnosis occasions with a boy in her school and would usu- and treatment of ectopic pregnancy in the United ally use a condom, but two times had not. She contin- States. Obstet Gynecol 2010; 115: 495–502. ued to deny vaginal bleeding and discharge. She denied 4. Menon S, Sammel MD, Vichnin M, Barnhart KT. Risk smoking, alcohol use, and drug use. factors for ectopic pregnancy: A comparison between The patient was identified as requiring resuscita- adults and adolescent women. JPediatrAdolesc Gynecol 2007; 20: 181–5. tion. IV access was established and resuscitation was initiated with normal saline. The patient was unable 5. Crochet JR, Bastian LR, Chireau MV. Does this woman have an ectopic pregnancy? The rational to provide a urine specimen for urine ␤-hCG. Labs clinical examination systematic review. JAMA 2010; were sent for CBC, basic metabolic panel, serum quan- 309: 1722–9. titative ␤-hCG, and type and crossmatch. Bedside U/S 6. Rui P, Kang K, Albert M. National Hospital was performed and the images demonstrated an empty Ambulatory Medical Care Survey: 2013 Emergency uterus with complex pelvic free fluid (Figure 8.8), department summary tables. See www.cdc.gov/nchs/ which tracked up the right pericolic gutter to Morri- data/ahcd/nhamcs emergency/2013 ed web tables son’s pouch (Figure 8.9). A live extrauterine pregnancy .pdf

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Figure 8.10 Live extrauterine pregnancy in the left adnexa.

7. ZivA,BouletJR,SlapGB.Emergencydepartment 13. Saxon D, Falcone T, Mascha E, et al. A study of utilization by adolescents in the United States. ruptured ectopic pregnancy. Obstet Gynecol 1997; 90: Pediatrics 1998; 101: 987–94. 46–9. 8. Goyal M, Hersh A, Luan X, et al. Frequency of 14. Stein JC, Wang R, Adler N, et al. Emergency physician pregnancy testing among adolescent emergency ultrasonography for evaluating patients at risk for department visits. Acad Emerg Med 2013; 20: ectopic pregnancy: A meta-analysis. Ann Emerg Med 816–21. 2010; 56: 674–83. 9. CauseyAL,SeagoK,WahlNG,VoelkerCL.Pregnant 15. Richardson A, Gallos I, Dobson S, et al. Accuracy of adolescents in the emergency department: Diagnosed first trimester ultrasound in diagnosis of tubal or not diagnosed. Am J Emerg Med 1997; 15: 125–30. pregnancy in the absence of an obvious extrauterine 10. Birkhahn RH, Gaeta TJ, Bei R, Bove JJ. Shock index in embryo: Systematic review and meta-analysis. the first trimester of pregnancy and its relationship to Ultrasound Obstet Gynecol 2016; 47: 28–37. ruptured ectopic pregnancy. Acad Emerg Med 2002; 9: 16. Kirk E, Bottomley C, Bourne T. Diagnosing ectopic 115–19. pregnancy and current concepts in the management of 11. Greene DN, Schmidt RL, Kamer SM, et al. Limitations pregnancy of unknown location. Hum Reprod Update in qualitative point of care hCG tests for detecting 2014; 20: 250–61. early pregnancy. Clin Chim Acta 2013; 415: 317–21. 17. Murtaza UI, Ortmann MJ, Mando-Vandrick J, Lee AS. 12. Creanga AA, Shapiro-Mendoza CK, Bish CL, et al. Management of first-trimester complications in the Trends in ectopic pregnancy mortality: 1980–2007. emergency department. Am J Health Syst Pharm 2013; Obstet Gynecol 2011; 117: 837–43. 70: 99–111.

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Case 1 r General: Listless but conscious and interactive toddler, with normal work of breathing and Contributing Author: Rebecca Jeanmonod normal perfusion. r HEENT: There are no signs of trauma. PERRL. History Thechildisorientedtopersonandplace.There A 3-year-old girl is brought to the ED by her mother are no oral lesions. Her mucous membranes for confusion. The child did not get up when she aremoist.Thereisnoevidenceoftongue usually does for daycare, so mom went to wake her biting. up. She noted that the child was difficult to rouse and r Neck:Neckissupple,withnoadenopathyor seemed sweaty and confused. The child had some odd masses. body jerks that were not rhythmic and not frequent, r Cardiovascular: Regular tachycardia, with no which mom describes as “spasms.” Mom attempted M/R/G. Normal capillary refill. to give the child some juice, but it dribbled out of the r Lungs: Clear bilaterally, with normal effort and child’s mouth. EMS was called, and on arrival to the good air movement. house, they checked the child’s glucose, which was r Abdomen:Soft,withnormalbowelsounds.No 34. An IV line was placed and the child was given masses. No hepatomegaly. dextrose. She is now acting “more normal” per mom, r Extremities and skin: Pale. No rashes or signs of but still “not quite herself.” The child’s IV line was trauma. dislodged during transport. r Neurologic: The child is drowsy but answers Past Medical History questions and follows commands. She has no focal deficits. Her reflexes are intact. r The child was a term neonate with no birth r Pertinent laboratory values: CBC normal. Na 138, complications. She is a small child, but has been K 5, Cl 103, bicarbonate 14, BUN 20, Cr 0.33, consistent in her growth curve between the 5th glucose 64, pH 7.25, 3+ urine ketones. and 10th percentile. She is fully immunized and r Pertinent imaging:HeadCTnegative. has met all her milestones. She is potty trained. There is no family history of diabetes or inherited metabolic diseases. Questions for Thought r What is the diﬀerential diagnosis for the Medications hypoglycemic toddler? r Multivitamins. r What labs are important to obtain in this child? r Should the IV be replaced? r Allergies If the child continues to be hypoglycemic, how r NKDA. would you manage her?

Physical Examination and Ancillary Studies r Vital signs: T 98.6 °F, HR 140, RR 42, BP 110/63, Diagnosis r O2 sat 100% on room air. Idiopathic ketotic hypoglycemia.

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Discussion metabolism may not be readily apparent, the r Epidemiology: Idiopathic ketotic hypoglycemia is provider should initiate the work-up for inborn the most common cause of hypoglycemia in errors of metabolism, including serum pH, urine children who do not have diabetes, occuring in studies for ketones, lactate, glucose testing, about 4 in 100,000 children.1 It is typically ammonia, serum ketones, and electrolytes, and diagnosed between the ages of 18 months and other tubes of blood should be drawn on 5years.2,3 presentation and held for further testing should r Pathophysiology: The exact pathophysiology the child be suspected of having an inborn error. of this disease process is incompletely There is more information on this in Chapter 7 understood. Unlike children with true inborn Case 1. When the child is hypoglycemic, with errors of metabolism, these children have intact positive blood and urine ketones and a history pathways for glycogenolysis and gluconeogenesis; inconsistent for other items on the hypoglycemia however, their gluconeogenesis may differential, a presumptive diagnosis of idiopathic 1 be inadequate because of low levels of amino acids ketotic hypoglycemia may be made. Diagnosis is used in gluconeogenesis.4,5 These children may confirmed when the child is unable to tolerate a also have limited glycogen stores (as the disease is ketogenicdietorafast. r more common in children with low birth weight Treatment:Illchildrenshouldberesuscitated, and who fall under the 50th percentile for height with careful attention to the ABC algorithm. and weight) as a contributor, or they utilize ketone Hypoglycemic children should receive 25% bodies less effectively.6 These children are usually dextrose, 2cc/kg. IV dextrose typically improves developmentally normal. As infants, children the child’s symptoms rapidly, in contrast to receive a steady source of glucose with regularly hypoglycemia from inborn errors of metabolism scheduled feeds, which precludes presentation of or intoxicants, where the child may take a long this disease. Presentation generally occurs when a period of time to return to baseline mental status. childbeginstoforgonight-timefeedsorswitches If the provider is assured that the child has to a lower carbohydrate diet. Presentation beyond idiopathic ketotic hypoglycemia, the best 5 years of age is rare. Most children with idiopathic treatment for the child is to eat a ketotic hypoglycemia will outgrow it by age 10.3 carbohydrate-rich meal. However, if the r Presentation: Children with idiopathic ketotic provider believes the child may have an inborn hypoglycemia will classically present in the error of metabolism or is unsure, the child morning after an overnight fast with altered should be made NPO to avoid ongoing mental status and hypoglycemia. Seizures are metabolism and creation of toxic substances. uncommon, but can be a presenting complaint, These children should be placed on dextrose and ketosis may lead to vomiting as well. Altered infusion at a rate that prevents catabolism, 7,8 mental status may take the form of lethargy, focal typically D10 at 1 to 1.5 maintenance. neurologic deficits, abnormal vital signs, or Long-term management of children with confusion. Children may have an infectious idiopathic ketotic hypoglycemia involves process that precipitates their symptoms, or they frequent non-ketotic meals and regular home may be otherwise well. They are classically age glucose and urine testing for hypoglycemia and 18 months to 5 years and, although most are of a ketonuria. r slender build, there are cases reported in larger Disposition: Most children with idiopathic ketotic children. Although this presentation is classic, it is hypoglycemia warrant an inpatient admission to not pathognomonic, and the ED provider should monitor their blood sugars and ascertain consider inborn errors of metabolism, definitive diagnosis. Although this condition is hyperinsulinemia, endocrine deficiencies, toxins generally benign and self-limited, with (specifically, oral hypoglycemics and alcohols), spontaneous resolution by age 10, recurrent and sepsis as part of the differential. episodes of hypoglycemia and ketonemia can lead r Diagnosis: Because the difference between this to complications such as brain abnormalities, 9 child and a child with an inborn error of lowered IQ, and seizures.

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Historical clues Physical findings Ancillary studies 9. Pollack ES, Pollack CV. Ketotic hypoglycemia: A case r r r report. JEmergMed1993; 11: 531–4. Developmentally r Lethargy r Hypoglycemia r normal Tachypnea Elevated anion Low body (signaling gap acidosis Case 2 weight acidosis) r Ketonuria r Toddler age r Negative head group CT Contributing Author: Abhishek Chaturvedi r No family members with History diabetes (i.e. no access to The patient is a 5-month-old full-term boy brought to hypoglycemic the ED for altered mental status with lethargy, fussi- agents) ness, and decreased feeding for 3 days. He has been exclusivelybreastfedsincebirthbuthasnotbeenlatch- Follow-Up ing well lately. His last bowel movement was 6 days ThechildwasmadeNPOforconcernforinborn ago despite two glycerin suppositories. According to errors. She became more lethargic, and an IV line hismother,heusuallystoolsthreetofourtimesaday. was placed for a glucose of 42. The child was given Yesterday, he had only four wet diapers compared to IVdextroseandwasstartedonadextroseinfusion. his usual eight to ten wet diapers per day. His mother She was transferred to a pediatric hospital where a denies any history of fever, vomiting, jaundice, or any full metabolic evaluation was performed, which was sick contacts except that the boy had some conges- largelyunremarkable.Shewasinthehospitalfor tion and cough 1 month back, which resolved with 10 days while adjustments were made to her diet to administration of tea prepared by a family friend. The prevent recurrent hypoglycemia. She was eventually child lives with his parents and two siblings. They have discharged home, and at 6-month follow-up was doing recently moved to a new neighborhood in California well with high carbohydrate meals every 4–6 hours. because of mom receiving a promotion at work. References Past Medical History r He is a developmentally normal, healthy term 1. Daly LP, Osterhoudt KC, Weinzimer SA. Presenting neonate who is UTD on immunizations. features of idiopathic ketotic hypoglycemia. JEmerg Med 2003; 25: 39–43. Medications 2. Soyka LF, Glass AG, Halldorsson TS. Ketotic r 400 international units of liquid vitamin D daily. hypoglycemia, an important cause of seizures. Clin Pediatr 1967; 6: 368–72. Allergies 3. Denmark TK. Inborn errors of metabolism. In r NKDA. Pediatric Emergency Medicine,BarenJ,ed. Philadelphia, PA: Saunders, 2008, pp. 273–6. Physical Examination and Ancillary Studies r 4. Pagliara AS, Kari IE, De Vivo DC, et al. Vital signs: T 99.1 °F, HR 155, RR 24, BP 80/50, O2 Hypoalaninemia: A concomitant of ketotic sat 92% on room air. hypoglycemia. JClinInvest1972; 51: 1440–9. r General: Awake but lethargic, poorly responsive, 5. Haymond MW, Karl IE, Pagliara AS. Ketotic overall well-nourished and well-developed. hypoglycemia: An amino acid substrate limited r HEENT: PERRL but sluggish, intact red reflex. disorder. J Clin Endocrinol Metab 1974; 38: 521–30. Normocephalic, atraumatic, with flat scalp veins 6. Huidekoper HH, Duran M, Turkenburg M, et al. and sunken fontanelle. Mucous membranes tacky. Fasting adaption in idiopathic ketotic hypoglycemia: r Amismatch.Eur J Pediatr 2008; 167: 859–65. Neck: Supple, with midline trachea and no adenopathy. 7. Fletcher JM. Metabolic emergencies and the r emergency physician. JPaediatrChildHealth2016; 52: Cardiovascular: Slightly tachycardic, with regular 227–30. rhythm. No M/R/G. r Lungs:CTAbilaterally,withnoW/R/R. 8. Long D, Long B, Koyfman A. Inborn errors of r metabolism: An emergency medicine approach. Am J Abdomen: Soft, non-tender, non-distended, with Emerg Med 2016; 34: 317–18. no organomegaly. Bowel sounds are decreased.

16:18:54 203 10 Chapter 9: Altered Mental Status r Extremities and skin: Extremities are flaccid and in contracting botulism, presumably because of extension, with no localizing signs. No rash, higher exposure to dust particles containing trauma, or edema noted. clostridium spores.2,4 Breastfeeding as a risk r Neurologic: Markedly decreased tone throughout, factor is controversial. Some studies show that it with minimal withdrawal to pain. Pupils are increases risk, whereas others suggest it may sluggish. The baby does not track and has a weak protect from rapidly progressive disease.2 suck,withlackofheadcontrol.Deeptendon Formula-fed infants tend to develop botulism at reflexes are 1+. earlier ages and may have a more fulminant r Pertinent laboratory values:CBC,comprehensive presentation.2 metabolicpanel,CRP,ABG,andCSFanalysisare Ingestionofcontaminatedhoneyhasbeen all normal. The child’s U/A is only remarkable for implicated in a number of cases of infant a specific gravity of 1.030. botulism. Microbiologic surveys of honey r Pertinent imaging:HeadCTisnormal.An products have reported the presence of abdominal radiograph was obtained due to his Clostridium botulinum spores in up to 25 percent constipation; however, there was no significant of products; however, it is worth noting that in stool burden appreciated. 85 percent of diagnosed cases, a definitive source of C. botulinum spores is never identified.2,4 Corn syrup was previously found to contain C. Questions for Thought botulinum spores, but no cases of infant botulism r What are the next important resuscitative to date have been definitively attributed to treatments to be undertaken for this infant? contaminated corn syrup. Nonetheless, the AAP r What is appropriate further testing? r continues to recommend against feeding What are the conditions that can have similar unpasteurizedcornsyrupandhoneytoinfants presentations? younger than 12 months of age. Constipation has r Why is it important to not delay the administration of the drug for a conﬁrmed been shown to represent an independent risk diagnosis? factor for botulism in infants older than 2 months r What is the most feared complication of this of age. This is presumably because decreased condition? colonic motility allows C. botulinum spores further time to germinate in the GI tract and produce toxins. There are multiple other recognized clinical Diagnosis forms of botulism, including wound botulism, in r Infant botulism. which wounds become contaminated with C. botulinum spores; and foodborne botulism, in Discussion which the preformed toxin is ingested from r Epidemiology:About70casesofinfantbotulism contaminated food sources. r are reported annually in the USA, although the Pathophysiology: C. botulinum is a sporulating, true incidence is likely higher due to obligate anaerobic, Gram-positive bacillus, under-recognition of the disease.1,2 Throughout present in soil and aquatic sediment. The bacteria theworld,mostcasesarereportedintheUSA, generate spores that can survive extreme weather likely due to under-reporting.2,3 Geographically, and temperature conditions. Unlike the toxin, the prevalence of infant botulism in the USA is which is heat-labile, the spores are relatively highest in California, Utah, and the eastern heat-resistant. Temperatures of 248 °Fmaybe Pennsylvania–New Jersey–Delaware area.2 required to kill the spores, although heating at 185 Up to 95 percent of infant botulism cases °F inactivates the toxin. Infant botulism occurs occurinchildrenyoungerthan6monthsofage.2 when the clostridial spores of C. botulinum are Young children are thought to be at increased risk inhaled, caught in saliva, and swallowed. The due to immaturity of their gut flora. Infants living cecum is thought to be the initial site of activity in rural/farm environments and around active and paralysis of the ileocecal valve might allow construction sites appear to be at higher risk for the colonizing bacteria to extend into the terminal

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ileum. In the large intestine, the spores then syndrome, sepsis, and inborn errors of germinate and multiply (with an incubation metabolism. Children with infant botulism are period of 3–30 days), allowing the release of classically afebrile and of normal mental status botulinum neurotoxin into the bloodstream. withmotorweakness,butmayhavealtered Botulinum neurotoxin then irreversibly binds mental status secondary to dehydration from cholinergic receptors in the presynaptic cell feeding difficulties, which may make their membrane of voluntary motor and autonomic diagnosis more challenging. neuromuscular junctions, preventing IntheED,diagnosisisclinical,andtreatment acetylcholine release. This creates the vast array of should not be withheld pending definitive symptoms with which these infants may present. diagnosis. Definitive diagnosis is made by More than 70 percent of the neuromuscular detection of botulinum toxin in the stool.2 junctions have to be impaired before impairment Following the initial exposure, the toxin may of voluntary muscles and autonomic function continue to be present in the stool for up to becomes evident, and when 90 percent are several months. Toxin is less commonly found in involved, diaphragmatic function becomes serum than in the stool and has been detected in impaired, leading to respiratory failure.2,4 only 1 percent of US infants with botulism. r Presentation: Clinically, botulism infection can On initial presentation, basic serum studies in cause a wide spectrum of presentations in infants, the infant with botulism will typically be normal, ranging from mild hypotonia to a combination of or they may demonstrate mild perturbations bilateral cranial nerve palsies, flaccid paralysis, relatedtodehydration.CSFmayshowmildly and diaphragmatic weakness necessitating elevated protein, again related to dehydration. mechanical ventilation.2,4 Typically, the first These studies are generally only helpful to rule out symptom noted in infant botulism is constipation other conditions. MRI and EEG are generally not (characterizedby3ormoredayswithout indicated, but if obtained, they will usually be defecation),whichisthenfollowedbysome unremarkable. combination of lethargy, decreased spontaneous Nerve conduction studies and activity, and diminished appetite.2,4 Infants then electromyography can be used to help confirm the go on to experience loss of head control secondary botulism diagnosis but are not used in the ED. to neck muscle weakness, typically followed by r Treatment: Supportive care, in particular, symmetric descending hypotonia and weakness, monitoring of respiratory function and ultimately progressing to involve the appropriate use of endotracheal intubation (for diaphragmatic muscles. Approximately half of airway protection and for mechanical ventilation) patients will require mechanical ventilation at are important. Non-intubated patients should be some point during their hospital course. positioned with the head of the bed elevated to Symmetric cranial nerve palsies (ptosis, sluggishly 30° above the level of the feet to minimize risks of reactive pupils, diminished gag reflex, bifacial aspiration. Fluid resuscitation is often necessary. weakness, poor suck, and difficulty swallowing) Aminoglycosides should be avoided because their are often particularly notable. Muscle stretch use can lyse bacteria, releasing additional reflexes are typically preserved. In advanced intracellular toxin into the infant gut. illness, autonomic disturbances may be present, IV botulism immunoglobulin was approved such as decreased heart-rate variability, dilated by the US Food and Drug Administration in 2003 and fixed pupils, xerostomia, intestinal ileus, and and should be given to all infants with suspected urinary retention. botulism prior to confirmatory testing.5 The r Diagnosis: The differential diagnosis for the floppy half-life of botulism immunoglobulin is about infant is broad. The neurologic presentation 28 days. It has been shown to reduce the hospital should prompt consideration of myasthenia length of stay from a mean of 5.7 weeks to 2.6 gravis, Guillain–Barre´ syndrome, tick paralysis, weeks.2,5 In addition, duration of intensive care, intracranial mass lesions, cerebrovascular mechanical ventilation, and tube or IV feeding are accident, toxins, and encephalitis. The clinician all significantly reduced in patients treated with should also consider abuse/shaken baby botulism immunoglobulin.5

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Gastric decontamination has historically been 4. Rosow LK, Strober JB. Infant botulism: Review and recommended to remove unabsorbed toxin from clinical update. Pediatr Neurol 2015; 52: 487–92. thebaby’sGItract,buthasnotbeenshownto 5. ChalkCH,BensteadTJ,KeezerM.Medicaltreatment shorten illness duration. If cathartic agents are for botulism. Cochrane Database Syst Rev 2014; 2: used, sorbitol is preferable to magnesium salts CD008123. because the latter may exacerbate neuromuscular blockade. Whole bowel irrigation with polyethylene glycol may have a theoretical role in Case 3 decontamination and it could be evaluated in severe poisoning. However, these procedures may Contributing Author: Denis R. Pauze´ be difficult and their efficacy may be reduced in History the presence of constipation/toxin-induced ileus. A 3-month-old boy is brought into the ED for persis- In some cases, neostigmine, which inhibits the tent crying, fussiness, and poor weight. He was seen enzymatic degradation of acetylcholine, appears twice in the ED over the past 2 weeks for similar com- to be useful in reversing ileus. plaints and both times diagnosed with colic. His PCP Antibiotics to eradicate the infection are saw him yesterday and told the parents it is colic and contraindicated, as they may cause an increased “he will get better soon and grow out of it.” The parents release of botulinum toxin.2 r brought the infant in again because he is now persis- Disposition: All children with suspected infant tently crying. botulism should be admitted to a monitored The parents state that he always cries with feeds and setting with access to critical care services. has not gained weight in the past several weeks. The parents state the infant is “sweaty” and is much more Historical clues Physical findings Ancillary studies r r r irritable, especially with feeds. He has no fevers, bil- Refusal to feed Hypotonia Normal ious vomiting, cough, or rash. He has good tone and is r Altered mental r Bilateral ptosis laboratory tests r r “always hungry” but isn’t feeding. r status Decreased bowel r Normal imaging r Constipation r sounds Clinical Exposure to Decreased dehydration Past Medical History high-risk area reflexes r Full term, normal spontaneous vaginal delivery, no prenatal complications. Follow-Up Medications The stool sample collected was positive for C. r botulinum toxin. The baby was transferred to the Acetaminophen. PICU. He did not require intubation, but was on R Allergies enteral tube feeds. He received BabyBIG and phys- r ical therapy was consulted for strength and range of NKDA. motion exercises. He began taking all of his feeds Physical Examination and Ancillary Studies orally and made a gradual but full recovery. He was r ° discharged home from the hospital on hospital day 14. Vital signs: T 100.2 F, HR 140, RR 40, BP 90/48, O2 sat 96% on room air. References r General: Non-toxic in appearance and in no acute distress. He is not crying. 1. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in r the United States: A clinical and epidemiological HEENT: Circumference at 50 percent; no scalp review. AnnInternMed1998; 129: 221–8. hematoma or facial bruising. Corneas appear normal. PERRL. Mucous membranes moist. 2. CoxN,HinkleR.Infantbotulism.Am Fam Phys 2002; r 65: 1388–93. Neck: Normal range of motion. No masses or adenopathy. 3. Koepke R, Sobel J, Arnon SS. Global occurrence of r infant botulism, 1976–2006. Pediatrics 2008; 122: Cardiovascular: Normal S1, S2. +S3. No e73–82. murmurs.Strongandnormaldistalpulses.

16:18:54 10 Chapter 9: Altered Mental Status r Lungs: Clear bilaterally, with good air movement. needs a very careful, detailed, and thorough No accessory muscle use. evaluation. Although the vast majority of true r Abdomen: Soft and non-distended. No masses. No colic is caused by benign or unknown factors, it is hernia. No splenomegaly. Liver feels mildly important to note the more critical diagnoses that enlarged. cannot be missed. Some potential causes of r Genitourinary: Circumcised penis. Testicles worrisome crying in the infant include descended. No masses or erythema. non-accidental trauma, (abusive head trauma and r Extremities and skin: No rashes. No signs of fractures), meningitis, corneal abrasion, hair trauma. Warm and well-perfused. tourniquets, incarcerated hernias, and testicular 4,5 r Neurologic: Intact reflexes, symmetric motor torsion. Cardiac issues such as supraventricular examination, social smile present. tachycardia or congenital heart anomalies must r also be considered.6 Pertinent laboratory values: WBC 23,000, Hb 12, r Plt normal. Na 129, K 3.3, Cl 88, bicarbonate 31. Pathophysiology: There is no known etiology for BUN and Cr normal. colic. Multiple hypotheses have been postulated, r Pertinent imaging: CXR reveals cardiomegaly. including GI issues such as feeding difficulties, milk or lactose intolerance, and intestinal flora Questions for Thought abnormalities. Some have hypothesized that colic is caused by increased serotonin release while r What is the diﬀerential diagnosis for the colicky others have suggested an infantile migraine as the baby? 7 r How is colic deﬁned? How is it diagnosed? cause for normal baby crying. Others have r Is it common for colicky babies to fail to gain or to postulated maternal smoking and family stress as lose weight? acause. r Presentation: Excessive and persistent crying is virtually always the chief complaint in true colic. Diagnosis Infants are usually brought in when the crying is r Anomalous left coronary artery with take-off persistent and the parents “don’t know what to do” from the pulmonary artery. and are at “their wits end.” Remember, excessive infant crying is very distressing to the parent. r Diagnosis: In general, the cause of crying is often Discussion r found in the history and physical examination. Epidemiology:“DuringthesecondcenturyBC,the Colic is really a diagnosis of exclusion. The Greek physician Galen prescribed opium to calm cardinal rule for not missing a critical cause of fussy babies, and during the Middle Ages in “crying or colic” involves a thorough, complete Europe, mothers and wet nurses smeared their history and a detailed “head-to-toe” physical nipples with opium lotions before each feeding. examination. 1 Alcohol was also commonly given to infants.” The history can give specific crucial clues for Colic is a common presentation for many primary diagnosis. The EM provider should determine the care offices and EDs. The exact prevalence is following: What is the pattern of crying, and how unknown because there are different definitions of long has it been going on? Does it only happen colicandnotallparentsreportorseetheirPCP during certain periods of the day? Have there for colic. Colic has many potential definitions, been any fevers, trauma, or (bilious) vomiting? with a common criteria (Wessel’s rule of 3s) being Are there any new medications or herbal an infant that cries for Ͼ 3hoursperday,Ͼ 3days supplement exposures? Has there been adequate per week, in an infant 3 months of age or weight gain? Any diaphoresis or cyanosis or 2,3 younger. Crying in infants is common, with the fatigue with feeds? For instance, a baby with 2 average infant crying 1–2 hours per day. This can weeks of crying at night time is much different be very distressing to parents. Cases of true colic than an infant with a corneal abrasion, who has are benign and self-limited. However, for the ED cried non-stop for the past 8 hours. A child with provider, a baby brought in for “persistent crying” inadequate weight gain or other symptoms such

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as vomiting should not be diagnosed with colic; r Disposition: Disposition depends upon the there is something else going on and a broader diagnosis. Infants with true colic can be work-up should be pursued. discharged home with close follow-up if their r Physical examination should be thorough and guardians are reliable and are coping well with the systematic. crying. r Vital signs canoftenhelpnarrowdownthe diagnosis. A febrile infant could harbor Historical clues Physical findings Ancillary studies r r r meningitis or infection as a cause for crying. Multiple visits Abnormal vital Labs A tachycardic infant may have supraventricular for same signs demonstrating complaint r Abnormal cardiac dehydration tachycardia. Infants with unequal distal blood r r Sweating with r examination CXR with pressures may have a coarctation of the aorta. r feeds Abnormal cardiomegaly r Failure to gain abdominal Head: Is the head circumference large? Are weight examination there any signs of head trauma? Does this infant have any bruises? These are concerning for non-accidental trauma. Follow-Up r Eyes: Is there any evidence of corneal abrasion Our patient had historical red flags, including numer- or infantile glaucoma? ousvisitsforthesamecomplaint,sweatingwithfeeds, r Cardiovascular:Anysignsofheartfailure? and failure to gain weight. He had an examination Unequal distal pulses? S3 gallop? which was remarkable for abnormal vital signs, abnor- r Abdomen: Any evidence of masses, mal cardiac examination, and hepatomegaly. These incarcerated hernia, or hepatomegaly? Is the findings led the EM provider to check laboratory tests abdomen distended? and CXR, both of which were abnormal. Because of r Genitourinary: Is there a bad diaper rash? Anal this, the provider performed an EKG, which revealed fissure? Phimosis or paraphimosis? Evidence of large Q waves in the anterior and lateral leads. Pedi- testicular torsion? Distended bladder? atric cardiology was consulted and an echocardiogram r Skin: Any rashes or vesicles? Any bruises that was performed. The patient was diagnosed with an could signify non-accidental trauma? Any hair anomalous left coronary artery with take-off from the tourniquets? pulmonary artery. This coronary artery anomaly in r Treatment: Treatment varies depending upon infants can cause pain (especially with “stress testing” what is uncovered in the history and physical such as feeding), myocardial infarction, and heart fail- examination. When no acute pathology is ure. The patient was admitted to the PICU and had suc- discovered, different interventions can be cessful corrective surgery the next day. discussed with the caregivers. Parents can try soothing techniques, such as pacifier use, using an References infant swing, car ride, or noise machines. 1. From Wikipedia. Their referenced source: Solter A. Once a thorough history and physical Tears and Tantrums: What to Do When Babies and examination has been performed, it is important Children Cry. Goleta, CA: Shining Star Press, 1998. to assess the parent/guardian. Persistent crying is 2. Harb T, Matsuyama M, David M, Hill RJ. Infant a risk factor for and may lead to non-accidental colic – what works: A systemic review of interventions trauma. Parents should understand that in most for breast-fed infants. J Pediatr Gastroenterol Nutr cases, crying in an infant is normal and will 2016; 62: 668–86. resolve. Providers should emphasize to the 3. Hall B, Chesters J, Robinson A. Infantile colic: A caregiverthattheyarenotdoinganythingwrong systematic review of medical and conventional to cause the crying. Additionally, parents/ therapies. JPaediatrChildHealth2012; 48: 128–37. caregiver may need a break from a crying child, 4. JennyC,HymelKP,RitzenA,etal.Analysisofmissed and it is okay for them to “walk away” from a cases of abusive head trauma. JAMA 1999; 281: 621–6. screaming infant. Additional resources can be 5. Sugar NF, Taylor JA, Feldman KW. Bruises in infants found at National Center on Shaken Baby and toddlers: Those who don’t cruise rarely bruise. Syndrome (www.dontshake.org). Arch Pediatr Adolesc Med 1999; 153: 399–403.

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6. Lardhi AA. Anomalous origin of left coronary artery child has otherwise been meeting her milestones, from pulmonary artery: A rare cause of myocardial andisabletositsupported.Sheisimmunized. infarction in children. J Family Community Med 2010; 17: 113–16. Medications 7. Qubty W, Gelfand AA. The link between infantile r Metoclopramide. colic and migraine. Curr Pain Headache Rep 2016; 20: 31. Allergies r None. Case 4 Physical Examination and Ancillary Studies r ° Contributing Author: Rebecca Jeanmonod Vital signs:T97 F, HR 175, RR 70, BP 75/42, O2 sat 96% on 2 L nasal cannula. History r General: The child is conscious and purposeful, A 5-month-old girl with history of failure to thrive is pushing at nasal cannula. She is ashen. brought to the ED for “not acting right.” Her parents r HEENT:Therearenosignsofheadtrauma.The report that she has been “lethargic” and “angry,” child’s anterior fontanelle is open and sunken. beginning 4 days ago and getting worse every day. The PERRL. Her mucous membranes are dry. child has been irritable and difficult to console. She has r Neck: Supple and non-tender, with no adenopathy. not had restful sleep, although she seems unusually r Cardiovascular: Regular tachycardia, with no sedate to them. She has seemed uncomfortable and M/R/G. Capillary refill 4 seconds. fussy when receiving feeds through her G-tube and r Lungs: Tachypneic and shallow, but clear has had high residuals. They have therefore reduced bilaterally with no adventitial sounds. the volume of her feeds and spaced their intervals. r She has been having decreased PO, as well. She was Abdomen: Soft and scaphoid, non-tender/ hospitalized about 2 weeks ago for fever and was in non-distended. G-tube in place with no the hospital for 5 days, during which time she was surrounding erythema or drainage. No organomegaly. treated for dehydration and discharged home with r resumption of her normal schedule. The child has Extremities and skin: Ashen and mottled with no signs of trauma. not had fever since then. She has not been vomiting, r and there has been no diarrhea. Her parents report Neurologic: The child is purposeful at times, at other times she is listless. Not interactive. that she is making very few wet diapers, and that they r “smell bad.” There has been no coughing or difficulty Pertinent laboratory values: Fingerstick glucose breathing. The parents are most concerned about 142. the G-tube not functioning well, and are requesting surgery be called to evaluate the G-tube. Questions for Thought r What are the appropriate initial steps to take to Past Medical History stabilize this child? r r Babywasbornat34weeksforprematurerupture What historical information should be elicited to make this diagnosis? of membranes. She spent 2 weeks in the hospital r for feeding difficulties, and went home on If you are unable to obtain IV access in this child, nasogastric feeds. She had a percutaneous G-tube what are other options for initiating treatment? placed about 3 months ago for ongoing feeding issues and failure to thrive. The family has tried many different formulations of nutrition and have Diagnosis been seen by a nutritionist as recently as her last r Hypernatremic dehydration from receiving hospitalization. The child has, over the last 6 concentrated feedings. weeks, been feeding somewhat regularly on her own, but still receives regular tube feeds. She has Discussion had a metabolic work-up, which has revealed no r Epidemiology: Dehydration is a common problem underlying source of her failure to thrive. The in the pediatric population, with annual

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admissions of 200,000 in the USA for dehydration parents may use a standard spoon rather than the relatedtogastroenteritisalone.1 Worldwide, appropriate commercial scoop, thus unwittingly diarrheal diseases affect 2 billion people each year, altering the electrolyte and carbohydrate killing about 1.5 million children.2 The specific concentration in the child’s food. The diagnosis of contribution of formula preparation mistakes to dehydration is clinical, and the most accurate and dehydration burden in children is unknown, but reproducible finding in dehydration is reduction errors during reconstitution of formula are of body weight.1 Unfortunately, the EM provider common, with overconcentration being the more may not have access to the child’s prior weights, frequent error.3 In the USA, 77 percent of women and scales may not be appropriately calibrated. breastfeed their infants, but this proportion falls Without knowing the child’s weight changes, the to under 50 percent by 6 months.4 most accurate physical signs for dehydration are r Pathophysiology: Children are at increased risk for decreased capillary refill, abnormal skin turgor, dehydration due to their relatively large body and abnormal respirations.6 The diagnosis of surface areas, resulting in increased evaporative hypernatremia is made on laboratory chemistry losses from skin, increased respiratory rate with studies, but may be suspected in irritable infants losses due to exhalation of hydrated air, and in whom a history of inappropriately prepared frequent illnesses which cause increased sensible feeds is elicited. (diarrhea and vomiting) and insensible losses r Treatment:Indehydratedinfants,theappropriate (tachypnea, fever, sweating). Hypernatremic therapyisaweight-basedbolusofisotonic dehydration in infants is most commonly crystalloid fluid at 20 cc/kg. For maintenance secondary to diarrheal disease, but receiving fluid, studies demonstrate that isotonic (and not hyperconcentrated feeds is another cause.5 The the traditional hypotonic) crystalloid with infant kidney is not able to excrete large sodium dextrose is the preferred fluid in both general loads, nor is it able to dilute as well as the adult pediatric patients and in the PICU.7,8 If IV access kidney. Therefore, hypernatremia may be is unable to be obtained, IO access (or umbilical secondary to relative water depletion, water access) is acceptable.9 In children with moderate depletion in excess of sodium depletion, or to severe dehydration with a working gut (without sodium excess with normal volume status. In intractable vomiting), nasogastric resuscitation is ambulatory pediatric and adult patients with as successful as IV.9 Therefore, it is not access to water, thirst usually prevents significant unreasonable to resuscitate a child through a hypernatremia; however, in small children and nasogastric tube, or in this case, a G-tube, when bedbound individuals, hypernatremia can be a IV access is not available. Hypernatremia should significant problem. be corrected slowly, no quicker than r Presentation: Children with dehydration may 0.5 mEq/hour, as more rapid correction may appear listless, with dry mucous membranes and result in cerebral edema and further decreased tear formation. Children with complications. hypernatremia, regardless of volume status, often r Disposition: Sick children should be resuscitated have irritability and altered mental status. according to the ABC algorithm. Most children Children will often present with symptoms with mild dehydration can be discharged home fromtheunderlyingsourceofdehydration, with instructions for oral hydration with such as fever, diarrhea, or respiratory appropriate fluids (NOT sports drinks with high illnesses. sugar contents) and close follow-up and return r Diagnosis: History is often not helpful in making precautions. Children with moderate or severe the diagnosis of dehydration, although it may give dehydration with unreliable follow-up, who important clues to underlying pathology, such as a cannot take oral fluids, should be admitted for IV history of recent diarrheal illness. It is important fluid therapy. Hypernatremic infants should be to obtain a full feeding history, including how the admitted for sodium correction and further caregiver mixes the formula, as this may be the evaluation to determine the underlying cause of only clue to the true diagnosis. Different scoops hypernatremia (such as adrenal or renal disease), from different brands of formula vary in size, and if the source is unclear.

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Historical clues Physical findings Ancillary studies intravenous fluid therapy in children: A systematic r r r review. Pediatr Nephrol 2015; 30: 1163–72. Reduced tube r Mottled skin Normal glucose r feeds Abnormal vital 8. Almeida HI, Mascarenhas MI, Loureiro HC, et al. The r Decreased PO r signs effect of NaCl 0.9% and NaCl 0.45% on sodium Reduced wet r Poor capillary refill chloride, and acid–base balance in a PICU population. diapers Sunken fontanelle J Pediatr (Rio J) 2015; 91: 499–505. 9. RouhaniS,MeloneyL,AhnR,etal.Alternative Follow-Up rehydration methods: A systematic review and lessons EDnursingwasinitiallyunabletoobtainanIV,sothe for resource-limited care. Pediatrics 2011; 127: PICU nursing team was called. During the 90 min- e748–57. utes it took to obtain IV access, the child suffered cardiac arrest. Her initial laboratory chemistries dur- Case 5 ing her code demonstrated the following: Na 165, K 7.3, Cl 118, bicarbonate 22. The child received full Contributing Authors: Tom Williams, Emily ACLS protocol, IV fluid bolus, and treatment of hyper- kalemia with calcium, insulin, and glucose. She had Miller, and Denis R. Pauze´ return of spontaneous circulation after 17 minutes of History cardiac arrest. After review of the family’s discharge A 9-day-old is brought into the ED by his parents for instructions and notes from the child’s prior admis- “not acting like himself.” He was born full term, with- sion, it became clear that there had been miscommuni- out complications, and was discharged home. The pre- cation between the parents and the nutritionist regard- vious week at home had been completely uneventful. ing feeding preparation, and that this error had likely Tonight, he started making funny noises and looked been responsible for her prior admission, as well. She gray and pale to them. They tried to suction his nose, wasadmittedtothePICUforaprolongedperiodand but he seemed limp and they did not like his breathing, was ultimately discharged to a rehabilitation facility so they brought him immediately to the ED. On arrival with spastic quadraparesis secondary to anoxic brain to the ED, the parents are screaming “my baby looks injury and hypernatremia. gray!” The child is immediately brought into a room where he is noted to be obviously mottled with grunt- References ing respirations. He is ashen-gray in appearance. As 1. Canavan A, Arant BS. Diagnosis and management of the baby is placed on the monitor and nursing works dehydration in children. Am Fam Phys 2009; 80: on IV access, you immediately start resuscitating the 692–6. child. Your medical student asks the parents a few 2. Diarrhoeal Disease Fact Sheet. Geneva: World Health quick questions. You establish that there have been no Organization, 2009. known fevers or vomiting episodes and that the child 3. Renfrew MJ, Ansell P, Macleod KL. Formula feed was eating normally up until tonight. preparation: helping reduce the risks; a systematic review. Arch Dis Child 2003; 88: 855–8. Past Medical History 4. National Center for Chronic Disease Prevention and r Born at 39 weeks, normal vaginal delivery. Normal Health Promotion, Division of Nutrition, Physical prenatal screening. No birth complications. Activity, and Obesity. Breastfeeding Report Card Discharged from the hospital on day 2. United States/2013. See www.cdc.gov/breastfeeding/ pdf/2013breastfeedingreportcard.pdf (accessed Medications October 2016). r 5. Leung C, Chang W-C, Yeh S-J. Hypernatremic None. dehydration due to concentrated infant formula: Report of two cases. Pediatr Neonatol 2009; 50: Allergies 70–3. r None. 6. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA 2004; 291: 2746–54. Physical Examination and Ancillary Studies r 7. Padua AP, Macaraya JRG, Dans LF, et al. Isotonic Vital signs:T99°F, HR 170, RR 70 and labored, versus hypotonic saline solution for maintenance BP in the right arm 70 systolic, unable to obtain

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lower extremity BP, O2 sat 92% in right arm, 79% diagnose congenital heart defects in the prenatal in left arm. period, less than 50 percent of coarctations are r General: He appears mottled and ashen-gray. He diagnosed before birth.5 has grunting respirations. r Pathophysiology:Inutero,thefetushasaunique r HEENT:Therearenosignsofheadtrauma. circulation that differs in several important ways Fontanelle soft. Sclera normal. from that of the infant. Oxygenated blood from r Neck:Tracheamidline. the placenta travels to the fetal heart via the r Cardiovascular: Tachycardic. Unable to palpate umbilical veins and right atrium. A large femoral pulses. proportion of this oxygenated blood is shunted r Lungs: Accessory muscle use and obvious distress. directly to the left atrium through the foramen Bilateral rhonchi. ovale, allowing oxygenated blood to flow to the r Abdomen: Soft and non-distended. No masses. No body’s tissues. Some of the blood from the right appreciable hepatomegaly. atrium enters the right ventricle and is pumped into the pulmonary artery. As the lungs are not r Extremities and skin: Mottled. No rash or vesicles. ventilated in utero, blood flow to the pulmonary There is delayed capillary refill. circuit is largely unnecessary. Pulmonary blood is r Neurologic:Listless. shunted from the pulmonary artery to the aorta r Pertinent laboratory values: WBC 14,000, Cr 1.1, via the ductus arteriosus. At birth, the pulmonary bicarbonate 14, Na 130, urine and blood culture circuit opens up as the foramen ovale and ductus sent. r arteriosus begin to close. The pressure difference Pertinent imaging: CXR reveals early pulmonary between the left and right atrium should snap edema. There is no obvious cardiomegaly, the foramen ovale shut within the first few pneumonia, or rib fractures. breaths, while ductus arteriosus closure is more gradual. Questions for Thought As mentioned, the ductus arteriosus connects the pulmonary artery and the aorta. Some r What is the diﬀerential diagnosis for the neonate in shock? patients with congenital heart lesions are r What medications should be started, even dependent upon an open and functioning ductus without a deﬁnitive diagnosis? arteriosus in order to survive. These lesions are r What are your management priorities? called ductal dependent lesions and come in two general categories: ductal dependent pulmonary blood flow lesions (right-sided obstructive lesions) and left-sided obstructive lesions. Diagnosis r Ductal dependent pulmonary blood flow Critical ductal dependent coarctation of the lesions compromise right-sided blood flow to the aorta. pulmonary circuit. These lesions rely on retrograde flow through the ductus arteriosus Discussion from the aorta to supply blood to the pulmonary r Epidemiology: Congenital heart defects occur at a artery. These lesions can be seen in anatomic rate of somewhere near 8 in every 1,000 live variants such as pulmonary atresia, critical births, depending on the specific definition of pulmonary stenosis, and Tetralogy of Fallot with congenital heart disease (CHD).1–4 About 1 in pulmonary atresia. 1,000 of patients with CHD will be discharged Left-sided obstructive lesions include home with a critical obstructive left heart anatomic lesions that impede flow of blood process.1,2 Coarctation of the aorta occurs at a through the aorta and to the peripheral rate of roughly 4 in 10,000 live births and circulation. These patients become dependent on accounts for approximately 5–8 percent of all the patent ductus arteriosus to bypass the congenital heart defects.5 Of these, approximately obstruction and supplement the systemic 60 percent are male. While advances in prenatal circulation. Examples include hypoplastic left screening and U/S are enhancing our ability to heart syndrome, critical coarctation of the aorta,

