Approach to a child presenting with anaphylaxis

Pathophysiology and Etiology

Anaphylaxis is a catastrophic, systemic hypersensitivity reaction characterized by the acute onset of multiorgan system dysfunction, which can rapidly progress to life-threatening cardiopulmonary compromise.
The fundamental pathophysiology involves the acute, massive release of histamine, leukotrienes, bradykinin, and other inflammatory chemical mediators from mast cells and basophils.
This mediator release is typically triggered by exposure to specific allergens, most commonly insect bites, medications, foods, and environmental agents in a sensitized individual.
Hemodynamically, anaphylaxis causes a classic distributive shock pattern: the sudden release of histamine induces profound peripheral vasodilation and increased capillary permeability.
This abnormal vasodilation drastically reduces systemic vascular resistance (SVR), leading to a sudden fall in both preload and afterload, accompanied by a maldistribution of blood flow away from vital organs.
The cardiovascular system initially attempts to compensate for this severe intravascular volume depletion (due to capillary leak and "third-spacing") with a marked increase in heart rate and cardiac output.

The onset of symptoms in anaphylaxis is typically sudden and catastrophic, presenting without a prodrome.
Diagnosis relies heavily on circumstantial history (e.g., specific food ingestion, insect sting) coupled with a constellation of classic signs across multiple organ systems.

Organ System	Characteristic Clinical Signs
Cutaneous / Mucosal	Pruritus, urticaria, facial swelling, erythema, and profound swelling of the lips and tongue.
Respiratory	Upper airway edema leading to stridor and hoarseness; lower airway narrowing manifesting as bronchospasm, wheezing, and dyspnea.
Cardiovascular	Tachycardia, flushed and warm extremities, bounding pulses, flash capillary refill (early), wide pulse pressure, and eventual profound hypotension leading to syncope or shock.
Gastrointestinal	Nausea, vomiting, and severe abdominal cramps.

Triage must be immediate; the child must be evaluated using the Pediatric Assessment Triangle (Appearance, Work of Breathing, Circulation to Skin).
A rapid and systematic evaluation of the Airway, Breathing, Circulation, and Disability (ABCD) must be initiated.
The child should be placed in the Trendelenburg position (supine with legs elevated) once any immediate airway threat or hypotension is recognized, to maximize venous return to the heart.
A bedside serum glucose test should be performed for any patient presenting with an altered mental status to rule out hypoglycemia.

Intramuscular epinephrine is the absolute first-line treatment of choice for anaphylactic shock and must be administered immediately upon recognition.
Epinephrine acts on alpha-adrenergic receptors to reverse peripheral vasodilation (increasing systemic vascular resistance and blood pressure) and on beta-adrenergic receptors to induce bronchodilation and suppress further mast cell mediator release.
The standard pediatric dose is $0.01$ mg/kg of the $1 : 1, 000$ ( $1$ mg/mL) solution, administered via the intramuscular (IM) route.
The maximum single dose is $0.5$ mg for an older child or adolescent.
This IM dose can and should be repeated $2 - 3$ times every $5 - 15$ minutes if the child's clinical condition does not rapidly improve or if symptoms recur.

Supplemental oxygen ( $100$ ) should be administered immediately via a non-rebreather face mask to aggressively treat hypoxemia.
Severe upper airway obstruction secondary to progressive epiglottic or laryngeal edema may necessitate emergency advanced airway management.
Endotracheal intubation must be anticipated and prepared for early, as impending respiratory failure can progress to complete obstruction rapidly.
If bronchospasm and wheezing are prominent features, nebulized beta-agonists such as salbutamol should be administered alongside epinephrine.

Because anaphylaxis induces distributive shock characterized by massive vasodilation and capillary leak, aggressive fluid resuscitation is critical to restore intravascular volume.
Intravenous (IV) or intraosseous (IO) access must be established promptly.
Isotonic crystalloids (Normal Saline or Ringer's Lactate) should be administered as rapid IV boluses of $20$ mL/kg.
Repeat fluid boluses may be necessary if hypotension or signs of poor perfusion persist, with continuous reassessment for signs of fluid overload.

Antihistamines and corticosteroids are considered second-line, adjunctive therapies and should never delay the administration of IM epinephrine.

Medication Class	Drug and Dosage	Clinical Indication
Antihistamines	Chlorpheniramine (or diphenhydramine) given intravenously or orally.	To relieve cutaneous symptoms such as severe pruritus and urticaria.
Corticosteroids	Hydrocortisone at a dose of $10$ mg/kg IV (maximum $100$ mg per dose).	Considered for severe symptoms or for known asthmatics with significant, persistent bronchospasm after other symptoms have abated.

In rare instances, persistent shock may reflect refractory anaphylaxis despite multiple doses of IM epinephrine and adequate volume expansion.
If hypotension is refractory to initial IM epinephrine boluses and fluid resuscitation, a continuous intravenous epinephrine infusion must be initiated.
The continuous epinephrine infusion should be started at $0.1$ $μ$ g/kg/min and can be titrated upwards to $1$ $μ$ g/kg/min based on continuous hemodynamic monitoring and clinical response.
Ensure the complete removal of the inciting agent if it is still present (e.g., removing a stinger, discontinuing an offending intravenous medication or blood product).
The child requires admission to a Pediatric Intensive Care Unit (PICU) for continuous cardiovascular monitoring, serial assessment of perfusion parameters, and airway observation.