What is anaphylaxis
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Here is a comprehensive overview of anaphylaxis based on authoritative emergency medicine textbooks:
Anaphylaxis
Definition
Anaphylaxis is a serious, rapid-onset allergic reaction that may cause death and requires emergent diagnosis and treatment. It is now used as a single term to describe both IgE-dependent (previously "anaphylactic") and IgE-independent (previously "anaphylactoid") reactions, because the final pathway in both is identical. It represents the most severe form of immediate hypersensitivity. — Tintinalli's Emergency Medicine, p. 110
Pathophysiology
Anaphylaxis arises primarily from activation of mast cells and basophils through crosslinking of IgE and aggregation of high-affinity IgE receptors. Upon activation, these cells rapidly release:
- Preformed mediators: histamine, tryptase, carboxypeptidase A, proteoglycans
- Newly synthesised mediators: prostaglandins, leukotrienes, platelet-activating factor (via arachidonic acid cascade)
- Cytokines: TNF-α (released both early and late)
Effects of key mediators:
| Mediator | Effect |
|---|---|
| Histamine | Vasodilation, ↑ vascular permeability, ↑ heart rate, bronchoconstriction |
| Prostaglandin D₂ | Bronchoconstriction, pulmonary/coronary vasoconstriction, peripheral vasodilation |
| Leukotrienes | Bronchoconstriction, ↑ vascular permeability, airway remodeling |
| Platelet-activating factor | Potent bronchoconstriction, ↑ vascular permeability |
| TNF-α | Neutrophil activation, chemokine synthesis |
— Tintinalli's Emergency Medicine, p. 110
Common Triggers
- Foods: peanuts, tree nuts, shellfish, milk, eggs, soy, mammalian meats (alpha-gal sensitization after tick bite)
- Medications: antibiotics (especially penicillins), NSAIDs, radiocontrast media
- Insect stings: hymenoptera venom (bees, wasps, ants) — occurs in up to 3% of adults stung
- Latex: natural rubber latex (NRL) — still common in many countries
- Allergen immunotherapy injections
- Idiopathic (no cause identified) — a significant proportion
NSAIDs are the most common trigger of drug-induced anaphylaxis, acting through non-IgE (arachidonic acid) mechanisms. — Rosen's Emergency Medicine, p. 2386
Clinical Features
The classic progression:
- Early: pruritus, cutaneous flushing, urticaria
- Developing: throat fullness, anxiety, chest tightness, shortness of breath, lightheadedness
- Severe: hoarseness/"lump in throat" (laryngeal edema), respiratory distress, hypotension, decreased consciousness
- Associated symptoms: abdominal pain, nausea, vomiting, diarrhea, bronchospasm, rhinorrhea, conjunctivitis
Diagnostic Criteria (Clinical)
Anaphylaxis is highly likely when any one of the following three criteria is met:
- Acute-onset skin/mucosal involvement (urticaria, itching, flushing, or edema) plus either respiratory compromise or reduced blood pressure/end-organ dysfunction
- Two or more of the following after exposure to a likely allergen: skin/mucosal involvement, respiratory compromise, reduced BP or shock symptoms, or persistent GI symptoms
- Reduced BP after exposure to a known allergen for that patient
— Tintinalli's Emergency Medicine, p. 111
Risk Factors
For having anaphylaxis:
- Pregnant women, infants, teenagers, elderly
- Parenteral > oral route of allergen exposure
- History of atopy, mastocytosis
- Emotional stress, acute infection, physical exertion
- Summer/fall seasonality
For increased severity and mortality:
- Cardiovascular or pulmonary disease (especially poorly controlled asthma)
- Beta-blockers and ACE inhibitors (impair compensatory response)
- Previous anaphylaxis episode
- Upright posture at onset
- Delayed epinephrine administration
— Rosen's Emergency Medicine, p. 2386
Treatment
First-Line (Immediate)
Epinephrine (adrenaline) — the cornerstone of treatment
- IM injection into the anterolateral thigh: 0.3–0.5 mg (0.3–0.5 mL of 1:1000) in adults; 0.01 mg/kg in children (max 0.5 mg)
- Repeat every 5–15 minutes as needed
- IV epinephrine infusion for shock refractory to IM dosing
- Delays in giving epinephrine worsen outcomes — administer immediately
Positioning:
- Supine (or Trendelenburg) with legs elevated if hypotensive
- Semi-recumbent if respiratory distress
- Avoid upright posture
Airway:
- Supplemental oxygen; early intubation for laryngeal edema (can be very difficult)
IV Fluids:
- 1–2 L isotonic crystalloid bolus (10–20 mL/kg in children) for distributive shock
Second-Line Agents
| Agent | Use |
|---|---|
| Corticosteroids (methylprednisolone 80–125 mg IV; hydrocortisone 250–500 mg IV) | Prevent protracted and biphasic reactions |
| H1 antihistamines (diphenhydramine 25–50 mg IV/IM) | Adjunct — symptom relief |
| H2 antihistamines (ranitidine) | Severe cases with circulatory shock |
| Inhaled β₂ agonists (albuterol) | Bronchospasm/wheezing |
| Vasopressors (dopamine, norepinephrine, vasopressin) | Shock refractory to epinephrine |
| Glucagon | Anaphylaxis in patients on beta-blockers (overcomes epinephrine resistance) |
| IV magnesium sulfate | Severe bronchospasm refractory to albuterol |
— Tintinalli's Emergency Medicine, pp. 111–113
Biphasic Anaphylaxis
A second wave of anaphylaxis can occur hours after the initial reaction without re-exposure to the trigger. Severe initial reactions and need for repeated epinephrine doses are risk factors. All patients should be observed after treatment. — Miller's Anesthesia, p. 1278
Epidemiology
- Lifetime individual risk: 1%–3%
- Incidence: ~50–2,000 episodes per 100,000 person-years
- Fatality: 0.7%–2% per case
- Fatal anaphylaxis represents <1% of all cases, but medication-induced fatalities are increasing
— Washington Manual of Medical Therapeutics; Rosen's Emergency Medicine
Key takeaway: Epinephrine is the only life-saving drug in anaphylaxis — antihistamines and corticosteroids are adjuncts. Early IM epinephrine is the single most important intervention.
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