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A Treatment of Anaphylaxis
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At the first suspicion of anaphylaxis, airway, breathing, and circulation are assessed If systemic anaphylaxis is suspected, aqueous epinephrine 1:1000 in a dose of 02 05 mL (02 05 mg) is injected intramuscularly Repeated injections can be given every 5 15 minutes as necessary Between 40% and 70% of patients suffering from severe anaphylaxis will require more than one injection of epinephrine Injection in the anterolateral thigh may lead to more predictable and rapid absorption compared with subcutaneous administration Epinephrine can stabilize hemodynamics, cause bronchodilation, and prevent further mast cell degranulation Rapid intravenous infusion of large volumes of fluids (saline, lactated Ringer s injection, plasma, colloid solutions, or plasma expanders) is essential to replace loss of intravascular plasma into tissues in patients with hypotension caused by marked vasodilation Other vasopressor drugs (high-dose dopamine, norepinephrine, phenylephrine) may be necessary if the patient remains hypotensive Airway obstruction is caused by edema of the larynx and hypopharynx or by bronchospasm The former is treated by maintenance of an airway with endotracheal intubation or tracheostomy Inhalation of selective 2-
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adrenergic agonists, such as albuterol, and intravenous administration of aminophylline (05 mg/kg/h IV with 6 mg/kg loading dose over 30 minutes) are effective for bronchospasm Antihistamines (H1- and H2-receptor antagonists) such as diphenhydramine (25 50 mg orally, intramuscularly, or intravenously every 4 6 hours) and ranitidine (150 mg orally every 12 hours or 50 mg intramuscularly or intravenously every 6 8 hours) may be useful adjuvant therapies for alleviating the cutaneous manifestations of urticaria or angioedema and pruritus and for the gastrointestinal and uterine smooth muscle spasms Corticosteroids will not reverse respiratory obstruction or shock but may reduce prolonged reactions or relapses Long-term combined oral antihistamine and prednisone therapy reduces the number and severity of attacks in patients with frequent lifethreatening episodes of idiopathic anaphylaxis Medical therapy does not reliably prevent true IgE-mediated hypersensitivity reactions There may be a clinical biphasic or late-phase response in anaphylaxis, causing a recrudescence of symptoms hours (most commonly 6 12 hours) after exposure to the allergen The incidence of late phase reactions is estimated to be between 1% and 20% Since this may occur after subsidence of the immediate-phase response, all patients with anaphylaxis should be monitored for up to 24 hours, discharged with injectable epinephrine, and educated about the possible recurrence of symptoms Anaphylaxis in a patient being treated with -adrenergic blocker drugs is a special problem because of refractoriness to epinephrine and selective -adrenergic agonists Higher doses of adrenergic drugs are required for the desired effect; glucagon (05 1 mg intravenously, intramuscularly, or subcutaneously may be repeated 30 minutes later) in patients taking -blockers may be beneficial Patients being treated with angiotensin-converting enzyme inhibitors may suffer from more severe hypotension due to blockade of renin-angiotensin-dependent compensatory mechanisms
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B Treatment of Urticaria and Angioedema
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These disorders are discussed fully in 6 If urticaria or angioedema is found to be secondary to underlying inflammatory or infectious processes, treatment of the primary disorder can lead to remission of cutaneous symptoms
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Patients demonstrating immediate hypersensitivity reactions to stinging insects (honey bees, wasps, hornets, yellow jackets, and imported fire ants) with documented venomspecific IgE on allergy skin testing should receive venom immunotherapy for prevention of anaphylaxis A 5-year course of venom-specific immunotherapy is indicated for persons suffering from generalized urticaria, angioedema, bronchospasm, or hypotension after insect venom exposure Large isolated local reactions to insect stings are not a predisposing factor for systemic anaphylaxis Untreated individuals have a 50 60% risk of anaphylactic response to
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after starting the drug, presence of other systemic involvement, coexisting illness, and concurrent drug use In previously sensitized individuals, immediate hypersensitivity is manifested by rapid development of urticaria, angioedema, or anaphylaxis Delayed onset of urticaria accompanied by fever, arthralgias, and nephritis may indicate the development of an immune complex-mediated disorder Drug fever and Stevens-Johnson syndrome probably act by immune hypersensitivity mechanisms In genetically slow acetylators and in AIDS patients with depleted hepatic glutathione levels, drugs such as sulfamethoxazole are not rapidly excreted during drug metabolism This altered drug metabolism favors the generation of haptenated immunoreactive metabolites as well as drug reactions, such as delayed morbilliform eruptions Other types of immune-mediated dermatologic drug reactions include lupus-like syndromes caused by procainamide, isoniazid, phenytoin, or hydralazine Drugs that have been associated with the development of systemic or cutaneous vasculitis include leukotriene receptor antagonists, allopurinol, phenytoin, thiazides, nonsteroidal anti-inflammatory drugs, furosemide, cimetidine, gold, hydralazine, and many antibiotics (eg, penicillin, sulfonamides, quinolones, and tetracycline) Cutaneous vasculitides are usually associated with fixed lesions, with histologically-proven immune-complex involvement Food hypersensitivity is manifest by symptoms consistent with IgE-mediated immediate hypersensitivity/anaphylaxis but commonly is also accompanied by abdominal pain, nausea, vomiting, or diarrhea More rarely, atopic dermatitis may be the sole clinical expression of food allergy The onset of allergic food reactions is rapid, usually within minutes to a couple of hours of ingestion, and the reaction is usually quite reproducible Oral allergy syndrome is a self-limited form of fruit and vegetable hypersensitivity, where symptoms are confined to the oropharynx Due to cross-reactivity between certain fruit and vegetable allergens and certain seasonal pollens, ingestion of these foods causes a contact allergy with pruritus of lips, tongue, and palate typically without other symptoms or signs of systemic anaphylaxis The most common cross-reacting foods and pollens are apples and carrots, which cross-react with birch pollen; melons and bananas, which cross-react with ragweed pollen Many of these antigens involved in oral allergy syndrome are heat labile and denature during cooking Immunologic cross-reactivity appears to also underlie the association of latex allergy and hypersensitivity to avocado, banana, chestnut, kiwi, and papaya Unlike the oral allergy syndrome, however, systemic anaphylaxis upon ingestion of these foods may develop in 35 50% of patients who are allergic to latex (so called latex-fruit syndrome)
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subsequent stings Venom immunotherapy is highly protective, affording 98% protection from life-threatening reactions on rechallenge Rarely, anaphylaxis has been associated with other biting insects, including Triatoma and mosquito, but diagnostic reagents and therapeutic extracts are not consistently available for these other species
Dibbern DA Jr Urticaria: selected highlights and recent advances Med Clin North Am 2006 Jan;90(1):187 209 [PMID: 16310530] Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology The diagnosis and management of anaphylaxis: an updated practice parameter J Allergy Clin Immunol 2005 Mar;115(3 Suppl 2):S483 523 [PMID: 15753926] Moffitt JE et al Stinging insect hypersensitivity: A practice parameter update J Allergy Clin Immunol 2004 Oct;114(4): 869 86 [PMID: 15480329] Simons FE Anaphylaxis, killer allergy: long-term management in the community J Allergy Clin Immunol 2006 Feb;117(2): 367 77 [PMID: 16461138] Weiler CR et al Genetic test indications and interpretations in patients with hereditary angioedema Mayo Clin Proc 2006 Jul;81(7):958 72 [PMID: 16835976]
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