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critical aortic stenosis, and interrupted aortic While there are findings on physical examination arch. that can strongly suggest a ductal dependent For our patient with a critical coarctation of lesion, the spectrum of ductal dependent systemic the aorta, once the ductus arteriosus closes, blood blood flow and ductal dependent pulmonary can no longer bypass this severe obstruction. This blood flow lesions is variable and not all findings increases the left ventricle afterload, thus causing may be present.1–4 However, a focused physical a decrease in the left ventricle ejection fraction. As examination can uncover findings that should cardiac output diminishes, manifestations of poor alert the examiner to the presence of a cardiac perfusion can be seen as infants develop signs and anomaly. On cardiovascular examination, one symptoms of shock, including mottled skin, cool may palpate a hyperactive precordium, auscultate extremities, decreased urine output, and central a systolic heart murmur, or find a single S2 or the cyanosis.6,7 presence of an S3. When palpating central and r Presentation: Ductal dependent lesions typically peripheral pulses, a critical ductal dependent share common aspects of history and systemic blood flow lesion will produce weakened, presentation. The degree of clinical distress or even absent, pulses in the lower extremities. depends a great deal on the severity of the However, a ductal dependent pulmonary blood underlying lesion. For instance, the clinical flow lesion has no impediment to systemic flow presentation of coarctation depends on the degree andthuswillhaveintactperipheralpulses. of stenosis. Ductal dependent lesions may present Generally, however, these children are cyanotic. anywhere along the spectrum of illness from Use your vital signs! A key finding in non-specific and mild symptoms to frank heart diagnosing coarctation is a difference in oxygen failure.1,6–8 Neonates may present with poor saturation between the right upper extremity and feeding and fussiness, or may be seen with more the lower extremities. With the ductal dependent drastic symptoms such as irritability, tachypnea, systemic blood flow lesion in coarctation, the or cyanosis.1,6,7 In the extreme, they may present preductal flow will produce a normal oxygen with hypotension, mottled skin, frank shock, or saturation in the right upper extremity while cardiac arrest.1,6–8 About 40 percent of patients post-ductal flow, which is supplemented with with coarctation are symptomatic within the first deoxygenated blood, will produce a reduced 2 days of life. Therefore, the majority will present oxygen saturation level in the lower extremities. outside of the hospital in offices or EDs. Others Four-extremity pulse oximetry has become a may present later in life, with claudication, life-saving neonatal screening that should happen headaches, and hypertension. It should be noted in all well-baby nurseries.2 Pre- and post-ductal that coarctations can present at any age. oxygen saturation and BP gradients are Neonatal cardiogenic shock may easily be non-invasive and incredibly informative. confused for septic shock.8 In the extreme, it can A CXR is always indicated if you suspect be incredibly difficult to tell these two etiologies cardiac or pulmonary disease. In the case of apart. Additionally, some infections may cardiac defects, CXR can reveal helpful clues. exacerbate a cardiac lesion. Therefore, all infants Increased vascular markings can indicate less than 2 weeks old with shock should be pulmonary congestion and heart failure while the considered to have a ductal dependent congenital cardiac silhouette may show classic findings such heart lesion and be treated with prostaglandin E1 as cardiomegaly or the “boot shape” of Tetralogy (PGE1) until a confirmatory echocardiogram can of Fallot (very rare). While not always present, be performed by pediatric cardiology.1,7 These there are some X-ray findings that may be seen infants should also undergo full septic evaluation with coarctation. The “3” sign of coarctation is and be treated with broad-spectrum antibacterial formed by the pre-stenotic aortic dilation, agents as well as antivirals. followed by the indentation of the stenotic lesion, r Diagnosis: The diagnosis of a ductal dependent followed by the post-stenotic aortic dilation. lesion is suggested by history, physical Notching of the inferior rib margins may be seen examination, and clinical suspicion. Confirmation as collateral intercostal vessels enlarge to help is made by imaging, typically an echocardiogram. supply the post-ductal portion of the aorta,

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eroding the associated rib margins as they grow and CHD. These infants should expediently be (this isn’t seen in infants, only older patients who given antibiotics (ampicillin–gentamycin or have had time to develop collaterals). In reality, ampicillin–cefotaxime as well as acyclovir). PGE1 the clinician should focus on looking for treatment should be started immediately to open pulmonary congestion or cardiomegaly because and maintain the ductus arteriosus and must not these are likely the only abnormalities on CXR. be delayed for a definitive diagnosis. The dose Additionally, cyanotic CHD should be considered used to open the duct is 0.05–0.1 mcg/kg per if there is persistent hypoxia but the lungs are minute while the dose to maintain an open duct is clear. CHD is discussed further in Chapter 3, 0.01 mcg/kg per minute. The response to Case 7. treatment should be swift and is measured by EKG may also be useful in suspected CHD. improvement of femoral pulses in the case of Evidence of ventricular hypertrophy or hypoplasia ductal dependent systemic blood flow lesions and or conduction abnormalities may give clues to improvement of cyanosis in ductal dependent underlying pathology. pulmonary blood flow lesions. Potential side The definitive diagnosis of cardiac defects is effects of PGE1 include respiratory depression, made by echocardiography, in which the lesion is apnea, hypotension, bradycardia, fever, and rash.9 visualized using either a transthoracic or While the extent of respiratory depression is transesophageal approach.1 However, a formal, dose-dependent, it is often recommended to detailed echocardiogram may not be practical or intubate the patient prior to initiation of PGE1 to feasible during the initial ED presentation. ED secure the airway and avoid significant episodes of point-of-care U/S is growing in availability, hypoxia from apnea. Neonates on PGE1 who need quality, and extent of use and can guide the ED to be transferred should be intubated prior to work-up. One particular approach is to use the transfer. Hypotensive children should be given BLEEP examination, in which the ED provider pressor support, such as dobutamine or examines the inferior vena cava, observes the dopamine. quality of myocardial contractility, and evaluates r Disposition: Once a patient has been stabilized, for the presence and extent of pericardial he/she should be admitted for further evaluation effusion.1 Imaging the arch is extremely and definitive diagnosis. The level of care under challenging and definitive diagnosis should be which the patient will be admitted, whether it is done by pediatric cardiology. an ICU (for infants in shock) or lower level of r Treatment: ED management of a patient with a monitoring, will depend on the individual patient, ductal dependent lesion does not need to wait for his or her clinical status, and local protocol definitive diagnosis. The initial management of (NICU vs. PICU). Pediatric cardiology will need any patient in undifferentiated shock should to be engaged to diagnose and delineate the obviously focus on the ABC algorithm.1 One lesion. Once the diagnosis is confirmed, pediatric particular treatment challenge for these unstable cardiothoracic surgery becomes involved for infants is vascular access. The shock state will surgical management. leavetheneonateclampeddownand Many of these patients will need to be hypoperfused. Potential sites include umbilical transferred to a children’s hospital with the vein access and IO access. Scalp veins may also be appropriate specialists. It should be emphasized a potential site of access. that these are fragile infants with highly complex For the neonate, it may be difficult in the and unusual physiology, with a high probability initial stages to differentiate between cardiogenic for serious decompensation. They require 1:1 shock and septic shock, particularly in children nursing care with attention to minutiae. These with left-sided ductal dependent lesions, who may neonates should be transported by experienced not be hypoxic.8 They appear similar to infants neonatal or pediatric transport teams, whenever with shock from dehydration, trauma, or inborn possible. Ventilator settings, oxygen, fluids, and errors of metabolism. Therefore, as mentioned, sedation must be finely titrated to maintain work-up and management should address many stability and prevent an unexpected potential etiologies, especially infectious diseases decompensation.

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Historical clues Physical findings Ancillary studies Case 6 r r r Sudden r Tachycardia CXR with deterioration Hypotension pulmonary Contributing Author: Rebecca Jeanmonod r Rapid, shallow r Respiratory edema breathing distress History r Altered mental r Absent femoral An11-year-oldboyisbroughttotheEDbyEMSwith status r pulses r Discordant O2 sat his mother for acting strangely. Mom states that the Abnormal lung childdidn’tcomedowntodinner,andwhenshewent examination up to his room to retrieve him, she found him sitting on the floor with his eyes closed, his hands grasp- Follow-Up ing at the air. There was vomit on his shirt. She called The patient was immediately intubated. Fortunately, hisname,buthedidn’trespondtohervoice,soshe a nurse was able to obtain IV access. A blood and shookhim.Hefeltsweatytoher.Heopenedhiseyes urine culture as well as laboratory tests were sent. An and seemed startled, stated “I am made of wood,” and LP was not performed because of the instability of closed his eyes again. She could not get him to accom- the patient. Ampicillin, cefotaxime, and acyclovir were pany her down the stairs to the car to bring him in for started. PGE1 was also initiated in the ED. After 30 evaluation, so she called EMS. EMS reports that the minutes of PGE1, the infant’s color improved dramati- child has been tachycardic en route, with a heart rate cally. A call was made to the pediatric cardiologist and of about 125, and had a normal blood glucose. He was the child was admitted to the PICU. Shortly thereafter, otherwise“fineforus,”stableandnotcombative.Mom an echocardiogram revealed a coarctation of the aorta. states she has never seen the child like this before. He had been previously healthy, and is a 6th grader who References generallygetsBsinschool.Hehadbeenplayingvideo 1. Strobel AM, Nu LN. The critically ill infant with games in his room throughout the day today with sev- congenital heart disease. Emerg Med Clin N Am 2015; eral friends, but his friends went home an hour before 33: 501–18. mom found him. The child provides no meaningful 2. Liske MR, Greeley CS, Law DJ, et al. Report of the history. Tennessee Task Force on Screening Newborn Infants for Congenital Heart Disease. Pediatrics 2006; 118: Past Medical History e1250–6. r Healthy and developmentally normal, has 3. Brown K. The infant with undiagnosed cardiac disease received all immunizations. in the emergency department. Clin Pediatr Emerg Med 2005; 6: 200–6. Medications 4. Hoffman JIE, Kaplan S. The incidence of congenital r None. heart disease. JAmCollCardiol2002; 39:1890–900. 5. Centers for Disease Control and Prevention. Facts Allergies about coarctation of the aorta. See www.cdc.gov/ r None. ncbddd/heartdefects/coarctationofaorta.html (accessed January 2017). Physical Examination and Ancillary Studies 6. Savitsky E, Alejos J, Votey S. Emergency department r Vital signs: T 99.6 °F, HR 132, RR 22, BP 100/62, presentations of pediatric congenital heart disease. JEmergMed2003; 24: 239–45. O2 sat 100% on room air. r General: The child is sitting upright on the 7. Lee YS, Baek JS, Kwon BS, et al. Pediatric emergency room presentation of congenital heart disease. Korean stretcher with his eyes closed, picking at the air. Circ J 2010; 40: 36–41. He is not in any obvious distress. r 8. Ramby AL, Nguyen N, Costello JM. Cardiogenic shock HEENT:Therearenosignsofheadtrauma.The masquerading as septic shock. Clin Pediatr Emerg Med child’s pupils are small, but reactive. When he 2014; 15: 140–8. opens his eyes, his eye movements are generally 9. Sharma M, Sasikumar M, Karloopia SD, et al. roving, but he occasionally seems to fixate on his Prostaglandins in congenital heart disease. Med J mother. His mucous membranes are moist. His Armed Forces India 2001; 57: 134–8. oropharynx is clear.

16:18:54 215 10 Chapter 9: Altered Mental Status r Neck: Supple and non-tender, with no adenopathy. poisonings annually presenting for treatment.3 r Cardiovascular: Regular tachycardia, with no Almost half of these patients are between the ages M/R/G. Capillary refill is brisk. of 12 and 20, with the majority of poisonings r Lungs:CTAbilaterally. intentional (for the purpose of getting high), 3 r Abdomen: Soft, without distension or tenderness. although some are suicide attempts. r No masses or organomegaly. Normal genitalia. Pathophysiology: Poisoning is ultimately a matter r Extremities and skin: Diaphoretic, warm, and of dosing. Even substances that are non-toxic, like well-perfused, no signs of trauma. water, can be intoxicating and even fatal in high r Neurologic: The child resists movements of his doses. Because children are generally smaller than extremities and does not follow commands. He adults, they are at increased risk of toxicity when does move his extremities spontaneously and ingesting substances because the substance symmetrically. His face is symmetric. His sensory distributesthroughasmallertotalvolume.Thisis examination, cerebellar examination, and gait are why a single tablet of a calcium channel blocker or unable to be assessed due to his mental status. a beta blocker may be fatal in a small child. Many r Pertinent laboratory values: Fingerstick glucose 81. over-the-counter medications have not been studied in children, and most dosing guidelines for children are based on child age, rather than Questions for Thought size, even though size can vary widely for a given r What sort of laboratory and ancillary tests are age. For these reasons, the AAP states that important to get in this patient? r children age 6 and younger should not receive Are there medications that should be given to over-the-counter cough or cold preparations.4 this child? r Dextromethorphan and its metabolites have a If the child returns to his baseline, can he be host of pathophysiologic effects, including NMDA discharged home? Why or why not? receptor antagonism, inhibition of catecholamine reuptake, and agonism of serotonin receptors.3 Additionally, dextromethorphan is usually Diagnosis combined with other agents in a given cold r Dextromethorphan overdose. preparation, most commonly pseudoephedrine, acetaminophen, or anticholinergics. This can Discussion make these overdoses harder to recognize, as r Epidemiology: In the USA, there are over 5 million anticholinergic findings or catecholamine excess poisonings each year.1 Seventy-five percent of may predominate in the clinical picture. these are acute ingestions, while 25 percent The pathophysiology for how any given toxin represent chronic toxicity or remote ingestion.1 works depends on what the toxin is. A complete Ingestions may be accidental or intentional, and discussion of all intoxicants is beyond the scope of may be recreational or as an attempt at self-harm. this book; however, the clinician should be aware Ingestions account for 5–10 percent of all ED of the major classes of toxidromes: visits, but the majority of overdose patients are sympathomimetic, anticholinergic, opioids, released to home, with an admission rate of only sedatives, and cholinergics. These are described in about 5 percent.1,2 The patients who get admitted, Table 9.1. however, may be quite ill. Intoxicated patients r Presentation: Presentations for intoxication vary account for more than 5 percent of ICU with the agent ingested. Patients may present with admissions. The most common intentional local GI irritation (vomiting and diarrhea) from overdoses involve pain medications, such as an agent that may not have systemic harm (such over-the-counter NSAIDs or prescription as rhododendron). They may present with a narcotics, but psychiatric medications, illegal toxidrome related to specific effects of the agent drugs, vitamins, and cardiac medications are also on neurotransmitters in the CNS and systemically common. Dextromethorphan, a compound in (Table 9.1), such as diphenhydramine, cocaine, or many over-the-counter cough and cold selective serotonin reuptake inhibitors. They may medications, accounts for about 13,000 cases of present with non-specific altered mental status,

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Table 9.1 Examination findings with specific toxidromes HR RR BP T Pupils Skin Sympathomimetics Elevated Elevated Elevated Elevated Mydriasis Moist Anticholinergics Elevated Either Either Elevated Mydriasis Dry Opioids Decreased Decreased Decreased Decreased Miosis Dry Sedatives Decreased Decreased Decreased Decreased Either Dry Cholinergics Either – Either – Miosis Moist

either on the sedation spectrum or the agitation andisopropylalcoholmaycauseanelevated spectrum, such as with zolpidem. They may osmolar gap (calculated as [laboratory osmoles – present with hemodynamic instability (common (2Na) – (glucose/18) – (BUN/2.8)], abnormal in cardiac medications), hypoglycemia (with oral being Ͼ10 or Ͻ –10). Low glucose can occur from hypoglycemics, beta blockers, or insulin), or alcohols, oral hypoglycemics, insulin, or beta hallucinations (as with anticholinergics, LSD, blockers. A host of toxins may cause renal failure phencyclidine, or dextromethorphan). Because of or liver failure. Anemia can suggest iron toxicity the wide variety of possible presentations, the or isopropyl alcohol ingestion. An EKG with a clinician should at least consider the possibility of wide QRS or a prolonged Q–T should raise poisoning during formulation of the differential concern for ingestion of psychiatric medications for virtually all chief complaints. Most diagnoses (such as tricyclics or antipsychotics), are ultimately based on history, but there are clues antihistamines (diphenhydramine), or cardiac that may be provided on physical examination or medications (type 1a and 1c anti-arrhythmics or on laboratory evaluation. amiodarone). Urine tests are available for a host of r Diagnosis: History is the mainstay of diagnosis of intoxicants, including methadone, a specific intoxicant. Obtaining a history from benzodiazepines, cocaine, and marijuana. Specific family members and friends, reviewing details of blood tests are available to identify many toxins, the scene with EMS, calling pharmacists to such as acetaminophen, salicylates, ethanol, toxic ascertain the patient’s medication lists, and review alcohols, cardiac glycosides, and many seizure of the medical record may all prove valuable in medications, but further toxicologic testing is narrowing down the toxin involved. Vital signs, often not available in real time in the ED for the pupil examination, and assessment of skin is purpose of making clinical decisions. helpful in making diagnosis of a toxidrome r Treatment: For most intoxicants, including (Table 9.1). A careful neurologic examination may dextromethorphan, treatment is quite simply reveal clonus (pathognomonic for serotonin supportive care. This includes the ABC syndrome) or rigidity (which may occur with algorithm, establishment of an IV line, and fluid neuroleptics), as well as evidence of hallucinations resuscitation. Symptomatic patients with an (patient responding to internal stimuli) or ingestion should be placed on a monitor and seizures. Visual and tactile hallucinations are observed. Agitated and hallucinating patients more likely to be toxic in etiology, while auditory like this patient should have external stimuli hallucinations are more likely to be psychiatric. minimized and may be given benzodiazepines Serum electrolytes may be helpful, as in cases for further symptom control. If the ingestion was where a patient displays an elevated anion gap within 1 hour of evaluation, the believed substance acidosis (anion gap Ͼ12), calculated as [sodium – is harmful and known to adsorb to charcoal, (chloride + bicarbonate)]. Methanol, ethylene and the patient has an intact airway, activated glycol, salicylates, paraldehyde, iron, isoniazid, charcoal at a dose of 1 g/kg should be given.2 carbon monoxide, and cyanide can all cause an There has been no demonstrated benefit and some elevated anion gap. Measurement of serum harm to whole bowel irrigation, gastric lavage, or osmolarity and calculation of an osmolar gap may forced vomiting, and these practices are generally be helpful, as methanol, ethanol, ethylene glycol, not indicated in intoxicated pediatric patients.

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Table 9.2 Specific poisons and their antidotes sustained-release, controlled-release, have long Poison Antidote half-lives (such as methadone), or delayed effects (such as bupropion) should prompt admission for Acetaminophen N-acetyl-cysteine observation. If the clinician is unfamiliar with the Narcotic analgesics Naloxone substance or has any questions about the Benzodiazepines Flumazenil management of the child, he or she should call the Methanol and ethylene glycol Fomepizole, ethanol Poison Control Hotline for recommendations. Isopropyl alcohol Dialysis Diphenhydramine (and other Sodium bicarbonate Historical clues Physical findings Ancillary studies agents that widen the QRS r Age group r Active r Normal glucose complex) r hallucinations Oral hypoglycemics Glucose, octreotide for r Tachycardia sulfonylureas Diaphoresis Beta or calcium-channel Glucagon, high-dose insulin blockers and glucose therapy Follow-Up Digoxin or other cardiac Digoxin-specific antibody (Fab) glycosides fragments The child seemed to be having visual hallucinations, Iron Deferoxamine and was medicated with lorazepam for his symptoms. Mom was able to provide the phone number to the Mercury, lead Dimercaprol, EDTA child’s friends, who provided the history that the child Organophosphates Pralidoxime had been drinking cough syrup in order to get high Cyanide Hydroxocobalamin earlier in the day, and they had left when he “started Isoniazid Pyridoxine acting weird.” The child’s laboratory tests did not show Local anesthetics and dapsone Methylene blue any significant electrolyte or renal abnormalities, and (cause methemoglobinemia) his LFTs were normal. The child had a negative serum toxicology screen for ethanol, salicylates, and acetaminophen, and had a negative urine toxicology Some intoxicants have specific antidotes, the screen. His EKG showed sinus tachycardia with nor- most notable of which is acetaminophen. malintervalsandnoectopy.Thechildwasadmitted Acetaminophen is a common co-ingestant and for observation, and his sensorium improved over may cause fatal hepatotoxicity, which is thefollowing8hours.Thechildadmittedtotaking completely preventable with treatment with the syrup recreationally, and stated that he had not N-acetyl-cysteine within 12 hours of the done it before, but had heard it was fun from an ingestion. Likewise, salicylates and toxic alcohols older child on the school bus. He denied suicidal may be treated with dialysis, digoxin is treated intent. He was evaluated and cleared by the crisis staff. with digoxin-specific antibody (Fab) fragments, The child was ultimately discharged home with his and heavy metals are treated with chelation parents, after observation, and has had no further therapy (see Table 9.2 for a list of poisons with problems. their antidotes). For this reason, in the patient with an unknown intoxicant, it is important to check levels of substances that would require a References change in therapy, especially in the critically ill 1. Watson WA, Litovitz TL, Rodgers GC Jr, et al. 2004 patient, as failure to treat appropriately may result Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. in death. Am J Emerg Med 2005; 23: 589–666. r Disposition: Sick children should be resuscitated 2. Chyka PA, Seger D, Krenzelok EP, et al. Position according to the ABC algorithm. In most patients paper: Single-dose activated charcoal. Clin Toxicol with a known ingestion, who are asymptomatic, (Phila) 2005; 43: 61–87. an assessment for suicidal ideation (possibly with 3. Chyka PA, Erdman AR, Manoguerra AS, et al. psychiatric consultation in the right clinical Dextromethorphan poisoning: An evidence-based scenario) and observation for 4–6 hours is consensus guideline for out-of-hospital management. appropriate. However, substances that are Clin Toxicol (Phila) 2007; 45: 662–77.

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r 4. Lowry JA, Leeder JS. Over-the-counter medications: HEENT: Normocephalic and atraumatic. Anterior Update on cough and cold preparations. Pediatr Rev fontanelle is soft and flat. PERRL. 2015; 36. See http://pedsinreview.aappublications.org/ r Neck: Supple, with a midline trachea. content/36/7/286 (accessed November 2016). r Cardiovascular: Regular rate, with no M/R/G. r Lungs: Clear and equal, with no W/R/R. Case 7 r Abdomen: Soft, non-distended. Palpable mass in the right lower quadrant. Guaiac positive. Contributing Author: Kinsey Leonard r Extremities and skin:Skiniswarmanddry. ˂ History Capillary refill 3seconds.Norash.Nobruises, lacerations, or other signs of trauma. A 7-month-old male is brought to the ED by his r Neurologic: Patient withdraws all extremities to parents. He is sleeping in his mother’s arms. His painful stimuli. Examination appears non-focal. parents state that they have not been able to wake him r up for the last 3 hours. He typically takes a 1.5-hour Pertinent laboratory values: Fingerstick glucose is afternoon nap. Today, after 1.5 hours, mom tried to normal. Toxicology screen is negative. Electrolytes and divalents are normal. WBC 17,000. wake him but was unsuccessful. She figured the infant r was tired and let him sleep longer. When she couldn’t Pertinent imaging:CTheadnormal. arouse him after an additional 1.5 hours, she became concerned. She states that the infant was acting nor- Questions for Thought mally earlier in the day. Mom states that he had taken a r What are the appropriate initial steps in bottle every 3 hours, he had been making normal wet managing this child? diapers, and he had a normal bowel movement in the r What ED work-up is necessary to diagnose this morning. entity and exclude other entities? r On review of systems, mom states that he is a How does this condition usually present? r healthy male and denies recent illness. She denies What is the deﬁnitive treatment for this condition? fevers, rhinorrhea, cough, decreased PO intake, diar- r rhea, vomiting, melena, hematochezia, or decreased What is the disposition of this patient? urination. She denies increased fussiness. The infant is UTD on all immunizations. He is breast fed. He has met all developmental milestones. He does not attend Diagnosis daycare, mom stays at home with the infant and his r Intussusception. older brother. Discussion Past Medical History r Epidemiology: Children are at greatest risk for r Normal spontaneous vaginal birth at 39 weeks’ intussusception before the age of 3 years, although gestation, no medical problems, UTD on it can occur at any age. Males are at an increased immunizations. risk compared to females. Intussusception is the leading cause of intestinal obstruction in Medications children. r r Vitamin D. Pathophysiology: Intussusception occurs when a proximal segment of bowel “telescopes” into a Allergies more distal segment. The most common location r is ileocolic. The proximal segment and the NKDA. associated mesentery become edematous due to decreased venous return, which can result in Physical Examination and Ancillary Studies ischemia. Seventy-five percent of cases are r Vital signs:T99°F, HR 110, BP 90/60, RR 30, O2 idiopathic. Intussusception has been postulated to sat 100% on room air. be caused by viral illness, with increase lymphoid r General: The patient is asleep in his mother’s arms. tissue at Peyer’s patches acting as the lead point. Unarousable. Withdrawals from painful stimuli. Intussusception has also been linked to Meckel’s

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diverticulum, polyps, duplication cysts, diagnosed on CT scan, but this is not the modality lymphomas, and hematomas from of choice due to the risks of radiation exposure Henoch–Schonlein¨ purpura. Some studies report and the expense of the modality. increased risk of intussusception in children with r Treatment: The child should be resuscitated with cystic fibrosis, celiac disease, and Crohn’s IV fluids and close attention to the ABC disease.1–3 algorithm. A nasogastric tube is often used to r Presentation: Most commonly, children present decompress the stomach before the child has an with colicky abdominal pain and vomiting. More air contrast enema performed. The treatment of information on this presentation is present in the choice for intussusception is a pneumatic enema, chapter on vomiting. The triad of intermittent using either air or carbon dioxide, rather than a abdominal pain, emesis, and currant-jelly stool is hydrostatic enema, which has a higher risk of seen in about 20 percent of presentations. Both perforation, although either may be used. The vomiting and grossly bloody stool occur as a later enema is usually performed under U/S or complication of intussusception; however, guaiac fluoroscopic guidance to confirm reduction of the testing is most often positive even in early intussusception, with U/S being the preferred presentations. A palpable, “sausage-shaped,” modality. Perforation occurs in about 1 percent of abdominal mass is found in the majority of cases, cases that are treated with enemas.5 but the absence of an abdominal mass should not r Surgery is indicated in cases where the pneumatic be falsely reassuring. or hydrostatic enema is unsuccessful, when there In 10–20 percent of cases, lethargy, or altered are multiple recurrences, when perforation is mental status may be the sole presenting suspected, or when the patient is complaint or a component of the presentation, as hemodynamically unstable or has a peritoneal in this case.4 abdomen. A pediatric surgeon should be r Diagnosis: Diagnosing intussusception is easier consulted in all intussusception cases in case when the patient presents with the typical triad. In surgery needs to be performed. this presentation, the clinician may only want to r Disposition: Children are usually observed for order U/S to confirm the suspected diagnosis. U/S 24 hours after reduction. Intussusception recurs not only diagnoses the condition (demonstrating in about 10 percent of children.6 In these cases, a “target sign,” in which loops of bowel are seen enema reduction can be attempted again. If the invaginated within one another), it can also intussusception keeps recurring, surgical confirm the location and whether or not a treatment is indicated.6,7 pathologic lead point exists. If the history is extremely suggestive of intussusception and the Historical clues Physical findings Ancillary studies physical examination supports the diagnosis, r r r Age 3 months Mass in the r Leukocytosis some institutions recommend proceeding directly to3years abdomen Negative r Guaiac positive metabolic, to air enema, which will simultaneously confirm trauma, and toxic the diagnosis and treat the condition. work-up If the child presents atypically, as in this case with altered mental status, a more comprehensive work-up is indicated, to exclude other pathology. Follow-Up Evaluation for metabolic, endocrine, infectious, The child had IV fluid resuscitation and was admitted neurologic, traumatic, and toxicologic sources of to the hospital for observation. On hospital day 2, he altered mental status should be undertaken. In became less stable and underwent CT which demon- children with altered mental status of unclear strated intussusception and free fluid in the abdomen. etiology, the clinician should consider performing An example of a CT with intussusception is shown in U/S of the abdomen as part of the child’s Figure 9.1. He was flown to a pediatric center where evaluation. he underwent exploratory laparotomy during which Plain films of the abdomen are not specific for he had the necrotic bowel excised. His post-operative the diagnosis of intussusception and may be course was uncomplicated and he was discharged after entirely normal. Intussusception may be 7 inpatient days.

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and also speaking out loud as if in conversation with someonewhenheisaloneinhisroom.Thepatient denies drug or alcohol use, but does not answer further questions. His parents report that he is a healthy male and deny any recent illness. Mom states that he had several friends at his high school, but has not been hanging out with them for the past few months. To the best of her knowledge, she concurs that he does not use drugs, drink alcohol, or smoke cigarettes.

Past Medical History r Asthma. r UTD on immunizations. Figure 9.1 CT of the abdomen showing intussuscepted bowel (white arrow) in the left lower quadrant. Medications r Albuterol. References 1. Holmes M, Murphy V, Taylor M, et al. Allergies Intussusception in cystic fibrosis. Arch Dis Child 1991; r NKDA. 66: 726–7. 2. MushtaqN,MarvenS,WalkerJ,etal.Smallbowel Physical Examination and Ancillary Studies intussusception in celiac disease. JPediatrSurg1999; r 34: 1833–5. Vital signs: T 98.2 °F, HR 73, BP 120/70, RR 18, O2 3. Cohen DM, Conard FU, Treem WR, et al. sat 100% on room air. r Jejunojejunal intussusception in Crohn’s disease. General: The patient is awake and alert. J Pediatr Gastroenterol Nutr 1992; 14: 101–3. r HEENT: Normocephalic and atraumatic. PERRL. 4. KleizenKJ,HunckA,WijnenMH,etal.Neurological There is no nystagmus. Oropharynx clear. symptoms in children with intussusception. Acta r Neck: Supple, with a midline trachea. Paediatr 2009; 98: 1822–4. r Cardiovascular: Regular rate, with no M/R/G. 5. Maoate K, Beasley SW. Perforation during gas r Lungs: Clear and equal, with normal work of reduction of intussusception. Pediatr Surg Int 1998; 14: breathing. 168–70. r Abdomen: Soft, with no tenderness, distension, 6. YangCM,HsuHY,TsaoPN,etal.Recurrenceof rebound, or guarding. intussusception in childhood. Acta Paediatr Taiwan r 2001; 42: 158–61. Extremities and skin:Skiniswarmanddry. 7. Weihmiller SN, Buonomo C, Bachur R. Risk Superficial lacerations to the second-fourth stratification of children being evaluated for metacarpophalangeal joints on the right hand. intussusception. Pediatrics 2011; 127: e296–303. Bleeding well controlled. r Neurologic:Alertandoriented× 4. No focal Case 8 neurologic deficits. Patient ambulated into the ED with a normal gait. Contributing Author: Kinsey Leonard r Psychiatric: The patient appears anxious. He is looking around the room and seems to be History listening to something because he keeps shaking A 15-year-old male presents to the ED with altered his head. He seems agitated, is moving rapidly and mental status. The patient’s parents state that he unexpectedly. He demonstrates echolalia when he became very agitated at home and punched the tele- is asked questions directly. vision set, injuring his hand. The parents report that r Pertinent laboratory values: Urine toxicology is they have heard the patient talking to the television negative. Ethanol level is undetectable.

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r Questions for Thought Bipolar disorder: During manic episodes, the r patient may have delusions of grandeur that What components of the work-up may may appear to the clinician as psychosis. diﬀerentiate a psychiatric psychosis from an r Brief psychotic disorder:Delusions, organic cause? r What laboratory values might be helpful? hallucinations, or disorganized speech is r What is the goal of the emergency physician in present acutely for less than 1 month. The child evaluating psychiatric patients? completely recovers back to baseline after the r What determines the disposition of the patient? episode. An acute stressor precipitates the episode. r Schizophreniform: Diagnosis requires two of Diagnosis the following five symptoms – hallucinations, r Acute psychosis. delusions, disorganized thoughts, abnormal/ catatonic behavior, and/or negative symptoms, Discussion present for more than 1 month, but less than r Epidemiology: The prevalence of schizophrenia is 6months. about 1 percent, with equal prevalence in females r Schizophrenia: Continuation of the psychotic and males.1,2 A strong genetic predisposition has disturbance for at least 6 months, with two of been found. The prevalence of bipolar disorder in the five symptoms (hallucinations, delusions, the pediatric population is 2–3 percent.2,3 The disorganized thoughts, disorganized/catatonic prevalence of depression ranges depending on age behavior, negative symptoms) present for the of the child, with less than 1 percent in children majority of 1 month. under5yearsandabout4percentinlate r Schizoaffective disorder:twoofthefivecriteria adolescence.2,3 for schizophrenia are present, with r Pathophysiology:Psychosiscanbecausedbymany intermittent mood disorder, either bipolar or underlying problems beyond primary psychiatric majordepression,foratleast1month.The disease. The clinician should consider underlying psychotic symptoms of the illness are present medical causes, such as metabolic/electrolyte foratleast2weekswithoutthemooddisorder. derangements, toxins, CNS disease and infections, r Schizoid and schizotypal personality disorder seizures, autoimmune disease, and vitamin also may have psychotic features. deficiencies. Primary psychiatric disease should r Presentation: An abrupt, acute onset of psychosis only be considered once these other processes are in children is more likely secondary to an eliminated through history, physical examination, underlying medical/organic cause, while a more and ancillary studies as indicated. gradual onset is more likely psychiatric in origin. Psychiatric disease often has its first Most patients with primary psychiatric disease presentation as psychosis in the ED. There is will have normal vital signs. They typically have usually a history of progressively worsening an unremarkable physical examination, with symptoms over several weeks to months.1,2 The normal neurologic examination, level of alertness, most common psychiatric diseases with psychotic and orientation. The only abnormal findings on features are depression with psychotic features, examination are typically psychiatric: evidence of bipolar disorder, brief psychotic disorder, abnormal thinking, hallucinations, a tangential schizophreniform, schizophrenia, and thought process, pressured speech, disorganized schizoaffective disorder.2 Personality disorders or catatonic behavior, and agitation. Patients with andconductdisordercanalsopresentwith hallucinations from a psychiatric cause are psychosis. These are each described in brief below. typically auditory, while those from an underlying r Depression with psychotic features:Thepatient medical/toxic process are more commonly visual meets criteria for major depressive disorder or tactile.2 r and has delusions or hallucinations during the Diagnosis: In the ED, if there is any doubt that the mood disorder. The mood disorder occurs at child’s psychosis is psychiatric in origin, times without psychosis. alternative medical causes should be sought.

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Glucose testing, electrolytes, divalents, thyroid patients. Providers should be familiar with their studies, and LFTs may all be indicated for a newly state’s laws concerning the restraint and psychotic child. All children with psychosis involuntary admission of psychiatric patients, as should undergo toxicology screening, and these laws vary in different regions. appropriately aged female patients should have a Crisis/psychiatric consultation should be pregnancy test done. If toxins are suspected, EKG obtained, and social workers may also assist in should also be performed to look for evidence of disposition issues and follow-up. QRS widening or dysrhythmias. Neuroimaging r Disposition:Ifthechildisinasafeenvironment andLPmightbeindicatedintherightclinical with reliable follow-up and poses no harm to setting. him/herself or others, he/she may be discharged If a psychiatric cause is suspected, the with close follow-up. All others require inpatient evaluation should be tailored to determining the admission. patient’s risk as an immediate threat to him/herself or someone else. This includes an Historical clues Physical findings Ancillary studies r r r assessment of suicidal or homicidal ideation. It is Auditory r Normal vital signs Negative urine important to remember that a child may be a hallucinations Normal toxicology r Gradual onset neurologic r Negative ethanol threat to him/herself without being suicidal. A r examination psychoticpatientwhoisunabletointeractwith Normal eye and attend to his/her environment in an examination appropriate way may be at risk for accidental death (for example, walking into traffic) or Follow-Up self-harm. Either scenario necessitates inpatient The child was admitted to psychiatry, where he was hospitalization. The majority of newly psychotic ultimately diagnosed with schizophrenia. He is cur- children should have a psychiatric/crisis rentlyonastabledrugregimenthatallowshimto evaluation, and admission versus close outpatient function, and has returned to school. treatment should be decided in concert with psychiatric professionals. References r Treatment: Acutely psychotic patients should be 1. Holder SD, Wayhs A. Schizophrenia. Am Fam Phys placed in a quiet area of the ED, with decreased 2014; 90: 775–82. stimulation, preferably in an area designed for 2. Griswold KS, Del Regno PA, Berger RC. Recognition such patients. They should be provided with and differential diagnosis of psychosis in primary care. verbal redirection and de-escalation. Sedatives Am Fam Phys 2015; 91: 856–63. such as benzodiazepines or antipsychotics may be 3. American Psychiatric Association. Diagnostic and necessary for the violent psychotic patient, and StatisticalManualofMentalDisorders, 5th edition. physical restraints may also be required to Washington (DC): American Psychiatric Association, preserve the safety of the ED staff and other 2013.

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Case 1 Physical Examination and Ancillary Studies r Vital signs: T 100.4 °F, HR 113, BP 97/50, RR 25, Contributing Author: Sonika Raj O2 sat 98% on room air. r History General: Teenage female lying supine and in distress secondary to headache. She is The patient is a 14-year-old girl who was brought to intermittently somnolent. the ED immediately after her mother found her uncon- r HEENT: Normocephalic and atraumatic. PERRL. scious on the bedroom floor. The patient had been No photophobia. No pharyngeal erythema or complaining of headache and dizziness for 1 day, but exudates. thoughtitwas“juststress”foranupcomingexamina- r Neck: Supple, with midline trachea. tion. Shortly after arrival, the child suffers cardiopul- r Cardiovascular: Tachycardic and regular. No monary arrest; after a short course of CPR and resusci- M/R/G. tative efforts, she regains cardiac function but remains r Lungs:CTAbilaterally,withnoW/R/R. unconscious. While you prepare for endotracheal intu- r bation, she regains consciousness and starts to com- Abdomen: Soft, non-distended, non-tender, with plain of nausea and a headache. normoactive bowel sounds and no hepatosplenomegaly. The mother states she has had no recent ill- r nesses, fevers, or other complaints. According to her Extremities and skin:Pale,mildlycyanotic extremities with no edema. mother, the patient is a happy, generally healthy young r teenager,withagoodsupportsystemoffamilyand Neurologic: She has generalized difficulty friends. She earns top grades in school and her mother concentrating during the examination. Somnolent often finds her working late into the night on school but responsive. Cranial nerves II–XII intact. assignments. There is no history of drug or alcohol use, Muscle strength 4/5 and symmetric throughout. depression, being bullied, or suicide attempts. Sensory and vibratory examinations intact and symmetric throughout. Reflexes 3+ and Past Medical History symmetric throughout. Patient has significant difficulty with rapid alternating movements, r Tension headaches, approximately 1 per month heel-to-shin test, and finger-to-nose test. Positive since the start of the school year. Romberg test. Negative pronator drift. When r Immunizations UTD. asked to demonstrate gait, patient refuses due to Medications fatigue. r r Ibuprofen 200 mg PO every 6 hours as needed for Pertinent laboratory values: Fingerstick glucose tension headaches. 110. Na 140, K 5, Cl 106, bicarbonate 11. Thyroid and drug screen negative. EKG shows sinus Allergies tachycardia. r r NKDA. Pertinent imaging:HeadCTunremarkable.

