Anaphylaxis - briefly describe
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Anaphylaxis
Definition
Anaphylaxis is a serious, life-threatening systemic hypersensitivity reaction with rapid onset, capable of causing death if not treated promptly. It represents the most severe form of immediate hypersensitivity. The older terms "anaphylactic" (IgE-mediated) and "anaphylactoid" (non-IgE-mediated) are no longer used separately - both are now simply called anaphylaxis, since the final pathway is identical.
- Tintinalli's Emergency Medicine, p. 3673; Rosen's Emergency Medicine, p. 2386
Epidemiology
- Lifetime risk: 1-5% (up to 5% in the US)
- Prevalence appears to be increasing, with food-related fatalities rising in Australia and drug-related fatalities in North America
- Fatal anaphylaxis is rare: <1% of cases
- Incidence: ~50-2,000 episodes per 100,000 person-years
- Frequently underdiagnosed
Pathophysiology
The core mechanism is mast cell and basophil activation, primarily via crosslinking of IgE antibodies and aggregation of high-affinity IgE receptors (FcεRI). This triggers degranulation and release of:
| Mediator | Effect |
|---|---|
| Histamine | Vasodilation, increased vascular permeability, increased heart rate, bronchospasm |
| Prostaglandin D2 | Bronchoconstriction, pulmonary/coronary vasoconstriction, peripheral vasodilation |
| Leukotrienes | Bronchoconstriction, increased vascular permeability, airway remodeling |
| Platelet-activating factor (PAF) | Potent bronchoconstriction, increased vascular permeability |
| TNF-α | Neutrophil activation, chemokine synthesis |
| Tryptase, carboxypeptidase A | Released from secretory granules |
The net result is widespread vasodilation, increased capillary leak, and bronchoconstriction - leading to circulatory collapse and/or asphyxia.
Non-IgE mechanisms (direct mast cell activation) can also trigger anaphylaxis - e.g., radiocontrast media, NSAIDs, opioids, exercise, cold.
- Tintinalli's Emergency Medicine, p. 3684-3686
Common Triggers
| Category | Examples |
|---|---|
| Foods (most common) | Peanuts, tree nuts, shellfish, fish, soy, cow's milk, eggs |
| Medications | Antibiotics (penicillin), NSAIDs, chemotherapy, monoclonal antibodies |
| Insect stings | Hymenoptera (bee, wasp), fire ants |
| Latex | Natural rubber latex |
| Physical factors | Exercise, cold, heat, sunlight |
| Idiopathic | No identifiable cause (up to 60% of adults) |
Food reactions typically begin within 5-30 minutes; a notable exception is alpha-gal syndrome (mammalian meat allergy after tick bite), which is delayed 3-6 hours.
Clinical Features
The classic presentation progresses as:
- Cutaneous (most common, ~90%): Pruritus, flushing, urticaria, angioedema
- Respiratory: Throat fullness, hoarseness, stridor, bronchospasm, dyspnea
- Cardiovascular: Hypotension, tachycardia, syncope, cardiac arrest
- GI: Nausea, vomiting, abdominal pain, diarrhea
- Neurologic: Anxiety, altered consciousness
The more rapid the reaction onset after exposure, the more likely it is to be severe and fatal.
Biphasic anaphylaxis: A second wave of symptoms occurring 1-72 hours after the initial reaction (even without re-exposure). Risk factors include severe initial reaction and repeated epinephrine dosing.
Diagnosis
Anaphylaxis is a clinical diagnosis based on the following criteria (any ONE of three):
- Acute onset of skin/mucosal symptoms + respiratory compromise or hypotension
- Two or more of the following after allergen exposure: skin/mucosal symptoms, respiratory compromise, hypotension, or persistent GI symptoms
- Hypotension after exposure to a known allergen
Differential includes: vasovagal syncope, panic attack, acute asthma, hereditary angioedema, carcinoid syndrome, MCAS.
Serum tryptase peaks 1-2 hours post-onset and can support the diagnosis retrospectively; a normal tryptase does not rule out anaphylaxis (especially food-triggered).
Treatment
First-line: Epinephrine (ALWAYS)
- IM injection into the anterolateral thigh: 0.3-0.5 mg (1:1,000 solution) in adults; 0.01 mg/kg in children (max 0.5 mg)
- May repeat every 5-15 minutes
- Auto-injector (e.g., EpiPen): 0.3 mg adult, 0.15 mg child
- Delayed epinephrine is associated with increased fatality
Adjuncts (NOT substitutes for epinephrine):
| Drug | Role |
|---|---|
| IV fluids | Rapid bolus for hypotension (fluid shifts out of vasculature) |
| H1 antihistamine (diphenhydramine) | Relieve urticaria/pruritus; do not treat shock |
| H2 antihistamine (ranitidine/famotidine) | Adjunct for cutaneous symptoms |
| Corticosteroids | May reduce biphasic reactions (evidence modest) |
| Bronchodilators (salbutamol) | Treat bronchospasm as adjunct |
| Glucagon | For patients on beta-blockers (bypasses beta-receptor blockade) |
Positioning: Supine with legs elevated (upright posture at onset is a risk factor for mortality).
Airway: Early intubation if upper airway edema is progressing.
Observation: All patients should be monitored for 4-6 hours minimum; those with severe reactions or risk factors for biphasic reactions should be observed for 24 hours.
Risk Factors for Severity/Mortality
- Extremes of age (very young, elderly)
- Comorbid asthma, cardiovascular disease
- Concurrent beta-blockers or ACE inhibitors (worsen severity, resist treatment)
- Delayed epinephrine administration
- Absence of skin findings at presentation
- Peanut/tree nut allergy
- History of mastocytosis
Secondary Prevention
- Prescription of two epinephrine auto-injectors at discharge
- Allergy/immunology referral for trigger identification
- Medic-alert bracelet
- Patient education on trigger avoidance and self-injection technique
- Consider venom immunotherapy for insect-sting anaphylaxis (can reduce recurrence risk to <5%)
Sources: Rosen's Emergency Medicine 9e, Ch. 106; Tintinalli's Emergency Medicine 9e, Ch. 14; The Washington Manual of Medical Therapeutics
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