I: Anaphylactic or immediate hypersensitivity
IgE-mediated mast cell degranulation and activation
Anaphylaxis, allergic rhinitis, allergic asthma, acute urticaria, insect sting allergy
II: Antibody-mediated cytolytic reactions
IgM or IgG against antigens bound to cell membrane structures
Autoimmune or drug-induced hemolytic anemia, Goodpasture's disease, Rh hemolytic disease
III: Immune- complex mediated
Complexes of IgM or IgG and circulating antigens
Serum sickness, SLE, vasculitis, poststreptococcal glomerulonephritis
IV: Delayed hypersensitivity
Tuberculin skin test reactions, GVHD, contact dermatitis
- Immediate hypersensitivity skin test (IHST): Stop antihistamines for 5 days before testing. Use the prick technique (introduce antigen intracutaneously via pricking or puncturing). Positive predictive value is good for inhalants, moderate for foods (high rate of false-positive results); negative predictive value is excellent for foods and inhalants.
- Serum tests: Serum eosinophilia is often present (low diagnostic value); serum IgE is often elevated with atopic dermatitis (low diagnostic value); serum allergen-specific IgE assays (eg, RAST) measure circulating Ag-specific IgE and have similar predictive value to skin testing.
- Definition: A serious allergic reaction that is rapid in onset and may cause death
- Differential Diagnosis:
- Vasovagal syncope, panic attack, hyperventilation, systemic mastocytosis, scombroid fish poisoning. Rare causes include carcinoid syndrome, pheochromocytoma, and idiosyncratic causes.
- Anaphylactoid reactions, which have complement activation, but are not IgE mediated.
- Example: Radiocontrast media, drugs (NSAIDS, opiate), blood products, exercise induced, and idiopathic. Clinical presentation and treatment are the same as for anaphylaxis.
- Major Trigger: Food (most commonly peanut, tree nuts, shellfish, fish, eggs, milk), insect venom, latex, drugs, immunotherapy
- Pathophysiology: Production of IgE in a susceptible individual (sensitization)→ IgE-sensitized mast cells and basophils→ exposure of allergen and then allergen binding leads to mast cell degranulation.
- Clinical Symptoms and PE
- Variable symptoms: Angioedema, shortness of breath, wheezing, flushing, urticaria, pruritus, hypotension, chest pain, syncope, abdominal pain, vomiting, diarrhea, aura of impending doom.
- Time pattern: Uniphasic, biphasic (recur up to 8 h later in 3%–20%), or protracted syndrome.
- Diagnostic Studies
- Markers of mast cell degranulation, including plasma histamine (only elevated for 1 h after the onset of symptoms), urinary histamine and metabolites (elevated for longer), or serum tryptase level (peaks is 90 minutes and stays elevated for as long as 5 h) may be useful when the diagnosis is uncertain. Undetectable levels do not rule out anaphylaxis (tryptase is positive <50%).
- In vitro allergen-specific IgE assays or IHST may be used later to confirm. IHST may not be reliably positive in sensitized individuals for up to 4 to 6 weeks after an episode of anaphylaxis. In sensitized individuals, the test should be repeated if results are negative.
- Monitor patients with mild reactions limited to flushing, urticaria, angioedema, and mild bronchospasm in the ED for a minimum of 6 to 8 hours. Consider longer observation of patients with mild symptoms who have received epinephrine because epinephrine may have minimized the symptoms.
- Provide ...
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