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r Questions for Thought Presentation: Acute CO toxicity may present with a range of symptoms. The most common r What is your diﬀerential diagnosis for an symptom is headache.2,3 Additional complaints unconscious teenager? 2,3 r Does this condition have a “typical” presentation? include dizziness, fatigue, and visual changes. If so, what are the signs/symptoms? Neurologic symptoms include changes in r What further diagnostic modalities (if any) should memory/concentration, disorientation, and 2,3 be used to evaluate this patient? coma. Cardiovascular (chest pain secondary to r What treatments should be initiated in the ED? myocardial ischemia), GI (nausea/vomiting), or r What is the deﬁnitive treatment of this condition? pulmonary symptoms (shortness of breath) may also be seen. Some patients may have long-term, undiagnosed exposure to CO. These patients may Diagnosis present with a myriad of non-specific symptoms, r Carbon monoxide (CO) poisoning. such as cognitive decline, sleep problems, memory difficulty, and emotional lability.2,3 r Diagnosis: Diagnosing CO toxicity requires a high Discussion index of suspicion, as well as careful questioning r Epidemiology: Thousands of patients visit the ED regarding potential sources for CO exposure (the eachyearforCOpoisoning.Itisaleadingcauseof patient’s work environment, heat sources in the death by accidental poisoning, and accounts for home, and recreational activities). Household severalthousandhospitaladmissionseachyear.In members with similar symptoms represent a national study of adolescent poisoning deaths in another diagnostic clue. the USA between 1979 and 1994, CO inhalation Venous carboxyhemoglobin levels are helpful caused 38.2 percent of the deaths, and 65.1 percent in confirming the diagnosis of CO poisoning, of these were suicides.1 The true incidence of CO although it is important to remember that this test toxicity is unknown, as symptoms may be mild has limitations.2,3 Patients may be exposed to CO (and patients do not seek care) as well as vague at their house, then have their levels decrease (resulting in misdiagnoses). Sources of exposure when they leave the source. By the time they reach include house fires, fuel-burning devices which the ED for diagnostic testing, which may be are inadequately vented (i.e. inhalation of car several hours later, their CO levels can normalize. exhaust in a closed garage), and damaged heating Information from the fire service/EMS at the units (i.e. space heaters or gas radiators). While scene with environmental CO measurements is CO toxicity is more common in the winter when important to obtain for CO evaluation, when people use alternate heat sources, it can occur at possible. Pulse oximetry has no role in screening any time of the year. for CO poisoning. r Pathophysiology: CO is an odorless and colorless In patients with confirmed CO poisoning, gas that is absorbed into the pulmonary vascular other tests may be useful. Blood glucose testing bed where it attaches to hemoglobin. Since may reveal hypoglycemia, creatine kinase levels hemoglobin has a much stronger affinity for CO may demonstrate secondary rhabdomyolysis from than oxygen, most hemoglobin molecules will tissue hypoxia, and EKG/troponin may show attach to CO. This shifts the oxygen–hemoglobin cardiac ischemia or infarction. For those patients saturation curve to the left, which in turn reduces in whom exposure was secondary to house or oxygen delivery to peripheral tissues. This chemical fire, evaluation for cyanide toxicity is produces tissue hypoxia and, secondarily, lactic also very important. acidosis. CO also causes anoxia by integrating into In the undifferentiated teen with altered the intracellular oxygen–cytochrome oxidase mental status, toxicologic screening and other system, where it blocks cellular oxidation. The laboratory tests may rule out other metabolic and sequelae are the sequelae of hypoxia: seizure, toxic sources of mental status changes. CT cardiopulmonary arrest, and death. imaging may help rule out other central causes,

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such as subarachnoid hemorrhage or mass. In Follow-Up severe cases of CO toxicity, CT may show Upon further questioning, it was discovered that the 2,3 hypodensities in the basal ganglia. The childwasusingaspaceheaterinherroom,withthe detection of such changes within 24 to 48 door closed at night to keep warm. The child’s carboxy- hours of the poisoning is associated with a poor hemoglobin level was checked, and measured 20 per- prognosis. cent. Given her neurologic symptoms, she underwent r Treatment: The initial treatment for CO toxicity is hyperbaric oxygen therapy, which was successful. Her to remove the patient from the source and headache, nausea, and disorientation resolved. She was immediately start 100 percent oxygen via a instructed to avoid using the space heater with inade- non-rebreather mask;2,3 100 percent oxygen quate ventilation. She has no lasting neurologic deficits should be administered until symptoms have secondary to this isolated exposure. resolvedandthecarboxyhemoglobinlevelis below 10 percent. Tracheal intubation should be References performed when clinically indicated. 1. Shepherd G, Klein-Schartz W. Accidental and suicidal Hyperbaric oxygen significantly decreases the adolescent poisoning deaths in the United States, half-life of CO. Indications for hyperbaric oxygen 1979–1984. Arch Pediatr Adolesc Med 1998; 152: therapy include patients who are unconscious, 1181–5. those with a neurologic deficit, those with EKG 2. Colomb-Lippa D. Acute carbon monoxide exposure: changes and/or infarction, and those with a Diagnosis, evaluation, treatment. JAmAcadPhys carboxyhemoglobin level greater than Assist 2005; 18: 41–6. 25 percent.2,3 Because fetal hemoglobin has an 3. Weaver LK. Carbon monoxide poisoning. NEnglJ especially high affinity for CO, pregnant patients Med 2009; 360: 1217–25. with a carboxyhemoglobin level greater than 20 percent should be considered for hyperbaric therapy.2,3 Case 2 Rhabdomyolysis, seizures, and myocardial ischemia should be treated as indicated. Contributing Author: Rebecca Jeanmonod CO poisoning may be intentional, and each patient should be evaluated by a psychiatrist if History clinically indicated. A15-year-oldboyisbroughttotheEDcomplaining r Disposition: Asymptomatic patients with elevated of headache. The child was at school, where he is a carboxyhemoglobin levels should be treated with sophomore, when he began to complain of a severe high-flow oxygen therapy until their levels headache.Hewassenttothenursewherehewasnoted normalize. Symptomatic patients who do not to be diaphoretic and pale. He vomited twice, and meet criteria for hyperbaric therapy should be was sent by EMS from the school. He is accompanied admitted for high-flow oxygen therapy and by a school representative, who states that the nurse monitoring. Patients who meet criteria for was concerned enough about the boy that she did not hyperbaric therapy should be transferred to a wait for his parents to transport him. The boy has an facility with capability for this therapy, when action plan in place at the school for an underlying possible. condition of migraine headaches. He has been having intermittent severe headaches for the last 2 years, and his pediatrician has been managing him with NSAIDs Historical clues Physical findings Ancillary studies and sumatriptan. The child’s headaches are episodic r r r and severe, occipital in location, pounding in charac- Loss of Abnormal vital r Negative head CT r consciousness r signs Negative tox ter, and usually accompanied by vomiting, pallor, and Headache and Abnormal screen diaphoresis. The child states that he occasionally has nausea neurologic r Anion gap r palpitations and “sometimes I feel like I can’t breathe Use of space examination r acidosis heater Elevated carboxy- because I’m vomiting so hard.” This headache is sim- hemoglobin ilar in character to his typical headaches, but more level severe. The child denies trauma. He has not had fevers

16:26:06 11 Chapter 10: Head and Neck Pain or chills. He denies abdominal pain or diarrhea. His Diagnosis review of systems is otherwise negative. r Hypertensive emergency secondary to pheochromocytoma. Past Medical History r Immunizations UTD. Discussion r Migraine headaches. r Epidemiology: Hypertension in children, defined r Occasional marijuana use. as a blood pressure higher than the 95th percentile for age, is increasing in incidence in the Medications USA, mostly secondary to increasing obesity.1,2 r Sumatriptan. The current incidence is estimated to be r Ibuprofen. approaching 4 percent.2 That said, hypertension in a child should never be considered essential Allergies hypertension without a work-up, as most r Penicillin. hypertension in children is secondary to underlying disease, typically renal/renovascular 1 Physical Examination and Ancillary Studies or endocrine. Pheochromocytoma is exceedingly rare, with about 0.3 cases in a million in the r ° Vital signs: T 99.6 F, HR 125, RR 24, BP 223/128, general populous, and only 10–20 percent O2 sat 100% on room air. 3 r presenting in the pediatric age group. These are General:Heisanxious.Hehasareceptaclefor associated with a specific genetic mutation or vomit on his lap. He is pale and diaphoretic and familial syndrome (such as von Hippel–Lindau looks dyspneic and uncomfortable. and multiple endocrine neoplasia) in r HEENT: No signs of head trauma. PERRL. 40–56 percent of pediatric patients.3,4 Extraocular movements intact. Papilledema r Pathophysiology: Although patients frequently present. Slightly dry mucous membranes. state that they get headaches from having elevated Oropharynx clear. blood pressure, it may well be that in most cases, r Neck:Supple,withnoadenopathyorJVD. the pain of the headache precipitated the r Cardiovascular: Regular tachycardia, with no hypertension, and not the other way around. M/R/G. Patient has delayed capillary refill. Generally, in a patient without chronic r Lungs: Clear bilaterally. Patient is tachypneic. hypertension, cerebral autoregulation keeps r Abdomen: Soft, non-tender/non-distended, no cerebral blood flow constant at mean arterial masses or organomegaly. Normal genitourinary pressures (calculated as [diastolic BP + examination. 1/3(systolic BP – diastolic BP)]), anywhere from r Extremities and skin: Diaphoretic and generally about 60–120. When blood pressure climbs above pale. No deformity. that level, however, cerebral autoregulation fails, r Neurologic: Normal cranial nerves, strength, which results in increased cerebral blood flow and sensation, reflexes, and coordination cerebral edema. Therefore, in patients with no r Pertinent imaging:HeadCTnormal. history of hypertension who complain of severe headache with mean arterial pressures above 120, the provider should consider the diagnosis of Questions for Thought malignant hypertension. Malignant hypertension r is diagnosed when severe hypertension causes any What should be the treatment priorities in this end-organ damage, and this damage is generally patient? secondary to failure of autoregulatory r Does the child require further diagnostic imaging or blood work? mechanisms in the affected organ. For the r What is your diﬀerential for this presentation? purposes of most patients, these presentations r Do you need to wait for his parents to be present involve hypertensive encephalopathy (cerebral to initiate treatment? edema, sometimes confusion or focal neurologic deficits, headache), cardiac damage (acute

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myocardial infarction or acute congestive heart secondary to extremely high vascular tone and failure secondary to pressure overload), and renal profound volume depletion, or may present more failure. subtly, with intermittent non-specific symptoms. Pheochromocytoma causes malignant r Diagnosis:Thediagnosisofhypertensive hypertension through secretion of emergency, although supported through catecholamines, most commonly norepinephrine. laboratory studies, EKG, and radiographic studies, These catecholamines activate both alpha- and is generally a clinical one. In emergency medicine, beta-adrenergic receptors. Alpha activation leads it is easy to overlook a BP that is not low, but it is to vascular constriction in the brain, GI tract, critically important to recognize the high value kidney, and skin, which causes cool, pale that is outside the range of the body’s extremities in the setting of severe hypertension. autoregulation, especially in more subtle Beta activation leads to increased heart rate as presentations. The differential in a teenager with well as stroke volume, increased renin secretion, malignant hypertension should include and increased glucagon secretion. Therefore, the renovascular hypertension and endocrine hypertension caused by a secretory syndromes, but toxins (such as pheochromocytoma is multifactorial; not only sympathomimetics, some prescribed psychiatric secondary to vascular constriction, but also due to medications) pre-eclampsia/eclampsia, increased cardiac output and activation of the coarctation of the aorta, and underlying lung renin–angiotensin system. Because of disease should also be considered.1 longstanding vasoconstriction in most of these For a definitive diagnosis of patients, they are commonly very volume pheochromocytoma, biochemical testing of urine depleted in spite of their hypertension. (24-hour urine metanephrines) and blood r Presentation: Patients with malignant (fractionated metanephrines) is the initial step. hypertension present with elevated blood pressure Thismaybeperformedasanoutpatientinstable, and signs of end-organ damage. Patients with asymptomatic adult patients with good follow-up, hypertensive encephalopathy may have headache, but, in general, children with suspected vomiting, altered mental status, and focal pheochromocytoma or significant hypertension neurologic deficits. Their head CTs may be shouldundergoevaluationasaninpatient.6 If normal or may show regional or generalized blood work suggests pheochromocytoma, edema or intracranial hemorrhage. Patients with imaging studies should be performed to locate the cardiac involvement may have complaints of chest tumor. There is debate as to whether CT or MRIis pain, shortness of breath, palpitations, or the preferred imaging modality. CT exposes the peripheral edema. Their examinations and child to significant radiation, but MRI has inferior ancillary studies may demonstrate rales, spatial resolution for this entity and is more jugulovenous distension, hepatomegaly, EKG expensive.7 Tagged radioisotope studies using changes (ischemia or evidence of ventricular iodine-131 MIBG (which resembles hypertrophy or conduction abnormalities), norepinephrine) have a 77–90 percent sensitivity elevated troponin, or elevated BNP. Those with and 95–100 percent specificity for identification of renal involvement may present with edema or pheochromocytoma.7,8 laboratory evidence of renal failure. r Treatment:Thediagnosisofthespecificcauseof For malignant hypertension secondary to malignant hypertension can be time- and pheochromocytoma, most patients present with resource-consuming. That said, this is a headache (70–90 percent), palpitations dangerous diagnosis that needs aggressive (50–70 percent), and diaphoresis initial management. Initial therapy should follow (60–90 percent).5 Because neurotransmitter the ABC algorithm. In patients with secretion may be episodic, the hypertension +/– pheochromocytoma or with malignant tachycardia that occurs with pheochromocytoma hypertension from toxins or renovascular causes, may also be episodic. These patients may present the blood pressure should be treated initially with dramatically, with cardiovascular collapse an alpha-adrenergic blocker, such as hydralazine

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or nicardipine. Monotherapy with Follow-Up beta-adrenergic blockade is contraindicated, as The child’s medical record was reviewed, and it this can cause decreased cardiac output with no was noted that he had incidental hypertension on reductionintheactualvasculartension,andcan numerous unrelated visits for sports injuries. He was result in unopposed alpha effect and started on a nicardipine drip for his hypertension cardiovascular collapse. If the patient additionally and was fluid resuscitated with 2 L normal saline. has significant tachycardia, beta-blockade can be The provider did not wait for his parents to arrive, undertaken after adequate alpha-blockade has as his entire evaluation was considered a “screen- been achieved. If the hypertension is believed to ing examination for medical emergency” as required be secondary to congenital heart disease, your by law, and in his case, his condition was found to best course of action is to consult with cardiology constitute a medical emergency warranting immedi- regarding medication choices. In undifferentiated ate treatment and stabilization. The patient’s symp- malignant hypertension, initial medical toms improved with BP control. He was admitted to management can be attempted with nicardipine the ICU for further testing. The child’s metanephrine or nitroprusside. It is important to remember levels were high, and he had a negative renovascu- that many of these patients are profoundly lar evaluation. He underwent CT scanning, which dehydrated, and all require IV fluid resuscitation, demonstrated a concerning mass in his pelvis. He was usually with several weight-based boluses of discharged home and returned for elective surgery crystalloid. after3weeks.Themasswasidentifiedasanextra- The long-term treatment of these patients is adrenal malignant pheochromocytoma. The child initially with oral alpha-blockade, most hassincehadthemassresectedandisundergoing commonly with phenoxybenzamine, which binds chemotherapy. the alpha-receptor irreversibly. Oral beta-blockade may be added after adequate alpha-blockade. Most patients undergo resection References of their tumors, but resection is not performed 1. Brady TM, Feld LG. Pediatric approach to until the child is adequately resuscitated and has hypertension. Semin Nephrol 2009; 29: 379–88. adequate alpha- and beta-blockade. Typically, the 2. Riley M. High blood pressure in children and resection is performed in an elective fashion and adolescents. Am Fam Phys 2012; 85: 693–700. the child is observed in an ICU setting 3. Waguespack SG, Rich T, Grubbs E, et al. A current before and immediately after the procedure. All review of the etiology, diagnosis, and treatment of children with pheochromocytoma should pediatric pheochromocytoma and paraganglioma. undergo evaluation for inherited endocrine J Clin Endocrinol Metab 2010; 95: 2023–37. syndromes. 4. Havekes B, Romijn JA, Eisenhofer G, et al. Update on r Disposition:Childrenwithmalignant pediatric pheochromocytoma. Pediatr Nephrol 2009; hypertension should be admitted to an ICU 24: 943–50. setting where they have appropriate monitoring. 5. Adullah I, Cossey K, Jeanmonod R. Extra-adrenal Children with asymptomatic hypertension require pheochromocytoma in an adolescent. West J Emerg close outpatient follow-up to determine causes of Med 2011; 12: 258–61. secondary hypertension. Hypertension in children 6. Eisenhofer G, Goldstein D, Walther M, et al. always requires an evaluation, and should never Biochemical diagnosis of pheochromocytoma: How to be presumed to be primary in etiology. distinguish true- from false-positive test results. JClin Endocrinol Metab 2003; 88: 2656–66. 7. Guller U, Turek J, Eubanks S, et al. Detecting Historical clues Physical findings Ancillary studies pheochromocytoma: Defining the most sensitive test. Ann Surg 2006; 243: 102–7. r Episodic r Marked r Negative head CT 8. Ilias I, Pacak K. Current approaches and r headaches r hypertension r Diaphoresis r Tachycardia recommended algorithm for diagnostic localization of r Vomiting r Diaphoresis pheochromocytoma. J Clin Endocrinol Metab 2004; 89: Palpitations Dyspnea 479–91.

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Case 3 Contributing Authors: Tom Dittrich, Denis R. Pauze,´ and Matthew Adamo History The patient is a 16-year-old male who fell from his skateboard approximately 30 minutes prior to arrival. He was riding the skateboard when the board came out from under him and he fell backwards, striking the back of his head on concrete. He was not wearing a helmet. The fall was from a standing height and he briefly lost consciousness. An ambulance was called. He was awake and alert and vomited once during transport. He complained of a severe headache described as pressure, originating from the posterior of the occiput. He reports neck pain. He repeatedly asks for an emesis bag throughout the ride to the hospital. He denies chest pain, shortness of breath, abdominal pain, extremity pain,visualchanges,ordizziness. Figure 10.1 Head CT demonstrating an occipital epidural Past Medical History hematoma. r UTD on immunizations. motion and no tenderness on examination. Medications Superficial abrasions over the right posterior r None. thorax. r Neurologic: Child is sleepy but rouses easily. No Allergies focal deficits. r r NKDA. Pertinent laboratory values: WBC 17,000, Hb 14, complete metabolic panel normal. Physical Examination and Ancillary Studies r Pertinent imaging:CXRandCTnecknormal. r Vital signs: T 98.6 °F, HR 112, BP 128/74, RR 16, Head CT shown in Figures 10.1 and 10.2. O2 sat 99% on room air. r General: Healthy-appearing 16-year-old male, Questions for Thought somnolent but easily arousable. r r When is a head CT indicated in the pediatric HEENT: Round abrasion and hematoma on the patient? posterior occiput, about 4 cm in diameter, no r What are the diagnostic studies this patient lacerations or active bleeding. No skull should receive in the ED? r depressions or Battle’s sign. Face and jaw What are the treatment options for this condition in the ED? What are options for consultants? non-tender. Teeth intact. r r Neck: No step-offs, tender at C6, c-collar in place. What are important management strategies in patients with traumatic brain injury (TBI)? r Cardiovascular:Regular,withnoM/R/G. r Lungs: Clear bilaterally, with no W/R/R, no chest-wall tenderness. Diagnosis r Abdomen: Soft and non-tender, with no distension r Occipital epidural hematoma. or signs of trauma. r Extremities and skin: No thoracic or lumbar Discussion midline tenderness. Pelvis is stable, all peripheral r Epidemiology: Head injuries, including falls with joints ranged and palpated with full range of “bump on the head,” concussions, and TBIs are

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damage to an underlying vessel (such as the middle meningeal artery), which subsequently bleeds in the extradural space between the dura and the skull. As blood fills this space the hematoma tends to thrust inwards, displacing the brain. This yields the classic convex appearance of blood visualized on CT imaging. If left untreated, this bulging can lead to the brain herniating through the foramen magnum at the skull base, leading to death. Symptoms are related to the pressure from the bleeding site. r Presentation: The presentation for an epidural hematoma varies considerably by age group. In patients younger than 12 months, the open fontanelles may allow for expansion of bleeding in the skull. This is important to note, as active bleeding may result in a large amount of blood accumulation in the skull, even before signs of Figure 10.2 Head CT with bone windows demonstrating an clinical deterioration. Initially, these infants may occipital skull fracture. present with non-specific symptoms, such as vomiting, fussiness, irritability, or lethargy.3 Seizure and unresponsiveness may also be seen. commonly encountered scenarios for the EM Physical examination should pay particular clinician. It is estimated that more than 1.5 attention to signs of head trauma, which includes million TBIs occur annually, with a resultant more scalp bruising, hematoma, or cephalohematoma. than 50,000 yearly deaths.1,2 From 2001 to 2010, Although a late clinical finding, a large and TBI ED visits, hospitalizations, and deaths have bulging fontanelle may also be seen. Classic increased, with 715 TBI-related visits per 100,000 changes of bradycardia and pupillary changes are population in 2010.1,2 Children age 0–4 have had also delayed findings. The commonly described the greatest frequency of TBI, with a rate more “lucid interval” for temporal epidural hematoma than double that of any other age group.1,2 This is often absent in children younger than 12 high-risk age group also has the greatest increase months.3 Rather, infants may present with in injury rate, with an approximately 50 percent vomiting, irritability, or hemorrhagic shock from increase in ED visits for TBI between 2001 and blood loss in the brain. It is important to note 2010.1,2 Common causes of TBI in children aged that, in cases of non-accidental head injury, there 0–14 include motor vehicle crashes, falls, and may be no history of trauma provided. assault. Varied presentations exist in older children, TBI encompasses a wide range of brain injury, andmayberelatedtothesizeandlocationofthe including edema, bleeding, herniation, and bleed.3 History may reveal a loss of consciousness contusions. Epidural hematomas represent a small and/or a lucid interval. Headaches with subset of TBIs. Causative factors will vary by age. nausea/vomiting are common complaints. Falls and abusive head trauma are more prevalent Patients with persistent bleeding may be confused in the younger patient, while motor vehicle or altered. Anisocoria, hemiparesis, or hemiplegia crashes account for the most common cause in the are late clinical findings and indicators of teenage population. Epidural hematomas that are significant bleeding and eventual herniation. promptly diagnosed and treated often have an Cushing’s triad of hypertension, bradycardia, and excellent outcome. respiratory depression may be seen in this age r Pathophysiology: Epidural hematomas typically group. arise from trauma to the temporal or occipital r Diagnosis: Not all children with head injuries need regions of the head. The skull is fractured, causing imaging. Certainly, an obtunded pediatric patient

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or one with a diminished GCS does not present as dioxide status, and glucose levels are paramount a diagnostic dilemma, as imaging is clearly to optimize treatment in the brain-injured child. needed. The indications for imaging include For patients with epidural hematomas, goals considering the mechanism of the injury, the include making the correct diagnosis, finding location of the head injury, neurologic additional injuries such as c-spine pathology, examination, and features such as a loss of timely neurosurgical consultation and care, and, if consciousness, irritability, lethargy, vomiting, or needed, airway protection. These will each be seizures. Clinical decision rules have been considered below. developed to help aid the clinician as to when r Airway and oxygenation: Maintaining appropriate CT imaging in children with a TBI is oxygenation and ventilation during care indicated. Examples of clinical decision rules for remains a high priority, as hypoxia worsens pediatric head injuries include CHALICE, secondary brain injury. Patients with a poor CATCH (Canadian Assessment of Tomography GCS (typically less than 9) or with rapidly 4 for Childhood Head Injury), and PECARN. The declining mental status should be intubated for PECARN decision rule is discussed in detail in airway protection. Special attention should be Chapter 2, Case 2, and Table 2.2. placed on maintaining oxygen saturation and When the decision is made to use preventing desaturation. Making sure the child radiographic imaging, the diagnosis of an is appropriately pre-oxygenated therefore epidural hematoma is made in the ED with a remains a crucial component of care. non-contrast head CT. Classically, a biconvex area Remember, children are rapid oxygen of hematoma is seen between the inside of the metabolizers and will desaturate quickly. A skull and the brain. Features to note include nasal cannula before and during intubation is midline shift, effacement of ventricles, “swirling” recommended. Etomidate may be used as an within the hematoma suggestive of active induction agent, as it may decrease intracranial bleeding, and evidence of herniation. Cranial U/S pressure and improve cerebral perfusion is not an appropriate diagnostic study to evaluate pressure.8,9 Intubated patients should be for an epidural hematoma, even in very young ventilated to maintain a PaCO2 of 35–40 to infants where cranial U/S is used for other keep the intracranial pressure relatively low.5 purposes. MRI may be used, but has a limited role Once intubated, the bed should be placed with in many institutions secondary to its lack of the head elevated to 30 degrees. availability. LP is contraindicated for the r Cerebral perfusion pressure and systolic blood theoretical risk of inducing herniation. pressure:Aspreviouslymentioned,when Patients with a suspected epidural hematoma cerebral blood flow is compromised, harmful typically also meet criteria for imaging of the secondary brain injury results. Therefore, c-spine. Patients with multi-trauma, altered maintaining blood perfusion through the brain mental status, or a complaint of pain and bony is of paramount importance. Cerebral tenderness should be strongly considered for perfusion pressure is measured by the mean c-spine imaging. Further discussion of c-spine arterial pressure minus the intracranial imaging may be found in Chapter 2, Case 3. = r pressure (CPP MAP – ICP). Thus, Treatment:ThegoaloftreatmentintheEDisto optimizing blood pressure is another vital prevent secondary brain damage caused by the component to maintaining appropriate initial TBI. Secondary brain damage leads to cerebral perfusion pressure.8 It is estimated increased intracranial pressure, cerebral edema, that an episode of hypotension during the first 5–7 and subsequently poor neurologic outcomes. 6hoursaftertheinitialTBIisapredictorof Therefore, maintaining and optimizing blood poor neurologic outcome. It is therefore perfusion throughout the brain is a paramount recommended that blood pressure be component of therapy for TBI, as hypoxia and maintained at least at the 75 percent range for 5–7 hypotension lead to worse outcomes. Special the patient’s age. Fluid resuscitation and/or attention to oxygenation, blood pressure, carbon pressors to maintain mean arterial pressures

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should be implemented in order to maintain r Disposition: All patients with an epidural cerebral perfusion. hemorrhage should be admitted to an ICU for r Hyperosmolar solution: If signs of herniation close monitoring of their neurologic status. If not are present, then treatment with hyperosmolar available, transfer to a capable trauma center is solution such as 3% saline or mannitol may be needed. Neurosurgery consultation is also indicated. Although debatable, 3% saline may indicated. be a more favorable option, especially in the hypotensive patient.9 Historical clues Physical findings Ancillary studies r r r r Neurosurgical consultation:Allpatientswith r Trauma r Signs of trauma Head CT with epidural hematomas require consultation with Vomiting Sleepiness epidural r Loss of hematoma and a neurosurgeon as early as possible. Operative consciousness skull fracture management is recommended for patients with a poor GCS or rapidly declining mental status, focal neurologic deficits such as signs of Follow-Up impending herniation, a midline shift on CT, The patient had an isolated occipital epidural or relatively large hemorrhages. The procedure hematoma and an otherwise unremarkable trauma involves opening the skull and evacuating the work-up.Hisbloodpressureandoxygensaturation hematoma. In the event that a neurosurgeon is were consistently within normal limits. Neurosurgery not available at the treating hospital, transfer to was consulted. He was made NPO and started on a trauma center with appropriate capabilities is IV fluids. He was deemed to be a candidate for non- required. operative management and was admitted to the PICU. r Burr hole:Veryrarely,theEMprovidermay He maintained a GCS of 15 throughout his hospital need to perform a burr hole. Certainly, this is a course and had an uneventful recovery without procedure that the vast majority of EM requiring surgical evacuation of the hematoma. physicians do not do, have never done, and are not trained to do. A scenario exists where a References child comes into the ED, is diagnosed with a 1. Centers for Disease Control and Prevention. Rates of large epidural hematoma, and has TBI-related emergency department visits, deteriorating mental status that subsequently hospitalizations, and deaths – United States, requires airway protection and intubation. If 2001–2010. See www.cdc.gov/traumaticbraininjury/ the hospital has no neurosurgical availability data/rates.html (accessed January 2017). andtransferisnecessary,itispossiblethata 2. Centers for Disease Control and Prevention. Annual long transport time is required to get to the number of TBIs. See www.cdc.gov/ nearest trauma center with neurosurgical traumaticbraininjury/pdf/tbi blue book capabilities. Unfortunately, the child described annualnumber.pdf (accessed January 2017) in this scenario may not survive a prolonged 3. Rocchi G, Caroli E, Raco A, et al. Traumatic epidural transport time. Active bleeding could cause hematoma in children. JChildNeurol2005; 20: herniation in a short period of time. This could 569–72. certainly occur at a rural hospital, many miles 4. Lyttle MD, Crowe L, Oakley E, et al. Comparing away from a trauma center. Bad weather could CATCH, CHALICE, and PECARN decision rules for paediatric head injuries. Emerg Med J 2012; 29: also prevent evacuation by helicopter and thus 785–94. force a lengthy ground transport. Faced with 5. KochenekPM,CarneyN,AdelsonPD,etal. this difficult and unusual scenario ofa Guidelines for the acute medical management of time-sensitive procedure and long transport severe traumatic brain injury in infants, children, and time, the EM provider should consider a burr adolesscents: Second edition. Pediatr Crit Care Med hole when herniation or death is likely. 2012; 13 Suppl 1: S1–82. Descriptions of this technique are available in 6. Vavilala MS, Bowen A, Lam AM, et al. Blood pressure the article Emergency burr holes: “How to do and outcomes after severe pediatric traumatic brain it.”10 injury. JTrauma2003; 55: 1039–44.

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7. ChaiwatO,SharmaD,UdomphornY,etal.Cerebral Physical Examination and Ancillary Studies hemodynamic predictors of poor 6-month Glasgow r Vital signs: T 98.6 °F, HR 90, BP 98/56, RR 20, O2 Outcome Score in severe pediatric traumatic brain sat 100% on room air. injury. JNeurotrauma2009; 26: 657–63. r General: Patient is calm, not distressed, but points 8. Allen BB, Chiu YL, Gerber LM, et al. Age specific tohisheadashesays“ithurts.” cerebral perfusion pressure thresholds and survival in r children and adolescents with severe traumatic brain HEENT: Tympanic membranes are clear without injury. Pediatr Crit Care Med 2014; 15: 62–70. erythema. No discharge. No rhinorrhea. No 9. Shein SL, Ferguson NM, Kochanek PM, et al. tonsillarerythemaorabscess.PERRL.Pain Effectiveness of pharmacological therapies for with extraocular movements. Funduscopic intracranial hypertension in children with severe examination not performed due to patient’s lack traumatic brain injury. Pediatr Crit Care Med 2016; 17: of cooperation. 236–45. r Neck: Supple, without masses or adenopathy. 10. Wilson MH, Wise D, Davies G, et al. Emergency burr r Cardiovascular: Regular rate and rhythm, with no holes: “How to do it.” Scand J Trauma Resusc Emerg M/R/G. Med 2012; 20: 24. r Lungs: Normal work of breathing, clear bilaterally. No W/R/R. r Abdomen:Soft.Notendernessordistension. Case 4 Positive bowel sounds. r Extremities and skin: No bruising, tenderness, or Contributing Authors: Anst Gelin and Janet rash. Young r Neurologic: The patient is alert and oriented. He History follows commands without difficulties. Positive dysmetria. Positive Romberg. No focal weakness The patient is a 4-year-old male, who is presenting to noted. the ED, accompanied by his mother, for headaches. r Pertinent laboratory values:CBC,comprehensive The patient’s mother reports that for approximately 1 metabolic profile, toxicologic screens all normal week the patient has been complaining of intermit- or negative. tent headaches. However, he has been “doing fine” in r Pertinent imaging:CTheadwithIVcontrast terms of eating, sleeping, and playing with his older shows a posterior fossa mass, which is located in sister (2 years older than the patient). Initially, she was the midline with homogeneous contrast not concerned because the child appeared to be act- enhancement. ing normally. After a week, she became concerned for several reasons: in the prior 24 hours, the patient had bumped into the doorway twice as he was coming out Questions for Thought ofhisroom,andheonceappearedtobedriftingtohis r left side when running during playtime. The mother What symptoms are concerning for intracranial mass? reportsthatthepatientisusuallyveryagile,andthe r What are some options for treatment? imbalance is very unusual for him. r What is the likelihood that this child will be alive and doing well in 10 years? Past Medical History r Full-term vaginal delivery with no complications. r Vaccinations UTD. Diagnosis Medications r Medulloblastoma. r None. Discussion Allergies r Epidemiology: In pediatric patients, brain tumors r NKDA. make up approximately one-fifth of solid tumors;

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of those, medulloblastomas are the most by the parent or other care provider is very common.1 They account for approximately 20 important, given the subtle changes that may percent of all intracranial tumors in children. be noticed by someone who knows the patient They are most commonly seen in children well. between the age of 1 and 10 years, with peak On physical examination, ataxia can be noted; incidence occurring from 3 to 5 years of age.1,2 abnormal gaze can also be found. Papilledema Over 250 children are diagnosed with this disease will be seen in the setting of elevated intracranial every year. As is true in most cases of brain pressure, which may be seen in the setting of tumors, the causes are unknown. There may be a headaches, ataxia, and other complaints. rare hereditary association with isochromosome Utilization of bedside U/S may non-invasively 17q, which is reported to be present in one-third diagnose papilledema, if the patient will tolerate to one-half of the cases, and it is thought that it. Once the possibility of intracranial lesion is some cases may be secondary to radiation considered, CT and MRI are both useful for exposure.2 diagnostic and treatment planning.5 While MRI is r Pathophysiology: Medulloblastomas are usually superior to CT, the cost, rapidity, and availability found in the cerebellum, and usually extend to the of CT makes it a valuable tool in the initial fourth ventricle. Although pressure can build up evaluation of intracranial masses. MRI of the in the intracranial space from a mass effect with spine may be necessary to evaluate for metastatic tumor growth, CSF obstruction at the fourth disease preoperatively. ventricle is usually the cause of the increased r Treatment: In the acute presentation, treatment intracranial pressure that leads to papilledema effortsshouldbefocusedonsymptomatic and the clinical findings that are seen. Although management and decreasing the intracranial rare, a tumor can metastasize to the spinal cord pressure to prevent herniation. Dexamethasone and, less commonly, to the bone marrow. There is should be given (1 mg/year of age, maximum dose more discussion of pathophysiology of brain of 10 mg). An actively seizing patient should tumors in general in Chapter 7, Case 6. receive appropriate dosing of benzodiazepines in r Presentation: Like other brain lesions in children, addition to the consideration of cerebral diuretics the initial presentation of a medulloblastoma can (mannitol), antihypertensives (carbonic be vague and non-specific. Considering the push anhydrase inhibitors, loop diuretics), or to limit unnecessary radiation in children, the hypertonic (3%) saline. examiner must perform a very thorough history Definitivetreatmentintheabsenceof and physical examination to include brain tumors metastasis involves resection followed by in the differential diagnosis. The most common radiation and/or chemotherapy. With the current symptoms include headaches, vomiting, treatments available, the survival rate for the clumsiness, ataxia, loss of fine motor functions, disease is estimated to reach 80 percent in mild and cognitive decline.3,4 As in other tumors of the cases and approximately 60 percent in patients posterior fossa, early-morning or post-nap with metastatic spread. Younger patients do have headaches and vomiting is a classic presentation. higher mortality as compared to older children. Other reported symptoms include back pain, One important factor affecting survival is the visual disturbance, seizures, somnolence, and ability for a complete surgical resection of the urinary and stool incontinence.3,4 Other tumor. non-specific symptoms can be social in nature, Tumor recurrence is a concern that exists, such as behavioral changes and sleeping with one study reporting survival around 65 disturbances. Many of the symptoms listed are percentat30yearsofageforapatientdiagnosed due to intracranial hypertension. at age 0–19 years.6 Alargeportionofthosedeaths r Diagnosis:Thediagnosisofamedulloblastoma were due to primary tumor recurrence and other relies on historical clues and physical examination malignancies.6 findings, which should lead a provider to Seizures can be seen in patients who have been consider the diagnosis. The history as provided treated for brain tumors.7 However, the incidence

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of seizures in medulloblastomas is much less Case 5 when compared to other intracranial tumors such as glioneuronal tumors, high-grade gliomas, and Contributing Authors: Christine M. George oligodendrogliomas.7 Long-term antiepileptic medications can be considered in consultation and Melanie K. Prusakowski with a neurologist. History r Disposition:Patientsdiagnosedwith The patient is a 5-year-old girl who presents with 3 days medulloblastomas or other unknown brain of headache. It began with a generalized headache, lesions should be admitted for evaluation and which improved with ibuprofen. The child developed multidisciplinary planning with neurosurgery, a fever 2 days ago to 101 °F. She still complained of oncology, and radiation oncology. the headache, and was less active and more irritable. Yesterday, she continued with her symptoms and Historical clues Physical findings Ancillary studies also vomited twice. Her mother has been alternating ibuprofen and acetaminophen every few hours with r Headache r Positive Romberg r Head CT with r Bumping into r Dysmetria posterior fossa minimal relief. This morning her headache became worse. She has associated photophobia, intermittent r wall mass Gait instability abdominal pain, and multiple episodes of non-bilious emesis. Her mother also notes she has been very tired and “not herself.” There is no reported seizure Follow-Up activity. Her mother believes a few children at day- The child was admitted to the hospital for neurosur- care were recently sick but cannot provide further gical consultation and malignancy staging. He under- details. Mom reports no recent travel or known head went primary resection and radiation therapy, and is trauma. currently in remission. Past Medical History References r Healthy and UTD on immunizations. 1. Johnson KJ, Cullen J, Barnholtz-Sloan JS, et al. Childhood brain tumor epidemiology: A brain tumor Medications epidemiology consortium review. Cancer Epidemiol r Ibuprofen last taken 3 hours ago. Biomarkers Prev 2014; 12: 2716–36. r Acetaminophen last taken 7 hours ago. 2. Wrensch M, Minn Y, Chew T, et al. Epidemiology of primary brain tumors: Current concepts and review of the literature. Neuro Oncol 2002; 4: Allergies 278–99. r NKDA. 3. Purdy RA, Kirby S. Headaches and brain tumors. Neurol Clin 2004; 22: 39–53. Physical Examination and Ancillary Studies 4. Wilne S, Collier J, Kennedy C, et al. Progression from r Vital signs: T 99.3 °F, HR 97, RR 20, BP 103/55, O2 first symptom to diagnosis in childhood brain sat 99% on room air. tumours. Eur J Pediatr 2012; 171: 87–93. r General: Well-developed girl, laying on stretcher 5. Toriori-Donati P, Fondelli MP, Rossi A, et al. in moderate distress. Upsets easily throughout Medulloblastoma in children: CT and MRI findings. Neuroradiology 1996; 38: 352–9. examination and continually complains of headache. 6. NingMS,PerkinsSM,DeweesT,etal.Evidence r of high mortality in long term survivors of HEENT: Normocephalic and atraumatic. Mucous childhood medulloblastoma. JNeurooncol2015; 122: membranes are dry. Tympanic membranes are 321–7. clear. No oropharyngeal exudate or erythema. No 7. Ullrich NJ, Pomeroy SL, Kapur K, et al. Incidence, oral ulcers. Unable to perform funduscopic risk factors, and longitudinal outcome of seizures in examination due to poor patient cooperation. long-term survivors of pediatric brain tumors. PERRL, although child complains of increased Epilepsia 2015; 56: 1599–604. head pain when light is shined into her eyes. No

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conjunctivae discharge. No scleral erythema or Diagnosis icterus. r Meningitis, most likely enteroviral. r Neck: No cervical lymphadenopathy. Range of movement and nuchal rigidity difficult to assess secondary to patient cooperation. Discussion r r Cardiovascular: Regular rate and rhythm. No Epidemiology:Meningitisisinflammationofthe murmur. Brisk capillary refill. leptomeninges and subarachnoid space, and is r Lungs:Effortnormal.CTAbilaterally. most often the result of an infectious agent. In the r Abdomen: Bowel sounds are normal. Soft, USA, bacterial meningitis is much more rare than non-tender, no mass, no organomegaly. other kinds of meningitis, and has a mortality of about 10 percent.1–4 In developing nations where r Extremities and skin: Normal range of motion. No routine immunization is less common, bacterial joint swelling, redness, or tenderness. meningitis affects 1 of 250 children in his or her Erythematous, blanchable, papular rash on the first year of life.2,3 Since the successful chest, without extremity or face involvement. introduction of conjugate vaccines for r Neurologic: Very irritable but able to answer Haemophilus influenzae type b (Hib) and questions appropriately after being consoled by Streptococcus pneumoniae, the incidence of mother. Extraocular movements are intact. Facial bacterial meningitis in the USA has decreased.2 muscles activate symmetrically. Tongue midline. Peak incidence occurs in infants less than 2 Palate elevates symmetrically. Spontaneously months of age (80.69 cases per 100,000 population moves all four extremities equally, without in 2006–2007).1,5 Patient age and host immunity obvious focal weakness. She is able to ambulate likely have the greatest effect on the etiology of with a steady gait. 4 r bacterial meningitis. For example, lack of Pertinent laboratory values: immunization, asplenia, sickle cell disease, HIV r WBC 7,600, with a normal differential; infection, otitis media, sinus infection, and r Glucose 92; cochlear implants are predisposing risk factors for r U/A with 40+ ketones and trace protein, pneumococcal and Hib meningitis. otherwise normal; Immunodeficiency and diabetes mellitus are risk r CSF: factors for S. pneumoniae and Listeria r Glucose 56 mg/dL; monocytogenes meningitis. Terminal complement r CSF protein: 54 mg/dL; deficiency and living in certain environments (e.g. r Tube 1: WBC 253, RBC 1,489; dormitory or military barracks) are risk factors r Tube 3: WBC 333, RBC 15; for Neisseria meningitidis meningitis, which has a r WBC differential: neutrophils 68%, peak incidence in older adolescence. lymphocytes 26%, mononuclear cells 6%, Aseptic meningitis refers to inflammation of and absolute neutrophils 226.4/mm3; the meninges without the presence of visible r Gram’s stain: 2+ WBC, no organisms microorganisms on routine CSF Gram’s stain. The seen. causative agent may be viral, fungal, or parasitic. It may also be secondary to atypical bacteria that are not well seen on Gram’s staining, such as Questions for Thought Mycobacterium or Borrelia. Viral meningitis is r How does the clinical presentation of this more common than bacterial meningitis and all condition vary by patient age? other causes of aseptic meningitis combined.1,4 r What other laboratory tests could help narrow Enteroviruses, such as echovirus, Coxsackie virus the diagnosis? B, and enterovirus-71, account for more than 80 r How do the typical laboratory ﬁndings in this percent of all cases of viral meningitis in the USA, condition vary by etiology? r with a majority of these occurring in children less What are some indications for the use of than 5 years of age.1,4 In temperate climates, the radiographic diagnostic modalities? incidence of enteroviral meningitis peaks in the r What treatment should be initiated in the ED? summer and early fall.

16:26:06 7 11 Chapter 10: Head and Neck Pain r Pathophysiology: Pathogens enter the CNS via is important to recognize these findings, any hematogenous spread or as a direct extension specific finding suffers from either poor sensitivity from a contiguous site, such as the inner ear or or poor specificity or both, and clinician gestalt is sinuses. Direct communication with the CSF can still an important predictor for meningitis.2,6 occurincasesoftraumaandinpatientswith r Diagnosis: Initial laboratory evaluation should cochlear implants. Ventriculoperitoneal shunts, include a CBC with differential, peripheral and/or congenital dural defects, such as dermal glucose, and blood culture(s). CSF should sinus or meningomyelocele, are also causative evaluate the WBC with differential, RBC, glucose, factors. In neonates, pathogen exposure most protein, and Gram’s stain. A CSF culture should often occurs after contact with maternal also be obtained. CRP should not be used as a secretions during delivery. The most common screening tool for meningitis. bacterial pathogens associated with neonatal LP with CSF examination is indicated for all meningitis include Streptococcus agalactiae (group patients with suspected meningitis, unless B streptococcus), Escherichia coli,andListeria contraindicated due to clinical instability, monocytogenes.2–4 In infants and children, coagulopathy, or suspicion of a space-occupying organismsoftenspreadafterfirstcolonizingthe intracranial lesion. Head CT should be confirmed upperrespiratorytractandthencrossingthe priortoLPifthepatientisimmunocompromised, blood–brain barrier. The presence of infectious has a history of CSF shunt placement, organisms results in the release of cytokines, hydrocephalus, prior neurosurgery, or if there are which can cause fever, subarachnoid concerns for a CNS space-occupying lesion.2 inflammation, and altered blood flow. These Patients with papilledema or a focal neurologic pro-inflammatory mediators ultimately manifest deficit (other than cranial nerve VI or VII) on as meningismus and impaired cerebral glucose physical examination should also have a metabolism. This may lead to vasculitis, radiographic study prior to LP.2 Initiation of seizures, coma, and potentially may progress to empiric antibiotic therapy should not be delayed if death. LP must be deferred. Early antibiotics decrease r Presentation:Theclinicalpresentationof morbidity and mortality, and should not be meningitis can vary significantly based on the delayedforanyreasonwhatsoever. causative pathogen, patient age, duration of The Bacterial Meningitis Score has been illness, and host response to infection. Infants utilized for augmenting clinical distinction of younger than 1 month of age who have either viral bacterial from viral meningitis.7 Bacterial or bacterial meningitis often present with a meningitis is very unlikely in children without: constellation of non-specific, “sepsis-like” signs, r Bacteria on Gram’s stain; including fever or hypothermia, lethargy, r CSF protein Ͼ 80 mg/dL; irritability, and poor feeding.2 Older infants and r Peripheral absolute neutrophil count Ͼ 10,000 young children may instead demonstrate signs cells/mm3; and symptoms of meningeal inflammation and r CSF absolute neutrophil count Ͼ 1,000 increased intracranial pressure, including cells/mm3; paradoxical irritability (does not wish to be r Seizures. handled and prefers to remain motionless), vomiting, apnea, and seizures.2,6 Older children If any of these criteria are present, meningitis and adolescents with meningitis more often cannot be ruled out and empiric antibiotics experience malaise, headache, photophobia, and should be continued.7 These criteria are less neck stiffness.6 Bulging fontanelle, neck stiffness, reliable in children with recent antibiotic use, or seizure can occur. Some patients may exhibit a which has been shown to increase CSF glucose petechial or purpuric rash. Cranial nerve palsy and protein levels as well as the likelihood of a (most often III, IV, and/or VI) can be present with positive CSF culture. bacterial and Lyme meningitis. In general, a child For children with a CSF pleocytosis, with viral meningitis does not appear as critically additional testing should be dictated by the ill as a child with bacterial meningitis. Although it clinical scenario. Enteroviral PCR testing can

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confirm a viral infection and shorten the duration In general, there is no specific therapy for viral of hospitalization and IV antibiotics.8,9 HSV PCR meningitis. Mainstays of treatment include IV testingshouldbeconsideredinneonates.10 Lyme fluids, analgesics, and antiemetics. For patients meningitis is a consideration in children with CSF with suspected HSV meningitis, empiric IV pleocytosis who live in Lyme endemic areas, such acyclovir should be initiated pending CSF HSV as the northeast, mid-Atlantic and upper midwest PCR results. of the USA. However, it can often be difficult to r Disposition: Infants and young children with distinguish between Lyme meningitis and other meningitis should be admitted to the hospital for causes of aseptic meningitis in the ED. One definitive diagnosis, treatment, and supportive validated clinical prediction rule to help identify care. Children should be admitted to a PICU if children at low risk for Lyme meningitis is the they have focal neurologic findings, signs of “rule of 7s”: less than 7 days of headache, less than impending neurologic collapse, or signs of shock CSF 70 percent mononuclear cells, and no or respiratory compromise. Older children and (including seventh) cranial nerve palsy teenagers with confirmed viral meningitis will (sensitivity 96 percent, specificity 41 percent, have a self-limited illness and may be appropriate negative likelihood ratio 0.1).11,12 Lyme serology for discharge home. and CSF antibodies should be ordered if Lyme meningitis is suspected. There is more information on Lyme disease in this chapter, Historical clues Physical findings Ancillary studies Case 7, and Chapter 6, Case 5. r r r r Headache r Photophobia Elevated WBC in r Treatment: Treatment of meningitis begins with Fever Irritability CSF r Vomiting r Negative Gram’s an assessment of respiratory, circulatory, and r r Irritability stain neurologic status. Fluid resuscitation may be Photophobia required in patients with shock. Airway protection may also be needed. Empiric antimicrobial therapy for suspected bacterial Follow-Up meningitis varies based on patient age and specific The child received IV antibiotics in the ED for bacte- predisposing conditions. In neonates, empiric rial meningitis and was admitted for IV fluids, antibi- therapy consists of ampicillin plus cefotaxime or otics, and observation. The child’s PCR came back pos- an aminoglycoside. In older infants and children, itive for enterovirus, and the child’s antibiotics were empiric treatment is a third-generation stopped. She was discharged home after 3 days and had cephalosporin (ceftriaxone or cefotaxime) plus afullrecovery. vancomycin. Empiric therapy in the setting of penetrating trauma, recent neurosurgery, or a CSF shunt is vancomycin plus cefepime, ceftazidime, References or meropenem. If the patient is unimmunized and 1. Thigpen MC, Whitney CG, Messonnier NE, et al. Bacterial meningitis in the United States, 1998–2007. Hib meningitis is suspected, the administration of NEnglJMed2011; 364: 2016–25. dexamethasone prior to antimicrobial therapy is associated with less severe hearing loss, but does 2. DorsettM,LiangSY.Diagnosisandtreatmentof central nervous system infections in the emergency notconsistentlyaffectmortalityortheriskof department. Emerg Med Clin N Am 2016; 34: 917–42. other serious neurologic sequelae.13 3. Tacon CL, Flower O. Diagnosis and management of Dexamethasoneisthusindicatedincasesof bacterial meningitis in the pediatric population: A suspected or confirmed Hib meningitis (e.g. the review. Emerg Med Int 2012; 2012: 320309. unimmunized child) if the patient is 6 weeks of 4. Centers for Disease Control and Prevention. age or older and the steroid can be administered Meningitis. See www.cdc.gov/meningitis/ (accessed just before or concurrently with the first dose of January 2017). 13 antimicrobial therapy. The efficacy of 5. Nigrovic LE, Kuppermann N, Malley R, et al. Children corticosteroid use in children with meningitis with bacterial meningitis presenting to the emergency caused by organisms other than Hib is department during the pneumococcal conjugate controversial. vaccine era. Acad Emerg Med 2008; 15: 522–8.

