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KembaraXtra-Medicine – Anaphylaxis
Anaphylaxis is a severe, rapid-onset, life-threatening allergic reaction. It occurs when IgE-mediated and non–IgE-mediated systemic mast cell degranulation leads to release of inflammatory mediators, producing respiratory, cardiovascular, gastrointestinal, and/or mucocutaneous symptoms. A common synonym is anaphylactic reaction. Relevant ICD-10CM codes include T78.2 (anaphylactic shock, unspecified, initial encounter), T78.00XA (anaphylactic reaction due to unspecified food, initial encounter), T80.52XA (anaphylactic reaction due to vaccination, initial encounter), and T63.94XA (toxic effect of contact with unspecified venomous animal, undetermined, initial encounter).
In the United States, the incidence is estimated at 50 to 2000 episodes per 100,000 persons, with a lifetime prevalence of 1.6% to 5.1%. Emergency department visits for anaphylaxis increased by 101% from 2005 to 2014, yet fatalities have remained stable at about 0.7 per million adults per year. In adults, medications and insect stings are leading triggers, while in children and adolescents, foods and insect stings are the leading triggers.
Risk factors depend on the trigger and severity. Atopy increases risk for anaphylaxis triggered by food, exercise, and latex. Risk factors for severe anaphylaxis include cardiovascular disease, asthma, older age, mast cell disorder, beta-blocker use, and ACE inhibitor use.
Clinical presentation commonly includes involvement across multiple systems. Mucocutaneous findings include urticaria, pruritus, flushing, and angioedema. Respiratory symptoms include dyspnea, cough, wheezing, hypoxia, stridor, and rhinitis. Cardiovascular features include hypotension, tachycardia, weakness, dizziness, syncope, malaise, and vascular collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, dysphagia, and abdominal pain.
Anaphylaxis results from a sudden systemic release of histamine and other mediators from basophils and mast cells via IgE-dependent and non–IgE-dependent mechanisms, and almost any substance can trigger it. In acute settings, the cause is often not identified, accounting for 30% to 60% of cases. Common triggers include foods and additives (notably peanuts, tree nuts, eggs, shellfish, fish, cow’s milk, fruits, soy). A notable food-related mechanism is alpha-gal syndrome, where a lone star tick bite can cause IgE sensitization to alpha-1,3-galactose, leading to delayed anaphylaxis after eating mammalian (red meat) products. Medication triggers include antibiotics (especially penicillins and sulfa agents), insulin, allergen extracts, opiates, vaccines, NSAIDs, contrast media, streptokinase, immunomodulators, and IV iron. Environmental exposures include bee/wasp stings, snake venom, and fire ant venom. Other triggers include blood products (plasma, immunoglobulin, cryoprecipitate, whole blood), latex, and exercise. Mechanistically, immune (often IgE-mediated) triggers include foods, venoms, many medications, latex, seminal fluid, and sometimes radiocontrast; IgE-independent immune triggers include radiocontrast (in most cases), dextrans, some monoclonal antibodies (e.g., rituximab), and some medications; and nonimmunologic triggers include certain drugs such as opioids and protamine. “Idiopathic” anaphylaxis refers to cases where known causes (including mastocytosis) have been excluded. Non–IgE mechanisms may involve complement activation, kinin production, potentiation, or direct mediator release, and more than one mechanism can occur together (for example, exercise-induced reactions following food). ACE inhibitors are a notable cause of unexplained angioedema, occurring in up to 1 in 200 users and may occur at any time after starting the medication.
The differential diagnosis is broad and includes allergic reactions without anaphylaxis, other causes of shock such as sepsis or pulmonary embolism, endocrine conditions such as carcinoid, adrenal crisis, paradoxical pheochromocytoma, systemic mastocytosis, serum sickness, severe asthma (distinguished by abrupt onset in anaphylaxis versus progressive worsening), scombroid poisoning, localized angioedema, acute urticaria, vasovagal/presyncopal syndromes, airway foreign body, vocal cord dysfunction, and anxiety-related symptoms such as globus hystericus.
