Anaphylaxis is a sudden-onset, life-threatening event characterized by bronchial contractions in conjunction with hemodynamic changes. Its clinical presentation may include respiratory, cardiovascular, cutaneous, or gastrointestinal manifestations.
The term anaphylaxis describes ‘a serious allergic reaction that is rapid in onset and may cause death. It arises as an acute, generalized IgE-mediated immune reaction involving specific antigen, mast cells and basophils. The reaction requires priming by the allergen, followed by re-exposure. To provoke anaphylaxis, the allergen must be systemically absorbed, either after ingestion or parenteral injection and a range of allergens have been identified:
* foods: nuts (peanuts (protein-arachis hypogaea Ara h 1-3), Brazil, cashew), shellfish (shrimp (allergen Met e 1), lobster), dairy products, egg (and more rarely citrus fruits, mango, strawberry, tomato)
* venoms: wasps, bees, yellow-jackets, hornets
* medications: antisera (tetanus, diphtheria), dextran, latex, some antibiotics.
Anaphylaxis is rare, and the symptom/sign constellation ranges from widespread urticaria to cardiovascular collapse, laryngeal oedema, airway obstruction and respiratory arrest leading to death. Fatal reactions to penicillin occur once every 7.5 million injections; between 1 in 250 and 1 in 125 individuals have severe reactions to bee and wasp stings, and a death takes place every 6.5 million stings; such stings cause between 60 and 80 deaths per year in North America, and 5-10 in the UK. Central to the pathogenesis of anaphylaxis is the activation of mast cells and basophils, with systemic release of some mediators and generation of others. The initial symptoms may appear innocuous: tingling, warmth and itchiness. The ensuing effects on the vasculature give vasodilatation and oedema. The consequence of these may be no more than a generalized flush, with urticaria and angio-oedema. More serious sequelae are hypotension, bronchospasm, laryngeal oedema and cardiac arrhythmia or infarction. Death may occur within minutes. Serum plateletactivating factor (PAF) levels correlate directly with the severity of anaphylaxis whereas PAF acetylhydrolase (the enzyme that inactivates PAF) correlated inversely and was significantly lower in peanut sensitive patients with fatal anaphylactic reactions. Early recognition and treatment are essential.
The best treatment is prevention. Avoidance of triggering foods, particularly nuts and shellfish, may require almost obsessive self-discipline. Patient education is necessary and many are instructed in the self-administration of adrenaline (epinephrine) and carry pre-loaded syringes. Desensitization has a well established place in the management of this disorder, particularly if exposure is unavoidable or unpredictable, as in insect stings.
Anaphylactoid reaction is closely related to anaphylaxis. It is caused by release of mast cells and basophil mediatros triggered by non-IgE-mediated events.
EPIDEMIOLOGY & DEMOGRAPHICS
INCIDENCE: 20,000 to 50,000 persons/yr in the U.S. Anaphylaxis rates are 0.0004% for food, 0.7% to 10% for penicillin, 0.22% to 1% for radiocontrast media, and 0.5% to 5% after insect stings. It is estimated that 1 in every 3000 inpatients in U.S. hospitals develops an anaphylactic reaction.
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Urticaria, pruritus, skin flushing, angioedema, weakness, dizziness
• Dyspnea, cough, malaise, difficulty swallowing
• Wheezing, tachycardia, diarrhea
• Hypotension, vascular collapse
Virtually any substance may induce anaphylaxis in a given individual.
• Commonly implicated medications are antibiotics, insulin, allergen extracts, opiates, vaccines, NSAIDs, contrast media, streptokinase
• Foods and food additives, nuts, egg whites, shellfish, fish, milk, fruits, and berries
• Blood products, plasma, immunoglobulin, cryoprecipitate, whole blood
• Venoms such as snake venom, fire ant venom, bee sting (Hymenoptera stings)
• Endocrine disorders (carcinoid, pheochromocytoma)
• Globus hystericus, anxiety disorder
• Systemic mastocytosis
• Pulmonary embolism, serum sickness, vasovagal reactions
• Severe asthma (the key clinical difference is the abrupt onset of symptoms in anaphylaxis without a history of progressive worsening of symptoms)
Workup is aimed mainly at eliminating other conditions that may mimic anaphylaxis (e.g., vasovagal syncope may be differentiated by the presence of bradycardia as opposed to the tachycardia seen in anaphylaxis; the absence of hypoxemia in ABG analysis may be useful to exclude pulmonary embolism or foreign body aspiration).
• Laboratory evaluation is generally not helpful, because the diagnosis of anaphylaxis is a clinical one.
• ABG analysis may be useful to exclude pulmonary embolism, status asthmaticus, and foreign body aspiration.
• Elevated serum and urine histamine levels can be useful for diagnosis of anaphylaxis, but these tests are not commonly available.
Generally not helpful.
• Chest x-ray is indicated in patients presenting with acute respiratory compromise.
• Radiologic evaluation for epiglottitis is useful in patients with acute respiratory compromise.
• ECG should be considered in all patients with sudden loss of consciousness or complaints of chest pains or dyspnea and in any elderly patient.
• IV access should be rapidly established, and intravenous fluids (i.e., saline) should be administered.
• Supplemental oxygen and cardiac monitoring are also recommended.
ACUTE GENERAL Rx
• Epinephrine should be rapidly administered as an SC or IM injection at a dose of 0.01 ml/kg of aqueous epinephrine 1:1000 (maximum adult dose 0.3 to 0.5 ml). The dose may be repeated approximately q5-10 min if there is persistence or recurrence of symptoms. Endotracheal epinephrine should be considered if IV access is not possible during life-threatening reactions.
• Administration of H1 - and H2 -receptor antagonists is also recommended in the initial treatment of anaphylaxis.
1. Administer diphenhydramine 50 to 75 mg IV or IM.
2. Cimetidine 300 mg IV over 3 to 5 min, or ranitidine 50 mg IV, should be given initially; subsequent doses of H1 - and H2 -blockers can be given orally q6h for 48 hr.
• Corticosteroids are not useful in the acute episode because of their slow onset of action; however, they should be administered in most cases to prevent prolonged or recurrent anaphylaxis. Commonly used agents are hydrocortisone sodium succinate 250 to 500 mg IV q4-6h in adults (4 to 8 mg/kg for children) or methylprednisolone 60 to 125 mg IV in adults (1 to 2 mg/kg in children).
• Aerosolized b-agonists (i.e., albuterol, 2.5 mg, repeat prn 20 min) are useful to control bronchospasm.
• Additional useful agents in specific circumstances: atropine for refractory bradycardia, dopamine for refractory hypotension (despite volume expansion), and glucagon in patients on b-blocking drugs.
PEARLS & CONSIDERATIONS
• Patient education regarding the nature of the illness and preventive measures is recommended. A documented history of previous anaphylactic episodes or known anaphylaxis triggers is the most reliable method of identifying individuals at risk.
• Prescription for prefilled epinephrine syringe (EpiPen) should be given, and the patient should be instructed on the use of this emergency epinephrine kit in case of recurrent anaphylactic episodes.
• Patients should also be advised to carry or wear Medic Alert ID describing substances that have caused anaphylaxis.
• Avoidance of radiologic contrast is also recommended.
• Venom immunotherapy immediately after a sting is effective and recommended for up to 5 years after the anaphylactic incident.