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6. Bilavsky E, Leibovitz E, Elkon-Tamir E, et al. The chills, rash, neck complaints, cough, or respiratory diagnostic accuracy of “classic meningeal signs” in complaints. Mom has a history of migraine headaches. children with suspected bacterial meningitis. Eur J Emerg Med 2012; 20: 361–3. Past Medical History 7. Nigrovic LE, Kuppermann N, Macias CG, et al. r None. Immunizations are UTD. Clinical prediction rule for identifying children with cerebrospinal fluid pleocytosis at very low risk of Medications bacterial meningitis. JAMA 2007; 297: 52–60. r Multivitamins. 8. King RL, Lorch SA, Cohen DM, et al. Routine cerebrospinal fluid enterovirus polymerase chain Allergies reaction testing reduces hospitalization and antibiotic r use for infants 90 days of age or younger. Pediatrics NKDA. 2007; 120: 489–96. Physical Examination and Ancillary Studies 9. Lyons TW, McAdam AJ, Cohn KA, et al. Impact of r in-hospital enteroviral polymerase chain reaction Vital signs: 98.8 °F, HR 82, RR 18, BP 114/72, O2 testing on the clinical management of children with sat 100% on room air. meningitis. JHospMed2012; 7: 517–20. r General: The patient is well-appearing, non-toxic, 10. Long SS, Pool TE, Vodzak J, et al. Herpes simplex virus andinnoacutedistress. infection in young infants during 2 decades of empiric r HEENT: Atraumatic and normocephalic. PERRL. acyclovir therapy. Pediatr Infect Dis J 2011; 30: 556–61. Extraocular movements intact. Sclera 11. Garro AC, Rutman M, Simonsen K, et al. Prospective unremarkable. Funduscopic examination validation of a clinical prediction model for Lyme unremarkable. Moist mucous membranes without meningitis in children. Pediatrics 2009; 123: e829–34. oropharyngeal lesions. 12. Cohn KA, Thompson AD, Shah SS, et al. Validation of r Neck: Supple, no cervical lymphadenopathy. No a clinical prediction rule to distinguish Lyme nuchal rigidity. Full range of motion. meningitis from aseptic meningitis. Pediatrics 2012; r 129: e46–53. Cardiovascular: Regular rate and rhythm, with no M/R/G. 13. Brouwer MC, McIntyre P, Prasad K, et al. r Corticosteroids for acute bacterial meningitis. Lungs:Clearbilaterally,withnoW/R/R. Cochrane Database Syst Rev 2013; 6: CD004405. r Abdomen: Soft, non-tender, non-distended, no flank tenderness present, no rebound or guarding, bowel sounds present. No masses palpated. r Extremities and skin: No rashes, petechiae, or Case 6 deformity. Normal capillary refill and good pulses. r Neurologic: Awake and alert. Cranial nerves Contributing Author: Carl Daniel II–XII intact. Speech fluent. Gait normal. 5/5 History upper extremity and lower extremity strength. The patient is a 12-year-old male who presents to the Childisalertandoriented,withintactmemory ED with a headache. The headache was preceded bya and insight. No suicidal ideation. loss of vision in his left eye’s field of vision, which he described as “snow on a TV.” This lasted for approx- Questions for Thought imately 15 minutes. As it resolved, a right temporal r What are the dangerous diagnoses you should crescendo headache started. It was accompanied by consider? r nausea, photophobia, and phonophobia. He has never What is the most likely diagnosis? r had a headache like this before, and given the nausea Does this child need imaging or laboratory studies? he went to the school nurse’s office. His father brought r him to the ED for further evaluation. What are two treatment strategies for this diagnosis? He describes that he has been under significantly r How would management change if he was more pressure at school lately, with several tests and febrile? If he had right-arm and right-leg projects in one week, as well as increased track prac- weakness? tice. No recent illnesses or sick contacts. No fevers,

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Diagnosis previous diagnosis of migraine. Indeed, to carry a r Migraine headache. diagnosis of migraine, a child must have a history ofatleastfivepriorheadaches.3 Other diagnostic requirements include two of the following: Discussion r bilateral or unilateral frontal or temporal location, Epidemiology:Headachesareacommon pulsating quality, moderate to severe intensity, or complaint among children, with a prevalence of aggravated by routine physical activities.3 The 70–80 percent in children under the age of 16 headache should be accompanied by either 1,2 years. Headaches are classified into primary nausea/vomiting or photophobia/phonophobia.3 headache disorders and secondary headache If the patient presents with a first-time disorders, which are caused by underlying headache or is having recurrent headaches pathology. Of the primary headache disorders without a confirmed etiology, a thorough history (tension, cluster, migraine, and chronic daily and physical examination should be performed, headaches), migraine is the most common in looking for any clues or red flags that indicate 1,2 children. Prior to the age of 12, migraines are significant underlying pathology. Establishing the more common in males, and after age 12, females initial diagnosis of “migraine” is not of paramount 1–3 tend to have more migraines. Migraines can importance for the EM provider. This can occur in any age range, and there is evidence certainly be completed in follow-up by a linking migraine to episodic syndromes such as neurologist. Rather, the EM provider should focus 4 colic. on ruling out dangerous secondary causes of r Pathophysiology: The exact pathophysiology of headaches.7 migraines is not clearly defined and remains The EM provider should evaluate for “red unknown. Although evidence exists for a genetic flags” of headache that could harbor significant etiology, or at least a genetic component, the true and even deadly pathology. Some examples of pathophysiology of migraine headaches is likely dangerous causes of secondary headaches include multifactorial. Clinicians and researchers have brain tumor, subarachnoid hemorrhage, postulated a multitude of potential causes, meningitis, encephalitis, carotid artery dissection, including a “hyperexcitable” brain, vasodilation of carbon monoxide poisoning, and traumatic brain blood vessels, alteration of cerebral blood flow, injury. In these patients, a careful and thorough serotonin release, elevation of specific history and physical examination will guide the neuropeptides, stimulation of specific neurons, need for further diagnostic evaluation. Sudden neurogenic inflammation, and even cardiac and severe headaches (“thunderclap” or “worst shunting.5,6 headache of life,” associated with cerebrovascular r Presentation: Patients with migraine headache events), headaches that are worse upon waking may present in a variety of ways. Episodic and associated with vomiting (concerning for migraines have different presentations than increased intracranial pressure and brain tumor), chronic migraines. Some migraines may have an headaches with neurologic deficits (concerning aura, such as visual changes (scotomas, loss of for mass lesions or strokes), headaches with fever vision, bright lights), paresthesias, or (concerning for infectious and autoimmune hallucinations. Other migraine headaches do not causes), headaches with visual symptoms have an aura involved. Headache description can (concerning for pseudotumor cerebri or also vary, and may be dull, heavy, vice-like, or glaucoma), and headaches in the very young child throbbing. The headache itself can be unilateral or are all concerning for significant underlying bilateral and can evolve over the course of hours pathology. Physical examination should focus on to days. Children may present with a known prior abnormal vital signs, a careful neurologic diagnosis of migraine, or with a first attack. examination to look for focal deficits, a r Diagnosis: The diagnosis of migraine headache is funduscopic examination, visual fields, careful eye madelargelybythehistoryandphysical examination, head circumference (in young examination. Most patients will present with a infants), and an assessment of skin (for history of headaches or as someone with a toxidromes as well as for rashes suggestive of

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systemic pathology). In the child with a reassuring may also contribute, such as alcohol, caffeine, history and physical examination, it is not chocolate, cheese, and shellfish. necessary to perform laboratory tests and Prophylaxis of migraine headaches in children neuroimaging. initially involves regular sleep and meal patterns, r Treatment: Treatment should begin by placing the avoidance of triggers, and regular exercise. If these patient in a quiet and dark room, and removing do not cause significant improvement, stimuli. Migraines characteristically are improved pharmacotherapy can be introduced. This is best by sleep.3 Medical therapy includes IV fluids, done by a neurologist who specializes in migraine acetaminophen, and NSAIDs.3,7 care. Triptans, which are serotonin receptor agonists, are a potential treatment option for the acute migraine, with good efficacy.7 They are Historical clues Physical findings available as an injectable or nasal spray, and orally. r r r Headache r Normal neurologic examination Rizatriptanisapprovedforchildrenaged6or r Classic scotoma r Normal eye examination older. The combination of a triptan and Family history Normal neck examination r Crescendo headache r Normal vital signs anti-inflammatory is found in r Nausea r sumatriptan–naproxen (Treximet R ). This Phonophobia medication remains a viable option and is approved for children of 12–17 years of age. Antiemetics are also part of the Follow-Up armamentarium for the treatment of acute migraine. Promethazine is an option, but should The child was placed in a dark, quiet room. An IV be used with extreme caution. There is a “US black line was inserted, and he was given IV fluids, ketoro- box warning” for pediatric respiratory depression lac, and metoclopramide. Imaging was not performed. and potential fatality. Because it may cause Over the next few hours, his pain completely abated. significant respiratory depression, it should not be A diagnosis of probable migraine was given. He was giventochildrenlessthan3yearsofage. asked to follow up with his pediatrician and the local Promethazine also has a “black box warning” for pediatric neurologist. causing serious tissue injury. Prochlorperazine is another option and may be used for migraine References treatment in children greater than 7 years of age. 1. Parisi P, Vanacore N, Belcastro V, et al. Clinical Metoclopramide may also be used but, as also guidelines in pediatric headache: Evolution of quality with the above mentioned phenothiazines, using the AGREE II instrument. JHeadachePain2014; 15: 57. dystonic reactions may occur. When metoclopramide is used, slow infusion over 15 2. Abu-Arefeh I, Russell G. Prevalence of headache and migraine in schoolchildren. BMJ 1994; 309: 765–9. minutes will usually reduce the incidence of akathisia. Prophylaxis with diphenhydramine is 3. Lewis DW. Headaches in children and adolescents. not needed if slow infusion takes place. Am Fam Phys 2002; 65: 625–33. Diphenhydramine has not been shown to 4. van Hemert S, Breedveld AC, Rovers JM, et al. decrease migraine severity. Other pharmacologic Migraine associated with gastrointestinal disorders: Review of the literature. Front Neurol 2014; 5: 241. options include ergotamine drugs, such as dihydroergotamine and IV valproate. Opioids 5. Malhotra R. Understanding migraine: potential role for neurogenic inflammation. AnnIndianAcadNeurol generally should not be utilized. 2016; 19: 175–82. r Disposition: Children whose symptoms can be 6. BursteinR,NosedaR,BorsookD.Migraine:Multiple controlledcanbedischargedhomewithfollow-up processes, complex pathophysiology. JNeurosci2015; with neurology. Children and parents should be 35: 6619–29. counseled regarding headache triggers, and 7. Damen L, Bruijn JK, Verhagen AP, et al. Symptomatic should be encouraged to keep a headache diary. treatment of migraine in children: A systematic Lack of sleep, stress, loud noises, bright lights, and review of medication trials. Pediatrics 2005; 118: dehydration may all be triggers. Dietary factors e295–302.

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Case 7 Contributing Authors: Michael Leonard and Rebecca Jeanmonod History The patient is a 12-year-old female who comes to the EDwithaheadacheforthelast6days.Thechildstates that she believed she had “slept wrong” while traveling with her parents on a hiking vacation in the southwest USA (the child lives in Pennsylvania), first noticing the pain upon awaking in a hotel room. The pain began behindherleftearandisconstantandaching,made worse by moving her head, and associated with nausea. The patient subsequently developed low-grade fevers, and her parents noticed that she had some swollen lymph nodes in her neck. They started her on ibuprofen every 6 hours for her symptoms, which seemed to help. The child had a single episode of vomiting on day 2 of her illness, and has had a poor appetite throughout. She had never complained of headache before. There has been no trauma. The child was out of school for spring break and traveling with her parents and Figure 10.3 Photograph of child’s face, demonstrating profound three siblings, two of whom developed fever, vomiting, left-sided facial palsy. and diarrhea during the trip. The parents did not bring the child in earlier because they believed she had the r General: The patient appears well, without signs of same viral infection as her siblings and that it would get distress. better on its own. Yesterday, prior to flying home, the r HEENT: Normal ear examination, without childawokeandstated“Ithinkmyfaceisstartingto evidence of erythema or bulging of the tympanic get paralyzed.” Her parents noted at that time that she membrane, normal funduscopic examination, seemed to have some left-sided facial weakness. Today, PERRL, extraocular movements intact. the child complains of inability to drink from a glass, r Neck:Supple,withseveraltenderprominent a watery and painful eye, and ongoing head and neck lymph nodes in the cervical chain. pain. r Cardiovascular: Regular rate, with no M/R/G. Child has brisk capillary refill. Past Medical History r Lungs: Clear bilaterally, with good air movement. r The child has a history of vasovagal syncope. She r Abdomen: Soft and non-tender, with no masses, is fully immunized and developmentally normal. rebound, or guarding. r Extremities and skin:Nosignsoftrauma.Beneath Medications the child’s hair, there is a faint 6-cm blanching r Ibuprofen every 6 hours. macule surrounding the left ear, with no central clearing. r Allergies Neurologic:Thechildisalertwithage-appropriate r interactions. She has a complete left facial palsy Dogs. that includes the forehead (Figure 10.3). She has decreased taste on the left. On hearing testing, she Physical Examination and Ancillary Studies complains of “double hearing” in her left ear. Her r Vital signs: T 98.9 °F, HR 75, RR 18, O2 sat 100% neurologic examination is otherwise completely on room air. normal.

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Questions for Thought associated with Lyme disease in a cluster in the Minnesota and Wisconsin area. The spirochete r What is the diﬀerential diagnosis of pediatric uses the blacklegged tick (Ixodes scapularis)inthe facial droop? r What additional testing or imaging would be northeastern and upper midwestern USA and the useful in this patient, if any? western blacklegged tick (Ixodes pacificus)as r What treatment is indicated in this patient? vectors. There are a number of ticks in the USA that are not vectors for Lyme disease, although identification of ticks can be challenging when Diagnosis they are engorged. Lyme disease is not considered r Lyme disease, early disseminated, with facial to be transmittable between persons or from pets, nerve palsy. althoughpersonsorpetsmayactasavectorfor infected ticks. Discussion r Presentation: Lyme disease presents variably based r Epidemiology: It is estimated approximately upon the stage of the illness: 329,000 cases of Lyme disease are diagnosed each r Early localized disease; 1 year in the USA. Because there are differences in r Early disseminated disease; the methods of diagnosis – clinical observation r Late disease. versus laboratory diagnostics – the reporting rate Although the characteristic rash of Lyme is highly variable. Although the disease is disease, erythema migrans, is the most common concentrated in a select number of northeastern finding – and the only finding that allows clinical and upper midwestern states (see Table 10.1), it diagnosis – fatigue and headache are the next accounts for the fifth most commonly nationally mostcommonfindingsintheearlystagesof reported disease.2 disease, with the benchmark study of 201 children The number of cases of Lyme disease in Connecticut indicating that 42 percent of diagnosed in the USA appears to have plateaued patients with early localized disease and 70 percent between 2010 and 2014 but the number of of patients with early disseminated disease have counties with reported cases continues to these complaints.4 Even in children diagnosed increase, representing an expanding area – though early, most did not have a known tick bite within continuing to be geographically localized.2 the past month, making diagnosis more elusive. According to the CDC, pediatric males between 5 If Lyme disease is not diagnosed in the early and 9 years old account for the largest number of localized stage, the pathogen enters the reported cases between 2001 and 2010, but all age bloodstream and spreads throughout the body groups and both genders are susceptible.3 Lyme including the CNS. Consequently, early disease occurs far more frequently in the summer disseminated disease commonly presents with (June–August) with an increase in outdoor multiple lesions of the characteristic rash and activities, and has a reduced incidence in the generalized non-specific systemic symptoms winter (December–March).3 including headache, fatigue, arthralgia, and fever. r Pathophysiology: Lyme disease is a common Although the rash is common, it is not universal, tick-borne illness transmitted primarily by the and, as stated above, many patients have no spirochete Borrelia burgdorferi in North known history of tick bite, making diagnosis America – although a second species, Borrelia elusive in those without rash. During this stage, a mayonii, has recently been identified as being child may also develop some of the more Table 10.1 States accounting for 96 percent of the reported characteristic findings of Lyme disease, including cases of Lyme disease in the USA3 facial palsy (9 percent), aseptic meningitis 3 Connecticut Pennsylvania New Jersey Maine (1 percent), and carditis (1 percent). Children may also develop Lyme arthritis, which Maryland Delaware Rhode Island Minnesota is dealt with further in Chapter 6, Case 5. New Hampshire Massachusetts Wisconsin New York Facialpalsyinachildisnotpathognomonic Virginia Vermont for Lyme disease, but a study of 313 children

16:26:06 11 Chapter 10: Head and Neck Pain presenting to the ED with facial palsy in an Co-infections should be considered in patients endemic area found Lyme as the source in 34 with unexplained symptoms or those with percent of cases.5 This study identified the onset persistent symptoms after treatment. of symptoms between June through October, r Diagnosis: The diagnosis of early Lyme disease presence of fever and headache, and absence of maybemadeclinicallywhenerythemamigransis herpetic lesions as clinical predictors of Lyme identified. At this stage in the disease, laboratory disease.5 Other sources of facial weakness to testing is typically falsely negative. Once the consider include infections with herpes viruses, patient progresses to early disseminated Lyme Guillain–Barresyndrome(particularlywhen´ disease, serologic testing is useful for diagnosis. associated with Zika virus), other tick-borne Laboratory testing of Lyme disease is completed encephalitides, mycoplasma, HIV, intracranial as a two-step method.3 The initial test is an mass lesions, parotid and acoustic tumors, enzyme immunoassay or immunofluorescence leukemia, trauma, botulism (most commonly in assay, which is highly sensitive in appropriately infants), and myasthenia gravis. Although limited selected patients (those demonstrating signs of to case reports, Lyme disease has been reported to disseminated disease), but is not very specific. If be among the rare contributors to bilateral facial this testing is equivocal or positive, a second set of droop.6 testing for IgM and IgG is completed as a Western Lyme meningitis presents as an aseptic blot, to improve diagnostic accuracy.3 If meningitis. In patients with aseptic meningitis of symptoms have been persistent for more than 30 unclear etiology, recognition and treatment when days, only the IgG component is necessary. If secondary to Lyme disease improves outcomes.7 these tests are negative and symptoms have been For children with aseptic meningitis without present for greater than 2 weeks, alternative clinical signs of Lyme disease, who live in endemic diagnoses should be considered as it is unlikely areas, rapid identification is challenging as thepatienthasLymedisease.Individualswho serologic testing may require additional time for have previously been diagnosed with Lyme disease completion. A “rule of 7s” was developed as a have unpredictable antibody titers that variably clinical prediction rule for children to identify low decline over time.10 As such, repeat testing for risk for Lyme meningitis to limit treatment, which individuals previously diagnosed is generally not includes: less than 7 days of headache, less than 70 necessary and clinical diagnosis is recommended. percent CSF mononuclear cells, and absence of For patients with concerns for Lyme seventh nerve or other cranial palsy.8 Those meningitis, LP may be useful to guide early meeting all criteria had a less than 2 percent treatment. The decision to perform an LP can be chance of Lyme meningitis.8 Certainly, the finding complicated. The Infectious Disease Society of of erythema migrans is pathognomonic for Lyme America (IDSA) recommends LP in patients with disease,andpointstothecorrectdiagnosiswhen symptoms consistent with strong clinical present in a child with clinical meningitis. suspicion of CNS involvement, such as severe Carditis, which most commonly occurs in late headache or nuchal rigidity.11 In cases of disease, usually presents as complete heart block. diagnostic uncertainty, as previously discussed, It is a rare presentation for Lyme in children.4 the proportion of mononuclear leukocytes in the Partial heart block may be more common but is CSF can assist in distinguishing viral meningitis likely unrecognized due to the lack of clinical versus Lyme meningitis to guide early treatment.8 manifestation. Most cases of Lyme carditis are Serologic testing of CSF is challenging due to self-limited and rarely require a temporary limitations in laboratory quality control to reliably pacemaker.9 handle PCR testing and is not universally It is important for the clinician to remember recommended unless appropriate facilities can be that the vectors that spread the spirochete identified.11 That said, in the setting of known involved in Lyme disease are host to a number of Lyme disease, diagnosis of Lyme meningitis may other transmittable diseases, including notalterthecourseoftreatmentandmay anaplasmosis, babesiosis, deer tick virus, therefore not add any additional benefit to patient Ehrlichiosis, and Borrelia miyamotoi. care.

16:26:06 5 11 Chapter 10: Head and Neck Pain r Treatment: The IDSA recommends that treatment ofLymediseaseinchildrenisbaseduponthe clinical stage. For early Lyme disease, treatment is amoxicillin or cefuroxime (for children less than 8 years old) or doxycycline (for children greater than 8 years old without a known allergy). For those with isolated facial nerve palsy and without abnormal LP results, the IDSA guidelines recommend treatment as in early Lyme disease for 14–21 days.11 The cranial nerve palsy usually resolves within a few weeks regardless of antibiotic treatment but therapy prevents later complications and should be initiated in all cases.11 These children require close follow-up with outpatient providers, who can carefully monitor response to therapy. For children with neurologic manifestations of meningitis or any abnormal CSF results, treatment with parenteral antibiotics is currently the standard of care in the USA (ceftriaxone, cefotaxime, or penicillin G). Patients exhibiting papilledema may require treatment with additional measures. Expert consultation is warranted to ensure optimal treatment based on Figure 10.4 Photograph of child’s face 6 months after treatment, the most recent evidence, considering the rarity of demonstrating marked improvement in facial weakness. the condition. All children requiring treatment facial palsy has not completely resolved at 6 months, with parenteral antibiotics likely warrant although it is greatly improved (Figure 10.4). admission and monitoring. There is evidence that oral doxycycline may be as effective as parenteral References antibiotics for the treatment of Lyme meningitis, 1. Nelson CA, Saha S, Kugeler KJ, et al. Incidence of as doxycycline has excellent CSF penetration, but clinician-diagnosed Lyme disease, United States, this evidence is from Europe where different 2005–2010. Emerg Infect Dis 2015; 21: 1625–31. 12 Borrelia species are prevalent. Nevertheless, this 2. Adams DA, Thomas KR, Jajosky RA, et al. Summary of represents a reasonable alternative when notifiable infectious diseases and conditions: United parenteral therapy is not an option or is refused. States, 2014. MMWR Morb Mortal Wkly Rep 2016; 63: r Disposition: Lyme is generally treated as an 1–152. outpatient except in cases of meningitis or carditis. 3. Centers for Disease Control and Prevention. Lyme disease. See www.cdc.gov/lyme/index.html (accessed Novemeber 2016). Historical clues Physical findings r r 4. Gerber MA, Shapiro ED, Burke GS, et al. Lyme disease Lives in endemic area Erythema migrans in children in southeastern Connecticut. Pediatric r Outdoor activities r Facial nerve palsy (including r Fever chorda tympani, with taste Lyme Disease Study Group.NEnglJMed1996; 335: r Headache deficits and hyperacusis) 1270–4. 5. Nigrovic LE, Thompson AD, Fine AM, et al. Clinical Follow-Up predictors of Lyme disease among children with a peripheral facial palsy at an emergency department in The child was diagnosed with early disseminated Lyme a Lyme disease-endemic area. Pediatrics 2008; 122: disease based on her classic presentation. Her par- e1080–5. ents declined LP. She was treated with doxycycline 6. Mlodzikowska-Albrecht J, Zarowski M, Steinborn B, for 3 weeks. The child had resolution of her rash and et al. Bilateral facial nerve palsy in the course of headache within 24 hours of starting therapy, but her neuroborreliosis in children: Dynamics, laboratory

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tests and treatments. Rocz Akad Med Bialymst 2005; 50 Medications Suppl 1: 64–9. r Loratadine as needed. 7. Halperin JJ. Diagnosis and treatment of the neuromuscular manifestations of Lyme disease. Curr Treat Options Neurol 2007; 9: 93–100. Allergies r 8. Cohn KA, Thompson AD, Shah SS, et al. Validation of Amoxicillin causes a rash. a clinical prediction rule to distinguish Lyme meningitis from aseptic meningitis. Pediatrics 2012; 129: e46–53. Physical Examination and Ancillary Studies r ° 9. Costello JM, Alexander ME, Greco KM, et al. Lyme Vital signs: T 102.9 F, HR 158, BP 95/70, RR 30, carditis in children: Presentation, predictive factors, O2 sat 97% on room air. r and clinical course. Pediatrics 2009; 123: e835–41. General: Well-developed, well-nourished boy, 10. Feder HM Jr, Gerber MA, Luger SW, et al. Persistence sitting in his mother’s lap with noticeable head of serum antibodies to Borrelia burgdorferi in patients tilt.Mildlyuncomfortable.Nodrooling.Mild treated for Lyme disease. Clin Infect Dis 1992; 15: inspiratory stridor is heard. 788–93. r HEENT:Theheadisangledtotheleftwith 11. Wormser GP. Clinical practice. Early Lyme disease. N rotation of the chin to right. There is marked Engl J Med 2006; 354: 2794–801. limitation of neck extension and mild limitation 12. Mygland A, Ljøstad U, Fingerle V, et al. EFNS of neck flexion. He uses his eyes to look upwards, guidelines on the diagnosis and management of limiting his neck motion. The head is European Lyme neuroborreliosis. Eur J Neurol 2010; normocephalic, without plagiocephaly. PERRL, 17: 8–16. extraocular movements intact. The oropharynx is erythematous. The right tympanic membrane is Case 8 bulging and injected, with white pus behind it. r Neck: There are several 0.5–1.0-cm tender mobile Contributing Author: Jason Schwaber lymph nodes in the left anterior cervical chain. History There is no tenderness over the sternocleidomastoid muscles. The patient is a 3-year-old boy who is sent from a retail- r basedwalkinclinicwithhisheadheldina“funnyposi- Cardiovascular:Tachycardic,butregular,with Ͻ tion.” His parents state that he had been well until 3 capillary refill 2 seconds. r Lungs: CTA bilaterally, without W/R/R. days ago when he began “clearing his throat,” which r his parents thought was due to a sore throat. They note Abdomen: Soft, non-tender and non-distended. thattodayheisholdinghisnecktiltedtotheleftand Normoactive bowel sounds. r refuses to bend his neck to look upwards. He had a cold Extremities and skin: Warm and well-perfused, 7daysago,buttodayhedevelopedafever.Hehasbeen without rash, or edema. r eating less, complaining that swallowing is painful, and Neurologic: Motor, sensory, gait, and cranial has a voice that “sounds funny.” The family denies nerves are intact and symmetric. emesis, rash, or swelling of the hands or feet. The r Pertinent laboratory values: WBC 22,000 with 91% urgent care had given him a dose of acetaminophen, neutrophils. performed a rapid strep test (negative), and referred him to the ED. He was born vaginally at 38 weeks. He is develop- Questions for Thought mentally normal. He lives at home with his parents and r an 8-year-old brother. He attends nursery school 3 days What is the diﬀerential diagnosis of pediatric a week. His immunizations are UTD for age. The fam- torticollis? r What is the role of advanced imaging in the ily has a pet turtle and two cats. management of this patient? What factors need to be considered? Past Medical History r r What is the role of antibiotics versus surgery in Otitis media. this patient? r Seasonal allergies.

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Diagnosis r Diagnosis: As these infections usually take place in r Retropharyngeal abscess with inflammatory small children who may not be verbal, diagnosis torticollis. There is further discussion of this can be challenging. Neck pain or stiffness should disease entity in Chapter 5, Case 9. prompt the clinician to consider referred pain (from head injury or shoulder injury), meningeal irritation (from subarachnoid hemorrhage or Discussion meningitis), oropharyngeal infection (tonsillitis, r Epidemiology: Retropharyngeal abscess is a epiglottitis, tracheitis, uvulitis), deep neck-space relatively uncommon head and neck infection infections (peritonsillar, parapharyngeal, and occurringprimarilyinchildrenlessthan5years retropharyngeal abscesses), ENT infection old.1 The incidence is estimated at 4 per 100,000, (mastoiditis), malignancy, dissection, and with most cases presenting in the winter or musculoskeletal pain (post-traumatic torticollis). spring.1 It exists as a spectrum of illness, ranging Therefore, it is important to do a complete head, from pharyngitis and deep neck cellulitis to neck,eye,neurologic,andmusculoskeletal life-threatening airway obstruction, with septic examination. If the child has abnormal vital signs complications throughout the neck, mediastinum, or any other findings on examination, the and chest. clinician should not assume the neck pain is r Pathophysiology: In young children, infections of musculoskeletal. Although many of these items the nasopharynx, eustachian tubes, and adenoids canbeassessedwithhistoryandexamination are common. Lymph nodes draining these areas alone, children with concerning findings warrant pass through the retropharyngeal space, and can further testing and imaging. suppurate, causing a cellulitis, phlegmon, or The diagnosis of retropharyngeal abscess is localized abscess. The swelling and mass effect can confirmed with imaging. Lateral neck X-rays may cause obstruction of the airway. An abscess can show a widening of the soft tissues anterior to the rupture into the airway, causing aspiration vertebrae (see Figure 5.5). These films should be pneumonia. The infection can spread, causing taken during inspiration, if possible. Typically, the mediastinitis, jugular vein thrombophlebitis, and width of the retropharyngeal space is less than sepsis. Retropharyngeal infections are typically that of the adjacent vertebral body at C2 or C3. A polymicrobial and include group A streptococci, CT scan with IV contrast has better sensitivity to anaerobes, and Staphylococcus aureus.2 MRSA detect retropharyngeal abscess and is the may also be an etiology. preferred study to clearly delineate the extent of r Presentation: Early presentation of the infection within the neck or beyond (see retropharyngeal abscess may be non-specific, Figure 5.6).3 However, some abscesses well often resembling a pharyngitis, with fever and identifiedonCTscandonotalwaysyield decreased oral intake. Children may also have an purulentmaterialatthetimeofsurgery.Therisk antecedent URI. Torticollis, neck stiffness, and of airway impingement should be considered refusal to move the neck should heighten the priortosendingachildwithstridorordroolingto index of suspicion.3 As upper-airway obstruction CT, as the imaging results may not significantly progresses, muffled voice and stridor may change the immediate management. r develop. Most older children have a prior Treatment: Treatment options are based upon the penetrating trauma to their pharynx. Other size and location of the abscess. All patients with infections such as peritonsillar abscess, bacterial suspected retropharyngeal abscess should receive tracheitis, or epiglottitis should be considered. antibiotics to cover typical oropharyngeal Advanced croup, anaphylaxis, and foreign bodies pathogens. Ampicillin–sulbactam or clindamycin are additional causes of airway obstruction. There are good options.2 Coverage against MRSA with have been a few case reports describing rare vancomycin should also be considered. For entities such as Kawasaki disease and cervical patients with airway compromise, immediate tuberculosis, mimicking retropharyngeal involvement with ENT is needed as airway abscess. protection and surgical drainage may be required.

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Children with a phlegmon or small Case 9 retropharyngeal abscess on imaging may be treated with IV antibiotics while being closely Contributing Authors: Jamaine Ortiz Jr., observed for progression or resolution of their symptoms. Rebecca Jeanmonod, Carl Daniel, Denis R. r Disposition: All children with suspected Pauze,´ and Matthew Adamo retropharyngeal abscess should be admitted to the History hospital. ENT should be involved as surgical drainage is required in about half of these cases. A lethargic 7-year-old female is brought into the ED Patients with concerns for airway compromise by a local EMS crew. She is accompanied by both of require monitoring in an ICU. her parents. The parents state that the child was having a push-up contest with her older brother approximately 30 minutes ago when suddenly, she started to Historical clues Physical findings Ancillary studies scream and complain of having a severe headache. The r r r patient put her hands up to her head and cried out r Recent URI r Fever Elevated WBC r Difficulty eating r Tachycardia with left shift to her parents “My head! It hurts!” The child has no Voice change Torticollis prior history of having migraines. The patient’s mother r Fever r Otitis media r Negative strep attempted to help relieve the pain by giving her a dose swab of acetaminophen and having her rest in bed. However, soon after the mother gave the medication, the child began to vomit. The mother states she was washing the Follow-Up vomit off the patient’s face when the child started to ThepatienthadaCTscanoftheneckwithIVcontrast, “talk extremely weird and slur her words like she was which revealed a 2-cm retropharyngeal phlegmon, drunk.” At that point, the parents called 911. While en without extension into the lateral pharyngeal space route to the hospital, the child had one other episode of or posterior mediastinum. The patient was treated vomiting. She remained rousable to stimuli, and com- with IV fluids, pain control, and clindamycin. He was plains of head pain when prompted. She has been quite admitted to a monitored bed. ENT evaluated him and lethargic. Parents deny that the child experienced any recommended outpatient adenoidectomy with tym- trauma, fevers, chills, vomiting, diarrhea, or abdomi- panostomytubeplacement.After48hoursofIV nal pain prior to this. antibiotics his neck stiffness and odynophagia had improved, and he was transitioned to oral clindamycin Past Medical History to complete a 14-day course at home. At outpatient r Attention deficit–hyperactivity disorder. follow-up his torticollis had resolved. r Asthma. r UTD on immunizations. References 1. Woods CR, Cash AM, Smith MJ, et al, Medications Retropharyngeal and parapharyngeal abscesses among r Adderal extended release. children and adolescents in the United States: r Epidemiology and management trends, Albuterol rescue inhaler. 2003–2012. JPediatrInfectDisSoc2016; 5: 259–68. Allergies r 2. Hoffman C, Pierrot S, Contencin P, et al. NKDA. Retropharyngeal infections in children. Treatment strategies and outcomes. Int J Pediatr Otorhinolaryngol Physical Examination and Ancillary Studies 2011; 75: 1099–103. r Vital signs: T 97.8 °F, HR 100, RR 20, BP 147/88, 3. Craig F, Schunk J, Retropharyngeal abscess in O2 sat 98% on room air. children: Clinical presentation, utility of imaging, r and current management. Pediatrics 2003; 111: General: Pale and diaphoretic. Vomit is present on 1394–8. chest and arms. Drowsy but rousable.

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Figure 10.5 (A) Non-contrast axial CT, demonstrating diffuse subarachnoid hemorrhage (arrow) as well as mild dilation of the temporal horns of the lateral ventricles (asterisks). (B) Three-dimensional angiography image of the left posterior carotid wall aneurysm (asterisk) associated with the left posterior communicating artery. For the color version, please refer to the plate section. r HEENT: No external signs of head trauma. r What are your treatment priorities in this patient? Tympanic membranes normal. Pupils sluggish but r What are the potential underlying causes of this reactive. diagnosis in a pediatric patient? r Neck: Supple, with no adenopathy, midline trachea. r Cardiovascular: Normal rhythm, with no M/R/G. Diagnosis Brisk capillary refill. r Subarachnoid hemorrhage. r Lungs: Clear and equal bilaterally, with no W/R/R. r Abdomen: No distension or masses. Normal bowel Discussion sounds. r r Epidemiology: Subarachnoid hemorrhage, or Extremities and skin: No signs of trauma. No bleeding into the subarachnoid space, is rare in rashes. children.1,2 The incidence of subarachnoid r Neurologic: Responsive to pain, opens eyes to hemorrhage in the general population is about 6 voice, unreliable following commands. cases per 100,000 patient-years, but only 1–2 r Pertinent laboratory values:CBCandelectrolytes percent of those occur in pediatric patients.1,3 The normal. most common cause of pediatric subarachnoid r Pertinent imaging: CT head shown in Figure 10.5. hemorrhage is trauma (with non-accidental trauma being more common than accidental Questions for Thought trauma), followed by aneurysmal bleeding, r Would any additional laboratory tests or arteriovenous malformation bleeding, and 1,2,4,5 diagnostic imaging be of use in this patient, and mass. Aneurysms in children are less why? common than arteriovenous malformations, but arteriovenous malformations are less likely to

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r present as isolated subarachnoid hemorrhage.1,4 Diagnosis:Diagnosisofsubarachnoidhemorrhage Comorbid disease, such as sickle cell anemia, is most commonly made on non-contrasted CT coarctation of the aorta, or connective tissue scan of the head.6 Although the traditional disorder, is common in patients with aneurysmal standard for diagnosis has been CT followed by disease, and family history is a risk factor for LP looking for xanthochromia and elevated red this.2 blood cells in the CSF if the CT is negative, with r Pathophysiology: Subarachnoid hemorrhage newer CT scan technology, this practice has been occurs when blood vessels become disrupted and called into question, since the likelihood of a leak blood into the subarachnoid space. subarachnoid hemorrhage in the setting of a Disruption can be due to trauma, or may be due negative CT is very low, and is only about 5 to blood vessel invasion from a tumor, increased percent even in the setting of a relatively high wall stress as occurs with aneurysm, increase pre-test probability.6 That said, in children with intravascular pressure as occurs with coarctation altered mental status, headache, or both, the of the aorta, abnormal anatomy as with differential includes numerous items besides arteriovenous malformations, or abnormal vessel hemorrhage,suchasinfectiousprocesses,and integrity as with connective tissue disorders. many of these children require LP for exclusion of Regardless of the cause, blood in the other dangerous diagnoses, independent of their subarachnoid space can cause mass effect, CT status. Unfortunately, if xanthochromia is not hydrocephalus, focal deficits, meningeal present but the RBC are elevated, it can be irritation, herniation, and death. In cases of difficult to distinguish traumatic LP from subarachnoid hemorrhage from subarachnoid hemorrhage, and there are no non-accidental trauma, the child may have definitive thresholds. multiple injuries. In children with concern for intracranial r Presentation: Children with subarachnoid bleeding or a symptomatic expanding aneurysm hemorrhage can present in a variety of ways. In or dissection, CT angiography can be helpful to non-verbal children, lethargy, seizures, poor tone, identify aneurysmal disease.2,6 MRI can also help altered level of consciousness, vomiting, apnea, elucidate intracranial pathology in children with feeding difficulties, and breathing difficulties may CNS symptoms. r be the predominant features.1 Older, verbal Treatment: Emergency physicians are not children may present with altered mental status, neurosurgeons, and do not provide definitive care vomiting, seizure, focal deficits, or complaint of for children with subarachnoid hemorrhage. The severe headache.1,2 It should be noted that the focus for care of these children needs to be severity of clinical presentation is the strongest reducing the secondary injury and getting the prognostic indicator in aneurysmal subarachnoid child to definitive care. The provider should start hemorrhage. The initial clinical severity can be with the ABC algorithm. Many of these children reliably categorized by use of simple validated will require airway management. Like other scales, such as that from Hunt and Hess, although brain-injured patients, these patients should not it is important to note that this scale has been be allowed to become hypoxic, as this can worsen criticized for its inter-observer variability. Higher their underlying injury. When intubating these grades, which are reflective of progressively children, care should also be taken to not higher hemorrhage severity and neurologic hyperventilate them excessively. Although dysfunction, are associated with higher overall hyperventilation decreases intracranial mortality. The Hunt and Hess scale is as follows: pressure, it can also cause cerebral vasospasm, grade 1 – asymptomatic or mild headache; and, therefore, children should be ventilated grade 2 – cranial nerve palsy or moderate to to keep their end-tidal carbon dioxide at severe headache/nuchal rigidity; grade 3 – mild about 35. focal deficit, lethargy, or confusion; grade 4– Optimal blood pressure management has not stupor and/or hemiparesis; grade 5 – deep beenstudiedinchildrenwithsubarachnoid coma, decerebrate posturing, moribund hemorrhage. In children with aneurysmal disease appearance. and concern for vasospasm, it is often appropriate

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to maintain higher blood pressures, to adequately Historical clues Physical findings Ancillary studies perfuse the brain, and antispasmodics r Sudden r Altered mental r CT with (nimodipine) are generally considered the r headache r status subarachnoid standard of care.2 Decisions regarding target Vomiting Sluggish pupils hemorrhage, CT r Slurred speech r Hypertension angiography with blood pressures in these exceedingly ill children aneurysm should be made in consultation with a pediatric neurosurgeon. Definitive therapy is not well studied in a Follow-Up controlled fashion due to the rarity of this process The child was diagnosed with subarachnoid hemor- and its multifactorial etiology, but in aneurysms, rhage from ruptured aneurysm based on her CT find- clipping as well as endovascular techniques are ings. She was transferred to a pediatric center and often performed.2 Ventriculostomy for underwent endovascular coiling of the aneurysm. She hydrocephalus and even craniectomy may be ultimately had a good neurologic outcome after a sev- necessaryinchildrenwithsignificant eral month rehabilitation stay. hydrocephalus. Arteriovenous malformations may require surgery, endovascular procedures, or References radiation therapy. Regardless of specialist 1. Westra DL, Colohan ART. Pediatric subarachnoid treatment, these children require management by haemorrhage. Acta Neurochir Suppl 2008; 104: 401–5. a multidisciplinary team of neurologists and 2. Beez T, Steiger H-J, Hanggi D. Evolution and neurosurgeons, and consultation should be made management of intracranial aneurysms in children: A to such specialists when a diagnosis of systematic review of the modern literature. JChild subarachnoid hemorrhage is made. Neurol 2016; 31: 773–83. r Disposition:Achilddiagnosedwitha 3. van Gijn J, Rinkel GJE. Subarachnoid haemorrhage: subarachnoid hemorrhage should be transferred Diagnosis, causes and management. Brain 2001; 124: to a center with pediatric neurosurgical capability. 249–78. The child should be closely monitored in a PICU 4. Stapf C, Mohr JP, Pile-Spellman J, et al. Epidemiology regardless of interventions performed. Frequent and natural history of arteriovenous malformations. neurologic assessments and blood pressure Neurosurg Focus 2001; 11: article 1. monitoring (and sometimes cerebrovascular 5. Wong G, Knuckey NW, Gubbay SS. Subarachnoid pressure monitoring) are important to prevent haemorrhage in children caused by cerebral tumour. J Neurol Neurosurg Psychiatry 1983; 46: 449–50. and/or detect vasospasm and secondary ischemic insult. Subsequent to being discharged 6. Carpenter CR, Hussain AM, Ward MJ, et al. from the hospital the child should begin physical Spontaneous subarachnoid hemorrhage: A systematic review and meta-analysis describing the diagnostic therapy to improve functionality as soon as accuracy of history, physical examination, imaging, possible and follow up with their neurologist and lumbar puncture with an exploration of test regularly. thresholds. Acad Emerg Med 2016; 23: 963–1003.

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Case 1 r Cardiovascular: Regular rate and rhythm, with no M/R/G. Contributing Author: Shellie Asher r Lungs: Normal work of breathing, with clear and equal breath sounds. No W/R/R. History r Abdomen: Soft, non-tender, and non-distended, The patient is a 12-month-old female who presents with normoactive bowel sounds throughout. with one episode of blood in her diaper. Per mom the Therearenopalpablemasses.Noapparent patient otherwise has been well. The child has not had tenderness. a fever, and has been eating and drinking without dif- r Genitourinary: Normal genitalia, with no signs of ficulty. The patient was exclusively breast fed through traumaandnobloodattheintroitus. 4 months, with the addition of table foods up until r Extremities and skin: No rashes or skin changes. this week, at which time the parents introduced whole No signs of trauma. cow’s milk. The patient normally has bowel move- r Neurologic:Appropriateforage,alertand ments every day, which are well formed. Today’s bowel interactive, no focal deficits. movement was softer and the parents noted blood in the diaper, which was bright red. Questions for Thought Past Medical History r What is the diﬀerential diagnosis for blood in the r UTD on immunizations. r diaper? Full-term spontaneous vaginal delivery without r What is the appropriate testing, should that complications. bleeding be determined to be GI in origin? r What is the ED management of this condition? Medications r None.

