Anaphylaxis

The patient is wheezing, hypotensive, and covered in hives after a contrast injection. You have seconds to act — and the order of your interventions determines survival.

Anaphylaxis management follows a fixed priority sequence. Epinephrine IM is always the first drug — not diphenhydramine, not a steroid, not a fluid bolus. Adult dose is 0.3–0.5 mg of 1:1,000 (1 mg/mL) concentration given intramuscularly in the lateral thigh (vastus lateralis). This can be repeated every 5–15 minutes if symptoms persist. IV epinephrine (1:10,000) is reserved for cardiac arrest or refractory shock and requires continuous monitoring. After epinephrine, establish large-bore IV access and infuse 1–2 L of 0.9% normal saline rapidly to counteract distributive vasodilation. Adjunct medications follow: diphenhydramine 25–50 mg IV for histamine blockade and methylprednisolone 125 mg IV to prevent biphasic reactions. Position the patient supine with legs elevated unless respiratory distress requires a semi-Fowler's position. Monitor for biphasic reaction — a second wave of symptoms occurring 1–72 hours later — which is why patients require observation for at least 4–6 hours post-event. Remove the causative agent immediately (stop the infusion, remove the stinger).

Key Distinctions

Don't confuse IM epinephrine concentration (1:1,000) with IV cardiac arrest concentration (1:10,000) — giving 1:1,000 IV can cause fatal arrhythmia. Students often prioritize diphenhydramine first because it treats hives, but antihistamines cannot reverse airway edema or cardiovascular collapse — only epinephrine does. Anaphylaxis fluid resuscitation uses crystalloid boluses like septic shock, but the root cause is massive vasodilation from histamine, not infection.

Clinical Pearl

Epi first, epi fast, epi in the thigh. Benadryl treats hives; epinephrine saves lives. Never let an antihistamine jump the line ahead of epinephrine.

Recognition & Triggers

Anaphylaxis is a severe, rapid-onset systemic allergic reaction mediated by massive IgE-triggered histamine and mediator release from mast cells and basophils. It is a form of distributive shock caused by widespread vasodilation and capillary permeability, not volume loss or pump failure. Recognition hinges on identifying involvement of two or more body systems within minutes to hours of exposure. The classic triad: skin (urticaria, flushing, angioedema), respiratory (laryngeal edema, stridor, bronchospasm, wheezing), and cardiovascular (hypotension, tachycardia, weak pulse). Skin signs are present in up to 90% of cases but can be absent — anaphylaxis without urticaria is the presentation students miss. GI involvement (cramping, vomiting, diarrhea) counts as a system. Onset is typically within 5–30 minutes of IV exposure, up to 2 hours for oral ingestion. A biphasic reaction can recur 1–72 hours after the initial episode without re-exposure, which is why observation periods of at least 4–6 hours are standard.

Key Distinctions

Don't confuse anaphylaxis (multisystem, requires epinephrine) with a localized allergic reaction (isolated hives, no respiratory or cardiovascular compromise). Students mistake vasovagal syncope post-injection (bradycardia, pallor, diaphoresis) for anaphylaxis — anaphylaxis produces tachycardia, not bradycardia. Angioedema of the lips and tongue signals airway threat even before wheezing begins; waiting for stridor means the window is closing.

Clinical Pearl

Two systems, think anaphylaxis. Hives plus wheeze? Hives plus vomiting? Wheeze plus hypotension? Stop the trigger and call for epinephrine — don't wait for all three.