One mast cell, four systems — epinephrine is the answer
✚ CRASH CARD
crashcard.co
18 × 24 IN · CLASSROOM REFERENCE
Anaphylaxis = an acute, systemic IgE-mediated (or non-IgE) hypersensitivity reaction —
mast cells & basophils dump mediators, hitting skin · airway · circulation · gut at once. The diagnosis is
clinical, the treatment is IM epinephrine, and delay kills.
Don't wait for tests. Don't reach for antihistamines first. Give epi.
Watch:Hereditary angioedema is bradykinin-driven — no urticaria, no response to epi / antihistamine / steroid.Scombroid mimics after spoiled fish and responds to antihistamines.
ONE CELL, FOUR TARGETS — EPI REVERSES EACH IgE crosslink · mediators
Airway β₂ · α₁
Edema + bronchospasm. Epi opens it & shrinks the mucosa.
Circulation α₁ · β₁
Leak + vasodilation. Epi tightens vessels, drives the heart.
Skin stabilize
Hives & angioedema. Epi halts further mediator release.
Gut ↓ mediators
Cramps & vomiting settle as the reaction is shut down.
3Diagnosisclinical — NIAID/WAO criteria
1Acute onset (min–hrs) with skin/mucosa involvement AND either respiratory compromise OR ↓BP / end-organ hypoperfusion.
2≥ 2 systems involved quickly after a likely allergen (skin, resp, CV, or persistent GI).
3↓ BP after exposure to a known allergen for that patient (isolated hypotension counts).
WAO 2020 also accepts isolated laryngo- or bronchospasm after a highly-probable allergen — skin need not be present.
Tryptase (draw 15 min–3 h, peak 1–2 h; repeat baseline ≥24 h) is confirmatory, not a gate — never delay epinephrine for a level.
▲Biphasic Reactionwhy we observe after resolution
ONE HIT, THEN A SECOND WAVE severity vs time · no re-exposure
Up to ~1 in 20 react a second time — hours after apparent resolution, with no re-exposure. That's why we observe, arm every patient with an auto-injector, and warn them to re-dose & return if it recurs.
4Treatmentepi first · adjuncts second · per protocol
Position supine, legs up — do NOT sit them upright (empty-vena-cava / collapse risk). Pregnant → left lateral.
High-flow O₂; monitor; prepare a difficult airway early if the throat is swelling.
Large-bore IV × 2 + crystalloid bolus1–2 L (peds 20 mL/kg) for shock — the tank is empty.
Adjuncts — SECOND-LINE only:antihistamines (itch/hives), steroids, inhaled β-agonist for bronchospasm. Never a substitute for epi.
Refractory:epinephrine infusion; add glucagon1–5 mg IV if on a β-blocker; vasopressors.
5Critical Proceduresthe airway only gets harder
⚠ Secure the airway before it closes
Progressing angioedema → intubate early — swelling only worsens; a delayed airway becomes a surgical one.
Have the double setup ready (cric kit, most experienced operator); anticipate distorted anatomy.
Epinephrine infusion for shock not responding to repeat IM + fluids — titrate to MAP.
On a β-blocker & refractory? Epi is blunted — give glucagon to bypass the β-receptor.
PPitfalls & Pearls
EPI FIRST. Antihistamines & steroids are not the treatment — they don't reverse shock or airway edema.
IM, not SC or IV push for the initial dose — IV push causes arrhythmia; SC is too slow.
Don't sit them up. Upright posture in shock has caused fatal cardiac arrest.
Delayed epi = deaths. The commonest error is giving it late, or not at all.
Observe for biphasic reactions — a second wave can come hours later without re-exposure.
Angioedema without hives + no epi response? Think hereditary angioedema (bradykinin) — different drugs.
REMEMBER — One cell, four systems: airway · circulation · skin · gut. EPI IM, thigh, repeat. Lay them flat, fill the tank, oxygen. Adjuncts are second. If tests delay epi → give epi anyway.
DDisposition
OBSERVE / ADMIT
Observe after response per local policy (risk-stratify; longer if severe / needed >1 dose)
Refractory, >1 epi dose, or β-blocker → admit
Poor access to care / prior biphasic
DISCHARGE
Epi auto-injector Rx ×2 + technique taught
Written action plan
Allergist referral
Avoidance counseling
Sheet
Anaphylaxis
Series / No.
GRAND ROUNDS 06
Part No.
CC-GR-06
Rev
A
Status
EDUCATION REFERENCE — NOT A PROTOCOL. VERIFY LOCALLY.