Workup is mainly aimed at excluding mimics, but treatment should never be delayed because anaphylaxis can be rapidly fatal. Diagnosis is primarily clinical. Laboratory testing is generally not helpful in the emergency setting, though serum/urine histamine and serum tryptase (drawn 30 minutes to 2 hours after symptom onset and compared with baseline) may support the diagnosis; importantly, normal levels do not exclude anaphylaxis and these tests may not be readily available. Imaging is usually not helpful; chest radiography is considered when evaluating foreign body aspiration or pulmonary pathology in acute respiratory compromise. An ECG should be considered in patients with sudden loss of consciousness, chest pain, dyspnea, and in elderly patients; ECG typically shows sinus tachycardia.
Clinical criteria make anaphylaxis highly likely when any one of the following is met: (1) an acute illness with skin/mucosal involvement plus either respiratory compromise or reduced blood pressure/end-organ dysfunction symptoms; (2) rapid onset of two or more after exposure to a likely allergen--skin/mucosal involvement, respiratory compromise, reduced blood pressure, or persistent GI symptoms such as crampy abdominal pain/vomiting; or (3) reduced blood pressure after exposure to a known allergen--age-specific hypotension or >30% systolic BP decrease in infants/children, or systolic BP <90 mm hg or>30% decrease from baseline in adults.
Immediate nonpharmacologic treatment begins with removing the trigger, rapidly establishing and protecting the airway, providing supplemental oxygen if needed, obtaining IV access, giving IV fluids (normal saline), and placing the patient on cardiac monitoring.
The cornerstone medication is intramuscular epinephrine. Adults and children >30 kg should receive 0.3 to 0.5 mg IM epinephrine (1:1000 concentration) in the anterolateral thigh; anyone >50 kg should receive 0.5 mg IM. Children <30 kg should receive 0.01 mg />g IM epinephrine (1:1000 concentration). IM administration is preferred because it produces a faster and more reliable rise to effective plasma levels, and the dose can be repeated within minutes if symptoms do not improve. Adjunct therapies include H1 and H2 antihistamines such as diphenhydramine and famotidine to improve itching and erythema, but they do not reverse airway obstruction, respiratory compromise, or hypotension, and their onset is delayed 1–2 hours. Corticosteroids do not help acutely because of slow onset and have not been shown to prevent prolonged or biphasic anaphylaxis, but they are commonly used as secondary treatment. Aerosolized beta-agonists help treat bronchospasm. If hypotension or cardiovascular collapse persists despite fluids and IM epinephrine, IV epinephrine (1:10,000 concentration) is used as vasopressor therapy, and small IV boluses may be used in the peri-arrest state. Patients on beta-blockers may respond poorly to initial treatment; in these cases, IV glucagon should be considered.
Disposition depends on severity and risk of recurrence. Patients with mild episodes should be observed for 1 hour after symptom resolution. Patients with severe symptoms—including cyanosis, pulse oximetry <92%, systolic bp <90 mm hg, confusion, loss of consciousness, or incontinence—those needing more than one epinephrine dose, those with a wide pulse pressure, unknown trigger, cutaneous signs />ymptoms, or a medication trigger in children should be observed for at least 6 hours to watch for biphasic anaphylaxis.
For discharge planning and chronic management, patients who are stable and remain asymptomatic should be prescribed two epinephrine autoinjectors, with clear instructions on when and how to use them. Referral to an allergist is helpful when the trigger is unclear in the emergency setting. Patient education is essential: a prior history of anaphylaxis or known triggers is the most reliable way to identify risk. Patients should be instructed to carry an epinephrine device at all times; school-aged children should have an additional autoinjector available at school with appropriate staff. Patients should also be advised to wear or carry MedicAlert identification listing substances that have triggered anaphylaxis. People with prior contrast reactions should avoid radiologic contrast when possible; however, pretreatment regimens with methylprednisolone or diphenhydramine may be used when contrast is unavoidable. For insect-sting anaphylaxis, venom immunotherapy initiated after the event is effective and is recommended for up to 5 years after the incident.
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