Medical School · Year 3 · Pediatrics · includes a quiz and discussion video

Seminar 18: Pediatric Emergencies

Unit 3: Pediatrics Clerkship

Learning Objectives

1. Apply Pediatric Advanced Life Support principles including the Pediatric Assessment Triangle and systematic primary assessment
2. Recognize and manage pediatric shock including differentiation between hypovolemic, distributive, cardiogenic, and obstructive types
3. Evaluate and treat respiratory emergencies including upper and lower airway obstruction in children
4. Identify causes of altered mental status in children and manage status epilepticus according to current protocols
5. Recognize and treat anaphylaxis and common pediatric toxicologic emergencies including identification of toxidromes
6. Apply pediatric trauma assessment principles including recognition of unique anatomic and physiologic considerations in children

Lecture Outline

Section 1: Pediatric Assessment Triangle and Primary Assessment

The Pediatric Assessment Triangle provides a rapid, visual assessment tool that allows clinicians to form an initial impression of a child's physiologic status within seconds of encounter, before touching the patient. The three components of the triangle include appearance, work of breathing, and circulation to the skin, each providing critical information about the child's cardiorespiratory and neurologic status. This "across the room" assessment identifies children who require immediate intervention and begins the process of determining the underlying physiologic abnormality. The PAT represents the foundation of systematic pediatric emergency assessment, guiding prioritization and initial stabilization efforts.

Appearance, assessed using the TICLS mnemonic, reflects the adequacy of oxygenation, ventilation, brain perfusion, and central nervous system function. Tone evaluates the child's muscle activity and resistance to passive movement, with normal children maintaining appropriate posture for age. Interactivity assesses the child's response to environmental stimuli and engagement with caregivers or examiners. Consolability determines whether a crying child can be soothed by caregivers, with inconsolable crying suggesting serious illness. Look or gaze evaluates whether the child fixes on faces or follows objects appropriately, while speech or cry assesses the strength and character of vocalizations.

Work of breathing provides visual assessment of respiratory effort and potential airway compromise. Abnormal positioning, such as tripoding, sniffing position, or refusal to lie down, suggests significant respiratory distress. Retractions at the intercostal, subcostal, or suprasternal locations indicate increased work to generate airflow. Nasal flaring represents recruitment of accessory muscles to maximize upper airway patency. Audible sounds including stridor, wheezing, and grunting can be heard without a stethoscope and provide clues to the location and nature of airway pathology.

The primary assessment follows the PAT and provides systematic evaluation using the ABCDE approach with immediate intervention for life-threatening abnormalities. Airway assessment determines patency and the ability to maintain an open airway, with interventions ranging from positioning to advanced airway management. Breathing evaluation includes respiratory rate, effort, breath sounds, and oxygen saturation, with supplemental oxygen and assisted ventilation provided as needed. Circulation assessment encompasses heart rate, blood pressure, peripheral perfusion, and pulse quality. Disability evaluation includes mental status using AVPU (Alert, Verbal, Pain, Unresponsive) or Glasgow Coma Scale, pupillary examination, and glucose measurement. Exposure involves complete examination for additional findings while preventing hypothermia.

<image>Panel A: Pediatric Assessment Triangle diagram showing the three components with visual cues for each assessment domain. Panel B: TICLS mnemonic breakdown with clinical examples of normal versus abnormal findings for each letter. Panel C: Photographs demonstrating visible signs of respiratory distress including retractions, nasal flaring, and abnormal positioning. Panel D: Flowchart showing progression from PAT through primary assessment with intervention decision points.</image>

Section 2: Pediatric Cardiopulmonary Resuscitation

Pediatric cardiac arrest differs fundamentally from adult cardiac arrest in that respiratory failure and shock are the predominant etiologies rather than primary cardiac arrhythmia. This difference in pathophysiology emphasizes the critical importance of effective oxygenation and ventilation in pediatric resuscitation, as hypoxia and acidosis frequently precede cardiopulmonary arrest. Most pediatric cardiac arrests begin with respiratory compromise that, if unrecognized or inadequately treated, progresses through respiratory failure to bradycardia and eventually asystole or pulseless electrical activity. Early recognition and treatment of respiratory distress and shock can prevent progression to cardiac arrest, which carries significantly poorer outcomes in children than in adults.