Allergies Diagnosis r r NKDA. Blood in the stool due to milk protein allergy.

Physical Examination and Ancillary Studies Discussion r r Vital signs: T 98.4 °F, HR 105, RR 22, BP 98/56, O2 Epidemiology: GI bleeding in infants is rare, sat 100% on room air. accounting for approximately 0.3 percent of chief r General: The patient is awake, alert, and appears complaints to a pediatric ED. Upper GI bleeding comfortable. is less common than lower GI bleeding, occurring r HEENT: PERRL. Extraocular movements intact. in 1 in 10,000 children each year.1 GI bleeding in Moist mucous membranes. Tympanic membranes children increases in incidence with older age. normal. r Pathophysiology: The pathophysiology of GI r Neck:Supple,withnoadenopathy. bleeding is multifactorial and depends on age and

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Table 11.1 Causes of GI bleeding by age. Bold type indicates more common reasons, regular font indicates less frequent etiologies.1–3 Neonate 1 month to 1 year > 1 year

r Anal fissures r Esophagitis/GERD r Peptic ulcer disease r Milk protein allergy r Gastritis r Juvenile polyp r Bacterial enteritis r Anal fissures r Meckel’s diverticulum r Intussusception r Intussusception r Infectious diarrhea r Swallowed maternal blood r Allergy r Arteriovenous malformations r Infantile peptic ulcers r Enteritis r Variceal bleeding r Adverse drug reaction r Volvulus r Duodenal ulcer r Stress gastritis r Foreign body r Esophagitis r Arteriovenous malformations r Variceal bleeding r Gastritis r Volvulus r Meckel’s diverticulum r Mallory–Weiss tears r Coagulopathies r Arteriovenous malformation r Inflammatory bowel disease r Meckel’s diverticulum r Henoch–Schonlein¨ purpura

presentation. Bleeding may be essentially estrogens. A rectal examination may be necessary asymptomatic or may cause chronic (iron to determine the source of bleeding. deficiency) anemia or acute blood loss The keys to diagnosis are a thorough history anemia (Table 11.1). There is more information and physical examination, as described above, on anemia and blood loss in Chapter 3, directed toward the common etiologies of GI Case 8. bleeding for the patient’s age and chief complaint r Presentation:Thehistoryandclinicalcourseof (i.e. bloody vomiting or blood in the stool). pediatric GI bleeding varies with the patient’s age Ancillary studies in the ED may include CBC, and specific diagnosis. Pertinent historical serum chemistries, fecal occult blood, and elements include the nature of the bleeding (blood coagulation studies. In addition, the Apt test can in the vomitus, blood in the stool, melena, acute be used to determine the presence of fetal vs. chronic bleeding), associated symptoms hemoglobin in a stool sample, to distinguish from such as fever or abdominal pain, medication the possibility of swallowed maternal blood in history, birth history, diet history, and family neonates or breastfeeding infants.1,2 If an history. infectious etiology is suspected, fecal leukocytes, On physical examination, close attention ova/parasites, and cultures can be obtained. should be paid to signs of shock, vital signs, any Abdominal U/S is indicated if intussusception is obvious sources of bleeding, abdominal suspected. Although often recommended, examination including tenderness, mass, or nasogastric irrigation and/or aspiration has very organomegaly, and rectal/anal examination for poor sensitivity for upper GI bleeding, incurs a gross blood and evidence of anal fissure. significant amount of discomfort to the patient, r Diagnosis: The first step to the complaint of and should not routinely be used as a diagnostic “blood in the diaper” is to determine if it is in fact maneuver. For significant blood loss or recurrent blood. Parents have brought their children in to bleeding, esophagogastroduodenoscopy or the ED for bloody diapers that were later colonoscopycanbeperformedbyapediatric discovered to be markers, crayons, beets, sports gastroenterologist for a definitive diagnosis. r drinks,foodcoloring,andclothingdyes.Thiscan Treatment:Mostchildrenwithafirstepisodeofa be assessed using hemoccult. Once it is small amount of blood in vomitus or stool, determined that there is in fact blood in the normal vital signs, and an unremarkable physical diaper, the next step is to determine the source. examination can be managed conservatively, with Blood may be urinary in origin, secondary to a observation at home and primary care follow-up. UTI, or can be vaginal in origin. Vaginal bleeding If anal fissures are noted on examination, stool may be from vaginal foreign body, sexual abuse, softeners should be prescribed. Children with trauma, or, in the first weeks of life, from larger amounts of bleeding or who appear ill or normal physiologic withdrawal from maternal unstable require IV fluid resuscitation and,

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potentially, transfusion. Intussusception is often Case 2 reduced with barium or air enema, but may require surgical intervention. Depending on the Contributing Author: Shellie Asher suspected cause of bleeding, medical management History may include H2 antihistamines, proton pump inhibitors, antacids, or hormone analogs such as The patient is a 4-month-old male who presents with octreotide or vasopressin. Significant GI bleeding parents who report a bulge in the baby’s diaper area. of other etiologies may be treated endoscopically The patient’s mother noticed this when changing his by a gastroenterologist, and surgical intervention diaper earlier today. She states that he has been feed- may be indicated if the bleeding cannot be ing well, with no vomiting and normal stools. He has controlled. not had any fevers or other systemic symptoms. The r Disposition:Theappropriatedispositionof patient is bottle-fed and has been taking his usual children with GI bleeding depends on the severity amounts of formula. of the bleeding and associated symptoms. Past Medical History Children with a first episode of a small amount of r bleeding in the setting of normal vital signs, Full-term delivery with no complications. r benign physical examination, and no other UTD on immunizations. associated symptoms can be discharged home Medications with careful observation and primary care r follow-up. Children who have more than a scant None. amount of bleeding, have abnormal vital signs, or Allergies appear ill require admission to a pediatric r NKDA. intensive care setting. Children presenting to a facility without these resources should be Physical Examination and Ancillary Studies stabilized and transferred in an expeditious r Vital signs: T 98.4 °F, HR 105, RR 22, BP 100/65, manner. O2 sat 100% on room air. r General: The patient is awake, alert, and appears Historical clues Physical findings r r comfortable. Blood in diaper Normal vital signs r HEENT: PERRL. Red reflex intact. Moist oral r Change in diet r Benign abdominal examination mucosa. Tympanic membranes normal. r Follow-Up Neck: Supple, with midline trachea and no adenopathy. The baby was found to have heme-positive stools. This r patient was diagnosed with milk protein allergy. The Cardiovascular: Regular rate and rhythm. No M/R/G. patient’s parents were instructed to stop cow’s milk, r and the patient was referred back to her pediatrician Lungs: Clear, with normal respiratory effort. No W/R/R. and an allergist for further dietary and allergy testing r and counseling. The patient did well without any recur- Abdomen: Soft, non-tender, and non-distended, rence of GI bleeding. with normoactive bowel sounds throughout. No apparent tenderness. References r Genitourinary:Thereisabulgeintheright inguinal area, with fullness in the right scrotum. 1. Owensby S, Taylor K, Wilkins T. Diagnosis and There is no erythema. No obvious tenderness. management of upper gastrointestinal bleeding in r children. JAmBoardFamMed2015; 28: 134–45. Extremities and skin: No rashes, deformity, or signs of trauma. 2. Hillemeier C, Gryboski JD. Gastrointestinal bleeding r in the pediatric patient. Yale J Biol Med 1984; 57: Neurologic: Normal mental status, interactive and 135–47. consoleable, symmetric strength, intact reflexes. r 3. Padilla BE, Moses W. Lower gastrointestinal bleeding Pertinent laboratory values:CBCandchemistry and intussusception. Surg Clin N Am 2017; 97: 173–88. studies are normal.

16:22:39 255 12 Chapter 11: Genitourinary Complaints r Pertinent imaging:U/Sdemonstratesaright reflecting associated pain. If the hernia is indirect inguinal hernia containing a small loop of incarcerated (abdominal contents are trapped in bowel. the defect), the patient may present with irritability or poor feeding. If strangulation (loss Questions for Thought of blood flow to entrapped bowel) has occurred, the patient may additionally present with r What are typical causes of this condition? r vomiting, decreased stool output, firm abdomen, What is the ED management for this condition? or fever.1–3 r What signs and symptoms associated with this r Diagnosis:Thekeystodiagnosisareathorough condition would be a cause for concern? history and physical examination. Other differential considerations include testicular Diagnosis torsion, epididymal appendage torsion, r epididymitis, orchitis, hydrocele, skin infection, Inguinal hernia. or tumor. Torsions, inflammatory syndromes, and incarcerated hernias are painful, while hydrocele, Discussion r tumor, and most uncomplicated hernias are not. Epidemiology: The incidence of indirect inguinal In situations where the diagnosis is in question, hernia in the USA is between 1 percent and U/S can help differentiate among these 5 percent, with highest rates in premature infants possibilities,andisoftendiagnosticfortorsion, 1,2 and males. Inguinal hernias demonstrate the tumor, or hernia. same predilection for children of all races, as A history of previous episodes of bulging, opposedtoumbilicalhernias,whicharemore birth history, changes in feeding, vomiting, fever, common in African American infants. Most irritability/crying, and a family history should be hernias are detected in the first year of life, obtained. On physical examination, a palpable although asymptomatic hernias may present smooth mass can often be felt in the inguinal 2 later. region. If there is no mass felt with the child lying r Pathophysiology:Abdominalherniaisadefectin supine, reassess in the setting of increased the ventral wall of the abdomen, which results in abdominal pressure (crying or straining, or an opportunity for intra-abdominal structures bearing down if the child is old enough to such as omentum or bowel to protrude into cooperate) or in an upright position. Girls should extra-abdominal space. Indirect inguinal hernias be assessed for palpable herniated ovary (often are the most common type in children, and are confused with an enlarged lymph node in the the result of failure of the processus vaginalis to inguinal canal) and boys should be assessed for close(afterthedescentofthetestisthroughthe the presence of both testes in the scrotum. Signs inguinal canal in males).2 Other hernias of the of an incarcerated hernia on examination include ventralwallincludedirectinguinalherniasand signs of pain such as crying/irritability, a tender, femoral hernias (both of which are acquired firm mass in the area of the hernia, which is rather than congenital, and are rare in children), unable to be reduced, and discoloration of the umbilical hernias, epigastric hernias, and overlying skin. If strangulation occurs, the bowel incisional hernias. Failure of the processus is at risk for necrosis and perforation. In this vaginalis to close may also result in hydrocele, setting,theabdomenmaybefirmanddiffusely when peritoneal fluid enters the scrotal sac.1–3 tender. Ancillary studies in the ED may include r Presentation: Infants or children with hernia CBC, serum chemistries, and U/S to evaluate for typically present with an apparent bulge at the hernia and/or incarceration or strangulation. In inguinal canal or in the scrotum. The majority of boys, hernia and hydrocele often cannot be hernias occur on the right side, and a small differentiated on clinical examination and U/S number are bilateral. Bilateral hernias are more may be helpful to delineate between these common in females.1 This bulge may be constant diagnoses. or intermittent, often occurs with crying or r Treatment: Well-appearing children who present straining, and may be associated with irritability with inguinal hernia should have reduction

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attempted in the ED. Children with signs of an 2. Wang KS. Assessment and management of inguinal incarcerated hernia should have reduction hernia in infants. Pediatrics 2012; 130: 768. attempted as long as there are no signs of systemic 3. Davis JE, Silverman M. Scrotal emergencies. Emerg toxicity such as unstable vital signs, peritoneal MedClinNAm2011; 29: 469–84. abdominal examination, fever/leukocytosis, or severe discoloration of the hernia contents. If Case 3 these signs are present, urgent surgical consultation is indicated. Definitive therapy is Contributing Author: Abhishek Chaturvedi surgical repair of the hernia. Early repair is warranted in young children, as the risk of History incarceration is high with delay in repair.1,2 The patient is a 4-year-old boy who was brought to the r Disposition: Reducible simple inguinal hernias ED by his caretaker for a 5-hour history of swelling without incarceration or strangulation can be and redness of the penis. The caretaker stated that the referred to a pediatric surgeon for close outpatient child became restless and started crying about 4 hours follow-up and repair. Surgical referral is always ago and did not stop, even after giving him his favorite indicated, as the hernia defect will not candies and toys. On further questioning, the caretaker spontaneously close and there is a 7–17 percent stated that about 5–6 hours ago, while giving a bath, risk of incarceration if it is left untreated.1,2 she retracted the foreskin over the penis to clean it Parents should be counseled regarding the signs but subsequently could not move it back. She thought and symptoms of incarceration or strangulation thatitwouldgobackonitsown.Whenshesawthat which should prompt immediate return to the ED the child’s penis was swollen and red, she immediately forurgentevaluationandmanagement.Children came to the ED to seek medical help. Review of systems with an unreducible hernia or signs of systemic is otherwise negative. toxicity should have urgent surgical consultation or be transferred to a facility where such Past Medical History consultation is available. r Healthy, immunizations UTD.

Historical clues Physical findings Ancillary studies Medications r r Bulge found r Palpable inguinal r U/S showing None. during diaper r hernia indirect inguinal r change Benign r hernia Allergies Normal feeding/ abdominal Normal laboratory r stools examination tests NKDA. r Lack of other symptoms Physical Examination and Ancillary Studies r ° Follow-Up Vital signs: T 98.8 F, HR 112, BP 100/70, RR 28, O2 sat 99% on room air. This patient was diagnosed with a simple, reducible, r General: Crying, irritable, appears well-nourished, indirect inguinal hernia. He was discharged home well-developed. with next-day surgical follow-up, and the parents were r HEENT: PERRL, mucous membranes moist. instructed regarding signs and symptoms of incarcer- r Neck: Supple and non-tender, with no adenopathy. ation and strangulation. The patient had an uncompli- r cated laparoscopic hernia repair and recovered with- Cardiovascular: Tachycardia, with regular rhythm. out sequelae. No M/R/G. r Lungs: Clear, with normal work of breathing. No References W/R/R. r Abdomen:Soft,withnodistension,masses,or 1. Chang SJ, Chen JY, Hsu CK, et al. The incidence of tenderness. No organomegaly. inguinal hernia and associated risk factors of r incarceration in pediatric inguinal hernia: A Genitourinary: Irritable with examination of the nation-wide longitudinal population-based study. genital area. Uncircumcised, the glans penis is Hernia 2016; 20: 559–63. edematous, erythematous, and congested, with a

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collar of edematous foreskin (like a “doughnut” cleaning, or following urinary catheter insertion.3 around the shaft near the glans). The remainder of Adolescents may have a delayed presentation the penile shaft is unremarkable. Testes are because of embarrassment, and in this age group, descended bilaterally, with normal cremasteric paraphimosishasbeenreportedinassociation reflex. No discharge from the urethral meatus. No with activities including sexual intercourse, evidence of foreign-body insertion. genital piercing, or prolonged erotic dancing.2,3 r Extremities and skin: No deformities noted. No Poor hygiene and balanitis at any age are also swelling, redness, tenderness, rashes. Full range of associated with increased risk, as the motion at all the joints with 5/5 muscle strength inflammation can result in contracture of the in all four extremities. distal foreskin. Ischemia can occur within hours, r Neurologic: Interactive, age appropriate, normal although some children will have minimal reflexes. vascular compromise even in the setting of several days of symptoms.3 Patients may complain of pain, or they may be agitated or fussy. Children Questions for Thought may also present with urinary retention or r What are the typical causes of this condition? abdominal distension. r What is the ED management for this condition? r r Diagnosis: Diagnosis is based upon physical What signs and symptoms associated with this examination. As such, it is critically important to condition would be a cause for concern? completely examine all patients, particularly the pre-verbal child who cannot tell you what hurts. Other items to consider include hair tourniquet Diagnosis r and phimosis. In cases of hair tourniquet, it may Paraphimosis. be very difficult to visualize the embedded hair. Phimosis, which is the inability to retract the Discussion r distal foreskin over the glans penis, is Epidemiology: According to the National Hospital physiologically normal in infants and children up Discharge Survey, circumcision rates in the USA to age 5–7, and considered pathologic only if it declined from an all-time high of 78–80 percent occurs after the foreskin was previously 1 in the mid to late 1960s to 55–60 percent in 2003. retractable, or after puberty. Parents should be While paraphimosis can occur at any age, its counseled to never forcibly retract the foreskin of distribution is bimodal, occurring in a young child, as this increases the risk of injury, uncircumcised young boys and adolescents and infection, and both phimosis and paraphimosis. 2 then again in older adult males. Young patients with phimosis can be followed by r Pathophysiology: Paraphimosis is the inability to their PCP, and older patients can be referred to completely reduce the penile foreskin distally back urology for outpatient follow-up and to its natural position overlying the glans penis management. after retraction. The entrapped foreskin forms a Once paraphimosis has been diagnosed, constricting band on the penile shaft. it is important to consider the underlying Compressioninhibitsvenousdrainageofthe predisposing contributor to the paraphimosis. glans and results in a vicious cycle of progressive Although most cases are spontaneous or glans edema, which further prevents reduction of secondary to poor hygiene, paraphimosis may be the foreskin. Glans edema may become so severe secondary to Plasmodium falciparum,chancroid, that arterial inflow is compromised and may lichen sclerosis, or contact dermatitis (application result in necrosis and gangrene of the glans, which of celandine juice on the prepuce).2 Paraphimosis rarelymaybecomplicatedbythedevelopmentof may also be secondary to iatrogenic injury or necrotizing fasciitis. neglect in disabled children who require r Presentation: More common in young children assistance for activities of daily living.2,3 and infants, paraphimosis is often discovered at a r Treatment: Paraphimosis is a urologic emergency diaper change, but may be seen after the foreskin that must be treated promptly to prevent glans is forcibly retracted in an attempt to facilitate necrosis. The treatment approach depends on the

16:22:39 12 Chapter 11: Genitourinary Complaints presence of glans ischemia and the duration of the The first layer is applied loosely, with the symptoms. In patients with no evidence of acute following two layers progressively tighter.4 ischemia and symptoms less than 12 hours, the r Iced glove: After topical anesthesia, a glove is EM physician may attempt reduction of edema half-filled with ice and water, and then tied off with osmotic agents and a single attempt to like a balloon. The penis is placed into the reduce the paraphimosis with adequate invaginated thumb of the glove for 5 minutes. sedation/analgesia.2–4 Patients with evidence of The glove is then compressed against the possible ischemia or symptoms for more than 12 pubis.4 hours should receive urgent urologic consultation r Osmotic agents: Glucose, granulated sugar, or and management. mannitol-soaked gauze may be wrapped The first step in reduction is adequate around the paraphimosis for 30–45 minutes, to analgesia. Topical local anesthetic options include draw out edema fluid.4 EMLR (2.5% lidocaine and 2.5% prilocaine) NOTE: Ice and osmotic agents may take 1–2 hours cream or lidocaine gel. Regional anesthesia (with to have an effect and should not be used when anxiolysis, as well) is accomplished with dorsal arterial compromise is suspected. penile nerve block using 1% lidocaine (or 0.5% Regardless of initial methods to reduce edema, bupivacaine if a longer-lasting analgesia is when the preputial swelling and edema have preferred after reduction).2–5 Calculate the subsided, correct the paraphimosis by gentle maximum safe dose according to the child’s body manual reduction. To reposition the prepuce, weight prior to injection. The total volume should placeboththumbsontheglanspenisandwrap notexceed2mL(1mLoneachside)–thiswill the fingers behind the prepuce. Apply gentle reduce the risk of any additional tourniquet effect steady pressure to the prepuce with counter- from the local anesthetic. Local anesthetic should pressuretotheglanspenisastheprepuceispulled be infiltrated from the dorsal surface, as close to down. the base of the penis as possible. Insert the needle If there is any concern for ischemia of the at the 2 o’clock and 10 o’clock positions, and wait glans penis or after an initial failed attempt at for a “give” as it passes through the fascia. manual reduction under adequate sedation/ Discomfort can be minimized by using a analgesia, a urologic surgical consultation should small (i.e. 29-gauge) needle and injecting slowly. be obtained emergently. If surgical intervention is Procedural sedation may also be not immediately available and an attempt at necessary. non-surgical intervention has failed, the following Non-manipulative methods of reduction are invasive techniques can be attempted (by an considered first-line measures in the absence of experienced provider or in consultation with a any signs of ischemia in patients with symptoms surgical expert): less than 12 hours’ duration. r Hyaluronidase method: Injection of 1-mL r EMLA R glove technique: An appropriately aliquots of hyaluronidase (using a tuberculin sized surgical glove is cut at the base of the syringe) into one or more sites of the thumb. A single tube of EMLAR is emptied edematous prepuce. Hyaluronidase disperses into the sleeve, which is advanced over the extracellular edema by modifying the penis and left for approximately 30 minutes. permeability of intercellular substance in The sleeve provides sufficiently prolonged local connective tissue. anesthesia and also allows it to soften the r Aspirationisamethodusingatourniquet foreskin. Manual reduction can then be appliedtotheshaftofthepenis,andthen attempted.5 inserting a 20-gauge needle parallel to the r Compression bandage (Colorado CoFlex R urethra to aspirate 3–12 mL of blood from the technique): After topical anesthesia or glans. This reduces the volume of the glans sedation,thepenisiswrappedinthreelayersof sufficiently to facilitate manual reduction. flexible self-adherent bandage, beginning at the r The Dundee technique involves multiple edematous area, then the entire penile shaft. needle punctures to drain out the collected

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fluid, thereby leading to manual reduction of 2. Dubin J, Davis JE. Penile emergencies. Emerg Med Clin the foreskin. NAm2011; 29: 485–99. r Dorsal slit procedure and emergent 3. Clifford ID, Craig SS, Nataraja RM, et al. Paediatric circumcision are the last resorts for reducing paraphimosis. Emerg Med Australasia 2016; 28: 96–9. paraphimosis. For the dorsal slit procedure, a 4. Pohlman GD, Phillips JM, Wilcox DT. Simple method vertical incision is placed in the 12 o’clock of paraphimosis reduction revisited: Point of position to incise the constricting band of the technique and review of the literature. JPediatrUrol foreskin. This frees the constricting ring and 2013; 9: 104–7. allows for reduction of the paraphimosis. The 5. Khan A, Riaz A, Rogawski KM. Reduction of R incised margins can then be approximated paraphimosis in children: The EMLA glove technique. Ann R Coll Surg Engl 2014; 96: 168. using 4/0 nylon sutures. r Disposition: Patients with reduction of paraphimosis in the ED should be observed after Case 4 reductiontoassureadequatepaincontrolandthe ability to urinate. Patients meeting criteria for Contributing Author: Jennifer Pelesz discharge should be instructed not to retract the History foreskin for at least 2 weeks and counseled The patient is a 15-year-old female who comes in with regarding signs and symptoms of recurrence, her mom to the ED with a complaint of pelvic and phimosis, and infection. They should be referred abdominal pain. She states the pain is across her lower to urology for outpatient follow-up. Patients abdomenandbeganadayorsoago.Ithasbeeninter- requiring surgical intervention should be mittent but has become worse over the last day. She managed per the post-operative instructions of describes it as “pressure” and it is becoming more the surgical team. severe. She also has pain across her lower back. She deniesfeverorchills,anynauseaorvomiting,andhas Historical clues Physical findings been eating and drinking normally. She denies urinary r Penis pain r Paraphimosis on symptoms. She states her periods have been “irregu- r lar” and the last menstruation was “last month,” but History of retraction during r examination r cleaning No evidence of ischemia doesn’t recall the exact date. She denies any vaginal Penile erythema discharge. She denies being sexually active. She is a high school student and lives at home with her mother, Follow-Up father, and a younger sister. She denies use of tobacco, The paraphimosis was reduced after application of ice alcohol, or recreational drugs. packs, followed by a compression bandage and man- Past Medical History ual reduction of the prepuce over the glans. Follow- r Asthma. ing reduction, it was ensured that the child could pass r urine. On discharge, the parents and caretaker were Myringotomy tubes as an infant. r instructed not to retract the foreskin for at least 2 Immunizations UTD. r weeks and informed to expect dysuria and/or hema- Menarche at age 12, last menstrual period about a turia and the need to continue simple analgesia for month ago. 24–48 hours. They were also instructed to place triple antibiotic ointment on the prepuce and follow up with Medications r urology or their PCP for evaluation in 3–4 weeks, to Albuterol as needed. review clinical progress and to assess indications for circumcision. Allergies r NKDA. References Physical Examination and Ancillary Studies 1. Centers for Disease Control and Prevention. National r Hospital Discharge Survey. See www.cdc.gov/nchs/ Vital signs: T 98.7 °F, HR 108, RR 16, BP 143/72, nhds/ (accessed February 2017). O2 sat 100% on room air.

16:22:39 12 Chapter 11: Genitourinary Complaints r General: Patient is obese, appears uncomfortable, pregnancy, lower abdominal or pelvic pain is and is holding her abdomen as she walks into the often the presenting complaint in ectopic room. pregnancy, which is discussed in detail in r HEENT: PERRL. Extraocular movements intact. Chapter 8, Case 8. Placental abruption is the Moist oral mucosa. premature separation of the placenta from the r Neck: Supple and non-tender, with no adenopathy. uterus, and often presents with lower abdominal r Cardiovascular: Regularly tachycardic, with no pain and/or vaginal bleeding. The peak incidence M/R/G. of abruption is between the 24th and 26th week, r Lungs:Clearbilaterally,withnoW/R/R. although it may occur at any time. Uterine r Abdomen/genitourinary:Obese,diffuselytender, rupture is rare in first pregnancies, and generally firmmasspalpablefrompelvistoabovethe occurs in laboring women who have had previous umbilicus. Small amount of clear, thin discharge uterine surgeries. Both abruption and rupture are on vaginal examination. associated with high maternal and fetal mortality. Pregnancy may spontaneously miscarry, but if not r Extremities and skin: Warm and well-perfused, all products of conception are passed, the patient with no signs of trauma and no rashes. may become septic from superinfection. r Neurologic: Awake and appropriate, non-focal Domestic violence during pregnancy is frequently neurologic examination. directed at the gravid uterus, and adolescents in r Pertinent laboratory values:Urinepositivefor violent relationships may also present with pregnancy, 1+ leukocyte esterase, trace protein. abdominal pain or pelvic complaints. r Presentation: Because of denial in this age group Questions for Thought and the reluctance to seek care, adolescents may r What is the diﬀerential diagnosis for this patient? present with any number of complaints at any r What are the potential complications? time during the pregnancy. Vague complaints such r What social ramiﬁcations and issues are involved as dizziness, nausea and vomiting, or fatigue are with this patient? r common in the first trimester. Also, pelvic pain, What other tests/studies should be performed? cramping, and vaginal bleeding can occur. Later, weight gain or amenorrhea may prompt a visit to thePCP,urgentcare,orED.Often,adolescent Diagnosis females have irregular and sporadic menstrual r Third-trimester pregnancy, in active labor. cycles and missed menses go unnoticed, prompting presentation later in the pregnancy. It Discussion is important to separate the adolescent from adult r Epidemiology: Early and unplanned pregnancy caregivers and ask about menstrual history and and childbirth are significant consequences of sexual activity in all females of this age group. A adolescent sexual activity. The vast majority of routine pregnancy test should be considered in all pregnancies in this age group are unplanned. females who have reached sexual maturity. Pregnant adolescents are more likely to delay Pregnant adolescents may also present with seeking prenatal care, some not getting any care at miscarriage. Spontaneous abortion or miscarriage all until childbirth. Therefore, there are higher occurs in about 20 percent of all pregnancies. rates of unfavorable outcomes, such as Presenting symptoms commonly include crampy prematurity, infant mortality, and poor health and pelvic pain and vaginal bleeding, sometimes with developmentaloutcomesinthisgroup.1 the passage of clots and/or visible products of Additionally, adolescent mothers are more likely conception. Young women with irregular or to drop out of school and rely on public assistance sporadic menstrual cycles may mistake these for support.2 symptoms for their normal period. If not all tissue r Pathophysiology: The complications of pregnancy is passed, the patient may become septic from are among the life-threatening gynecologic causes bacterial superinfection and may present with of pelvic pain in adolescents. While pelvic pain is fever, diffuse abdominal and pelvic pain, and an uncommon primary complaint for intrauterine malodorous vaginal discharge.

16:22:39 261 12 Chapter 11: Genitourinary Complaints r Diagnosis: The key to diagnosis is a careful history, a spontaneous abortion. Abnormal increases physical examination, and urine or serum ␤-hCG can point to an ectopic pregnancy. testing. Once pregnancy is confirmed in an r CBC to assess for possible infection as well as adolescent female, there are several important anemia. studies/tests that should be performed. First, a r Blood typing, including determination of complete physical examination in these patients rhesus status. In the rhesus-negative patient, includes a speculum and bimanual pelvic administration of rhesus immunoglobulin is examination. This may be the patient’s first pelvic indicated in the setting of ectopic pregnancy or examination and it is important to take the time vaginal bleeding to prevent alloimmunization. to explain the details of the examination and r Testing for sexually transmitted infections: obtain informed consent. Important findings on Earlytreatmentduringpregnancyisimportant pelvic examination include vulvar, anal, or vaginal to reduce the risk of complications and trauma; cervical motion tenderness; vaginal potential for fetal transmission in certain bleeding or discharge; uterine tenderness; and cases.1–3 adnexal tenderness or masses. Bimanual examination should not be performed in girls Imaging studies should be performed in the with vaginal bleeding who are believed to be in pregnant adolescent with abdominal or pelvic the second trimester or later until it can be pain to determine the location of the pregnancy. ascertained that they do not have placenta previa In the absence of assisted fertility treatments, the (placenta overlying the cervical os). identification of an intrauterine pregnancy Pregnancy in a minor may be a presentation of effectively rules out ectopic pregnancy, as sexual abuse or assault. Care should be taken to spontaneous heterotopic pregnancy (one embryo evaluate for signs of trauma or injury during the in the uterus and additional embryo[s] in an ectopic location) is very rare. physical examination, and to interview the patient r in a safe and private environment. Treatment: The appropriate treatment of pregnant Socially, the pregnant adolescent faces many adolescents varies depending on the stage of challenges. Many feel stigmatized and socially pregnancy. Most early-pregnancy complaints isolated. The reported rates of postpartum other than ectopic pregnancy can be effectively depression range from 7 to 37 percent in managedasanoutpatientanddonotrequireany adolescents, and teenagers are at greater risk to specific treatment other than hydration, prenatal complete suicide. A history of mental illness or a vitamins, and treatment of pregnancy-associated prior suicide attempt places a patient at an nausea and vomiting as needed. Adolescents increased risk for a repeat attempt. The provider presenting in late pregnancy (later than 20 weeks) should assess the patient’s mental health as well as should be assessed for active labor and treated accordingly. her physical health. r Clinicians should be aware of the state laws Disposition: Patients with an intrauterine governing adolescent confidentiality and privacy, pregnancy earlier than 20 weeks’ gestation should as well as those involving mandatory reporting be referred to obstetrics for outpatient prenatal and notification of the legal guardians. A minor’s care and follow-up. Patients presenting with ability to consent for healthcare and/or treatment abdominal complaints after 20 weeks’ gestation varies from state to state. should have urgent obstetrics consultation in the In addition, laboratory testing should be ED or be transferred for urgent evaluation if they performed to include: are not in active labor. If an intrauterine pregnancy cannot be identified in the ED, the r Serum quantitative ␤-hCG: In the absence of a disposition should be determined in conjunction defined intrauterine pregnancy, serum ␤-hCG with obstetrics and gynecology, based on the can be performed serially to assist in the ␤-hCG levels and U/S findings. diagnosis of ectopic pregnancy or fetal demise. In addition to the medical concerns, there are ␤-hCG should double about every 48–72 hours many social and legal issues that surround in a normal pregnancy and should decrease in adolescent pregnancy. Currently, two-thirds of the

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states in the USA explicitly allow minors to 3. McCracken KA, Loveless M. Teen pregnancy: An consent for prenatal care. Some require the minor update. Curr Opin Obstet Gynecol 2014; 26: 355–9. to be of a certain age or be classified legally as a “mature minor.” The remaining states have no Case 5 relevant policy or laws. In some states, a legal guardian may need to be informed for certain Contributing Author: Pamela Young examinations, tests, or procedures. It is important to be familiar with local statutes when evaluating History the pregnant adolescent in the ED. The patient is a 15-year-old female who presents with For various reasons, the ED provider, rather complaints of foul-smelling, yellow, vaginal discharge. than the pediatrician or family physician, may be She states that this has been going on for about 3 the one to diagnose an adolescent’s pregnancy. days. She complains of mild lower abdominal pain. Depending on how far along the pregnancy is at Sheisunsureofherlastmenstrualperiod.Sheiscur- diagnosis, there are many medical, legal, and rently sexually active with one long-term boyfriend. social issues to consider. In a busy department this She states that she was taking birth control pills a few can be challenging. Medical emergencies must be months ago but forgot to take them for a while. She is promptly addressed and treated immediately, but currently waiting for her next period to begin so that the social and legal implications should not be shecanresumethemedication.Sheisnotcurrently ignored. It is important to ensure access to proper using any contraception. The patient denies any fever follow-up care and adequate support for the or chills. She denies any previous history of sexually adolescent who is found to be pregnant in the ED transmitted infections (STIs). She denies any vomiting prior to discharge. or diarrhea, but has felt nauseous at times.

Past Medical History Historical clues Physical findings Ancillary studies r r r r Attention deficit–hyperactivity disorder. Crampy Gravid uterus Positive urine r Allergic rhinitis. abdominal and (above umbilicus pregnancy test r back pain corresponds to UTD on immunizations. Ͼ 20 weeks’ gestation) Medications r Oral contraception (non-compliant). Follow-Up Allergies The patient initially denied the possibility of preg- r nancy, even after being told of the positive urine test. NKDA. She was then interviewed after mom stepped out of Physical Examination and Ancillary Studies the room and admitted to the provider that she was r ° sexually active and was not using any birth control. Vital signs: T 98.2 F, HR 72, RR 14, BP 98/62, O2 Her pain continued to increase in intensity and it was sat 98% on room air. r determined she was in active labor. She was transferred General:Normalbodyhabitus.Awakeandalert, to the labor and delivery department and later that in no acute distress. r evening gave birth to a healthy male child. HEENT: PERRL, moist mucous membranes, unremarkable examination. r Neck: Supple and non-tender, with no adenopathy. References r Cardiovascular: Regular rate and rhythm, normal 1. Fernandes de Azevedo W, Baffi Diniz M, Borges da S1 and S2, no M/R/G. Fonseca ES, et al. Complications in adolescent r pregnancy: Systematic review of the literature. Einsten Lungs: Clear and equal, with no W/R/R. Normal (Sao Paulo) 2015; 13: 618–26. respiratory effort. r 2. Centers for Disease Control and Prevention. Abdomen: Bowel sounds in all four quadrants Reproductive health: Teen pregnancy. www.cdc.gov/ normal; mild, diffuse abdominal tenderness, teenpregnancy/ (accessed February 2017). increased in suprapubic region. No organomegaly,

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no guarding or rebound. No costovertebral angle among young people aged 15–24.2 Recent percussion tenderness. epidemiologic data suggest that one in four r Genitourinary: External genitalia is normal, sexually active adolescent females has an STI such without any lesions noted. Cervix is non-friable. as chlamydial disease or human papilloma virus, Large amount of thick, yellow discharge noted at and 10 percent of asymptomatic adolescents cervical os as well as brownish bleeding noted. screened in a pediatric ED were positive for Bimanual examination notes normal uterus, Chlamydia trachomatis or Neisseria gonorrhoeae.3 cervical os closed, adnexa not palpable, no During 2013–2014, the rate of reported primary cervical motion tenderness. Mild bilateral and secondary syphilis cases increased by 11.6 inguinal lymphadenopathy. percent among persons aged 15–19 years and by r Extremities and skin: Warm and well-perfused, 13.1 percent among persons aged 20–24 years.1 with normal capillary refill and no signs of In addition to a high rate of primary infection, trauma. repeated acquisition of STIs is common, with as r Neurologic:Awakeandalert,grosslynon-focal. many as 40 percent of the annual incidence of r Pertinent laboratory values:U/Anegativefor chlamydial or gonococcal disease occurring in leukocytes, 3+ blood. Urine hCG negative, rapid adolescents previously infected with the causative HIV antibody negative. organisms. Many adolescents are re-infected within a few months of an index infection. Repeated acquisition of STIs is a risk factor for Questions for Thought subsequent development of HIV infection. r What are the most common STIs in teenagers? Certain groups have been identified as higher r What is the role for empiric treatment of STIs in a risk of HIV infection and co-infection with other patient with this presentation? r STIs. In a recent study of very young men who Is there any indication for imaging in this patient? have sex with men, urban and non-white status r What is the deﬁnitive treatment of this patient? r indicated a higher incidence of infection as well as Are their special concerns for STIs in sexually co-infection.4 Other risk factors included the use active teenagers? of alcohol or drugs during sexual activity.2,4 In very young pediatric populations, care must be takentoscreenforsexualabuseorassault.AnSTI Diagnosis may be the first hint of sexual assault in a victim r Chlamydial cervicitis and bacterial vaginosis. whohasnotreportedtheabuse. r Pathophysiology: STIs are typically transmitted Discussion via contact by an infected individual to the r Epidemiology:Theaverageageoffirstcoitusis oropharyngeal area or genitourinary tract of approximately 16 years among American another individual, where thin mucous adolescents, but the age is lower in certain membranes are susceptible to microbial passage. populations, such as inner-city youth.1 CausativeagentsincludebacteriasuchasC. Adolescents have barriers affecting access to STI trachomatis, N. gonorrhoeae,andTreponema prevention and management, including pallidum, viruses such as herpes, human transportation, conflict between clinic hours and papilloma virus, and HIV, and parasites such as school or work, and the inability to pay for the Trichomonas vaginalis, pubic lice, and scabies. examination and treatment. Embarrassment, r Presentation: STIs may present with localized risk-taking behavior, peer norms, and concerns complaints of discharge, drainage, or dysuria, about confidentiality and parent involvement also cutaneous complaints, or abdominal pain and factor into adolescent sexual activity and the systemic complaints. reluctance to seek medical care. As a result, adolescents are at very high risk for STIs. The r Urethral or vaginal discharge and dysuria are CDC estimates that nearly 20 million new the hallmarks of gonorrhea and chlamydia, as sexually transmitted infections occur every year well as trichomoniasis, bacterial vaginosis, and in the USA, approximately half of which occur candidiasis. Classically, chlamydial and

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gonorrheal cervicitis cause purulent drainage, adolescent males should be performed dependent trichomoniasis causes malodorous gray to uponriskfactors,i.e.analintercourse,reported green discharge with vulvar irritation, bacterial unprotectedsexualactivity,andsymptomsupon vaginosis causes a watery, foul-smelling presentation. The CDC recommended in 2006 discharge with minimal irritation, and candida that “opt-out” HIV testing be routinely offered to vaginitiscausesvulvarirritationwithscant allpatientsaged13to64years.2 This involves white discharge. Vaginitis and vulvitis are informing the patient, orally or in writing, that discussed in more detail later in this chapter, HIV testing will be performed unless he or she Case 7. Genital herpes is sometimes associated declines. The AAP recommends that routine HIV with dysuria and a scant, mucoid urethral screening be offered at least once to all adolescents discharge; however, these infections usually by 16 to 18 years.5 Annual HIV testing should be have associated skin findings. offered to high-risk adolescents who use IV drugs r Skin findings are typical of genital warts or have sex with multiple partners, or men who (condyloma acuminata), caused by human have sex with men. If a patient is being tested papilloma virus, herpes infections, syphilis, for other STIs, then HIV testing should be and disseminated gonococcal infection. The included. skin lesions of genital warts are typically not For symptomatic patients, diagnoses of painful and are soft and fleshy, and located on gonorrhea and chlamydia are most commonly the perineal area. Herpes infections nearly made by a DNA probe or nucleic acid always present with painful genital ulcers, amplification from either a genitourinary swab which may be confused with “hair bumps,” specimen or from urine testing. Gram’s stain is particularly in adolescents who shave the both sensitive and specific for the diagnosis of genital region. These are sometimes gonococcal urethritis in symptomatic males. accompanied by systemic complaints in Although cultures are not routinely indicated, primary infection, as opposed to recurrences. they may be warranted in the instance of They can appear very similar to Behc¸et’s suspected sexual abuse or assault. Herpes is disease. The rash of disseminated N. typically diagnosed on clinical examination, gonorrhoeae is erythematous and papular to although wound culture of active lesions provides pustular. It is painful, and is usually a definitive diagnosis. accompanied by joint pain. The rash of syphilis SerologictestingforHIVisperformedvia is typically genital in location and is painless. It ELISA screening for HIV-1 and -2. Positive results is associated with a high rate of HIV are confirmed via HIV-1/HIV-2 differentiation co-infection. assay or Western blot. r r Abdominalpainandsystemiccomplaintsare Treatment: The CDC routinely publishes updated common in adolescents presenting with pelvic treatment guidelines for STIs, most recently in inflammatory disease, and any adolescent with 2015, reflecting developing resistance patterns. It abdominal pain or tenderness should be hasbeenestimatedthatupwardsof30percent queried privately regarding sexual activity. of adolescents are non-compliant with STI Pelvic inflammatory disease is a common treatment.6 Therefore, single-dose therapy or sequela of untreated gonorrhea or chlamydia treatment at the time of examination, if there is a andshouldbesuspectedinthefemalepatient high index of suspicion, is preferable. Expedited presenting with severe lower abdominal pain, partner therapy allows for the provision of with or without associated fever. Pain with appropriate single-dose antibiotics to patients intercourse is another common presenting with chlamydia or gonorrhea for delivery to symptom. partners. This measure may help to reduce the incidence of re-infection by repeat exposure to an r Diagnosis: Screening of sexually active female untreated partner. Current recommendations also adolescents for gonorrhea and chlamydia should endorseatestofcurewithin3to12months, be performed at least annually and as indicated by particularly if there is a question regarding complaint or presentation.5 Screening of compliance or treatment of the partner.

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Briefly, the CDC recommends that chlamydia 2. Centers for Disease Control and Prevention (CDC). infection be treated with azithromycin 1 g orally Reproductive health: Teen pregnancy. See www.cdc or doxycycline 100 mg twice daily for 7 days. N. .gov/teenpregnancy/ (accessed February 2017). gonorrhoeae infections should be treated with 3. Schneider K, FitzGerald M, Bychzkowski T, et al. ceftriaxone 250 mg IM plus azithromycin 1g Screening for asymptomatic gonorrhea and chlamydia orally. First-line treatment of initial presentation in the pediatric emergency department. Sex Transm Dis 2016; 43: 209–15. of genital herpes is a 7–10-day course of acyclovir, though there may be increased compliance with 4. Garofalo R, Hotton AL, Kuhns LM, et al. Incidence of the once daily dosing of valacyclovir. The HIV infection and sexually transmitted infections and related risk factors among very young men who have complete recommendations may be found on the sex with men. JAIDS2016; 72: 79–86. CDC website. r 5. American Academy of Pediatrics. Recommendations Disposition: Patients presenting with signs and for preventive pediatric health care. See www.aap.org/ symptoms of sexually transmitted infections en-us/Documents/periodicity schedule.pdf (accessed should be screened for co-infections, with close February 2017). follow-up arranged for test results and ongoing 6. Schneider K, Byckowski T, Reed J. Treatment care, including a test of cure to assure eradication compliance among asymptomatic adolescents with of the current infection. Providers should be sexually transmitted infections. JAMA Pediatr 2015; watchful for signs of sexual abuse/assault and 169: 1065-6. offer forensic examination and notification oflaw enforcement as per local law and practice. Case 6 Historical clues Physical findings Ancillary studies Contributing Author: Leah A. Perez r Vaginal r Mucopurulent r Negative History r discharge r cervical discharge pregnancy test Sexually active Inguinal The patient is a 4-year-old female who presents with r Abdominal adenopathy pain a 24-hour history of urinary frequency and dysuria. Per mom the patient started complaining of pain when voiding yesterday after she came home from preschool Follow-Up which the patient attends all day. The mother reports This patient’s presentation of foul-smelling discharge the patient has had decreased appetite with nausea, but with mild lower abdominal pain is typical for chlamy- mom denies vomiting, diarrhea, abdominal pain, or dia infections, for which her nucleic acid amplifica- fever. The patient is toilet trained and per mom she had tion test was positive. The patient was notified of her an accident last night and woke up wet this morning positive test and prescriptions for doxycycline were which is unusual for her. The patient’s mother is also provided to the patient and her partner. The patient concerned as the patient appears more uncomfortable returned 1 month later with concerns for a STI as her when voiding this morning and is crying intermit- partner may not have been compliant with the treat- tently, which is causing her to stop mid-stream when ment regimen, and she tested positive for both N. gon- voiding. The patient is voiding more frequently as well. orrhoeae and C. trachomatis.ShewastreatedwithIM She has no previous history of UTIs. ceftriaxone and oral azithromycin. The patient denied any concerns for sexual assault/abuse or human traf- Past Medical History ficking and stated that she had a safe living environ- r Tonsillectomy and adenoidectomy. ment. Her partner was notified to seek treatment at the r UTD on immunizations. Department of Health. The patient was subsequently lost to follow-up. Medications r References Loratidine daily. 1. Kann L, Kinchen S, Shankin SL, et al. Youth risk behavior surveillance United States, 2013. MMR Suppl Allergies r 2014; 63: 1–168. NKDA.

