Allergic Reactions, Anaphylaxis, and Immunologic Emergencies - NREMT: Paramedic Level

Repeat every $5$–$15$ minutes if symptoms persist or worsen. This interval allows assessment of response while preventing delay in addressing persistent mediator effects and symptom progression.

$0.01$ mg/kg IM, maximum $0.3$ mg per dose. Weight-based dosing ensures efficacy while minimizing side effects, with the cap preventing overdose in larger children.

$0.3$–$0.5$ mg IM (=$0.3$–$0.5$ mL of $1$ mg/mL). This dose provides sufficient alpha and beta adrenergic stimulation to reverse hypotension and bronchospasm without excessive risk in adults.

Intramuscular injection into the lateral thigh (vastus lateralis). IM administration ensures rapid absorption and bioavailability, with the vastus lateralis providing optimal muscle mass for injection in emergencies.

Epinephrine. Epinephrine rapidly counteracts the effects of released mediators, stabilizing hemodynamics and relieving bronchospasm as the cornerstone of treatment.

Hypotension with tachycardia and weak pulses. Distributive shock in anaphylaxis arises from widespread vasodilation and capillary leak, resulting in compensatory tachycardia and diminished pulse quality.

Wheezing with increased work of breathing. Bronchospasm leads to airway constriction, manifesting as wheezing and labored breathing due to mediator effects on bronchial smooth muscle.

Stridor from laryngeal edema. Laryngeal edema causes upper airway narrowing, producing stridor as a sign of potential imminent airway compromise requiring immediate intervention.

Urticaria, pruritus, flushing, angioedema. These manifestations result from histamine-induced vasodilation and increased vascular permeability in dermal and mucosal tissues.

Skin/mucosa plus respiratory or cardiovascular involvement. Involvement of these systems meets diagnostic criteria for anaphylaxis, as they signify widespread mediator effects beyond isolated cutaneous reactions.

Exposure + rapid onset + airway/breathing symptoms or hypotension. These elements indicate an IgE-mediated response with systemic involvement, differentiating anaphylaxis from localized allergic reactions.

Alpha-1 vasoconstriction increasing SVR and reducing mucosal edema. Alpha-1 agonism constricts vessels to restore blood pressure and decreases edema by reducing vascular permeability in anaphylactic states.

H1 antihistamines and corticosteroids (adjunctive, not first-line). These classes mitigate histamine effects and inflammation but act too slowly to serve as primary therapy for acute life-threatening symptoms.

Within $1$–$72$ hours, most commonly within $8$–$12$ hours. This timeframe reflects the variable kinetics of mediator release and immune response reactivation without additional antigen exposure.

Isotonic crystalloid bolus to treat relative hypovolemia from capillary leak. Crystalloids expand intravascular volume to counteract fluid shifts from increased permeability, supporting blood pressure in distributive shock.

Early airway control with preparation for difficult airway and rapid deterioration. Stridor signals potential airway compromise, necessitating proactive management to secure the airway before edema worsens and complicates intubation.

Beta-2 bronchodilation. Beta-2 receptor activation relaxes bronchial smooth muscle, alleviating airway constriction caused by anaphylactic mediators.

Inhaled albuterol. Albuterol provides targeted beta-2 agonism for bronchodilation but lacks the systemic effects needed to address hypotension or edema in anaphylaxis.

Administer glucagon per protocol for beta-blocker associated refractory anaphylaxis. Glucagon bypasses beta-receptor blockade to increase cyclic AMP, enhancing cardiac output and reversing refractory symptoms in such patients.

Anaphylaxis. Hypotension following exposure fulfills diagnostic criteria for anaphylaxis, as cardiovascular collapse can occur independently of dermatologic signs.

Mild allergic reaction (not anaphylaxis). Isolated cutaneous symptoms without systemic involvement indicate a localized reaction, not meeting criteria for anaphylaxis requiring aggressive intervention.

IgE-mediated mast cell and basophil degranulation. This mechanism triggers the release of histamine and other mediators, leading to the rapid onset of symptoms characteristic of anaphylaxis.

Recurrence of symptoms after initial resolution without re-exposure. Biphasic reactions occur due to a secondary release of mediators, highlighting the need for prolonged observation after initial treatment.