Basic life support in pediatric patients differs from adult protocols in compression technique, compression-to-ventilation ratios, and pulse check location. For infants, the pulse is assessed at the brachial artery rather than the carotid, and compressions are performed using either the two-finger technique or the two-thumb encircling hands technique, compressing to a depth of approximately 1.5 inches or one-third the anterior-posterior diameter. For children aged one year through puberty, the pulse is assessed at the carotid artery and compressions are performed with one or two hands to a depth of about 2 inches. The compression rate is 100-120 per minute for all ages, with a compression-to-ventilation ratio of 30:2 for single rescuers and 15:2 for two healthcare provider rescuers.

Defibrillation in pediatric patients addresses the minority of children who present with shockable rhythms including ventricular fibrillation and pulseless ventricular tachycardia. The initial defibrillation dose is 2 joules per kilogram, with subsequent doses of 4 joules per kilogram up to a maximum of 10 joules per kilogram or the adult dose. Automated external defibrillators with pediatric dose attenuators should be used for children under 8 years when available, though standard AEDs are acceptable when pediatric systems are not available. For non-shockable rhythms (asystole and pulseless electrical activity), high-quality CPR with epinephrine administration every 3-5 minutes represents the primary treatment while reversible causes are identified and addressed.

Medications in pediatric resuscitation include epinephrine for all cardiac arrest rhythms and anti-arrhythmic agents for refractory ventricular fibrillation and pulseless ventricular tachycardia. Epinephrine is dosed at 0.01 mg/kg of the 1:10,000 concentration for intravenous or intraosseous administration, equivalent to 0.1 mL/kg, repeated every 3-5 minutes as needed. Amiodarone at 5 mg/kg is the preferred anti-arrhythmic for shock-refractory VF/pVT, with lidocaine at 1 mg/kg as an alternative. The reversible causes of cardiac arrest, summarized as the H's and T's (Hypovolemia, Hypoxia, Hydrogen ion, Hypo/hyperkalemia, Hypothermia, Hypoglycemia, Tension pneumothorax, Tamponade, Toxins, Thrombosis, and Trauma), guide investigation and treatment during resuscitation efforts.

<image>Panel A: Comparison of infant versus child chest compression techniques with proper hand positioning demonstrated. Panel B: Pediatric cardiac arrest algorithm flowchart showing decision points for shockable versus non-shockable rhythms. Panel C: Weight-based dosing chart for epinephrine and other resuscitation medications. Panel D: Visual summary of H's and T's reversible causes with key clinical features for each.</image>

Section 3: Pediatric Shock - Recognition and Classification

Shock represents a state of inadequate tissue perfusion resulting in insufficient oxygen and nutrient delivery to meet metabolic demands, manifesting through clinical signs of cardiovascular compromise. Pediatric shock may result from decreased circulating volume, inappropriate distribution of blood flow, impaired cardiac pump function, or mechanical obstruction to blood flow. Early recognition of shock is essential because children compensate effectively through tachycardia and increased systemic vascular resistance, maintaining blood pressure until compensatory mechanisms are exhausted. By the time hypotension develops, the child is in decompensated shock with cardiovascular collapse imminent without immediate intervention.

Hypovolemic shock, the most common type in pediatric patients, results from decreased circulating blood volume due to fluid loss or hemorrhage. Common causes include dehydration from vomiting and diarrhea (the most frequent etiology globally), hemorrhage from trauma, and third-space losses in conditions such as sepsis and burns. Clinical findings include tachycardia, delayed capillary refill, cool and mottled extremities, decreased urine output, and eventually hypotension. The child's blood volume is approximately 80 mL/kg, meaning that small absolute volume losses represent significant percentage decreases, and early recognition of compensated hypovolemic shock enables intervention before decompensation.