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Physical Examination and Ancillary Studies r Pathophysiology: Urine in the proximal urethra r Vital signs: T 98.4 °F, HR 95, BP 118/69, RR 18, O2 and urinary bladder is normally sterile. UTIs sat 99% on room air. develop when pathogens ascend to the bladder r General: The patient is awake, alert, and appears (cystitis, or lower tract disease) or to the kidneys comfortable. (pyelonephritis, or upper tract disease) via the r HEENT: PERRL. Oropharynx clear, with moist urethra. Pathogens may then enter the blood mucous membranes. stream and cause systemic illness (bacteremia). r Neck:Supple,withnoadenopathy. Poor containment of infection, including bacteremia, is most common in infants less than r Cardiovascular: Regular rate and rhythm, with no 2 months old. Pathogens may enter the urinary M/R/G. tract secondary to turbulent urinary flow during r Lungs: Clear and equal, with normal work of normal voiding, voiding dysfunction, or breathing and no W/R/R. 1 r catheterization. In addition, sexual intercourse or Abdomen:Soft,notdistended.Normalbowel genital manipulation may foster the entry of sounds throughout. There are no palpable masses. bacteria into the urinary bladder.1 More rarely, the There is suprapubic tenderness on palpation. r urinary tract may be colonized during systemic Extremities and skin: No rashes, deformity, or bacteremia (sepsis); this is more common in evidence of trauma. r infants than in older children. Pathogens can also Neurologic: Appropriate for age, non-focal. infect the urinary tract through direct spread via r Pertinent laboratory values:Urinedipstickwith the fecal–perineal–urethral route. specific gravity 1.020, pH 6.0, glucose negative, The majority of UTIs are caused by Escherichia ketones negative, leukocyte esterase moderate, coli, which accounts for 75–90 percent of UTIs.2 nitrite positive, protein trace, hemoglobin trace, Most of the remainder are also caused by bowel bilirubin negative, and urobilirubin negative. flora such as Enterococcus or Klebsiella species or other Gram-negative rods, but fungi such as Candida albicans and even viruses may cause Questions for Thought UTI. Staphylococcus and Streptococcus species also cause UTIs, particularly in neonates and r What are typical laboratory ﬁndings in this adolescent females. condition? r r What further laboratory testing should be Presentation:Thehistoryandclinicalcourseofa initiated in the ED? UTI vary with the patient’s age and specific r What items on the diﬀerential diagnosis are diagnosis. No one specific sign or symptom can be important not to miss? used to identify UTI in infants and children. Contributing factors to making a decision to pursue UTI testing includes a prior history of a UTI, circumcision history in very young boys, Diagnosis and, in older children, typical symptoms such as r Lower UTI/cystitis. increased urinary frequency, abdominal or suprapubic discomfort, loss of urinary continence, Discussion or dysuria. Typical presentations for children of r Epidemiology: UTI is one of the most common various age groups are as follows: pediatric infections, second only to otitis media, and accounts for 1.5 million office visits a year.1,2 r Children aged 0–2 months: Neonates and These infections distress the child, concern the infants up to age 2 months generally present parents, and may cause permanent kidney with upper tract disease, and the UTI is damage and hypertension.2 UTIs occur with equal discovered as part of an evaluation for neonatal frequency in boys and girls under 1 year of age, sepsis. They may present with jaundice, fever, butaremorecommoningirlsafterthatage.1,2 poor feeding, vomiting, or irritability.1,2 Circumcision offers some protection from UTI in r Infants and children aged 2 months to 2 years: boys.1,2 Infants with UTIs may present with poor

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feeding, fever, vomiting, strong-smelling urine, probability, a positive nitrite on U/A increases the abdominal pain, or irritability.2 They often lack probability of UTI to 75 percent (as the specificity local symptoms or are unable to communicate of nitrite is 98 percent).4 This may change the those symptoms, although parents may note provider’s threshold for antibiotic administration. crying with urination or increasing frequency. Likewise, the visualization of bacteria on r Children aged 2–6 years: Preschoolers with microscopy increases the probability of UTI to lower tract disease usually have voiding 35 percent, which may bring the likelihood of the symptoms such as urgency, frequency, disease sufficiently high for an individual provider hesitancy, dysuria, or incontinence, with no to choose to treat.4 If a child does not have fever. They may have suprapubic pain or sufficient urine for U/A and culture, culture is the tenderness. Upper tract disease may present diagnostic test of choice, and U/A should not be with vomiting, abdominal pain, fever, performed.4 strong-smelling urine, enuresis, or regression Urine should be cultured within 4 hours or the with milestones in terms of toilet training, as urine should be refrigerated to prevent bacterial well.1 overgrowth. Culture positivity is defined at r Older children and adolescents with lower different thresholds depending upon the method tract disease usually present with dysuria, of obtaining the specimen. Current established urgency, and frequency with or without thresholds are 10,000 colony forming units abdominal pain.1 Fever is usually absent. With (cfus) of a single pathogen per milliliter in a upper tract disease, children may have fever, catheter-obtained specimen and 100,000 cfus/mL flank pain, abdominal pain, and vomiting. It is in a clean-catch specimen.4 Some advocate for important to remember that adolescent girls treating at lower counts in patients who have with sexually transmitted infections or symptomatic disease.4 vaginitis may present with similar symptoms, When a UTI has been diagnosed, the medical and the history and physical examination provider should consider the underlying should consider these possibilities. associated risk factors to optimize management. Constipation is a common risk factor, as is r Diagnosis: The AAP recommends that all children diabetes.4 Voiding dysfunction and anatomic with fever with no source under the age of 2 years anomalies should be considered in patients with be evaluated for UTIs.3 Although peripheral recurrent disease.3,4 Arecenthistoryof blood collection may risk-stratify individuals broad-spectrum antibiotic use may alter from a sepsis standpoint and assess renal antibiotic choice, and should be specifically function, the diagnosis of a UTI is made by urine questioned. studies. Although the AAP does allow for r Treatment: Symptomatic relief in children is non-invasive collection of urine for analysis, generally supportive, with anti-inflammatory bagged urine samples should not be used for medications and increased fluid intake to enhance culture, as they have a very high false positive urine dilution. Antiemetics may also be used. rate.1,3,4 A negative bag urine culture is strong Urinary anesthetics, such as phenazopyridine, are evidence that there is no UTI present. However, not recommended for children under 12 years of giventhelimitationstothismodeofcollection, age. consideration for catheterization should be given Children with cystitis typically respond well to for children with a high suspicion of UTI who are appropriate antibiotic therapy and symptomatic unable to provide a clean-catch specimen.4 treatment. Antibiotic therapy is started on the U/A is insufficient to make a diagnosis of UTI, basis of clinical history, physical examination, and and lacks the sensitivity to rule it out.4 The data U/A results before the culture provides a definitive obtained may change the clinical suspicion of the diagnosis, in most cases. Certainly, all ill children disease, however, and therefore it is not an should receive antibiotics. In older children with unreasonable test to obtain along with the gold an unclear etiology of symptoms, observation standard, which is urine culture and microscopy. alone pending urine culture is not unreasonable For instance, with a 10 percent pre-test as many will clear their bacteriuria spontaneously

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and there are no untoward affects from delaying Historical clues Physical findings Ancillary studies therapy for a day.4 In patients who are not toxic, a r Frequency r Suprapubic r U/A suggestive of 4-day course of an oral antibiotic agent is r r Dysuria tenderness a UTI, with recommended for the treatment of cystitis.4 A Enuresis positive nitrites systematic review of treatments for cystitis in and leukocyte esterase children showed no difference in efficacy with 7–14 days of therapy compared with 2–4 days.4 Empiric antibiotic therapy should be based on resistance patterns for typical uropathogens in the Follow-Up patient’s community, with an appropriate first-line This patient was diagnosed with an uncomplicated agent such as sulfamethoxazole–trimethoprim, cystitis and discharged to home with ibuprofen and amoxicillin–clavulanic acid, cephalexin, cefixime, trimethoprim–sulfamethoxazole based on clinical his- cefpodoxime, or nitrofurantoin. Of note, the tory,examination,U/Aresults,andlocalpatternsof limited tissue penetration of nitrofurantoin limits antibiotic resistance. The patient and her mom were its use to cystitis and excludes its use for encouraged to increase PO intake and take warm baths pyelonephritis. If the clinical response is not for comfort and return to the ED with any new or wors- satisfactory after an initial course of empiric ening symptoms. therapy, antibiotic choice should be altered on the basis of antibiotic susceptibility. Children with upper tract disease (systemic symptoms or WBC References casts on urine microscopy diagnostic for 1. Becknell B, Schober M, Korbel L, et al. The diagnosis, evaluation, and treatment of acute and recurrent pyelonephritis) should be treated for longer, 4 pediatric urinary tract infections. Expert Rev Anti typically 10–14 days. Ill children, children less Infect Ther 2015; 13: 81–90. than 2 months old, and children unable to take 2. Copp HL, Schmidt B. Work up of pediatric fluids by mouth should be admitted for IV urinary tract infection. Urol Clin North Am 2015; 42: antibiotics. 519–26. Former recommendations included a voiding 3. Newman TB. The new American Academy of cystourethrogram in the follow-up for all first Pediatrics urinary tract infection guidelines. Pediatrics febrile UTIs, but newer guidelines from the AAP 2011; 128: 572–5. state that U/S should be performed in young 4. White B. Diagnosis and treatment of urinary tract children with first UTIs, particularly all boys and infections in children. Am Fam Phys 2011; 83: 409–15. girlsunder3years,andfebrilegirlswithUTIs, under age 7.3,4 The risk–benefit on more detailed imaging, using modalities requiring radiation Case 7 exposure, are best deferred to the primary care team. Likewise, decisions for antibiotic Contributing Authors: Shellie Asher and prophylaxis for recurrent UTIs should be made in Rebecca Jeanmonod concert with the primary care team. r Disposition: Neonates (birth to 6 weeks) with fever History andaUTIshouldbeadmittedandstartedon The patient is a 4-year-old female, who is brought in parenteral antibiotics pending culture results and bymomforvaginaldischarge.Thepatient’smother clinical response to therapy. The majority of older states that she was giving the child a bath this evening infants and children with simple cystitis or when she noted a foul-smelling vaginal discharge and pyelonephritis can be discharged home with oral a yellow stain in the patient’s underwear. There have antibiotics if they are well-appearing and can take been no recent fevers, vomiting, abdominal pain, or oral fluids and medication. Patients who have other illnesses. The patient complains that it “feels signs of sepsis and/or cannot take oral fluids/ itchy down there” but denies other complaints. The medications should be admitted to the hospital patient’s mother notes that the child recently com- for fluid resuscitation and parenteral antibiotic pleted toilet training and has been independently man- therapy. aging her toileting and associated hygiene.

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Past Medical History Discussion r None. r Epidemiology: Symptoms referable to the vulva and vagina are common in girls of all ages. The Medications exact incidence is difficult to determine, as the r None. underlying diagnoses are numerous. The cause of vulvovaginitis differs as a factor of the patient’s Allergies age, with post-menarcheal girls having pathogens r similar to adult women of reproductive age, and NKDA. pre-menarcheal girls having non-specific vulvovaginitis or infections with respiratory flora. Physical Examination and Ancillary Studies r Pathophysiology: In prepubertal girls, most cases r ° Vital signs: T 98.4 F, HR 110, RR 22, BP 95/60, O2 of vulvovaginitis begin with irritation of the vulva, sat 98% on room air. followed by involvement of the vagina. The r General: Well-nourished and well-appearing anatomy and physiology of the pediatric vagina child, in no acute distress. and vulva is predisposed to irritation because of r HEENT: PERRL. Mucous membranes moist with the relatively small labia minora, the absence of no lesions. labial fat pads and pubic hair, low levels of r Neck: Supple, with no tenderness or adenopathy. estrogen with a resulting thin vaginal epithelium, r Cardiovascular:Regular,normalS1/S2,without and alkaline pH.1,2 Behavioral factors such as M/R/G. Good capillary refill. poor hygiene (particularly related to toilet r Lungs:Clearbilaterally,withnoW/R/R. training), self-exploration, foreign-body insertion, r Abdomen: Soft and non-tender with no masses, tight-fitting clothing, and chemical exposures rebound, or guarding. such as bubble baths and damp swim suits also 1,2 r Genitourinary:Tanner1.Slightlyerythematous play a role. While most cases are non-specific, vulva with a small amount of foul-smelling infectious agents such as respiratory pathogens discharge. There is a small foreign body at the (typically Streptococcus or Haemophilus species), vaginal introitus, which appears to be retained entericpathogens,STIs,viralinfections(suchas toilet tissue. There is no bleeding or other EBV), and parasitic infections may be associated 1–4 evidence of injury on external examination. with vulvovaginitis. Autoimmune and r idiopathic causes also occur, such as lichen Extremities and skin: Warm and well-perfused, 1 with no rashes or signs of trauma. sclerosis, vasculitis, psoriasis, or Behc¸et’s disease. Candidal vulvovaginitis is uncommon in r Neurologic: Normal mentation for age. Non-focal prepubertal girls, although it occurs in association examination. with diaper rash in children who are not toilet r Pertinent laboratory values:Wetmountwith3+ trained. WBC, Gram’s stain negative, culture with normal In girls who have reached puberty, the vaginal vaginal flora. mucosa is thicker, fat pads have developed, and pubichairispresent.ThepHofthevaginal Questions for Thought secretions is more acidic. All of these items offer r protection from the causes of vaginitis that plague What is the diﬀerential diagnosis for this the smaller child. Rather, the vast majority of all presentation? cases of vaginitis in post-menarcheal young r What are the possible causes of this diagnosis? women are caused by candidal species, r What social or safety concerns should you consider for this child? Gardnerella vaginalis,andTrichomonas vaginalis.5,6 These pathogens cause varying degrees of inflammation and discharge and displace normal vaginal flora. Diagnosis r Presentation:Patientswhoareindiaperswill r Non-specific vulvovaginitis. typically present with irritation, noted by the

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caregiver, or with discharge. Older children or on the caregiver’s lap. In extreme cases, such as adolescents may present with complaints of suspected abuse or irretrievable foreign body, the irritation or itching, or parents may note staining child may require an examination under or discharge in their underwear. Children may anesthesia. Older, post-menarcheal girls may also complain of burning, vaginal pain, and require a speculum examination, particularly if dysuria. sexually active and the diagnosis of vaginitis It is important to remember that versus cervicitis is unclear. Remember that vulvovaginitis exists on a spectrum. In cervicitis does not typically cause vaginal post-menarcheal girls with vulvovaginitis, irritation, although it does cause discharge. candidal infections most commonly present with The provider should carefully inspect the significant irritation but a paucity of discharge, vulva and vaginal introitus, with attention to although patients may complain of a thick plaque color, signs of injury, foreign body, or discharge. or discharge present at the introitus. Those with Vulvovaginitis should be distinguished from other bacterial vaginosis typically have copious common vulvar disorders including lichen discharge, which is thin and malodorous, but very sclerosis (which presents with intense pruritus little true inflammation. Those with and sharply demarcated, white, finely wrinkled trichomoniasis have both inflammation and skin around the vagina and anus), trauma, and discharge. The provider should have a high index labial adhesions (inability to separate the labia of suspicion for vaginal and vulvar pathology in minora, which may be associated with girls of all ages who complain of itching, concomitant vulvovaginitis). If inflammation and dysuria, drainage, irritation, or lower abdominal discharge are significant, diagnostic studies pain. including wet mount, Gram’s stain, and culture r Diagnosis: The diagnosis of vulvovaginitis may be performed. depends on a careful history and physical Wet mount, pH, and a whiff test are by far the examination. While the diagnosis is typically best immediate diagnostic tools at the disposal of derived clinically, there are many potential causes the clinician in the setting of post-menarcheal of vulvovaginitis that may need to be investigated, girls, as candida species, G. vaginalis, and T. including infection, chemical irritation, foreign vaginalis are all identifiable with sensitivities in bodies, allergy, systemic diseases, and sexual the mid 80s for these pathogens.5 Candidal species abuse. Important historical elements include will demonstrate budding yeast and a pH Ͻ5, with hygiene habits, recent illnesses (particularly no significant odor to the discharge in the clinical respiratory and GI), chemical irritant exposure, setting of intense vulvar/vaginal irritation.5 history of foreign body or masturbation, and Bacterial vaginosis will present with pH Ͼ5, clue sexual abuse. The provider should interview cells on microscopy, and a positive whiff test in verbal children privately to query regarding the clinical setting of copious malodorous inappropriate touching and abuse. The provider discharge.5 Trichomoniasis will present with a pH should do this in a way that is not frightening to Ͼ5.4 and a positive whiff test in the setting of the child. discharge and irritation with a strawberry cervix.5 The provider should perform a complete ADNAprobeforT. vaginalis is appropriate in this physical examination, paying attention to other patient population, as well. Testing for specific signs of injury, abuse, or neglect. When pathogens (such as sexually transmitted performing a vaginal examination on an infant, infections and pinworms) may also be the easiest method is to perform an external performed as indicated by the history and examination in frog-legged position. As children examination. becomeolder,theymaybeveryresistenttobeing r Treatment: Mainstays of treatment for examined. Other ways to examine a child that are non-specific vaginitis are good hygiene and local sometimes more acceptable to the child is to have care of inflamed tissues. The area should be the child on knees and elbows on the bed, or to cleaned gently with a mild fragrance- and dye-free have the child in frog-legged position while seated soap and gently dried. Clothes similarly should be

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washed with mild fragrance- and dye-free Follow-Up detergents, and the child should be dressed in The patient and mother were queried separately about loose, breathable clothing. Small amounts of the possibility of child abuse, and no concerns were non-medicated ointment or barrier cream may be identified. Symptoms were attributed to the retained applied to protect tissues during the healing foreign body secondary to inadequate hygiene. The process. Cases refractory to these measures may foreign body was removed and the vulva cleaned gently be treated with short courses of topical with warm water and mild soap. The patient’s mother low-potency corticosteroid creams. was counseled regarding supervision of hygiene at this Antimicrobials may be administered if history, age, and the patient’s pediatrician was contacted to examination, and testing suggest a specific assure close follow-up. microbiologic cause or for cases that do not respondtothepreviouslydiscussedmeasures.In References post-menarcheal girls in whom wet mount does 1. Van Eyk N, Allen L, Giesbrecht E, et al. Pediatric not provide a diagnosis, treatment for all three vulvovaginal disorders: A diagnostic approach and common causes of vaginitis is appropriate, as this review of the literature. JObstetGynaecolCan2009; covers more than 90 percent of all cases of 31: 650–62. vulvovaginitis in this age group. It is important to 2. Yilmaz AE, Celik N, Soylu G, et al. Comparison of determine pregnancy status prior to initiation of clinical and microbiological features of vulvovaginitis treatent, as treatment regimens differ in pregnant in prepubertal and pubertal girls. JFormosanMed Assoc 2012; 111: 392–6. and non-pregnant patients. r Disposition:Mostpatientscanbedischarged 3. Beyitler I, Kavukcu S. Clinical presentation, diagnosis, and treatment of vulvovaginitis in girls: A current home with supportive care as noted above. approach and review of the literature. World J Pediatr Arrangements should be made for outpatient 2017; 13: 101–5. follow-up with the patient’s PCP. 4. Kim H, Chai SM, Ahn EH, et al. Clinical and microbiologic characteristics of vulvovaginitis in Korean prepubertal girls, 2009–2014: A single center Historical clues Physical findings Ancillary studies experience. Obstet Gynecol Sci 2016; 59: 130–6. r r r 5. Hainer BL, Gibson MV. Vaginitis: Diagnosis and Vaginal r Vaginal discharge WBC on wet r discharge Retained foreign r mount treatment. Am Fam Phys 2011; 83: 807–15. Recent toilet body Normal flora on 6. Zeger W, Holt K. Gynecologic infections. Emerg Med training culture Clin N Am 2003; 21: 631–48.

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Case 1 r General: The patient is a well-appearing, playful girl in no distress. Contributing Author: Efrat Rosenthal r HEENT: The patient’s extraocular eye movements History are intact, she has moist mucous membranes and a clear oropharynx. No overt trauma. The patient is a 6-year-old female, who presents with r Neck: No obvious trauma. Her neck is supple with a painful lesion on her right buttocks. The lesion has no lymphadenopathy. been present for the last week, mildly red and elevated, r Cardiovascular:Theheartrateandrhythmare and tender to touch. The patient has been seen by her regular and there are no murmurs. The distal pediatrician, who had started her on trimethoprim– pulses are normal. sulfamethoxazole, which she has taken for 5 days, with r no improvement or change in symptoms. She has not Lungs: There are clear breath sounds bilaterally, with comfortable work of breathing. had any fevers and denies any discharge from the r lesion. Her pediatrician saw her in the office again Abdomen: The abdomen is soft, non-tender, today and gave a prescription for cephalexin, and then non-distended, with no masses or hepatosplenomegaly. sent her to the ED for possible incision and drainage. r Shehasotherwisebeeninherusualhealth.Ofnote,the Extremities and skin:Thepatienthasan patient was on vacation about two weeks ago and was approximately 1-cm erythematous lesion on her playing on a wooden structure. She did incur a splinter right buttock that is mildly swollen, with no inthesameareaatthetime;however,momwasableto induration or fluctuance appreciated. The lesion pull it out (approximately 1 cm in length). is tender to palpation and has a punctate center with an overlying scab. Extremities are Past Medical History normal. r r Healthy with no medical problems. Neurologic: Normal mental status and non-focal r UTD on immunizations. examination. r Pertinent imaging: Bedside U/S performed and Medications shown in Figures 12.1 and 12.2. r Currently taking trimethoprim–sulfamethoxazole. r Has prescription for cephalexin, but has not Questions for Thought started it yet. r What is the diﬀerence between inert and organic cutaneous foreign bodies? Allergies r r What are some complications that may stem NKDA. from retained foreign bodies? r What is the best diagnostic imaging to visualize Physical Examination and Ancillary Studies an organic foreign body? r r Vital signs: T 98.8 °F, HR 88, RR 18, BP 105/68, O2 Is antibiotic therapy necessary? sat 100% on room air.

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Figure 12.1 Bedside U/S (long-axis view) demonstrating a thin, elongated, approximately 1-cm foreign body about 1.5 cm deep in the tissue. No fluid collection or abscess visualized.

Diagnosis presenting to the pediatric ED.2 They are more r Foreign-body granuloma. frequent in the summer months, and penetrating wounds of the lower extremities are common, Discussion with more than half occuring in the foot.1,2 Most r Epidemiology: There are millions of ED visits puncture wounds occur as isolated minor events annuallyintheUSAduetoopenwounds.1 There and medical care is generally not sought or is more information on uncomplicated soft-tissue required. Any object becomes a foreign body wounds in Chapter 6, Case 4. Puncture wounds when it penetrates the skin and lodges in the soft account for 3–5 percent of traumatic injuries tissue. It is estimated that 38 percent of foreign

Figure 12.2 U/S Short-axis view of the foreign body, with the probe rotated by 90 degrees.

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bodies are overlooked on initial examination, are most commonly missed. Erythema, swelling, although history and imaging increase the or persistent pain in the area of the puncture site diagnostic yield and make discharge of patients suggests a retained foreign body. Chronic or with an acute wound with a retained foreign body recurrentinfectionsataspecificsitearealsovery relatively uncommon. The majority of the injuries suspicious for a retained foreign body. are caused by wood, metal, and glass; many are Foreign-body granulomas can also present as caused by thorns or fragments of wood that are pseudotumors of both bone and soft tissue years retained in the limb, creating a foreign-body after the initial injury. Depending on the time granuloma.1–4 since the initial injury, a puncture wound r Pathophysiology: A retained foreign body may overlying the lesion may or may not be visible. result in allergic, inflammatory, and infectious r Diagnosis: A thorough history, exploring the complications. The inflammatory response varies possibility of a foreign body, is an important first in intensity based on the composition of the step. Superficial foreign bodies can sometimes be object: inert materials (glass, plastic, metal) are palpated or visualized; however, relying solely on non-reactive and generate less response than a clinical examination may lead to many missed organic materials (bones, wood, rubber, soil, foreign bodies on the initial examination.1,3 stones, or vegetative materials).1,2,5 Inert Gently running a gloved finger over the suspected materials are relatively low risk for infection and foreign-body site can elicit a characteristic can be left in place if they are inaccessible and will foreign-body sensation in the patient.2,3,5 Deeper not cause tissue damage or function deficit, while foreign bodies may require imaging or surgical organicmaterialsposeahigherrisk.1,5 Organic exploration to localize. Radiographs have objects can cause a variety of bacterial and fungal traditionally been the first images obtained as infections, including synovitis from joint they can detect approximately 80 percent of all penetration, periosteal reactions, foreign-body foreign bodies, even the size of a pinpoint, if the granulomas, draining fistulas, and pseudotumors foreign body is radiodense. Almost all types of of the soft tissue. Wood is notorious for glass (95 percent) 2 mm in size can be seen by splintering and fragmenting, which is part of the X-ray, although smaller fragments are often reasonitishighriskforbeingleftasaforeign missed.1,3 Wooden foreign bodies have been body and why extraction is so difficult.1–3,5 reported to be visible by radiography in only Missed foreign bodies are a frequent cause of about 10–15 percent of all cases, however, these wound infections that are resistant to antibiotic may become invisible after 48 hours due to fluid therapy. Foreign-body granuloma, a chronic absorption. U/S is a non-radiation modality that inflammatory process, may occur with foreign has been shown to accurately demonstrate the bodies left in place over time. Tissue becomes size, shape, and location of soft-tissue foreign inflamed, and histolytic and macrophage bodies that are 2 mm or larger and it is superior to reactions occur, forming multinucleated giant cell CT in the ability to detect objects.6,7 Wood has a infiltration.5 The foreign body may then become distinct signature on U/S; hyperechoic foci, often encapsulated with fibrous tissue and form a with acoustic shadowing and a hypoechoic halo; granuloma. The patient may present with chronic which is helpful in the identification of these pain or inflammation at the skin site. otherwise difficult-to-find foreign bodies.1,6 r Presentation: In acute foreign body, most patients Though it has its limitations, U/S is portable, can will relate a history (such as breaking glass or be used real time, and does not utilize ionizing stepping on an object) that suggests the possibility radiation, making it the preferred modality for the of a foreign body. In most cases of a retained initial investigation of foreign bodies.1,6,7 foreign body, there is no clear history and patients r Treatment: The first step in treatment is to decide cannot reliably report its presence, but a high whether a removal attempt should be made in the index of suspicion is needed. Patients may present ED. Removal is more likely to be successful if the for evaluation several months or even years after object has been under the skin for less than the initial injury. Any injury with glass should 1week,theentrywoundisfresh,theobjectis raise the suspicion of a retained fragment, as these visible, the object can be localized with imaging,

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or the object can be felt during probing. Foreign References bodies within or proximal to joints, flexor 1. Wagstrom Halaas G. Management of foreign bodies in tendons, or blood vessels may require surgical the skin. Am Fam Phys 2007; 76: 683–90. consultation and removal within the OR.7 Local 2. Baldwin G, Colbourn M. Puncture wounds. Pediatr anesthesia should be limited to minimize swelling Rev 1999; 20: 21–3. near the foreign body, which can make 3. Levine MR, Gorman SM, Young CF, et al. Clinical localization more difficult. Using a number 15 characteristics and management of wound foreign scalpelblade,anincisionovertheentrypoint bodies in the ED. Am J Emerg Med 2008; 26: 918–22. should be made and a small curved clamp can be 4. Strecker-McGraw MK, Jones TR, Baer DG. Soft tissue used to explore the incision site for the foreign wounds and principles of healing. Emerg Med Clin N body.5 Raking through the site to feel for the Am 2007; 25: 1–22. foreign body may assist localization. Raking is not 5. Trott AT. Common wound care problems. In Wound recommended over delicate structures (i.e. nerves, and Lacerations: Emergency Care and Closure,4th flexor tendons) such as in the palm.5 Once edition. Philadelphia, PA: Saunders, 2012, pp. 220–35. localized, the foreign body is grasped and 6. Graham DD. Ultrasound in the emergency removed. If the foreign body is wood, a small department: Detection of wooden foreign bodies in incisionparalleltothecourseandangleofthe the soft tissues. JEmergMed2002; 22: 75–9. object should be made so the splinter can be 7. Boyse TD, Fessell DP, Jacobson JA, et al. Ultrasound of removed without leaving behind smaller splinters. soft-tissue foreign bodies and associated complications After removal, the wound should be irrigated. with surgical correlation. Radiographics 2001; 21: Suturing of small incisions is not recommended as 1251–6. thesiteshouldbeleftopentodrain,ifnecessary. Antibiotics should only be prescribed if there is Case 2 evidence of an infection and tetanus prophylaxis should be given as necessary.1 If a foreign body Contributing Author: Efrat Rosenthal cannot be removed within 5 to 10 minutes, History surgery should be consulted. r Disposition: Most patients with foreign bodies are The patient is a 12-year-old boy with history of autism, discharged from the ED after successful removal.3 presenting with a rash on his lower legs bilaterally Patients with objects that cannot be extracted for 2 days. The patient has otherwise been in his require outpatient surgical follow-up. usual state of health, afebrile, with no cold symptoms, Complications of foreign bodies can also dictate cough, vomiting, diarrhea, fatigue, or weakness. The the patient disposition, such as infections rash is not itchy or painful. It is located mostly on requiring IV antibiotics and, therefore, admission. his lower legs, with some spots on his upper legs and trunk. Of note, the patient presented about 1 week Historical clues Physical findings Ancillary studies ago to the ED with a chief complaint of left knee pain. r r r The pain was thought to be secondary to a possible History of r Normal vital signs U/S with foreign recent splinter Tender body trauma at school because the patient does occasionally removal erythematous fall, though this injury was unwitnessed. At that r Persistent pain lesion r Punctate center visit the patient had an X-ray that was normal, and, (entry site) given the history and normal physical examination, he was discharged home with acetaminophen and Follow-Up ibuprofen. The ED provider felt the foreign body was amenable to attempt at removal. A small incision was made and Past Medical History r prior to probing, a splinter was easily extracted with Autism. r external pressure. The wound was then irrigated and UTD on immunizations. dressed. The patient was UTD with her vaccinations and did not require a tetanus booster. Her antibiotics Medications were discontinued. r Acetaminophen for knee pain.

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Allergies Discussion r NKDA. r Epidemiology: Childhood cancer is rare, with a Physical Examination and Ancillary Studies reported incidence in the USA of approximately 1 caseper7,000amongchildrenaged15yearsand r Vital signs: T 98.9 °F, HR 96, RR 18, BP 115/70, O 2 younger.1,2 Almost 40 percent of childhood sat 99% on room air. cancers are hematologic malignancies. Acute r General:Thepatientisalert,well-appearing,and leukemia is the most common form of childhood interactive. r malignancy, comprising approximately 30 percent HEENT: No signs of trauma. The patient has of all childhood cancers, with ALL being four to moist mucous membranes with no pharyngeal five times more common than acute myeloid erythema. He has a few petechial spots in his leukemia (AML).1,2 The incidence of ALL is posterior soft palate, with no vesicular or approximately 3.4 cases per 100,000, with a peak ulcerative lesions. The extraocular muscles are incidence occurring between 2 and 5 years of age, intact and PERRL. 1,2 r and more commonly among boys than girls. Neck: Supple and non-tender, with shotty cervical Several genetic disorders are associated with an lymph nodes. r increased risk of leukemia, including but not Cardiovascular: Regular rate and rhythm. Intact limitedtoDown’ssyndrome(trisomy21), andnormaldistalpulses. r ataxia–telangiectasia, Wiskott–Aldrich syndrome, Lungs: Clear breath sounds bilaterally, with easy Bloom syndrome, Fanconi anemia, Kostmann work of breathing. disease, Klinefelter syndrome, Blackfan–Diamond r Abdomen:Thepatient’sabdomenissoft, anemia, and neurofibromatosis.1 non-tender, non-distended, and there is no r Pathophysiology:Thereisstrongevidencethat hepatosplenomegaly. acquired genetic changes from environmental or r Extremities and skin: The patient’s skin shows a genetic predisposition are central to the non-blanching petechial rash on both his lower development of leukemia.1–3 The exact causal extremities, with a few isolated lesions appreciated factor is usually unknown, but the changes result on his trunk. He has no signs of limb deformity or in unregulated monoclonal cellular proliferation trauma. of hematopoietic or lymphoid cells, which then r Neurologic: Awake and interactive, with a grossly cause symptoms through bone-marrow normal neurologic examination. replacement or proliferation of the malignant cells r Pertinent laboratory values: WBC 42,000, Hb 7.9, in other organs. Plt 37,000. On his peripheral blood differential, r Presentation: Leukemia proliferation within the there are 31 percent blast forms. Electrolytes, bone marrow results in decreased production of phosphate, and uric acid normal. normal white blood cells, red blood cells, and r Pertinent imaging: Right knee radiograph from platelets. This decreased production of normal prior visit is normal. blood cells is often related to the initial signs and symptoms of leukemia, including fatigue, pallor, Questions for Thought petechiae (as in this case), ecchymoses, mucosal bleeding, and a higher risk of infection.1–4 The r What are the typical laboratory ﬁndings in this type of patient? leukemic expansion within the bone marrow may r What other imaging would you like to get in the alsocauseseverebonepain,limp,orrefusalto ED? walk; this presentation occurs in approximately r What are two complications from this illness with 25 percent of children with newly diagnosed which a patient can present to the ED? leukemia.4 The extramedullary organs that are most frequently involved with leukemic infiltration are the liver, spleen, and lymph nodes.1,2 Many affected children initially present Diagnosis with an enlargement of these organs on physical r Acute lymphoblastic leukemia (ALL). examination. Any body organ can be potentially

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involved in leukemia, including the CNS, testes, Historical clues Physical findings Ancillary studies skin, kidneys, lungs, pleura, pericardium, eyes, r Atraumatic leg r Petechial rash r CBC with breasts, ovaries, and GI tract. r r pain Lymphadenopathy elevated WBC r Diagnosis: Hematologic malignancy should be New rash and blast forms r Negative knee considered in children with longstanding, X-ray unexplained fevers, longstanding, unresolved adenopathy, organomegaly, petechial rash, atraumatic bone pain, or recurrent infection. Follow-Up Initial blood work with a CBC and manual The likely diagnosis of leukemia was recognized in differential will detect circulating leukemic blast this patient presenting with a petechial rash in the cells in most patients. There are other conditions, setting of left knee pain. Given the clinical finding such as infectious mononucleosis, that can result of petechiae and associated differential diagnoses, the in atypical white cells in the blood. A bone patient quickly had a CBC that revealed lymphoblastic marrow examination, therefore, is essential for cells, consistent with a leukemic process. The patient conclusive diagnosis of leukemia, as well as an subsequently had a CXR to rule out a mediastinal adjunct in identifying specific subtypes of mass. Hematology–oncology was consulted, and he leukemia, which may require different approaches had further blood tests to assess for possible tumor in management.3 Once the suspicion of leukemia lysis syndrome, the results of which were within nor- is high on the differential, a CXR should be mal range. He was started on IV fluids and admitted performed to evaluate for the presence of a for further evaluation, including LP and bone-marrow mediastinal mass, which may be present in the aspiration, followed by the initiation of chemothera- setting of a lymphoma. peutic treatment. r Treatment: Initial management includes initiation of IV fluids, blood work (including CBC with References manual differentiation, electrolytes, uric acid, 1. Campana D, Pui CH. Childhood leukemia. In renal and liver function tests, coagulation Niederhuber JE, Armitage JO, Dorshow JH, Kastan studies), and admission to a pediatric cancer MB, Tepper JE, eds., Abeloff’s Clinical Oncology,5th center. Patients then commonly receive edition. Philadelphia, PA: Elsevier, 2014, pp. 1849–72. transfusion support, treatment of suspected or 2. Hunger SP, Mullighan CG. Acute lymphoblastic proven infections with broad-spectrum leukemia in children. NEnglJMed2015; 373: 1541–52. antibiotics, and correction of any metabolic 3. Hutter JJ. Childhood leukemia. Pediatr Rev 2010; 31: imbalances that may be present in patients with 234–40. high tumor burden secondary to tumor lysis 4. Simone JV, Verzosa MS, Rudy JA. Initial features and syndrome. Rarely, a patient may require prognosis in 363 children with acute lymphocytic leukophoresis or exchange transfusion to control leukemia. Cancer 1975; 36: 2099–108. extreme leukocytosis.1 Patients are scheduled for urgent bone-marrow aspiration and biopsy for Case 3 diagnostic accuracy and cytogenetics, as well as LP to assess CNS involvement.3 These results are Contributing Authors: Sundeep M. Shukla used for a risk-group stratification of the patient and Rebecca Jeanmonod in order to reduce toxicity in low-risk patients while ensuring appropriate, more aggressive History therapy for those with high-risk disease or The patient is a 3-year-old male who presents relapse.3 Successful treatment of children with to the ED after pulling hot water onto himself. ALL involves the administration of a multidrug While the patient’s mother was boiling a pot of water regimen, which is divided into several phases: to make rice, the child used a stepstool and pulled induction, consolidation, and maintenance. down the pot of water. His mother ran in from the r Disposition: Children diagnosed with leukemia pantry closet to find him lying on the ground with hot should be referred to a pediatric cancer center for water over his trunk and hands. The patient did not admission and to undergo the above treatment. have any loss of consciousness and cried immediately.

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The mother applied calamine lotion to the effected r How does management of this patient diﬀer from regions and then brought the child in for evaluation. that of patients with staphylococcal scalded skin Past Medical History syndrome, Stevens–Johnson syndrome, toxic r epidermal necrolysis, or other desquamating Asthma. rashes? r Prior clavicle fracture.

Medications Diagnosis r Albuterol as needed. r Superficial and superficial partial-thickness burns. Allergies Discussion r NKDA. r Epidemiology: Burns are a common problem in Physical Examination and Ancillary Studies children, and scald burns are the most common r ° cause of burns in children younger than 5 years of Vital signs: T 98.6 F, HR 121, RR 27, BP 92/68, O2 1 sat 100% on room air. age. Hot-tap-water burns cause more hospitalizations than any other hot liquid. Burns r General: The child looks underweight and has are discussed in more detail in Chapter 2, Case 5. tattered clothes. The patient is crying but without Electrical burns are less common than scald cyanosis or stridor. burns, but can have significant morbidity and r HEENT: PERRL. Mucous membranes moist. mortality. Oropharynx clear. r Pathophysiology: Burns disrupt the integrity of the r Neck: Supple and non-tender, with no adenopathy. r skin, causing a local and systemic inflammatory Cardiovascular: Regular tachycardia, with no reaction, which ultimately results in fluid shifts M/R/G. r from the vascular space into the interstitial space. Lungs: Normal work of breathing, with clear and This occurs as a consequence of changes in equal breath sounds. r vascular permeability due to the presence of Abdomen: Soft and non-distended. No masses or mediators including histamine, serotonin, organomegaly. prostaglandins, platelet products, complement r Extremities and skin: There is erythema over the components, and kinin.2,3 There is more head, face, and neck, with blisters containing information on the pathophysiology of cutaneous serous fluid present on the anterior surface of the burns in Chapter 2, Case 5. neck. There is also erythema and blisters on the Electrical burns are caused by electrical anterior chest, epigastric region, and on the right current passing through the body to the ground, hand. The patient has 14 percent total burns on closing a circuit. Like cutaneous burns, electrical the body. There is no extremity deformity. burns disrupt tissue, increase capillary r Neurologic: All wounded skin has intact sensation permeability, and result in fluid shifts and to light touch. intravascular volume depletion. Unlike cutaneous r Pertinent laboratory values: WBC 8,000, Hb 12, burns, however, the extent of the tissue damage HCT 38, CPK 190, BUN 10, Cr 0.9, K 3.6, all other from electrical burns is difficult to assess based on laboratory values are normal. physical examination alone. This is because electricity travels along the course of least Questions for Thought resistance (neurovascular bundles) and creates r heat in areas of high resistance (bone), and Is the mother’s description of the injury therefore the tissue damage and destruction are consistent with the patient’s physical ﬁndings? not evident on skin examination. The provider r What management should be initiated in the ED? mayonlybeabletoappreciateanentrance r How does management of this patient diﬀer from that of patients who are victims of electrical wound/eschar and an exit wound/eschar. burns? Furthermore, an electrical current may cause involuntary muscle contraction (resulting in

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musculoskeletal injury, blunt/blast injury, or r Treatment: Initial management should focus on rhabdomyolysis), seizure, or cardiac arrest. the airway. Burn patients will need supplemental Staphylococcal scalded skin syndrome is oxygen immediately on arrival and a quick caused by infection with Staphylococcus aureus, examination of the airway, as singed facial hairs which releases an exfoliative toxin.4 It occurs and carbonaceous sputum are important signs predominantly in young children and neonates, that an inhalational injury has occurred. The use with almost all cases presenting before age 6.4 The of a nasopharyngoscope can help evaluate injury disease is typically contracted from asymptomatic from the burns. carriers of the bacteria. IV access and fluid resuscitation are an Toxic epidermal necrolysis (which involves important aspect of burn care management. greater than 30 percent of the skin surface) and Many resuscitation formulas are available, with Stevens–Johnson syndrome (which involves less the most prominent being the modified than 10 percent of the skin’s surface, but has Parkland formula. The patient is to receive IV mucosal involvement) occur most commonly due fluids at 4 mL/kg per percentage burn area, with to pharmacologic agents, athough infections, half of the volume given in the first 8 hours radiation, sunlight exposure, connective-tissue (starting from when burn occurred) and the disorders, and malignancies may also be remaining half administered over the next involved.5 Although the cleavage site within the 16 hours. In addition, adding maintenance fluids skin differs in staphylococcus scalded skin hasalsobeenvitaltoresuscitatingtissuesin syndrome as compared to toxic epidermal children and is widely practiced in most burn necrolysis and Stevens–Johnson syndrome, the centers.6–8 Superficial or first-degree burns are end result is disruption of the barrier function of not used in calculating the total body surface area the skin, just like in a cutaneous burn. Thus, involved when using the modified Parkland patients undergo the same fluid shifts and formula. pathophysiologic consequences as burn Careful volume resuscitation is also important patients. in children with other exfoliating conditions, r Presentation:Mostpatientswithaburnwill following typical resuscitation endpoints, such as present with a consistent history for the injuries urine output. Children believed to have you see. Presentation depends upon the type of staphylococcus scalded skin syndrome should burn, the depth of the burn, and the burn location. receive anti-staphylococcal antibiotics. There is no There is more information on burn presentation role for routine antibiotic use in other exfoliating inChapter2,Case5.Incasesofanelectricalburn, dermatoses or in cutaneous burns. patients may present with severe pain, seizure, Care of cutaneous burns is outlined in detail in renal failure, rhabdomyolysis, hypotension, or Chapter 2, Case 5. cardiac arrest. They may also present with r Disposition: Depending on what burns are isolated mouth burns from chewing on electrical encountered the patient can be managed at home, wires. in the hospital, or may need to be transferred to a r Diagnosis: It is critically important to assess the burn center. Transfer to a burn center should total surface area involved in cutaneous burns. All occur in the following circumstances, which are patients must be completely disrobed and outlined in criteria established by the American examined. When available, the Lund and Browder Burn Association:1 chart is a reliable method to assess burn area in r Partial-thickness burns greater than 10 percent children. Otherwise, a modified rule of 9s may be of the total body surface area. used (Figure 2.7). r Burns that involve the face, hands, feet, In children with exfoliating rashes and no genitalia, perineum, or major joints. history of a burn, a history should be sought for r new pharmacologic agents and infectious disease Full-thickness burns in any age group. r symptoms.Theinvolvedsurfaceareashouldbe Electrical burns, including lightning injury. calculated for these children, as well, and a note r Chemical burns. made of mucosal lesions. r Inhalation injury.