Distributive shock results from inappropriate vasodilation with maldistribution of blood flow, most commonly from sepsis but also from anaphylaxis and neurogenic causes. Septic shock may present as either "warm shock" with vasodilation, bounding pulses, and flash capillary refill, or "cold shock" with vasoconstriction, weak pulses, and prolonged capillary refill, with cold shock being more common in pediatric patients. Anaphylactic shock features similar vasodilation with additional manifestations including urticaria, angioedema, and bronchospasm. Neurogenic shock occurs with spinal cord injury and features hypotension with paradoxical bradycardia due to loss of sympathetic tone.

Cardiogenic and obstructive shock result from pump failure and mechanical impedance to blood flow, respectively, and require specific interventions targeting the underlying cause. Cardiogenic shock in children may result from myocarditis, arrhythmias, congenital heart disease, or cardiomyopathy, presenting with poor perfusion, hepatomegaly, and pulmonary edema. Obstructive shock occurs when mechanical factors prevent adequate cardiac output, as seen in tension pneumothorax, cardiac tamponade, and massive pulmonary embolism. These shock types require smaller fluid boluses or drainage procedures rather than aggressive volume resuscitation, which can worsen cardiac function or fail to address the underlying obstruction.

<image>Panel A: Physiologic diagrams comparing the four types of shock with cardiac output, vascular resistance, and perfusion patterns. Panel B: Clinical comparison chart of compensated versus decompensated shock with vital sign patterns. Panel C: Photographs showing clinical signs of shock including mottled skin, delayed capillary refill testing, and weak pulses. Panel D: Diagnostic algorithm for differentiating shock types based on clinical assessment and response to initial fluid bolus.</image>

Section 4: Septic Shock Management

Septic shock in pediatric patients represents a medical emergency requiring recognition and protocolized intervention within the first hour to optimize outcomes. Recognition requires identification of systemic inflammatory response criteria including abnormal temperature, heart rate, respiratory rate, and white blood cell count in the context of suspected or confirmed infection. Perfusion abnormalities manifest differently in cold shock versus warm shock, with cold shock characterized by vasoconstriction, prolonged capillary refill, weak peripheral pulses, and cool extremities, while warm shock features vasodilation, flash capillary refill, and bounding pulses. Altered mental status, decreased urine output, and elevated lactate provide additional evidence of inadequate tissue perfusion.

The first-hour sepsis bundle emphasizes early recognition, rapid antimicrobial administration, and aggressive fluid resuscitation. Blood cultures should be obtained as quickly as possible, but antibiotic administration should not be delayed beyond one hour from recognition, as mortality increases significantly with each hour of delay. Empiric antibiotic selection depends on patient age and suspected source, with typical pediatric regimens including ceftriaxone plus vancomycin for community-acquired infection or broader coverage for healthcare-associated or immunocompromised patients. Fluid resuscitation begins with 20 mL/kg isotonic crystalloid boluses, repeated up to 40-60 mL/kg within the first hour if shock persists, with reassessment after each bolus.

Fluid-refractory shock, defined as persistent hypoperfusion despite 40-60 mL/kg of crystalloid, requires vasoactive medication support. Epinephrine is the first-line vasoactive agent for cold shock, providing both inotropic support and vasoconstriction to improve cardiac output and blood pressure. Norepinephrine is preferred for warm shock, providing primarily vasoconstriction to address pathologic vasodilation. Dopamine serves as an alternative first-line agent, with dobutamine added when additional inotropic support is needed. Central venous access facilitates administration of vasoactive medications, though peripheral administration is appropriate when central access would delay therapy.

Ongoing management of septic shock includes source control, continued hemodynamic monitoring, and prevention of secondary complications. Source control measures including abscess drainage, foreign body removal, and debridement should be pursued as soon as the patient is stabilized. Lactate clearance and clinical perfusion parameters guide continued resuscitation efforts. Stress-dose hydrocortisone is considered for catecholamine-refractory shock with suspected adrenal insufficiency. Blood product transfusion maintains hemoglobin above 7-10 g/dL depending on clinical status. Glucose monitoring prevents hypoglycemia, while careful attention to sedation and analgesia maintains patient comfort during intensive resuscitation.

<image>Panel A: Side-by-side comparison of cold shock versus warm shock clinical features with arrows indicating typical progression. Panel B: First-hour sepsis bundle timeline showing parallel tasks for laboratory, antibiotic, and fluid resuscitation. Panel C: Vasoactive medication selection flowchart based on shock phenotype and response to initial therapy. Panel D: Goal-directed resuscitation monitoring parameters with target values for each parameter.</image>

Section 5: Respiratory Emergencies

Respiratory emergencies in children may involve the upper airway, lower airway, or lung parenchyma, with anatomic location determining clinical presentation and management approach. The pediatric airway differs from adults in several important ways: the airway is smaller and more collapsible, the tongue is proportionally larger, the larynx is more anterior and cephalad, and the narrowest point is at the cricoid cartilage in young children rather than the vocal cords. These differences make children more susceptible to airway obstruction and require modifications in airway management techniques. Clinical signs of upper airway obstruction include stridor, drooling, and inspiratory distress, while lower airway obstruction produces wheezing and expiratory distress.

Croup, caused primarily by parainfluenza virus, represents the most common cause of upper airway obstruction in young children, typically affecting those aged 6 months to 3 years. The classic presentation includes a barky, seal-like cough, inspiratory stridor, and hoarse voice, often worse at night and preceded by upper respiratory symptoms. Severity is assessed by the presence of stridor at rest, degree of retractions, and level of distress, with severe cases featuring stridor and retractions even when calm. Treatment includes systemic corticosteroids (dexamethasone 0.6 mg/kg) for all severity levels, with nebulized racemic epinephrine added for moderate-to-severe cases. Children receiving nebulized epinephrine require 3-4 hours of observation for potential rebound worsening.

Epiglottitis, though rare since widespread Haemophilus influenzae type b vaccination, remains a life-threatening emergency requiring immediate recognition and airway management. The classic presentation features a toxic-appearing child with high fever, drooling, tripod positioning, muffled voice, and rapid progression of symptoms over hours. The child should be kept calm and undisturbed, as agitation can precipitate complete airway obstruction. Direct examination of the pharynx should be avoided outside the operating room setting. Management requires preparation for emergency airway intervention with experienced personnel and equipment for both intubation and surgical airway immediately available.

Lower airway emergencies include asthma exacerbation, bronchiolitis, and foreign body aspiration. Acute asthma exacerbations present with wheezing, prolonged expiration, tachypnea, and use of accessory muscles, with severity stratified to guide treatment intensity. Management progresses from intermittent bronchodilator administration to continuous nebulization, with systemic corticosteroids indicated for all but the mildest exacerbations. Magnesium sulfate, terbutaline, and BiPAP are considered for severe, refractory cases, with mechanical ventilation reserved for impending respiratory failure. Foreign body aspiration should be suspected with sudden-onset respiratory distress, unilateral wheezing, or choking history, requiring bronchoscopy for diagnosis and removal.

<image>Panel A: Comparative anatomy of pediatric versus adult airway with key differences highlighted. Panel B: Croup severity assessment scale with corresponding management for each severity level. Panel C: Lateral neck radiograph examples showing normal epiglottis versus "thumb sign" of epiglottitis. Panel D: Asthma exacerbation severity stratification with stepped treatment algorithm.</image>

Section 6: Altered Mental Status

Altered mental status in pediatric patients encompasses a spectrum from subtle behavioral changes to complete unresponsiveness, requiring systematic evaluation to identify potentially life-threatening etiologies. The AEIOU TIPS mnemonic provides a comprehensive framework for considering causes: Alcohol and Abuse, Encephalopathy and Electrolytes and Endocrine, Insulin (hypoglycemia), Opiates and Oxygen, Uremia, Trauma and Temperature, Infection, Psychiatric and Poisoning, and Seizure, Stroke, and Shock. Immediate assessment of airway, breathing, and circulation takes priority, followed by rapid glucose measurement as hypoglycemia represents a readily reversible cause of altered mental status across all age groups.