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r Burn injury in patients with preexisting complication is compartment syndrome, which medical disorders that could complicate could limit blood flow and cause irreversible management, prolong recovery, or affect tissue damage. Pain may intensify, necessitating mortality. narcotic medications, but return precautions r Any patient with burns and concomitant should be given for severe pain as this could also trauma (such as fractures) in which the burn indicate infection or compartment syndrome. injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the Historical clues Physical findings Ancillary studies r r r greater immediate risk, the patient may be History of Cutaneous Unremarkable pulling down blisters laboratory tests initially stabilized in a trauma center before boiling water r Splash burns being transferred to a burn unit. Physician judgment will be necessary in such situations andshouldbeinconcertwiththeregional Follow-Up medical control plan and triage protocols. This patient had superficial partial-thickness burns r Burned children in hospitals without qualified greater than 10 percent of the body surface area and personnelorequipmentforthecareof required transfer to a burn center. His injury was con- children. sistent with the mechanism described by his mother. r Burn injury in patients who will require special He received appropriated pain medications and IV social, emotional, or rehabilitative fluids per the modified Parkland formula. His care intervention. included several weeks of follow-up within a burn clinic after discharge from the inpatient burn center. Some patients may need to be admitted to a The patient had a full recovery. The mother was also hospital, but not necessarily transferred to a burn educated on using a back burner and other ways to pre- center. Cases in which there is concern that the vent injury. caretaker may not be able to provide appropriate wound care is one example. Inability to provide adequate pain management, poor access to References follow-up care, and concern for child abuse are 1. Kramer CB, Rivara FP, Klein MB. Variations in US other indications for admission. pediatric burn injury hospitalizations using burn repository data. JBurnCareRes2010; 31: 734–9. Patients who are discharged home must have adequate training on dressing changes. 2. Merz J, Schrand C, Mertens D, et al. Wound care of the Methodical dressing changes are required to keep pediatric burn patient. AACN Clin Issues Adv Pract Acute Crit Care 2003; 14: 429–41. the burn sites clean. Adequate supplies of dry gauze and ointments should be arranged for 3. Reed J, Pomerantz W. Emergency management of pediatric burns. Pediatr Emerg Care 2005; 21: 118–29. home. Instructions should be given detailing the procedure for dressing changes and also providing 4. Mishra AK, Yadav P, Mishra A. A systematic review on staphylococcal scalded skin syndrome: A rare and recommendations for close follow-up. Patients critical disease of neonates. Open Microbiol J 2016; 10: may also benefit from a visiting nurse to help with 150–9. dressing changes. As previously discussed, 5. Usatine RP, Sandy N. Dermatologic emergencies. Am appropriate pain control is essential when Fam Phys 2010; 82: 773–80. administering dressing changes, and also ensuring 6. Alharbi Z, Piatkowski A, Dembinski R, et al. adequate comfort of the burn patient at home. Treatment of burns in the first 24 hours: Simple and Providers need to educate the patient and practical guide by answering 10 questions in a guardians about potential complications, such as step-by-step form. World J Emerg Surg 2012; 7: 13. infections. Variations such as discharge color, 7. Hettiaratchy S, Papini R. Initial management of a worsening appearance of the wound, and bleeding major burn: II – Assessment and resuscitation. BMJ from the wound should promptly lead to 2004; 329: 101–3. notification of their provider. Photos taken during 8. Sharma RK, Parashar A. Special considerations in dressing changes can help evaluate the progress of paediatric burn patients. Ind J Plast Surg 2010; 43: wound healing. Another possible delayed S43–50.

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Case 4 posterior oropharynx is patent. There is no nasal or ear involvement. Contributing Author: Amanda Shorette r Neck: There is no swelling or tenderness to the neck. She has full range of motion. History r Cardiovascular: Mildly tachycardic but regular, The patient is a 5-year-old female, who presented from without M/R/G. an outside hospital after sustaining a dog bite to the r Lungs: Respirations are non-labored, with no face. She had been bitten by a pitbull, who was owned stridor or adventitious upper-airway noise. There by a family friend, while visiting the child’s home. The are clear lung sounds bilaterally and no evidence attack was witnessed by the patient’s older sister and of chest-wall trauma. the dog’s owner but neither were present in the ED to r Abdomen: Her abdomen is soft, non-tender, and provide exact details. The dog’s vaccination status was non-distended, with normal bowel sounds. unknown but the animal was taken into custody by r Extremities and skin:Noevidenceofextremity animal control. The child was evaluated at a commu- injury. nity ED, where she was noted to have extensive injuries r Neurologic: The patient is alert and oriented. She to the right side of her face, including several complex has good postural tone. She has a GCS of 15. She lacerations, with eyelid and intraoral involvement. IV is able to appreciate touch to the right side of her antibiotics and analgesia were provided and she was face but the examination is limited by pain and subsequently transferred to a tertiary hospital. the extent of the injury. There is right upper lid weaknessandlimitedsmileontheright.The Past Medical History remainder of her cranial nerve examination is r UTD on immunizations. r intact. No significant medical problems. r Pertinent laboratory values: Hb 11.8, HCT 33.1. r Pertinent imaging: CT reconstruction shown in Medications Figure 12.3. r None. Questions for Thought Allergies r Which animal bite wounds should be closed r NKDA. primarily? r When should prophylactic antibiotics be used for Physical Examination and Ancillary Studies animal bites? r Vital signs: T 99.0 °F, HR 129, RR 24, BP 107/73, r When is post-exposure prophylaxis (tetanus, O sat 98% on room air. rabies) indicated? 2 r r General: The patient is awake, alert, sitting up in When should you consider ancillary testing, such bed. She is anxious but responds appropriately. as imaging, in this kind of patient? r When should you consider urgent/emergent r HEENT:Thepatient’sglobesaregrosslyintact specialty consultation? bilaterally, with intact extraocular movements. PERRL. There is a 2-cm full-thickness laceration of the right lower lid. Her vision is grossly intact. She has a complex 8-cm laceration to the right Diagnosis r fronto-temporal scalp and forehead, just lateral to Severe facial dog-bite injury, complicated by the right orbit. There is a separate 2-cm laceration complex maxillofacial fractures. to her right cheek. In addition, there are multiple puncture wounds on her right cheek and along Discussion the angle of the mandible. There is a large r Epidemiology: Animal and human bites represent intraoral laceration seen at the gum line at the a significant health issue in the USA with 3–6 right lateral jaw. There is mobility of the right million occurrences per year. Dogs cause lower jaw and right lower teeth. There are no 80–90 percent of these animal bite wounds, with lacerations or trauma noted to the tongue. The 800,000 Americans seeking medical attention for

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teeth and their claws, with injuries typically presenting as abrasions or small, deep puncture wounds.2,3 Bite wounds tend to colonize with the native oral flora of the animal that inflicted the injury, notably anaerobic (i.e. Pasteurella), Staphylococcus,andStreptococcus species. Dog bites are known to inoculate wounds with Prevotella species and Capnocytophaga canimorsus,whichcanrarelyresultinfulminant systemic infection characterized by a profound inflammatory response, leading to shock, disseminated intravascular coagulation, and multi-system organ failure. r Presentation:Inchildrenlessthan9years,the head and neck are the most common sites of dog-bite injury, while in people older than 10 years, the extremities, particularly the hand, are mostly affected.2,3 Dog-bite patients tend to Figure 12.3 CT of head and face. There is no acute intracranial present either within 8–12 hours after the injury injury. There are numerous comminuted facial fractures, notably a comminuted orbital floor fracture, comminuted for acute wound management and concern for zygomaticomaxillary complex fracture, zygomatic arch fracture, rabies prophylaxis or much later after the fracture of the greater wing of the right sphenoid, and open development of signs of infection. Patients with comminuted mandible fracture–dislocation, with displacement of multiple primary teeth. The right orbit is also noted to be displaced infectiontendtopresentaround35hoursafter inferiorly but without radiographic evidence of globe injury or optic the bite. Dog bites have an infection rate ranging nerve injury. For the color version, please refer to the plate section. from 1.6 to 30 percent.2,3,6 Cat bites typically present later than dog bites, often only after the patient has developed an infectious complication. dog bites.1–4 Dog attacks kill approximately 20–35 Cat wound infection rates are high, with an people each year, mainly infants and small incidence of 15–50 percent.6 The penetrating children.1 Most affected individuals know the dog nature of cat bites predisposes patients to deep that attacked them. Children are especially abscess formation and osteomyelitis. Signs of vulnerable to dog attacks because of their small infection can occur rapidly, often within size and proximity to the dog’s mouth as well as 12–24 hours, which is typical of Pasteurella their uninhibited behavior around dogs. Cat bites infections.3 Animal-bite patients may also present are the second most common type of animal bite with wounds infected after primary repair, which with 400,000 annual cases, representing can manifest as fever, erythema, swelling, 5–15 percent of animal bite wounds. Feline attacks tenderness, purulent drainage, and lymphadenitis typically are underreported because they are near the site. These patients typically present perceived as less serious than other forms of 24 hours or later after the time of injury. animal bites; however, approximately 6 percent of r Diagnosis: A detailed history of the circumstances patients inflicted with cat bites will require surrounding the injury is critical, including 2,3 hospitalization. Compared to dog bites, cat (1) time and location of the bite event, bites tend to affect older individuals, with females (2) type/breed of the animal, (3) vaccination 2,3 being predominantly affected. history of the animal, (4) vaccination history of r Pathophysiology: Dog bites can lead to a range of the victim, (5) behavior of the animal and its injuries, but given their rounded teeth and current whereabouts, (6) provoked versus powerful jaws they typically cause crush unprovoked attack, (7) anatomic location of the injuries.3,5 Abrasions, lacerations, puncture wound(s), (8) any pre-hospital treatment, and wounds, and even avulsion injuries or amputation (9) any underlying medical factors that may can be seen.3,5 Cats inflict wounds with both their impair wound healing or increase the risk of

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infection (i.e. immunocompromised state, patient is stable and no emergent intervention is diabetes, asplenic patients).2–4,6 These factors are needed, then the clinician can proceed with important in determining the risk of wound wound care. Meticulous wound care is central to infection and the need for rabies prophylaxis. The treating animal bites. Copious pressurized wound should be thoroughly inspected under irrigation with 5–8 psi (18–20-gauge blunt needle local anesthesia to assess the extent and depth of attached to a 30–60-mL syringe using 250–500 the injury, to identify an injury to deeper mL of solution) is the most important means of structures, including neurovascular or tendon preventing infection by reducing bacteria counts injuries, to visualize devitalized tissue, and to in the wound.2–4,6,7 This method may reduce determine the presence of a foreign body.6 The infection rates fivefold, although it should be bottom of the wound should be visualized and noted that this is less effective for puncture examined under range of motion, if possible. wounds.Anydevitalizedtissueshouldbe Laboratory studies are indicated only in patients debrided as this has been shown to be effective in who present with infected bite wounds and signs preventing infection by removing a potential of systemic infection; in such cases, the clinician infection nidus.2–4,6,7 Careful wound exploration should consider a CBC, CRP, and ESR but should and foreign-body removal should be done, with know that normal values may still be seen in special attention to any fascial or joint capsule patients with cellulitis, joint infection, violation. Puncture wounds are more challenging osteomyelitis, and even sepsis. Wound cultures to manage since no specific wound treatment should be obtained in infected bites when possible method has been proven to reduce infection rates; before initiating antibiotic therapy and the however, the general consensus states that any laboratory should be notified that the sample is an superficial debridement of non-viable tissue animal bite, since oral flora common in infected should be performed. “Coring,” or removal of bite wounds (Pasteurella multocida in cats and deep tissue, is not recommended. dogs)tendtobefastidiousandeasily There is an abundance of literature addressing misidentified. Wound cultures are not indicated how to repair animal bites; however, the evidence in clinically uninfected bites since they do not is conflicting. The general consensus suggests that correlate with a risk of subsequent infection or when considering whether or not to close a pathologic organism in later-occurring infections. wound primarily, by delayed primary closure, or Consider radiography if there is concern for an by secondary intention, the clinician should underlying fracture, such as with deep bite consider the location, the complexity, and the age wounds or bites near joints. Also obtain of the wound.2,3,7 Untreated bites more than radiographs if there is concern for retained 6–12 hours old are at higher risk of infection. foreign bodies such as embedded teeth. Plain Primary closure of wounds can be performed in radiographs may be indicated in markedly simple lacerations, those that are clinically infected wounds to assess for bony injury, uninfected, face and scalp wounds, and bites less subcutaneous gas, and a change associated with than 12 hours old on the extremities or body.2,3 osteomyelitis. U/S is helpful when assessing for Wounds at higher risk for infection with primary abscess formation or radiolucent foreign bodies. closure include (1) crush injuries, (2) puncture Dog bites to the head can result in penetration of wounds, (3) bites involving the hands and feet, (4) the skull and even meningitis or brain abscess wounds more than 24 hours old on the face and formation; head CT scans are warranted with more than 12 hours old elsewhere, (5) cat and deep dog bites and puncture wounds to the scalp human bites not located on the face, and (6) bite or face to assess for fracture, especially in children wounds in immunocompromised hosts.2,3 Hand less than 2 years of age. bites have an infection rate of 30–40 percent.7 In r Treatment: All wounds should be assessed for contrast, scalp and facial bites demonstrate a low active bleeding and a neurovascular assessment infection rate and it is therefore recommended to should be performed. Direct pressure should be closeallofthesewhenpresentingwithin24hours. applied to any active bleeding, and resuscitation Facial injuries presenting greater than 24 hours should be promptly initiated when needed. If the are more controversial, but the consensus shows

16:24:29 13 Chapter 12: Skin Complaints that primary closure for uninfected wounds and theanimalappearsill,oriftheanimaliswildora delayed primary closure for contaminated- stray. The rabies vaccination status of the dog or appearing wounds are acceptable approaches. cat should be determined when possible. The Deep sutures and cyanoacrylate tissue adhesive CDC provides guidelines regarding the risk of (glue) should be avoided when possible as these contracting the rabies virus and when to repair methods can create an anaerobic administer post-exposure prophylaxis.1 environment and inhibit drainage of infected Previously unvaccinated individuals with material, if wound infection should occur.2,3 potential rabies exposure should receive both the Wounds that cannot be closed primarily should be rabies vaccine and rabies immune globulin. leftopentodrain,dressedwithwet-to-dry Surgical consultation should be considered for dressings twice a day, and examined daily to assess deep wounds that penetrate bone, tendons, and for infection, with debridement as needed. If after joints.3 Complex facial lacerations, wounds 72 hours the wound does not appear clinically associated with neurovascular compromise, and infected and it is in a cosmetically important area, woundswithcomplexinfections(abscess then delayed primary closure can be performed. formation, osteomyelitis, and septic joint), Secondary intention should be allowed for especially of the hand, also warrant surgical very-high-risk wounds and wounds complicated consultation. by infection. r Disposition: Patients with simple bite wounds can Evidence is especially mixed on the use of betreatedintheEDanddischargedhomewith antibiotic prophylaxis in animal-bite wounds. Cat good wound care instructions, close follow-up, bitesaswellasotherdeeppuncturewounds and prophylactic antibiotic therapy, if warranted. should receive prophylaxis due to the high risk of Superficial wound infections can be managed infection.2–7 Antibiotics should also be strongly with wound debridement as needed, oral considered in moderate to severe injuries with antibiotic therapy, and close outpatient follow-up. associated crush injury; wounds located on the Wounds complicated by abscess formation require hands, genitalia, or in close proximity to bones or surgical intervention. Wounds with either joints; bites in compromised hosts; and human infection involving deep structures, associated bites through the dermis.2–7 Prophylaxis should signsofsystemicinfection,orpersistentinfection be given for 3–5 days. When clinically infected, despite outpatient antibiotic therapy require antibiotic courses should be for at least 10 days, admission for IV antibiotics and possible surgical and any suture material from a prior repair should management. Admission should also be be removed. Antibiotic choice should be directed considered for immunocompromised individuals toward coverage of anaerobes and Staphylococcus, and those with poor follow-up or history of Streptococcus,andPasteurella species. First-line medication non-adherence. choice is amoxicillin–clavulanate. Alternative therapies include an agent with activity against P. Historical clues Physical findings Ancillary studies multicoda (doxycycline, trimethoprim– r r r r Dog bite Obvious facial Unremarkable sulfamethoxazole, penicillin VK, cefuroxime, r Pitbull deformity and r laboratory tests moxifloxacin) plus an agent with anaerobic UTD injury Head CT with immunizations r Intact airway orbital and activity (metronidazole, clindamycin). for both dog r Unstable facial mandibular Animal bites are tetanus-prone wounds, and child and jaw bones fractures therefore the immunization status of the patient should be addressed and tetanus toxoid vaccine administered when indicated. The need for Follow-Up tetanus immune globulin should also be assessed. The patient was managed by an interdisciplinary team Children with no immunizations require both of surgical specialists and required multiple recon- tetanus immune globulin and tetanus structive surgeries. Post-operatively, she does have immunization. some facial scarring and ptosis of her right eyelid but The patient’s risk for rabies exposure should be has preserved vision and intact function of her face and evaluatedespeciallyinunprovokedanimalbites,if jaw.

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References Medications r 1. Centers for Disease Control and Prevention (CDC). None. Preventing dog bites. See www.cdc.gov/features/ dog-bite-prevention/ (accessed February 2017). Allergies r 2. Ellis R, Ellis C. Dog and cat bites. Am Fam Phys 2014; NKDA. 90: 239–43. Physical Examination and Ancillary Studies 3. Eilbert WP. Dog, cat and human bites. Providing safe r and cost-effective treatment in the ED. Emerg Med Vital signs: T 99.1 °F, HR 95, RR 24, BP 96/60, O2 Pract 2003; 5: 1–20. sat 100% on room air. r 4. Aziz H, Rhee P, Pandit V, et al. The current concepts General: The patient is alert, awake, and acting in management of animal (dog, cat, snake, scorpion) appropriately for her age. She is happy, smiling, and human bite wounds. J Trauma Acute Care Surg and playful with staff. 2015; 78: 641–8. r HEENT: PERRL. No subconjunctival or retinal 5. Chhabra S, Chhabra N, Gaba S. Maxillofacial injuries hemorrhages. Mucous membranes are moist. due to animal bites. J Maxillofac Oral Surg 2015; 14: There is a large bruise over the patient’s left cheek, 142–53. which has petechiae and purpura in parallel lines. 6. Nakamura Y, Daya M. Use of appropriate There are no other regions of petechiae or antimicrobials in wound management. Emerg Med ecchymoses. There are no obvious facial fractures, Clin N Am 2007; 25: 159–76. Battle’s sign, raccoon eyes, or hemotympanum. 7. Kennedy SA, Stoll LE, Lauder AS. Human and other r Neck: Supple and non-tender, with midline mammalian bite injuries to the hand: evaluation and management. JAmAcadOrthopSurg2015; 23: 47–57. trachea and no adenopathy. r Cardiovascular: Regular rate and rhythm, with no M/R/G. Case 5 r Lungs: Clear and equal, with normal work of breathing. No W/R/R. Contributing Author: Benjamin Kitt r Abdomen: The patient has normoactive bowel History sounds. Her abdomen is soft and non-tender to The patient is a 24-month-old female accompanied by palpation. No signs of trauma or noticeable her mother, who presents to the ED with a complaint bruising. r ofamarkonhercheekthatmombelievesissecondary Extremities and skin:Thereisnoswellingor to some kind of trauma incurred while playing with tenderness. Full range of motion with good her brother. The mother reports that she was in the capillary refill. r kitchen when she heard her daughter start crying in Neurologic: Intact cranial nerves. Non-focal the bedroom, where she was playing with her 4-year- examination. old brother. When her mother entered the room, she found the patient crying and holding her face. The Questions for Thought patient told her mother that her brother hit her in r What concerns do you have about the bruise? the face, but the brother denied this and reported that r What reasons might the history be concerning? the patient hit her face on the door. The mother is now r Would you order any laboratory or radiographic concerned about the bruise on her daughter’s face and imaging? wants to make sure “everything is alright.” Since the r What is the patient’s disposition? incident, the patient has been acting normally, has not vomited, and is not complaining of pain. The child lives with mom, mom’s boyfriend, and her older brother. Diagnosis r Child abuse with facial hand-slap bruising. Past Medical History r UTD on immunizations. Discussion r No medical problems or known bleeding r Epidemiology: According to the US Department of diathesis. Health and Human Services, a 2013 report

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estimated that 679,000 children were victims of questioning should be open-ended.3 Open-ended abuse and neglect, which roughly translates to an questions can be followed by more specific incidence of 1 percent amongst the population.1 questions but yes or no questions should be Although the rate of child abuse has been avoided.3,4 Forpatientswhoarenon-verbal,the declining, physicians need to be aware that history will be based on the parent or family roughly 1 out of 100 children they see will be a account of what happened. Clinical gestalt will be victim of neglect or abuse. Most victims of abuse important when assessing the validity of the orneglectarebelowtheageof5(47percent)with parent’s story. Concerning factors for abuse 27.3 percent below 3 years old and 19.7 percent include a vague history or the injury not matching between3and5yearsold.1 Males and females are the history. An account not matching the patient’s victims of abuse or neglect in similar percentages: developmental abilities and inconsistent histories 48.7 percent for males and 50.9 percent for are also more concerning for abuse. More females. According to the 2013 data, 82 percent of information on presentation of child abuse is abusers are the biological parent and 18 percent available in Chapter 2, Case 4. are others, such as another relative, foster parent, A thorough physical examination must be daycare worker, etc.1 performed if abuse is suspected, which includes a r Pathophysiology: According to the Child Abuse head-to-toe examination with the patient Prevention and Treatment Act the term “child undressed. Examine the skin looking for bruising abuse and neglect” means, at a minimum, any in different stages of healing or in centrally located recent “act or failure to act on the part of a parent areas. Children who are walking commonly have or caretaker, which results in death, serious bruising on their anterior shins, but centrally physical or emotional harm, sexual abuse or located bruising such as to the abdomen, ears, and exploitation, or an act or failure to act which neck are concerning for abuse. presents an imminent risk of serious harm.”2 Look at the pattern on the bruise. Does it look According to the act, “The term ‘child’ means a like a hand slap, belt, or cord? In the case person who has not attained the lesser of the age described above the slap was in the shape of a of 18; or except in the case of sexual abuse, the age hand and contained multiple parallel lines, which specified by the child protection law of the State in occur when capillaries break between the fingers. which the child resides.”2 The risk factors for When assessing burns, assess to see if the abuse are hard to identify and track; however, a distribution of burned area matches with the few have been described. The greatest risk factor story. If the story is a cup of hot tea pulled down for a patient is age. If the child is younger than from the table, is the burn consistent with a splash 5 years old he or she falls into the age range with or is it uniform and suggestive of submersion in the highest percentage of abuse. Parental risk hot water? Look for signs of fractures and order factors include but are not limited to lack of child appropriate imaging studies. A thorough care skills, substance abuse, and history of child ophthalmologic examination should be maltreatment. Child abuse is divided into four performed to assess for signs of “shaken baby types of abuse and includes neglect, physical syndrome,” such as bilateral retinal hemorrhages. abuse, emotional abuse, and sexual abuse.1,2 Assess the genitalia and perineum for signs of Neglect is the most common type of trauma or lesions. maltreatment, followed by physical abuse, with r Diagnosis: If there are any red flags in the history emotional and sexual abuse having roughly or physical examination, a physician should similar percentages. pursue the appropriate investigation for child r Presentation: Child abuse and neglect can present abuse. The diagnostic work-up is guided by your in a variety of ways, and therefore physicians must physical examination. The AAP recommends a be vigilant in performing a thorough history and skeletal survey for children under the age of 2 who physical examination on any patient where abuse are suspected victims of physical abuse.5 The or neglect is suspected. Obtaining a history from skeletal survey can assess for both acute and the patient is often difficult as over half of the healing fractures. A typical skeletal survey has children abused are under the age of 5. Initial specific radiographic view requirements of the

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skull, spine, pelvis, femur, legs, feet, humerus, child abuse was consulted. It was determined that the forearms, and hands. The diagnosis for child mother’s boyfriend was responsible for the bruise. The abusebecomesmorelikelyifthepatienthas child was discharged in the care of her mother, with multiple fractures, multiple rib fractures, femoral, appropriate social services follow-up. humeral, or skull fractures.6 The AAP recommends neuroimaging in suspected child References abuse patients with head trauma, altered mental 1. Heisler K. US Department of Health and Human status, or skull fracture seen on X-ray to assess for Services. Child maltreatment 2013. See www.acf.hhs intracranial bleeding. Liver enzymes, specifically .gov/sites/default/files/cb/cm2013.pdf (accessed ALTandAST,canbeusefulinassessingfor February 2017). intra-abdominal trauma without external signs.7 2. Child Abuse Prevention and Treatment Act (CAPTA). CPS must be contacted and their investigation can United States Code title 42, chapter 67, reenacted also help make the diagnosis. 2010. r Treatment: Any life-threatening injuries should be 3. LambME,SternbergKJ,OrbachY,etal.Age treated according to the ATLS protocols, and differences in young children’s response to appropriate consultations should be made open-ended invitations in the course of forensic interviews. JConsultClinPsychol2003; 71: 926–34. according to the child’s injuries. Once medical management is addressed, social workers, CPS, 4. LambME,OrbachY,HershkowitzI,etal.Structured and physicians who specialize in child abuse forensic interview protocols improve the quality and informativeness of investigative interviews with should be consulted. Chapter 2, Case 4 has more children: A review of research using the NICHD information about this. investigative interview protocol. Child Abuse Negl r Disposition: Hospitalization is necessary for all 2007; 31: 1201–31. patients with serious medical conditions 5. American Academy of Pediatrics. Diagnostic imaging secondary to their abuse; however, consider of child abuse. See http://pediatrics.aappublications hospitalization if you are concerned that the child .org/content/123/5/1430 (accessed February 2017). will be returning to an unsafe environment or 6. Kemp AM, Dunstan F, Harrison S, et al. Patterns of CPS is unavailable to assess the patient until a skeletal fractures in child abuse: a systematic review. later time. Hospitalization will allow for close BMJ 2008; 337: a1518. monitoringofthepatientwhileprovidingasafe 7. LaneWG,DubowitzH,LangenbergP.Screeningfor environment for the child until an appropriate occult abdominal trauma in children with suspected investigation can be undertaken. The physician’s physical abuse. Pediatrics 2009; 124: 1595–602. primary responsibilities are to help in the identification of possible child abuse, provide Case 6 medical treatment, ensure detailed documentation, and contact CPS, who will Contributing Author: Rebecca Jeanmonod ultimately determine the social disposition of the child. History A 14-month-old girl presents to the ED accompanied Historical clues Physical findings by her grandfather for a rash. Grandpa states that he r r Story inconsistent with Parallel bruising pattern babysits the child most weekends, and when she was examination findings consistent with hand slap droppedofftodayhehadnotedredbumpsonher r Trauma being attributed to a arms and ankles. When he changed the child’s diaper, r small sibling Patient in high-risk age he realized the bumps actually involved most of the group for abuse child’s bilateral legs as well, and he saw a lesion or two on the back of her neck. He did not see anything Follow-Up in the diaper area. The child has seemed bothered Social work and CPS were consulted and felt that the by the rash, scratching at it and saying “boo-boo.” patient was unsafe to return home until a represen- Shehasotherwisebeenactinglikeherself.Shehas tative could assess the home. The patient was admit- been playful with Grandpa, and he states she ate ted to the hospital and a physician specially trained in herbreakfastandherlunchwithusualappetite.She

16:24:29 13 Chapter 12: Skin Complaints has not had fever, vomiting, cough, runny nose, or Diagnosis diarrhea. She has been making a usual number of wet r Insect bites. diapers, and has not had any recent dietary changes.

Past Medical History Discussion r r Eczema. Epidemiology: Rashes are a common presenting r Seasonal allergies. complaintinprimarycareandEDs.Theycanbe seen in any age group, and can be localized or r UTD on immunizations. generalized, painful, pruritic, or essentially Medications asymptomatic. They can be evidence of an isolated skin process or secondary to a systemic process, r Topical steroids as needed, although no recent use. r arising from infectious, inflammatory, immune, Loratidine. or toxicologic causes. Most importantly, they can be dangerous or benign, and although the clinical Allergies diagnosis of the exact etiology of a rash may be r Amoxicillin – rash. challenging,theprovidershouldbeableto recognize the rash that suggests severe disease. A Physical Examination and Ancillary Studies full discussion of every specific rash is outside the r Vital signs: 98.7 °F, HR 110, RR 25, BP 97/61, O2 scope of this book. sat 100% on room air. r Pathophysiology: Rashes are caused in a number of r General:Awake,alert,interactive,and ways. Wheals and hives are a result of increased well-appearing. capillary permeability, leading to extravasation of r HEENT: PERRL. Oropharynx without lesions. fluid into the skin, often secondary to a typeI Mucous membranes moist. hypersensitivity reaction (acute allergy/ r Neck: Supple and non-tender, with no adenopathy. anaphylaxis). Fluid-filled papules/vesicles and Midline trachea. bullae may also be secondary to a hypersensitivity r Cardiovascular:Regularrhythm,withnoM/R/G. reaction (topical dermatitis, such as with poison Capillary refill Ͻ 2 seconds. ivy exposure) when localized, or secondary to r Lungs: Normal work of breathing, clear lung viral infection (varicella, disseminated herpes) sounds, with no W/R/R. when generalized. Diffuse, non-descript r Abdomen:Soft,withouttenderness,masses,or maculopapular rashes may be secondary to drug guarding. Normal bowel sounds. eruptions or viral infections. Exfoliating rashes r Extremities and skin: Warm and well-perfused. may be caused by erythema multiforme, toxic There are several scattered erythematous shock syndrome, staphylococcal scalded skin blanching papules of about 7–10 mm in diameter, syndrome, or immune-mediated disease. which are located on the patient’s extremities. Petechiae may be caused by malignancy, They are not confluent. The child has no lesions vasculitis, meningococcemia, or Rocky Mountain on the palms or soles. There are several lesions on spottedfever.TherashofLymediseaseis the child’s posterior neck. The child does not have pathognomonic for the disease and is discussed lesions on the trunk. The lesions are not pustular elsewhere. Finally, scaling rashes may be from or vesicular. The child is scratching at the lesions. underlying chronic conditions, such as psoriasis or eczema, or can be from fungal infections. r Neurologic: Non-focal neurologic examination. r Presentation: Small children may present when parents notice a rash in an otherwise Questions for Thought asymptomatic child, or they may present for a r What ﬁndings in rashes are worrisome? complexofsymptomsofwhichtherashisonlya r What is the diﬀerential diagnosis for generalized small part. It is important to do a thorough rash? physical examination in all pediatric patients so as r How should this child be treated? not to miss serious pathology. It is also important to obtain the relevant history that contributes to

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the rash: recent travel, time of year, outdoor presence of blood in the tissue. This occurs activity (for insect, arthropod, and allergen because of injury to blood vessels or disease to exposure), medications, immunization history, platelets. In other words, these rashes are progression and migration of the lesions, sick evidence of underlying vasculitis or contacts or others with lesions, joint symptoms or coagulopathy, such as occurs with autoimmune fever, and involvement of palms, soles, and or idiopathic vasculitis, leukemic crises, mucosae. meningococcemia, or Rocky Mountain spotted r Diagnosis: The differential diagnosis for a rash is fever. Although children may have localized large, and not one that can be easily committed to petechiae to the face from forceful vomiting, memory.However,intheED,itisimportantto petechiae elsewhere are concerning for narrow down the differential diagnosis to exclude dangerous disease processes. It is important to dangerous items. One way to begin is to divide note that the rash of Rocky Mountain spotted rashes into “localized” rashes and “systemic” fever or meningococcemia may initially appear rashes. benign, so if there is any concern at all for these Localized rashes do not involve the entire body diagnoses, the child should be observed for by definition. Contact dermatitis from exposure several hours to assess for evolution of lesions, to poison ivy as well as insect bites often present and a low threshold should be maintained for in this way, and have a paucity of other symptoms initiation of treatment. beyond rash and pruritis, as in our patient. It is r Rashes that involve the palms and soles are also importanttonotethepatternoftherash.Isiton concerning. Although the clinician should be exposedareasthatarelikelytobesusceptibleto awareofbenigncommoncausesofpalmand insect bites? Is the rash localized to intertriginous sole rashes (such as hand–foot–mouth disease, areas (more common in streptococcal or candidal a self-limited, highly contagious disease of infections) or between fingers and toes (common early childhood – see Figure 12.4), rashes in in scabies)? A single lesion may also be evidence these regions can be evidence of erythema of cellulitis or, in the right clinical setting, primary multiforme, Kawasaki disease, Rocky Lyme disease. In all these scenarios, there is Mountain spotted fever, staphylococcal scalded generally no further testing needed for diagnosis skin syndrome, Stevens–Johnson syndrome, andtreatment–thechildmaybetreatedbasedon toxic epidermal necrolysis, and toxic shock the clinical diagnosis alone. syndrome, all of which may present with hand Generalized rashes are more challenging, as and foot involvement. the differential diagnosis is larger and contains r Rashes with blistering, exfoliation, or skin many concerning items. When facing these sloughing are generally “bad” rashes. rashes, the provider should begin by assessing the Blisters/vesicles suggest viral disease, such as overall status of the patient, and whether or not disseminated herpes or varicella. Rashes with the patient appears ill. Ill children with skin loss not only imply a significant benign-appearing rashes are ill children underlying disease (such as toxic shock nonetheless and require resuscitation, treatment, syndrome, staphylococcal scalded skin and diagnostic testing. Likewise, well-appearing syndrome, or toxic epidermal necrolysis) but children with dangerous-appearing rashes also the rash causes breakdown of the skin’s barrier typically require evaluation beyond examination. function to further infection and fluid loss. It is only the well-appearing child with a Therefore, these children are at risk for benign-appearing generalized rash who requires dehydration and electrolyte imbalances, and nothing more than symptomatic care. should be treated similarly to burn patients. What makes a rash “dangerous-appearing?” Further discussion of this can be found in this r Although there are exceptions to every rule, chapter, Case 3. rashes that do not blanch when pressed are r Rashes with significant systemic symptoms,such worrisome. Non-blanching rashes (e.g. as diffuse urticaria, with shortness of breath or petechiae and purpura) occur from the vomiting/diarrhea should always be taken

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or systemic steroids for allergic rashes (systemic steroids are often needed for extensive contact dermatitis) and antihistamine for pruritis. r Disposition:Mostcasesofrashcanbedischarged home with follow-up with pediatrics. Careful return precautions should address worrisome rash findings, which should prompt a repeat ED visit.

Historical clues Physical findings r Itchyrashonexposed r Papules consistent with insect areas bites located on areas not r No other complaints covered by clothing r Otherwise well child

Follow-Up Grandpa was encouraged to use symptomatic care for thechild’sinsectbitesandwascounseledregardingthe use of insect sprays to prevent further bites. The child was discharged home. Case 7

Figure 12.4 Rash on sole caused by hand–foot–mouth disease. Contributing Author: Dorka M. Jimenez´ For the color version, please refer to the plate section. Almonte seriously. The rash may be the presenting History complaint for anaphylaxis, sepsis, malignancy, A 10-month-old boy presents with fever, irritability, or significant infectious disease, such as and a rash of 8 hours duration. The parents report that measles, chickenpox, or rubella. the baby was doing well until approximately 8 hours r Rashes involving the mucosa should raise agowhenhewokeupfromhisnapwithahighfever. consideration for Kawasaki disease and The patient has been very fussy and crying incon- Stevens–Johnson disease. solably ever since. The parents gave acetaminophen Most rashes are benign. Most are non-specific, by mouth at home, which lowered the temperature blanching, non-exfoliating, and resolve butdidnotalleviatethefussiness.Theinfanthasbeen spontaneously. To distinguish among dangerous refusing to drink fluids or eat solids. He has had only rashes, CBC, blood cultures, pathogen assays, and one barely wet diaper in the last 8 hours. A couple of biopsy may be required, but the vast majority of hours ago, the parents noticed a reddish rash on his rashes require no further diagnostic work-up chest, abdomen, and legs. The child had two episodes beyond a good history and physical examination. of non-bilious vomiting at home, prompting the r Treatment: If the inciting process is known and parents to bring him in. En route to the ED, his rash treatable (for example, a child with a rash darkened in color. He has not had diarrhea or URI secondary to an antibiotic), the child should be symptoms. He has no known sick contacts. treated for the underlying cause. Children with Past Medical History concern for significant infectious disease should r receive antibiotics and admission to the hospital. Term normal spontaneous vaginal delivery. r The vast majority of non-specific rashes require UTD on immunizations. r only symptomatic care, which is typically topical Meeting developmental milestones with no issues.

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Medications r r What measures would you take to protect other Vitamin D supplement daily. patients and the medical staﬀ? Allergies r NKDA. Diagnosis r Physical Examination and Ancillary Studies Meningococcemia. r ° Vital signs: T 103.2 F, HR 180, RR 45, BP 85/45, Discussion O2 sat 99% on room air. r r General:Thepatient’ssizeandweightappears Epidemiology: Meningococcal disease is endemic appropriate for age. He is ill-appearing, crying to North America and the annual incidence varies from 0.5 to 1.5 cases per 100,000 in multiyear inconsolably,sittingonhismother’slap.Heisnot 1,2 producing tears despite crying. cycles. Globally,epidemicsoccuratirregular yearintervals,every7–10years,mostlyin r HEENT: No signs of trauma. Anterior fontanelle sub-Saharan Africa, known as the “meningitis is bulging. PERRL. Clear conjunctivae. Dry belt,” with rates as high as 1 case per 1,000 during mucous membranes. No oral lesions. these epidemics.2 Neisseria meningitidis,an r Neck: Supple, with no tenderness to palpation. The encapsulated Gram-negative diplococcus, is an range of motion appears intact as the patient obligate human pathogen. Humans are reservoirs moveshisheadinalldirectionswithout for N. meningitidis via asymptomatic restrictions. There is no evident nuchal rigidity. r nasopharyngeal carriage. Carrier rates increase Cardiovascular: Regular tachycardia, with no progressively with age from 0.7 percent of M/R/G.Femoralpulsesareequalbilaterally. children less than 4 years old to 10–20 percent in Capillary refill Ͼ 4 seconds. r adolescence and up to 30 percent in Lungs: Clear and equal bilaterally, with no W/R/R. 1,2 r 25-year-olds. Thisincreaseisthoughttobe Abdomen: The abdomen is not distended. It is soft secondary to changes in social behavior that occur and depressible and is not tender to palpation. with age (kissing, intimate contact) and There is no organomegaly. r overcrowding (e.g. poverty, military barracks). Extremities and skin: Extremities intact, with no Transmission occurs via close contact with signs of trauma. There are red macules and some infected respiratory droplets or secretions, and slightly raised maculopapular lesions on the trunk there is a 2–10-day incubation period.2 Rates of and extremities. There are a few non-blanching disease are significantly higher in children petechial lesions on the trunk and lower younger than 2 years of age, with a second peak extremities. There are approximately 3-mm during adolescence through young adulthood.1,2 purpuric, slightly elevated lesions on the dorsal Higher disease rates in less developed countries aspect of the feet. These purpuric lesions are are likely to be partially due to poverty, crowding, tender to palpation. poor sanitation, and malnutrition. The overall r Neurologic: Awake and crying, inconsolable. No mortality rate is 8–14 percent and the morbidity focal abnormalities. rate is 11–19 percent for those who survive.1–3 r Pertinent laboratory values: WBC 27,500 with 30% Long-term sequelae are typically devastating and bands, Plt 100,000, ESR 100. include hearing loss, neurodevelopmental delays, and amputations.2,3 r Questions for Thought Pathophysiology: N. meningitidis exclusively infects humans.1 Nasopharyngeal colonization by r How would you describe this patient’s condition? N. meningitidis is a prerequisite for the r What would be your initial steps to manage the patient? development of systemic infection. Invasive r What diagnostic tests would you obtain? meningococcal disease is only caused by six r What medications if any do you consider in this serogroups, classified by the polysaccharide patient? capsule surrounding the bacterium; serogroups A, B, C, W-135, X, and Y.2 The bacterium adheres to

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and invades the human epithelial and endothelial they can be present in any location. Purpura are cells. The polysaccharide capsule inhibits initially small, irregular, and painful. Multiple phagocytosis and uses numerous virulence factors large hemorrhagic lesions are associated with a to escape the human immune response, such as worseprognosis.Thehemorrhagicrashmay phase variation, antigenic variation, and progress to purpura fulminans, a cutaneous molecular mimicry of human antigens. manifestation of disseminated intravascular Nasopharyngeal carrier state, exposure to N. coagulation, which presents as a purpuric rash, meningitidis, and certain immune defects such as shock, and gangrene, often requiring asplenia and complement deficiencies are known amputation.2–5 Patients can also present a mixture risk factors for invasive meningococcal disease.2,3 of both meningitis and meningococcemia. An Damage to the nasopharyngeal epithelium initially mild condition may progress to a (changes in temperature, URIs, low humidity, and fulminant disease, multi-organ failure, and death sand particles) combined with host susceptibility within hours.2,3 Ill appearance, petechial rash leads to invasive disease.2,3 Vascular collapse and below the nipple line, and purpura measuring shock are caused by damage to the more than 2 mm have been identified in the microvasculature, resulting in increased vascular literature as predictors of meningococcal disease permeability (capillary leak), pathologic or serious bacteremia.2–5 In children, 95 percent vasoconstriction and vasodilation, and of cases of non-blanching petechial rash and fever intravascular coagulation. Microvascular are caused by viral pathogens such as enterovirus thrombosis is responsible for serious or adenovirus and not meningococcal disease.4 complications such as purpura fulminans. Early in meningococcemia the rash can have a r Presentation: Patients may present with one of maculopapular appearance. Given that it can be three syndromes: meningitis (30–50 percent), very difficult to distinguish early meningococcal meningitis with bacteremia (40 percent), or disease from a viral exanthem, a period of bacteremia alone (10 percent).1–3 Meningitis is observation is recommended for a well-appearing the most common presentation. Clinical childwithanacute,non-blanchingrash,tosafely presentation varies according to the age of the distinguish between the two. patient. Presentation in infants and young r Diagnosis:Inchildrenpresentingwithpetechial children is less specific and can present a rash and fever, laboratory studies including CBC, diagnostic challenge. Fever is typically the first blood culture, ESR, and CRP are usually symptom in infants and young children.2,3 warranted. Infants should also undergo Headaches are more common in children older age-appropriate fever work-up per current than 5 years of age.2,3 Many children initially guidelines. The diagnosis of N. meningitidis present with upper respiratory symptoms such as invasive disease is confirmed by positive cultures cough, sore throat, coryza, and otalgia.2,3 Most of the blood, CSF, or joint fluid. The CBC typically children are irritable and develop loss of appetite, showsleukocytosiswithleftshifting nausea, and vomiting. Symptoms rapidly evolve (predominance of granulocytes). The platelet (over a few hours) to a more serious presentation count may be decreased. The inflammatory with neck stiffness, altered mental status, and markers such ESR and CRP are usually elevated. If seizures.2,3 Bacteremia (acute meningococcemia) the patient has meningitis the CSF analysis will presents with non-specific symptoms, such as show pleocytosis (increased white blood cells), fever, lethargy, reduced oral intake, headache, decreased glucose, and increased protein. In the nausea, and vomiting, with or without clinical Gram’s stain, Gram-negative diplococci can be signs of sepsis, such as tachycardia, tachypnea, and seen. In advanced disease, coagulation studies can fever.2,3 Myalgias can be present in older children be used to evaluate for a consumptive and are typically more painful than those seen coagulopathy. BUN and Cr should also be with viral illnesses such as influenza. The cardinal obtained to evaluate renal function and presentation is a non-blanching, hemorrhagic electrolytes. Electrolyte disturbances are common (petechial or purpuric) rash.1–6 The lesions are in patients who have shock. Other etiologies that commonly seen on the trunk and extremities but present with fever and a hemorrhagic rash should

16:24:29 293 13 Chapter 12: Skin Complaints

be considered, such as vasculitis Historical clues Physical findings Ancillary studies ¨ (Henoch–Schonlein purpura), Rocky Mountain r Age r Fever r Leukocytosis with spotted fever, toxic shock syndrome, enteroviral r r r Fever Bulging left shift (elevated infection, leptospirosis, and bacteremia that is Rapid symptom fontanelle bands) progression r Irritability r Thrombocytopenia caused by other pathogens such as Streptococcus r Rash r Clinical findings r Elevated ESR pneumoniae.4,5 r of dehydration r Treatment: This is an infectious emergency Purpuric lesions and treatment must not be delayed. If the diagnosis is seriously considered, blood cultures Follow-Up must be drawn and antibiotics administered within 30 minutes. It is of utmost importance that A petechial and purpuric rash developed within antibiotic therapy is not delayed for diagnostic an hour of presentation to the ED. The patient was procedures such as LP. The drug of choice to promptly identified as requiring resuscitation and was treat suspected or culture-proven meningococcal placed on contact precautions. IV access was imme- infection is a third-generation cephalosporin, such diately obtained and fluid resuscitation was initiated as cefotaxime or ceftriaxone. If susceptible, the expeditiously. Laboratory tests were drawn including treatment could later be switched to penicillin G. CBC, ESR, CRP, electrolytes, glucose, BUN/Cr, and Serious complications, such as shock, disseminated blood culture. Additionally, coagulation studies were intravascular coagulation, and purpura fulminans obtained, given the presence of purpuric lesions. should be treated early and aggressively. The Antibiotic treatment was started with ceftriaxone patient should be placed on droplet precautions within 15 minutes. The patient was admitted to the until 24 hours after the initiation of effective PICU. One hour later an LP was performed. All antimicrobial therapy. Chemoprophylaxis household and daycare contacts were treated prophy- iswarrantedtointimatecontacts lactically. The next day the blood culture confirmed who have been exposed to the patient’s oral the diagnosis of invasive N. meningitidis infection. secretions (kissing, eating utensils, toothbrushes), such as household, daycare, nursery, References and school contacts. People who frequently 1. Centers for Disease Control and Prevention (CDC). slept in the same dwelling as the patient should Meningococcal disease incidence, United States, also receive prophylaxis. For healthcare staff, 1970–2015. See www.cdc.gov/meningococcal/images/ meningococcal-disease-incidence-lg.jpg (accessed chemoprophylaxis is not routinely recommended February 2017). except when involved in orotracheal intubation, 2. Sabatini C, Bosis S, Semino L, et al. Clinical suctioning of secretions, and examination presentation of meningococcus in childhood. JPrev of the eye area. Meningococcal quadrivalent Med Hyg 2012; 53: 116–19. vaccine is an adjunct to chemoprophylaxis 3. Pace D, Pollard AJ. Meningococcal disease: Clinical when an outbreak is caused by a serogroup presentation and sequelae. Vaccine 2012; 30 Suppl 2: covered by the vaccine (A, C, Y, and W-135). B3–9. r Disposition: Patients with a concern 4. Aber C, Alvarez Connelly E, Schachner LA. Fever and of meningococcal infection should be admitted to rash in a child: When to worry? Pediatr Ann 2007; 36: the hospital. If the child is ill-appearing or if there 30–8. are signs concerning for meningitis (neck stiffness) 5. Ramos-e-Silva M, Pereira AL. Life-threatening or septic shock (poor perfusion, hypotension), eruptions due to infectious agents. Clin Dermatol 2005; the child should be treated for meningococcal 23: 148–56. disease immediately and admitted to the 6. Klinkhammer MD, Colletti JE. Pediatric myth: Fever PICU for further monitoring and management. and petechiae. CJEM 2008; 10: 479–82.