Initial evaluation proceeds systematically while gathering historical information about symptom onset, preceding events, medications, possible ingestions, trauma, and fever. Vital signs including temperature identify potential infection, while pupillary examination and focal neurologic findings may suggest structural lesions or specific toxidromes. Laboratory evaluation typically includes glucose, electrolytes, blood gas, ammonia, and toxicology screening. Head computed tomography is indicated when trauma is suspected, focal neurologic findings are present, or no metabolic or infectious explanation is identified. Lumbar puncture should be performed when meningitis or encephalitis is suspected, after imaging excludes contraindications.

Status epilepticus, defined as continuous seizure activity or recurrent seizures without return to baseline for five minutes or longer, represents a medical emergency requiring prompt treatment to prevent neuronal injury. The approach prioritizes stabilization of airway, breathing, and circulation while simultaneously administering anti-seizure medication. First-line therapy consists of benzodiazepines: lorazepam at 0.1 mg/kg intravenously is preferred, with diazepam or midazolam (including intranasal, buccal, or intramuscular routes) as alternatives when intravenous access is not available. If seizures persist after two doses of benzodiazepine, second-line agents including fosphenytoin, levetiracetam, or valproate are administered.

Bacterial meningitis requires high clinical suspicion and empiric antibiotic treatment while awaiting diagnostic confirmation. Classic findings of fever, headache, neck stiffness, and altered mental status may not all be present, particularly in infants who may present only with irritability, poor feeding, and bulging fontanelle. Lumbar puncture provides diagnostic cerebrospinal fluid analysis, with bacterial meningitis characterized by pleocytosis with neutrophil predominance, elevated protein, and decreased glucose. Empiric antibiotics should be administered immediately when meningitis is suspected, with the regimen covering likely pathogens based on age: ceftriaxone plus vancomycin for most children, with ampicillin added for infants under one month. Dexamethasone administered before or with the first antibiotic dose may reduce neurologic complications.

<image>Panel A: AEIOU TIPS mnemonic diagram with examples of common causes for each category. Panel B: Neurologic examination summary showing pupillary findings, motor patterns, and associated diagnoses. Panel C: Status epilepticus treatment algorithm with medication dosing and timeline. Panel D: CSF analysis comparison chart for bacterial versus viral meningitis with treatment implications.</image>

Section 7: Anaphylaxis

Anaphylaxis represents a severe, potentially life-threatening systemic allergic reaction requiring immediate recognition and treatment with intramuscular epinephrine. Diagnostic criteria require involvement of multiple organ systems: skin or mucosal symptoms (urticaria, angioedema, flushing) plus either respiratory compromise (stridor, wheezing, dyspnea) or cardiovascular symptoms (hypotension, tachycardia, syncope). Gastrointestinal symptoms including nausea, vomiting, and abdominal pain may accompany the reaction. Symptoms typically develop within minutes to hours of exposure to an allergen, though delayed reactions can occur. The most common triggers in children include foods (peanuts, tree nuts, milk, eggs, shellfish), medications (antibiotics, NSAIDs), and insect stings.

Epinephrine is the first-line and most critical treatment for anaphylaxis, addressing bronchospasm, vasodilation, and mucosal edema through its alpha and beta adrenergic effects. The dose is 0.01 mg/kg of 1:1000 concentration (maximum 0.5 mg) administered intramuscularly in the anterolateral thigh, which provides more rapid absorption than subcutaneous injection or injection in other sites. The dose may be repeated every 5-15 minutes if symptoms persist or recur. Delay in epinephrine administration is associated with increased mortality, making prompt recognition and treatment essential. Patients should be placed in supine position with legs elevated unless this position compromises respiration.

Adjunctive treatments support the primary intervention but should never delay epinephrine administration. Intravenous fluid boluses of 20 mL/kg isotonic crystalloid address hypotension from vasodilation and capillary leak. Nebulized albuterol provides additional bronchodilation for persistent wheezing. H1-antihistamines such as diphenhydramine address urticaria and pruritus but do not reverse the life-threatening components of anaphylaxis. Corticosteroids may reduce the risk of biphasic reactions and protracted symptoms but have no immediate effect on acute symptoms. For refractory hypotension despite epinephrine and fluids, vasopressor infusion may be required.

Discharge planning following anaphylaxis treatment includes epinephrine auto-injector prescription, anaphylaxis action plan education, and allergist referral. Patients should receive prescriptions for two epinephrine auto-injectors and demonstration of proper use before discharge. The anaphylaxis action plan provides written instructions for recognizing symptoms and administering epinephrine, with clear direction to call emergency services after use. Observation for 4-6 hours is recommended due to the risk of biphasic reactions, which occur in up to 20% of cases. Medical alert identification and school emergency action plans help ensure appropriate response to future reactions.

<image>Panel A: Clinical photographs showing cutaneous manifestations of anaphylaxis including urticaria, angioedema, and flushing. Panel B: Anatomic diagram showing multi-system effects of anaphylaxis with epinephrine's reversal mechanisms. Panel C: Epinephrine auto-injector demonstration images showing proper technique for intramuscular injection. Panel D: Sample anaphylaxis action plan template with triggers, symptoms, and treatment steps.</image>

Section 8: Toxicologic Emergencies

Toxicologic emergencies in pediatric patients require systematic evaluation and management focused on supportive care, decontamination when appropriate, and antidote administration when available. The initial approach follows standard resuscitation principles: stabilization of airway, breathing, and circulation takes priority regardless of the suspected toxin. Identification of the ingested substance guides specific treatment, though in many cases the agent is unknown or multiple substances are involved. Poison control centers (1-800-222-1222 in the United States) provide expert consultation and should be contacted for guidance on evaluation and treatment. Activated charcoal for gastrointestinal decontamination is considered within 1-2 hours of ingestion for appropriate toxins, but is not universally indicated.

Recognition of toxidromes, characteristic constellations of signs and symptoms associated with specific drug classes, guides evaluation and treatment when the ingested substance is unknown. The anticholinergic toxidrome features dry skin, flushing, mydriasis, urinary retention, decreased bowel sounds, tachycardia, hyperthermia, and altered mental status ("hot as a hare, dry as a bone, red as a beet, mad as a hatter, blind as a bat"). The cholinergic toxidrome produces the SLUDGE mnemonic: Salivation, Lacrimation, Urination, Defecation, GI distress, and Emesis, along with bradycardia, miosis, and bronchospasm. The opioid toxidrome presents with respiratory depression, miosis, and decreased mental status. The sympathomimetic toxidrome includes tachycardia, hypertension, hyperthermia, diaphoresis, and agitation.

Certain medications represent particular danger in pediatric patients, with even small amounts potentially causing severe toxicity or death. Calcium channel blockers can cause profound cardiovascular collapse with a single tablet ingestion, requiring aggressive calcium replacement, glucagon, and high-dose insulin therapy. Sulfonylureas cause delayed and prolonged hypoglycemia that may persist for 24 hours or longer, requiring admission for glucose monitoring. Opioids cause respiratory depression rapidly reversed by naloxone but may require repeated dosing or infusion given the short half-life of the antidote compared to many opioid agonists. Tricyclic antidepressants cause sodium channel blockade with QRS prolongation, arrhythmias, and seizures, treated with sodium bicarbonate.

Antidote administration can be life-saving when specific antidotes exist for identified toxins. N-acetylcysteine prevents hepatotoxicity in acetaminophen poisoning when administered within 8-10 hours of ingestion, with continued efficacy if given later. Deferoxamine chelates iron in cases of significant iron ingestion with systemic symptoms or high serum iron levels. Atropine and pralidoxime reverse cholinergic toxicity in organophosphate poisoning. Flumazenil reverses benzodiazepine effects but risks precipitating seizures in patients with benzodiazepine dependence or mixed ingestions. Fomepizole inhibits alcohol dehydrogenase to prevent toxic metabolite formation in methanol and ethylene glycol poisoning.