16:24:29 13 Case Key

Chapter Case Diagnosis Chapter Case Diagnosis 2 1 Multiple trauma 7 1 Inborn error of metabolism 2 2 Head trauma 7 2 Acute gastroenteritis 2 3 Cervical spine injury 7 3 Iron toxicity 2 4 Non-accidental trauma 7 4 Intussusception 2 5 Burns 7 5 Seizure 2 6 Drowning 7 6 Intracranial mass 2 7 Hypovolemic shock 7 7 Bulimia nervosa 2 8 Cardiogenic shock 7 8 Malrotation 2 9 Respiratory failure 7 9 Strep throat 2 10 Septic shock 7 10 Overfeeding 2 11 Anaphylaxis 8 1 Appendicitis 3 1 Foreign-body airway 8 2 Urinary retention, constipation 3 2 Periodic breathing 8 3 Diabetic ketoacidosis 3 3 Gastroesophageal reflux disease (GERD) 8 4 Ingested foreign body 3 4 Bronchiolitis 8 5 Sexually transmitted disease 3 5 Acute asthma exacerbation 8 6 Pneumonia 3 6 Brief resolved unexplained event (BRUE) 8 7 Torsion 3 7 Congestive heart failure, congenital heart 8 8 Ectopic pregnancy disease (CHF, CHD) 9 1 Idiopathic ketotic hypoglycemia 3 8 Symptomatic anemia 9 2 Infant botulism 4 1 Febrile seizure 9 3 Congenital heart disease 4 2 Neonatal fever 9 4 Hypernatremia 4 3 Neutropenic fever 9 5 Congenital heart disease 4 4 Neuroleptic malignant syndrome (NMS) 9 6 Intoxication 4 5 Fever with sickle cell disease 9 7 Intussusception 4 6 Fever with transplant 9 8 Acute psychosis 4 7 Aspirin overdose 10 1 Carbon monoxide poisoning 4 8 Environmental hyperthermia 10 2 Hypertensive emergency 4 9 Acute viral perimyocarditis 10 3 Epidural hematoma 5 1 Foreign body ENT 10 4 Medulloblastoma 5 2 Anterior epistaxis 10 5 Meningitis 5 3 Globe rupture 10 6 Migraine 5 4 Acute mastoiditis 10 7 Lyme disease 5 5 Orbital fracture 10 8 Retropharyngeal abscess 5 6 Lemierre syndrome 10 9 Subarachnoid hemorrhage 5 7 Peritonsillar abscess 11 1 Milk protein allergy 5 8 Otitis media 11 2 Inguinal hernia 5 9 Retropharyngeal abscess 11 3 Paraphimosis 6 1 Nursemaid’s elbow 11 4 Pregnancy 6 2 Ankle sprain 11 5 Sexually transmitted disease 6 3 Septic arthritis 11 6 Urinary tract infection (UTI) 6 4 Lacerations 11 7 Vaginitis 6 5 Lyme arthritis 12 1 Retained foreign body 6 6 Osteomyelitis 12 2 Acute lymphoblastic leukemia (ALL) 6 7 Supracondylar fracture 12 3 Burns 6 8 Shoulder dislocation 12 4 Animal bite 6 9 Fractures 12 5 Child abuse 12 6 General rash 12 7 Meningococcemia

16:25:32 295 14 Cambridge University Press 978-1-316-60886-9 — Pediatric Emergency Medicine Edited by Rebecca Jeanmonod , Shellie L. Asher , Blake Spirko , Foreword by Denis R. Pauze Index More Information

Index

AAP guidelines pathophysiology, 151 pathophysiology, 65 bronchiolitis, 51 presentation, 151 presentation, 65 BRUE, 56, 57 treatment, 151–2 treatment, 66 child abuse, 287 acute lymphoblastic leukemia (ALL), anesthesia febrile seizure, 69 35, 73, 276–8 lacerations, 131 HIV screening, 265 diagnosis, 278 paraphimosis, 259 infant botulism, 204 epidemiology, 277 shoulder dislocation, 143 infant feeding, 172 pathophysiology, 277 aneurysms, subarachnoid hemorrhage, iron supplements, 65 presentation, 277 250, 251, 252 otitis media, 115, 116 treatment, 278 animal bites, 282–5 over-the-counter preparations, acute myeloid leukemia (AML), diagnosis, 283–4 216 277 disposition, 285 UTIs, 268, 269 acute psychosis, 221–3 epidemiology, 282 ABCDE algorithm, 5 diagnosis, 222 pathophysiology, 283 abdominal pain, 173–200 epidemiology, 222 presentation, 283 appendicitis, 173–5 pathophysiology, 222 treatment, 284–5 constipation. See constipation presentation, 222 anion gap, elevated, 217 diabetic ketoacidosis, 180–3 treatment, 223 ankle fracture, 144–6 ectopic pregnancy. See ectopic acute respiratory distress syndrome ankle sprain, 123–6 pregnancy (ARDS) diagnosis, 125 foreign-body ingestion, 183–6 burns and, 21 disposition, 126 intussusception, 220 drowning and, 25 epidemiology, 123 pelvic inlammatory disease, 265 acute viral perimyocarditis, 91–4 grading, 124, 125 pneumonia. See pneumonia altered mental status, 201–23 pathophysiology, 123–4 pregnancy, 260, 261 acute psychosis, 221–3 presentation, 123, 124 referred, 190 brain tumors, 162 treatment, 125 STIs. See sexually transmitted coarctation of the aorta, 211–15 anorexia nervosa, 164–5 infections (STIs) coronary artery anomaly, 206–8 anosmia, 161 gonadal torsion, 192–5 hypernatremia, 209–11 anticoagulants, 111 urinary retention, 176–80 idiopathic ketotic hypoglycemia, antidotes, and poisons, 218 abscess 201–3 antiemetics, 242 drainage, 113 infant botulism, 203–6 aorta, coarctation of, 211–15 peritonsillar. See peritonsillar abscess intoxication, 215–18 apnea, 46 retropharyngeal. See retropharyngeal intussusception. See intussusception bronchiolitis and, 51, 52 abscess American Academy of Pediatrics deinition, 46 absolute neutrophil count (ANC), (AAP). See AAP guidelines apparent life-threatening event 75 American Burn Association, criteria, (ALTE). See also brief resolved abusive head trauma, 17 280 unexplained event (BRUE) acetaminophen, 218 anaphylaxis, 38–41 GERD and, 48 activated charcoal, 87 diagnosis, 40 periodic breathing vs., 46 acute asthma exacerbation, 52–5 disposition, 40 appendectomy, 175 diagnosis, 54 epidemiology, 39 appendicitis, 173–5 disposition, 55 pathophysiology, 39 diagnosis, 175 pathophysiology, 53 presentation, 40 epidemiology, 174 presentation, 53 red lags, 40 pathophysiology, 174 treatment, 54–5 treatment, 40 presentation, 175 acute gastroenteritis, 150–2 anemia, 64–7, 254 treatment, 175 diagnosis, 151 diagnosis, 65–6 Apt test, 254 epidemiology, 151 epidemiology, 65 arterial blood gas (ABG)

296

Index

drowning, 25 brain tumors. See medulloblastoma, epidemiology, 225 reference values, xvi intracranial mass pathophysiology, 225 respiratory failure, 34 breastfeeding, 172, 204, 210 presentation, 225 arteriovenous malformations, 250, 252 breathing diiculties, 42–67 treatment, 226 arthritis acute asthma exacerbation, 52–5 carboxyhemoglobin levels, 225, 226 Lyme. See Lyme arthritis anemia. See anemia cardiac arrest, 211 septic. See septic arthritis bronchiolitis, 49–52 cardiogenic shock, 29–32 arthrocentesis, 128, 129, 134, 135 congestive heart failure, 59–63 diagnosis, 31 aseptic meningitis, 237, 245 foreign-body aspiration, 42–4 epidemiology, 30 aspiration method, 259 GERD. See gastroesophageal relux pathophysiology, 30 aspirin overdose, 85–8 disease (GERD) presentation, 30 diagnosis, 86 periodic breathing, 45–6 septic shock and, 36, 213, 214 epidemiology, 85 respiratory failure, 32–5 treatment, 31 pathophysiology, 86 brief psychotic disorder, 222 cardiopulmonary resuscitation (CPR) presentation, 86 brief resolved unexplained event BRUE patient, 57, 58 treatment, 87 (BRUE), 55–8 drowning patient, 23, 25 asthma diagnosis, 57 carditis acute exacerbation. See acute asthma epidemiology, 56 endocarditis, 30, 31 exacerbation pathophysiology, 56 Lyme, 245 anaphylaxis and, 39 presentation, 56 myocarditis, 30 epidemiology, 53 treatment, 57–8 pericarditis. See pericarditis ataxia, 161 bronchiolitis, 48, 49–52 cat bites, 283, 285 atrial septal defect (ASD), 61, 63 diagnosis, 51 CATCH criteria, 232 autism spectrum disorder, 76, 183 disposition, 52 catheterization, 97, 101, 179, 186 axillary nerve, 142 epidemiology, 50 c-collar immobilization, 11 pathophysiology, 50 Centers for Disease Control and bacteremia, 267, 293 presentation, 51 Prevention (CDC), 264, 265 bacterial meningitis treatment, 51–2 Centor score, 170 epidemiology, 237 bronchoscopy, 43, 44 cerebral edema, 181, 182 pathophysiology, 238 bruising cerebral palsy, 178 Bacterial Meningitis Score, 238 BRUE and, 58 cerebral perfusion pressure, 232 balloon catheter, 97, 101 child abuse, 286–8 cerebrospinal luid (CSF) Bankart lesion, 142 B-type natriuretic peptide (BNP), 31 meningitis, 238 basilar skull fracture, 8 buckle fracture, 145 pleocytosis, 238 bee allergy, 38–41 bulimia nervosa, 163–5 reference values, xvi benzodiazepines, 70, 159 diagnosis, 164 CHALICE criteria, 232 beta-agonists, 54, 55 epidemiology, 164 chest pain, pericarditis, 93 beta-hCG levels, 197, 198, 199, 262 pathophysiology, 164 chest X-ray (CXR) beta-hydroxybutyrate, 181 presentation, 164 acute asthma exacerbation, 54 bicycle accidents treatment, 164 bronchiolitis, 51 head trauma, 7–10 burn center, transfer to, 22, 280, 281 CHD, 62 multiple trauma, 3–6 burn shock, 20 CHF, 59 botulism immunoglobulin, 205 burns, 19–23, 278–81 coarctation of the aorta, 213 biphasic reaction, 41 classiication, 20 foreign-body aspiration, 44 bipolar disorder, 222 diagnosis, 280 foreign-body ingestion, 185 bladder-bowel dysfunction, 176–80 disposition, 22, 280–1 pneumonia, 190, 191 BLEEP examination, 214 epidemiology, 20, 279 child abuse, 1, 286–8. See also blood typing, 262 pathophysiology, 20, 279–80 non-accidental trauma blowout fractures, 107, 108 presentation, 20, 280 diagnosis, 287 blue CHD, 60, 61 treatment, 21–2, 280 disposition, 288 blunt trauma, 5, 21 burr hole, 233 epidemiology, 286 bone conduction theory, 107 button batteries, ingestion, 186 pathophysiology, 287 bone marrow examination, 278 presentation, 287 Borrelia burgdorferi, 134, 244 Canadian C-spine Rule, 12 risk factors, 287 Borrelia mayonii, 244 cancer. See also speciic cancers sexual, 189, 262, 264, 271 botulinum neurotoxin (BoNT), 205 neutropenic fever and, 73–6 treatment, 288 botulism, infant, 203–6 Candida albicans, 188 Child Abuse Prevention and bougienage method, 186 carbon monoxide poisoning, 21, 224–6 Treatment Act, 287 bowel perforation, 183–6 diagnosis, 225 chlamydial infection, 187–9, 263–6

297

Index

choking episode, 43 crying, persistent, 206, 207–8 Down’s syndrome, 166 circumcision, 258, 260, 267 c-spine injury, 10–14 drainage clinical decision rules diagnosis, 12–14 abscess, 113 head trauma, 232 epidemiology, 11 joint, 128 neutropenic fever, 75 imaging, 232 mastoiditis, 106 Clostridium botulinum, 204 pathophysiology, 11 dressing changes, burns, 281 Clostridium diicile,82 presentation, 11–12 drowning, 23–6 coagulation reference values, xvi treatment, 15 disposition, 25 coarctation of the aorta, 211–15 CT scanning, 1 epidemiology, 24 diagnosis, 213–14 animal bite, 283 pathophysiology, 24 disposition, 214 appendicitis, 175 presentation and diagnosis, 25 epidemiology, 212 brain tumors, 162 prevention, 25 pathophysiology, 212–13 epidural hematoma, 230, 232 resuscitative measures, 23 presentation, 213 foreign-body ingestion, 185, 186 treatment, 25 treatment, 214 globe rupture, 103 ductal-dependent lesions, 211–15 cognitive behavioral therapy, 165 head trauma, 8 Dundee technique, 259 colic, 206–8 intussusception, 221 duodenal atresia, 166 deinition, 207 Lemierre syndrome, 111 dysentery, acute gastroenteritis and, diagnosis, 208 mastoiditis, 105, 106 151 epidemiology, 207 multiple trauma, 6 dysuria, 264 presentation, 207 non-accidental trauma, 18 colloid therapy, 28 orbital fracture, 108, 109 ear complaints. See eye, ear, nose, and Colorado CoFlexR technique, 259 peritonsillar abscess, 113 throat community-acquired pneumonia, retropharyngeal abscess, 118, 119, ear pain, 115, 116 189–91 248, 249 early disseminated Lyme disease, 244, compartment syndrome, 281 subarachnoid hemorrhage, 250, 251 245, 246 compensated shock, 27 cyanide, 21 early localized Lyme disease, 244 complete blood count (CBC), xv cyanotic CHD, 60, 61 echocardiography compression bandage, 259, 260 cystitis, 266–9 cardiogenic shock, 31, 32 congenital heart disease (CHD), 59–63 cytomegalovirus (CMV), CHD, 62, 63 coarctation of the aorta. See transplant-associated, 81–4 coarctation of the aorta, 214 coarctation of the aorta ectopic pregnancy, 195–9 coronary artery anomaly, 206–8 deep partial-thickness burns, 20 diagnosis, 196–7 cyanotic, 60, 61 deferoxamine, 154 epidemiology, 196, 197, 284 diagnosis, 61 dehydration pathophysiology, 196 epidemiology, 60, 212 acute gastroenteritis, 151 presentation, 196 pathophysiology, 60 diabetic ketoacidosis, 181, 182 treatment, 197–8 pink, 60, 61, 62 epidemiology, 209 elbow, supracondylar fracture, 138–40 congestive heart failure (CHF), 59–63 hypernatremic, 209–11 electrical burns, 279 deinition, 61 depression, 222 electrocardiogram (EKG) diagnosis, 61 postpartum, 262 acute viral perimyocarditis, 92, 94 pathophysiology, 61 dextromethorphan overdose, 215–18 cardiogenic shock, 31 presentation, 61 diabetes, types, 181 CHD, 62 treatment, 62–3 diabetic ketoacidosis, 180–3 CHF, 60 constipation, 176–80 diagnosis, 182 coronary artery anomaly, 208 diagnosis, 178–9 epidemiology, 181 electroencephalography (EEG), epidemiology, 176 pathophysiology, 181 seizures, 159, 160 foreign-body ingestion and, 184, 185 presentation, 181 ELISA, 134 infant botulism and, 204, 205 treatment, 182 EMLAR glove technique, 259 pathophysiology, 177–8 diarrhea, 210 endocarditis, 30, 31 presentation, 178 hypovolemic shock from, 27 endoscopy, 185 treatment, 179 digital rectal exam, 178 enema, 156, 157, 220 convulsions, seizures and, 158 diplopia, 161 enteroviral meningitis, 236–9 corn syrup, contaminated, 204 disseminated intravascular environmental hyperthermia, 88–91 coronary artery anomaly, 206–8 coagulation, 293, 294 diagnosis, 90 red lags, 208 distributive shock, 36 epidemiology, 88 cow milk protein intolerance, 48 dog bites, 282–5 pathophysiology, 89 cranial nerve palsies, 205 dorsal slit procedure, 260 presentation, 89–90 cricothyroidotomy, 5 double-bubble sign, 167 treatment, 90

298

Index

enzyme immunoassay, 245 luid resuscitation gait problems, 127 epididymitis, 188 aspirin overdose, 87 Gardnerella vaginalis, 188, 263–6 epidural hematoma, 230–3 burns, 21, 23, 280 Gartland classiication, 139 diagnosis, 231 cardiogenic shock, 31 gastric decontamination, 206 epidemiology, 230 hypovolemic shock, 28–9 gastric outlet obstruction, 153 pathophysiology, 231 septic shock, 37 gastroenteritis, 48 presentation, 231 luorescein staining, 103 acute. See acute gastroenteritis treatment, 232–3 Foley catheter, 101, 186 viral, 26–9 epilepsy forced expiratory volume in one gastroesophageal relux, 47 febrile seizure and, 69, 70 second (FEV1), 54 gastroesophageal relux disease seizures and, 158, 159 forced vital capacity (FVC), 54 (GERD), 48–9 epinephrine, 38, 40, 41 foreign body diagnosis, 48 epistaxis, 98–101 esophageal. See esophageal foreign diferential diagnosis, 48 diagnosis, 99–100 body epidemiology, 47 epidemiology, 99 eye, 102, 103 overfeeding and, 172 pathophysiology, 99 lacerations, 131 pathophysiology, 48 posterior, 101 nasal. See nasal foreign body presentation, 48 presentation, 99 vaginitis, 272 red lags, 48 treatment, 100–1 foreign-body aspiration, 42–4 treatment, 49 Epstein–Barr virus (EBV), 82, diagnosis, 43–4 gastrointestinal bleeding, 253–5 84 epidemiology, 43 diagnosis, 254 erythema migrans, 134, 244, 245 pathophysiology, 43 disposition, 255 Escherichia coli, 267 presentation, 43 epidemiology, 253 esophageal foreign body, 96 treatment, 44 iron toxicity, 154 diagnosis, 96 foreign-body granuloma, 273–6 pathophysiology, 253 presentation, 96 diagnosis, 275 presentation, 254 treatment, 97 epidemiology, 274 treatment, 254 extravaginal torsion, 193 pathophysiology, 275 gastrointestinal irritation, 153 eye, ear, nose, and throat, 95–120 presentation, 275 generalized rashes, 290 epistaxis, 98–101 treatment, 275 genital warts, 265 foreign body in, 95–8 foreign body in the ear, 95–8 genitourinary complaints, 253–72 globe rupture, 102–4 diagnosis, 96 inguinal hernia, 255–7 Lemierre syndrome, 109–11 epidemiology, 95 milk protein allergy, 253–5 mastoiditis, 104–6 pathophysiology, 96 paraphimosis, 257–60 orbital fracture, 106–9 presentation, 96 pregnancy. See pregnancy otitis media, 104, 105, 114–16 treatment, 97–8 STIs. See sexually transmitted peritonsillar abscess, 112–14 foreign-body ingestion, 183–6 infections (STIs) retropharyngeal abscess, 117–20 diagnosis, 185 UTIs. See urinary tract infection disposition, 186 (UTI) facial nerve palsy, 243–6 epidemiology, 184 vaginitis, 269–72 FASTexamination,4,5 pathophysiology, 184 Glasgow Coma Scale (GCS), 3, 6 febrile seizure, 68–70 presentation, 185 globe rupture, 102–4 diagnosis, 69–70 treatment, 185–6 diagnosis, 103 epidemiology, 69 formula feeding, 171, 172, 204 epidemiology, 102 pathophysiology, 69 overconcentration, 210 pathophysiology, 102 presentation, 69 four-extremity pulse oximetry, 213 presentation, 103 treatment, 70 fractures, 144–6 treatment, 103 fever, 68–94 diagnosis, 145–6 globe to wall theory, 107 acute viral perimyocarditis, 91–4 epidemiology, 144 glucocorticoids, 54 aspirin overdose, 85–8 maxillofacial, 282–5 glycerin suppositories, 179 environmental hyperthermia, pathophysiology, 144–5 gonococcus, 265 88–91 presentation, 145 gonorrhea, 127, 188, 264, 265 febrile seizure, 68–70 rib, 16, 17 greenstick fracture, 145 neonatal, 71–3 supracondylar, 138–40 growth centers, elbow, 139 neuroleptic malignant syndrome, treatment, 146 G-tube, feeding through, 209, 210 76–8 free radicals, 153 neutropenic, 73–6 full-thickness burns, 20 Haemophilus inluenzae, 115, 237, 239 with sickle cell disease, 78–80 Fusobacterium necrophorum, 110, hair tourniquet, 258 with transplant, 81–4 111 hallucinations, 217, 218, 222

299

Index

head and neck pain, 224–52 hypercarbia, 33 diagnosis, 205 carbon monoxide poisoning, 224–6 bronchiolitis and, 51, 52 epidemiology, 204 epidural hematoma, 230–3 hypernatremia, 209–11 pathophysiology, 204 hypertensive emergency, 226–9 diagnosis, 210 presentation, 205 Lyme disease, 243–6 disposition, 210 treatment, 205 medulloblastoma, 234–6 pathophysiology, 210 infant feeding guidelines, 172 meningitis. See meningitis treatment, 210 informed consent, 262, 263 migraine, 240–2 hypertonic saline solution, 233 inguinal hernia, 255–7 retropharyngeal abscess, 247–9 hypertensive emergency, 226–9 diagnosis, 256 subarachnoid hemorrhage, 249–52 diagnosis, 228 disposition, 257 head trauma, 5, 7–10. See also epidural epidemiology, 227 epidemiology, 256 hematoma, traumatic brain injury pathophysiology, 227–8 pathophysiology, 256 (TBI) presentation, 228 presentation, 256 abusive, 17 treatment, 228–9 treatment, 256 diagnosis, 8–9 hypertensive encephalopathy, 227, insect bites, 288–91 disposition, 9 228 intoxication, 215–18 epidemiology, 8 hyperthermia. See environmental diagnosis, 217 globe rupture in, 103 hyperthermia disposition, 218 pathophysiology, 8 hypoglycemia epidemiology, 216 presentation, 8 idiopathic ketotic. See idiopathic pathophysiology, 216 treatment, 9 ketotic hypoglycemia presentation, 216 headache inborn error of metabolism and, 148, treatment, 217 brain tumors, 161 149 intracranial mass, 160–3. See also epidemiology, 241 hyponatremia, 182 medulloblastoma episodic, 226 hypotension diagnosis, 162 migraine, 240–2 septic shock and, 37 epidemiology, 161 red lags, 241 hypotensive shock, 27 pathophysiology, 161 heart failure, 30–1. See also congestive hypothermia, induced, 25 presentation, 161 heart failure (CHF) hypovolemic shock, 26–9 treatment, 162 heat cramps, 89 cardiogenic shock and, 30 intracranial pressure, 232 heat exhaustion, 89 diagnosis, 28 intrathoracic injury, 5 heat stroke, 88, 89. See also epidemiology, 27 intubation environmental hyperthermia pathophysiology, 27 anaphylaxis, 39 classic, 89 presentation, 27 aspirin overdose, 87 exertional, 89 septic shock and, 36 drowning, 23 Heimlich maneuver, 42, 44 treatment, 28–9 epidural hematoma, 232 hematogenous seeding, 136 hypoxia, 33, 225 multiple trauma, 5 hemodialysis, 87 respiratory failure, 34, 35 hemorrhagic shock, 27, 28 iced glove, 259, 260 subarachnoid hemorrhage, 251 treatment, 29 idiopathic ketotic hypoglycemia, intussusception, 155–7, 219–20, hepatotoxicity, 153 201–3 255 herpes infections, 188, 265, 266 diagnosis, 202 diagnosis, 156–7, 220 heterotaxy, 166 epidemiology, 202 epidemiology, 156, 219 high ankle sprain, 124, 126 pathophysiology, 202 pathophysiology, 156, 219 high-low nasal cannula (HFNC), 52 presentation, 202 presentation, 156, 220 hip, septic arthritis, 126–9 treatment, 202 treatment, 157, 220 Hirschsprung’s disease, 178 immune system, chemotherapy and, ipratropium, 54 HIV infection, 188, 264, 265 74 iron supplements, 65, 66 HIV testing, 265 immunoluorescence assay, 245 iron toxicity, 152–5 homonymous hemianopsia, 161 inborn error of metabolism, 147–50 diagnosis, 153–4 honey, contaminated, 204 diagnosis, 149 epidemiology, 153 human papilloma virus, 264, 265 epidemiology, 148 pathophysiology, 153 Hunt and Hess scale, 251 idiopathic ketotic hypoglycemia and, presentation, 153 hyaluronidase method, 259 202 treatment, 154 hydraulic theory, 107 pathophysiology, 148 iron-deiciency anemia, 64–7 hydrocele, hernia and, 256 presentation, 148–9 irreversible shock, 27 hydrocephalus, GERD and, 48 treatment, 149 isotonic crystalloids, 210 Hymenoptera anaphylaxis, 39 induced hypothermia, 25 Ixodes paciicus, 244 hyperbaric oxygen, 226 infant botulism, 203–6 Ixodes scapularis, 244

300

Index

Kawasaki disease, 30 epidemiology, 244 presentation, 241 Kesselbach’s plexus, 99, 100 pathophysiology, 244 treatment, 242 Kingella kingae, 127 presentation, 244–5 milk protein allergy, 253–5 knee complaints. See limb complaints treatment, 246 miscarriage, 261 Kocher criteria, 128 Lyme meningitis, 239, 245 motor vehicle accidents c-spine injury, 10–14 lacerations, 129–32. See also skin magnesium sulfate, 54 statistics, 4 complaints magnets, ingestion, 186 MRI scanning diagnosis, 131 malignant hypertension, 226–9 brain tumors, 162 disposition, 132 malnutrition, hypovolemic shock and, osteomyelitis, 137, 138 epidemiology, 130 28 peritonsillar abscess, 113 pathophysiology, 130–1 malrotation, 48, 165–8 MRSA, 127, 137, 138, 248 presentation, 130, 131 diagnosis, 167 multiple trauma, 4–6 treatment, 131–2 disposition, 168 diagnosis, 5 Ladd’s procedure, 168 epidemiology, 166 epidemiology, 4 laparoscopy, 257 pathophysiology, 166 globe rupture in, 103 laparotomy, 198, 220 presentation, 167 pathophysiology, 4 laryngoscopy, 44 treatment, 167 presentation, 4–5 late disease, Lyme, 245 mastoiditis, 104–6 treatment, 5–6 latent phase, iron toxicity, 153 diagnosis, 105 myalgias, 293 lateral ankle sprains, 124 epidemiology, 105 myocarditis, 30 Lemierre syndrome, 109–11 pathophysiology, 105 myringotomy, 106 diagnosis, 111 presentation, 105 epidemiology, 110 treatment, 106 nasal foreign body, 96, 99 pathophysiology, 110 maxillofacial fractures, 282–5 diagnosis, 96 presentation, 110 mean arterial pressure, 232 presentation, 96 treatment, 111 medulloblastoma, 234–6 treatment, 97 vaccination and, 110 diagnosis, 235 nasal packing, 100 leukemia. See acute lymphoblastic epidemiology, 234 nasoethmoid fractures, 107 leukemia (ALL) pathophysiology, 235 neck. See also head and neck pain limb complaints, 121–46 presentation, 235 decreased mobility, 117, 119 ankle sprain, 123–6 treatment, 235–6 Neisseria gonorrhoeae, 127, 188, 189 fractures, 144–6 meningitis, 236–9, 293 Neisseria meningitidis, 237, 292, lacerations, 129–32 aseptic, 237, 245 293 Lyme arthritis, 133–5 bacterial, 237, 238 neonatal fever, 71–3 nursemaid’s elbow, 121–2 diagnosis, 238–9 diagnosis, 72 osteomyelitis, 135–43 epidemiology, 237 epidemiology, 71 septic arthritis, 126–9 GERD and, 48 pathophysiology, 72 shoulder dislocation, 141–3 pathophysiology, 238 presentation, 72 supracondylar fracture, 138–40 presentation, 238 treatment, 72 Listeria monocytogenes, 237 treatment, 239 neuroleptic malignant syndrome localized rashes, 290 meningitis with bacteremia, 293 (NMS), 76–8 lumbar puncture (LP) meningococcemia, 291–4 diagnosis, 77–8 febrile seizure, 69 diagnosis, 293 disposition, 78 Lyme meningitis, 245 epidemiology, 292 epidemiology, 77 meningitis, 238 pathophysiology, 292 pathophysiology, 77 subarachnoid hemorrhage, presentation, 293 presentation, 77 251 treatment, 294 treatment, 78 Lund and Browder chart, 21, mental status assessment neurologic disorders 280 c-spine injury, 12 constipation and, 177, 178 Lyme arthritis, 133–5, 244 multiple trauma, 6 intoxication and, 217 diagnosis, 134 metabolic acidosis, 25, 86, 87 neurosurgery, 162, 233 epidemiology, 134 metabolic decompensation, 28 neutropenic fever, 73–6, 82 pathophysiology, 134 methotrexate, 198 diagnosis, 75 presentation, 133, 134 migraine, 240–2 disposition, 75 treatment, 134 diagnosis, 241–2 epidemiology, 74 Lyme disease, 243–6 disposition, 242 pathophysiology, 74 cases by State in the USA, 244 epidemiology, 241 presentation, 74 diagnosis, 245 pathophysiology, 241 treatment, 75

301

Index

NEXUS criteria, 12–13 presentation, 172 foreign-body aspiration and, 43 non-accidental trauma, 16–18. See also treatment, 172 GERD and, 48 child abuse oxygen, hyperbaric, 226 pathophysiology, 190 BRUE and, 58 oxygenation, maintaining, 232 presentation, 190 burns and, 20 respiratory failure from, 33, 34 diagnosis, 17–18 Panayiotopoulos syndrome, 157–60 transplant-associated CMV infection disposition, 18 papilledema, 162, 235, 246 and, 82 epidemiology, 17 paraphimosis, 257–60 treatment, 191 persistent crying and, 208 diagnosis, 258 Poison Control Hotline, 218 pregnancy and, 261 disposition, 260 poisoning. See also intoxication presentation, 17 epidemiology, 258 BRUE and, 58 red lags, 17 pathophysiology, 258 carbon monoxide, 224–6 subarachnoid hemorrhage and, 250, presentation, 258 poisons, and antidotes, 218 251 treatment, 258–60 polyethylene glycol, 154, 179, 180, 213 treatment, 18 Parkland formula, 21 polymerasechainreaction(PCR) nose complaints. See eye, ear, nose, and Pasteurella infections, 283, 284 testing, 238 throat patent ductus ateriosus, 63 post-transplant lymphoproliferative NSAIDs, 93 PECARN criteria, 232 disease (PTLD), 82 nucleic acid ampliication, 188, 265, c-spine injury, 13 potassium levels, abnormal, 182 266 head trauma, 8, 9 pregnancy, 260–3 nursemaid’s elbow, 121–2 pediatricseveresepsis,37 diagnosis, 262 diagnosis, 122 pelvic examination, 262 disposition, 262–3 disposition, 122 pelvic inlammatory disease, 188, 189, ectopic. See ectopic pregnancy epidemiology, 121 265 epidemiology, 196, 261 pathophysiology, 121 pelvic pain, 260, 261 pathophysiology, 261 presentation, 122 penetrating trauma, globe rupture, presentation, 261 treatment, 122 102–4 treatment, 262 pericarditis, 91–4 Pregnancy Mortality Surveillance obesity, 171, 172 diagnosis, 93 System, 196 oculocardiac relex, 108 epidemiology, 92 pregnancy testing, 196, 261 ondansetron, 151 pathophysiology, 92 primary closure of wounds, 284 orbital fracture, 106–9 presentation, 93 prostaglandin therapy, 63, 214 diagnosis, 108 treatment, 93 psychosis. See acute psychosis disposition, 108 periodic breathing, 45–6 pulse oximetry, four-extremity, 213 epidemiology, 107 diagnosis, 46 puncture wounds, 274 pathophysiology, 107–8 epidemiology, 45 treatment, 284 presentation, 108 pathophysiology, 46 purpura fulminans, 293, 294 treatment, 108 presentation, 46 pyloric stenosis, 48 orbital wall fracture, 108, 109 peripheral perfusion, assessing, 6 osmolar gap, elevated, 217 peritonsillar abscess, 112–14 rabies prophylaxis, 284, 285 osmotic agents, 162, 259 diagnosis, 113 radial head subluxation. See osteomyelitis, 135–43 disposition, 113 nursemaid’s elbow diagnosis, 137 epidemiology, 112 radiation exposure, thyroid cancer epidemiology, 136 pathophysiology, 112 and, 14 pathophysiology, 136–7 presentation, 112 radiography. See X-rays presentation, 137 treatment, 113 rashes, 288–91 treatment, 137 pharyngitis, 110, 111 dangerous-appearing, 290–1 otitis media, 114–16 strep. See streptococcal pharyngitis diagnosis, 290–1 diagnosis, 115–16 pheochromocytoma, 226–9 epidemiology, 289 epidemiology, 115 phimosis, 258 pathophysiology, 289 mastoiditis and, 104, 105 physeal fractures, 145 presentation, 289 pathophysiology, 115 pink CHD, 60, 61, 62 treatment, 291 presentation, 115 placenta previa, 262 red blood cells (RBC) treatment, 116 placental abruption, 261 destruction, 65, 66 Ottawa Ankle Rules, 125 plastic deformity, 144 failure to make, 66 ovarian torsion, 193, 194 Pneumocystis jirovecii,82 loss of, 65 overfeeding, 170–2 pneumonia, 189–91 red lags diagnosis, 172 diagnosis, 190 anaphylaxis, 40 pathophysiology, 171–2 epidemiology, 190 coronary artery anomaly, 208

302

Index

GERD, 48 schizoafective disorder, 222 osteomyelitis and, 137 headache, 241 schizophrenia, 222 pathophysiology, 79 non-accidental trauma, 17 schizophreniform, 222 presentation, 79 reduction secondary brain damage, 232 treatment, 80 inguinal hernia, 256 Seidel’s sign, 103 SIRS criteria, 36 intussusception, 157 seizures, 157–60 skeletal survey, 287 paraphimosis, 259–60 diagnosis, 159 skin complaints, 273–94. See also shoulder dislocation, 143 drowning and, 25 lacerations referred abdominal pain, 190 epidemiology, 158 ALL. See acute lymphoblastic rehydration febrile. See febrile seizure leukemia (ALL) bulimia and anorexia, 164 inborn error of metabolism and, 147, animal bites, 282–5 oral, 90, 151 149 burns. See burns resection, tumor, 229, 235, 236 pathophysiology, 158 child abuse. See child abuse respiratory failure, 32–5 presentation, 158–9 foreign-body granuloma, 273–6 diagnosis, 33–4 treatment, 159 meningococcemia, 291–4 epidemiology, 33 tumors, 235 rashes, 288–91 pathophysiology, 33 septic arthritis, 126–9 slit-lamp examination, 103 presentation, 33 diagnosis, 127–8 sore throat, 110, 111, 113 treatment, 34 epidemiology, 127 spina biida, 178 respiratory rate, taking, 33 pathophysiology, 127 spinal cord injury without respiratory syncytial virus (RSV), presentation, 127 radiographic abnormality bronchiolitis and, 50, 51 treatment, 128 (SCIWORA), 11, 14 resuscitation, 3–41. See also luid septic shock, 35–8 spirometry, 54 resuscitation cardiogenic shock and, 36, 213, 214 staphylococcal scalded skin syndrome, anaphylaxis, 38–41 CHF and, 63 280 brain tumors, 162 diagnosis, 36–7 Staphylococcus aureus, 127 burns, 19–23 epidemiology, 36 MRSA, 127, 137, 138, 248 cardiogenic shock, 29–32 neonatal fever and, 72 Stevens–Johnson syndrome, 280 c-spine injury, 10–14 pathophysiology, 36 streptococcal pharyngitis, 168–70 drowning, 23–6 presentation, 36 diagnosis, 170 ectopic pregnancy, 199 treatment, 37 epidemiology, 169 head trauma, 7–10 serotonin syndrome, 78 pathophysiology, 169 hypovolemic shock, 26–9 serum iron levels, 153, 154 presentation, 169 multiple trauma, 3–6 serum reference values, xv treatment, 170 non-accidental trauma, 16–18 serum salicylate levels, 86 streptococci, 110 respiratory failure, 32–5 sexual abuse, 189, 262, 264, 271 Streptococcus pneumoniae, 115, 237 septic shock, 35–8 sexually transmitted infections (STIs), subarachnoid hemorrhage, 249–52 retinal hemorrhage, 18 187–9, 263–6 diagnosis, 251 retropharyngeal abscess, 110, 117–20, diagnosis, 188, 262, 265 disposition, 252 247–9 disposition, 189 epidemiology, 250 diagnosis, 248 epidemiology, 188, 264 pathophysiology, 251 epidemiology, 117, 248 pathophysiology, 188, 264 presentation, 251 pathophysiology, 119, 248 presentation, 188, 264–5 treatment, 251–2 presentation, 119, 248 treatment, 189, 265 subdural hematomas, 1 treatment, 119, 248 UTIs and, 268 sudden infant death syndrome (SIDS), rhesus status, 262 shaken baby syndrome, 287 49 rheumatic fever, 169 shockindex,197 supericial burns, 20 rib fractures, 16, 17 shock syndrome, 27 supericial partial-thickness burns, 20 RICE, 125 shoulder dislocation, 141–3 supracondylar fracture, 138–40 Rome IV criteria, 178 diagnosis, 142–3 diagnosis, 139–40 rotavirus, 151 epidemiology, 142 disposition, 140 rule of 7s, meningitis, 239, 245 pathophysiology, 142 epidemiology, 139 rule of 9s, burns, 21, 280 presentation, 142 nursemaid’s elbow and, 122 Russell’s sign, 164 treatment, 143 pathophysiology, 139 shunting, 60 presentation, 139 salpingectomy, 198 sickle cell disease, 78–80 treatment, 140 salpingostomy, 198 diagnosis, 79 sutures, lacerations, 132 Salter–Harris fractures, 125, 145, 146 disposition, 80 sweating, 89 Sandifer syndrome, 48 epidemiology, 79 syndesmotic sprain, 124, 126

303

Index

synovial luid, assessment, 128, 134, incidence, 8 epidemiology, 270 135 intermediate-risk patients, 9 pathophysiology, 270 syphilis, 188, 264, 265 low-risk patients, 9 presentation, 270 systemic toxicity, 153 secondary brain damage from, 232 treatment, 271 systolic blood pressure, 232 Trichomonas, 188, 271 ventricular septal defect, 60, 63 triptans, 242 viral gastroenteritis, 26–9 tension pneumothorax, 5 trismus, 113 viral perimyocarditis. See pericarditis testicular torsion, 192–5 trisomy 4–5, 165, 183 vital signs tetanus, 285 troponin, 31, 94 CHD, 208, 213 tetanus prophylaxis, 132 type 1 diabetes, 181 migraine, 241 Tetralogy of Fallot, 60 type 2 diabetes, 181 volvulus, 48 THE MISFITS diferential diagnosis malrotation with, 165–8 CHD, 62 ultrasound (U/S), 1 vomiting, 147–72 febrile seizure, 70 appendicitis, 174, 175 acute gastroenteritis, 150–2 malrotation, 167 ectopic pregnancy, 197, 198 bulimia nervosa, 163–5 seizures, 159 foreign body, 275 diabetic ketoacidosis, 182 thoracotomy, 44 globe rupture, 103 inborn error of metabolism, 147–50 throat complaints. See eye, ear, nose, intussusception, 156, 157, 220 intracranial mass, 160–3 and throat malrotation, 167 intussusception, 155–7, 220 thyroid cancer, 14 septic arthritis, 128 iron toxicity, 152–5 tick bites, 244 torsion, 194 malrotation, 165–8 tonsillitis, 112 urinary retention, 177, 180 overfeeding, 170–2 torsion, 192–5 upper GI series, 167, 168 seizures, 157–60 diagnosis, 193 upper respiratory infection (URI) strep pharyngitis, 168–70 epidemiology, 193 febrile seizure and, 69 pathophysiology, 193 peritonsillar abscess, 113 Wessel’s rule of 3s, 207 presentation, 193 retropharyngeal abscess and, 119 Western blot, 134, 245 treatment, 194 urethritis, 188 whirlpool sign, 167 torticollis, 119, 247–9 urinalysis, 194, 268 white blood cells (WBC) torus fracture, 145 urinary retention, 176–80 reference values, xv total body surface area (TBSA), burns, urinary tract infection (UTI), 48, septic shock, 36 20, 21 266–9 wound irrigation, 131 toxic epidermal necrolysis, 280 diagnosis, 268 wounds. See lacerations toxidromes, examination indings, 217 epidemiology, 267 transplant-associated CMV infection, neonatal fever and, 71–3 X-rays. See also chest X-ray (CXR) 81–4 pathophysiology, 267 ankle sprain, 123, 125 diagnosis, 83–4 presentation, 267–8 c-spine injury, 13 epidemiology, 81–2 treatment, 268–9 foreign body, 275 pathophysiology, 82 urine pregnancy tests, 197 osteomyelitis, 137 presentation, 83 urine reference values, xvi retropharyngeal abscess, 118, 119 treatment, 84 uterine rupture, 261 septic arthritis, 128 traumatic brain injury (TBI). See also shoulder dislocation, 142 epidural hematoma, head trauma vaginal discharge, 264 supracondylar fracture, 139, 140 epidemiology, 230 vaginitis, 188, 269–72 high-risk patients, 9 diagnosis, 271 zygomatic complex, 108

304