<image>Panel A: Clinical comparison chart of major toxidromes with pupillary, vital sign, and skin findings for each. Panel B: "One-pill killers" visual reference showing medications dangerous in small quantities to young children. Panel C: Acetaminophen treatment nomogram showing toxic versus non-toxic thresholds based on time since ingestion. Panel D: Antidote quick reference guide with toxin, antidote, and dosing information.</image>

Section 9: Pediatric Trauma

Pediatric trauma assessment requires understanding of anatomic and physiologic differences that affect injury patterns and clinical presentation in children compared to adults. The relatively larger head-to-body ratio in young children results in higher frequency of head injuries, while the more flexible skeleton allows internal organ injury without overlying fractures. Children have proportionally larger body surface area, increasing susceptibility to hypothermia during resuscitation. The blood volume of approximately 80 mL/kg means that small absolute blood losses represent significant percentage decreases. Children maintain blood pressure through tachycardia and vasoconstriction until 25-30% of blood volume is lost, then rapidly decompensate.

The primary survey in pediatric trauma follows the ABCDE approach with age-appropriate modifications for each component. Airway management accounts for the smaller, more anterior airway, potentially requiring smaller equipment sizes calculated by age or length-based systems. For children under 8 years, uncuffed endotracheal tubes or cuffed tubes with careful pressure monitoring are appropriate. Breathing assessment includes high respiratory rates normal for age and recognition that chest wall compliance may transmit force to underlying structures without rib fractures. Circulation assessment prioritizes recognition of compensated shock, as hypotension represents a late and ominous finding. Disability assessment uses age-appropriate Glasgow Coma Scale modifications, and exposure includes particular attention to temperature maintenance.

Head trauma represents the leading cause of pediatric trauma mortality, requiring careful evaluation and management. The PECARN (Pediatric Emergency Care Applied Research Network) clinical decision rule guides CT imaging decisions based on mechanism of injury, symptoms, and physical examination findings to avoid unnecessary radiation while identifying clinically significant injuries. Children with GCS 13-15, no loss of consciousness, no vomiting, and no severe mechanism may be observed rather than imaged. Severe head injury (GCS less than or equal to 8) requires intubation for airway protection and consideration of interventions to reduce intracranial pressure. Signs of herniation including asymmetric pupils and posturing require immediate intervention with hyperventilation and osmotic therapy while neurosurgical consultation is obtained.

Abdominal trauma in children is predominantly blunt, with the spleen and liver representing the most commonly injured solid organs. The pliable pediatric ribcage provides less protection for abdominal organs, and the relatively larger solid organs extend below the costal margin. Seat belt injuries should prompt evaluation for lumbar spine fractures and hollow viscus injury. Contrast-enhanced CT provides definitive imaging for hemodynamically stable patients with suspected abdominal injury. Importantly, the majority of solid organ injuries in children are managed non-operatively with observation and supportive care, reserving surgery for hemodynamic instability despite resuscitation or evidence of hollow viscus injury requiring repair.

<image>Panel A: Anatomic comparison of child versus adult body proportions highlighting trauma-relevant differences. Panel B: Length-based pediatric resuscitation tape demonstrating equipment sizing approach. Panel C: PECARN head CT decision algorithm for children under 2 and 2 years and older with different pathways. Panel D: Abdominal CT images showing solid organ injury grading with associated management for each grade.</image>

Section 10: Special Pediatric Emergencies

Diabetic ketoacidosis represents a metabolic emergency occurring in type 1 diabetes when insulin deficiency leads to hyperglycemia, ketosis, and metabolic acidosis. Diagnostic criteria include blood glucose greater than 200 mg/dL, venous pH less than 7.3 or bicarbonate less than 15 mEq/L, and ketonemia or ketonuria. DKA may be the initial presentation of new-onset diabetes in children or may occur in known diabetics during illness, insulin omission, or pump failure. Clinical features include polyuria, polydipsia, weight loss, abdominal pain, nausea, vomiting, fruity breath odor, and Kussmaul respirations. Severity is classified by degree of acidosis, with severe DKA defined as pH less than 7.1 or bicarbonate less than 5 mEq/L.

Management of DKA prioritizes fluid resuscitation followed by insulin administration, with careful attention to the risk of cerebral edema. Initial fluid resuscitation consists of 10-20 mL/kg normal saline boluses to restore intravascular volume, followed by calculated rehydration over 24-48 hours. Intravenous insulin infusion at 0.05-0.1 units/kg/hour begins after initial fluid resuscitation, with the rate adjusted to achieve gradual glucose decrease of 50-100 mg/dL per hour. Potassium replacement begins with the first bag of maintenance fluids if the patient is urinating and potassium is not elevated, as total body potassium is depleted despite potentially normal or elevated serum levels initially.

Cerebral edema represents the most serious complication of DKA treatment, occurring in approximately 1% of pediatric DKA episodes but accounting for significant morbidity and mortality. Risk factors include younger age, new-onset diabetes, severe DKA, and overly rapid correction of glucose or sodium. Warning signs include headache, altered mental status, bradycardia, hypertension, and neurologic deterioration. Treatment involves immediate reduction in fluid rate, elevation of the head of bed, and administration of hyperosmolar therapy with mannitol or hypertonic saline. Early recognition and treatment are essential, as progressive herniation can occur rapidly.

Brief Resolved Unexplained Events (BRUE), previously termed Apparent Life-Threatening Events (ALTE), describe episodes in infants characterized by color change, breathing change, tone change, or altered responsiveness that resolve by the time of medical evaluation. Risk stratification determines the extent of workup and disposition. Lower-risk infants are those older than 60 days, born at greater than or equal to 32 weeks gestation, with no prior BRUE history, single episode lasting less than one minute, requiring no CPR by trained provider, and no concerning features on history or examination. Lower-risk infants may be observed briefly and discharged with close follow-up, while higher-risk infants require more extensive evaluation including consideration of cardiac, neurologic, infectious, and metabolic etiologies.

<image>Panel A: DKA pathophysiology diagram showing the cascade from insulin deficiency through metabolic derangements to clinical manifestations. Panel B: DKA fluid and insulin management protocol with monitoring parameters and adjustment guidelines. Panel C: Cerebral edema recognition and treatment flowchart with warning signs and intervention steps. Panel D: BRUE risk stratification criteria with corresponding evaluation and disposition recommendations.</image>

Summary

• The Pediatric Assessment Triangle provides rapid assessment of Appearance (TICLS), Work of Breathing, and Circulation to identify critical illness immediately
• Pediatric CPR uses 15:2 compression-to-ventilation ratio with two rescuers; compression depth is 1.5 inches for infants and 2 inches for children
• Shock in children is recognized by tachycardia and poor perfusion before hypotension develops; fluid resuscitation begins with 20 mL/kg boluses with reassessment
• First-hour septic shock management includes obtaining cultures, broad-spectrum antibiotics, fluid resuscitation up to 40-60 mL/kg, and vasopressors if fluid-refractory
• Croup is treated with dexamethasone 0.6 mg/kg for all severity levels, with nebulized epinephrine added for moderate-to-severe cases
• Status epilepticus treatment begins with benzodiazepines (lorazepam 0.1 mg/kg IV), progressing to second-line agents if seizures persist after two doses
• Anaphylaxis requires immediate intramuscular epinephrine 0.01 mg/kg (maximum 0.5 mg), repeated every 5-15 minutes as needed
• One-pill killers in pediatrics include calcium channel blockers, sulfonylureas, opioids, and tricyclic antidepressants
• Pediatric trauma assessment recognizes that tachycardia indicates compensated shock while hypotension is a late, ominous sign
• DKA management involves fluid resuscitation first, then insulin, with vigilance for cerebral edema especially in younger children with severe acidosis

Key Terms

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