check tryptase for anaphylaxis
- related: ICU intensive care unit
- tags: #literature #icu
This patient presents with signs and symptoms concerning for anaphylaxis, with potential triggers including recent food and exercise exposure. Diagnostic evaluation is often performed to confirm a diagnosis of severe anaphylaxis, as a single life-threatening episode can result in significant long-term ramifications and lifestyle modifications. Tryptase levels peak at 60 to 90 min after an anaphylaxis event and remain elevated for at least 5 h, making it the preferred laboratory test in this setting.
Anaphylaxis is a common problem encountered by emergency and acute care providers, with an estimated prevalence between 1.6% and 5.1% in the United States. Although the presence of antigen-specific IgE antibodies is considered the key risk factor for the development of anaphylaxis following subsequent antigen exposure, immunologic mechanisms involve a wide variety of effector cells and complement-, leukotriene-, and prostaglandin-mediated inflammatory pathways in addition to mast cells and histamine. Prodromal symptoms include headache, dyspnea, flushing, pruritus, cough, abdominal pain, and rhinorrhea. The diagnosis of anaphylaxis requires an acute-onset illness (minutes to hours) that involves the skin (hives, urticaria, flushing, angioedema) or mucous membranes (lips, tongue, uvula) in combination with respiratory compromise (bronchospasm), hypotension, or evidence of end-organ dysfunction after exposure to a likely trigger.
Although these criteria are quite straightforward, the legion of potential allergic triggers and highly variable clinical presentation can make the diagnosis and subsequent management of anaphylaxis quite challenging. Common triggers include certain foods, drugs, insect stings, and physical factors (exercise, cold, or heat), but a substantial number of anaphylaxis cases remain idiopathic (without an identifiable trigger). The differential diagnosis includes other causes of shock and acute cardiopulmonary complaints, hereditary angioedema with rash, flushing syndromes (carcinoid, tumors secreting vasoactive intestinal polypeptide, mastocytosis, mast cell activating syndrome, and medullary thyroid cancer), restaurant syndromes, and nonorganic disease (panic attacks, vocal cord dysfunction syndrome).
Management recommendations include early administration of IM epinephrine (0.01 mg/kg, generally provided through a 0.3-mg commercially available autoinjector). Supplemental oxygen, β-agonists, and close monitoring are recommended for patients with respiratory distress and airway symptoms. Judicious crystalloid resuscitation should be considered in patients with hypotension that is not immediately responsive to epinephrine administration. IV epinephrine may be considered in patients who fail to respond to multiple injections of IM epinephrine and fluid resuscitation. Histamine receptor (H1 and H2) antagonists and corticosteroids are often administered as adjunctive therapy in more severe cases to reduce the risk of a late-onset, biphasic reaction that can often be seen 4 to 8 h after symptom onset. The duration of patient observation after treatment should take into account the severity and duration of the anaphylaxis episode, response to treatment, pattern of previous anaphylactic reactions, medical comorbidities, patient reliability, and access to subsequent medical care. Longer observation is suggested for more severe presentations, a potential allergen ingestion, or when pharyngeal edema is present.
Although serum histamine is a more sensitive marker of anaphylaxis than tryptase, it only remains elevated for 30 to 60 min after symptom onset and therefore has usually returned to normal by the time patients present to medical attention. Twenty-four-hour urinary histamine metabolites and prostaglandin D2 levels can also be helpful. Angioedema is self-limited, localized subcutaneous or submucosal swelling that can occur in isolation, with urticaria, or in association with anaphylaxis. Initial evaluation includes a complement protein C4 level. Low levels should prompt further evaluation for hereditary or acquired C1 inhibitor deficiency, including a C1 inhibitor antigen and functional levels. Serum IgE levels may be helpful to identify patients with severe, poorly controlled asthma who may benefit from the addition of targeted biologic therapy, but the absence of prior persistent asthma symptoms makes this test less likely to be beneficial in this setting.12345678
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Footnotes
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Giannetti MP. Exercise-induced anaphylaxis: literature review and recent updates. Curr Allergy Asthma Rep. 2018;18(12):72. PubMed ↩
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Lieberman P, Nicklas RA, Randolph C, et al. Anaphylaxis—a practice parameter update 2015. Ann Allergy Asthma Immunol. 2015;115(5):341-384. PubMed ↩
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Muraro A, Roberts G, Worm M, et al; EAACI Food Allergy and Anaphylaxis Guidelines Group. Anaphylaxis: guidelines from the European Academy of Allergy and Clinical Immunology. Allergy. 2014;69(8):1026-1045. PubMed ↩
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Reber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol. 2017;140(2):335-348. PubMed ↩
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Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. J Allergy Clin Immunol. 2006;117(2):391-397. PubMed ↩
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Simons FE, Ardusso LR, Dimov V, et al; World Allergy Organization. World Allergy Organization anaphylaxis guidelines: 2013 update of the evidence base. Int Arch Allergy Immunol. 2013;162(3):193-204. PubMed ↩
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Wood RA, Camargo CA Jr, Lieberman P, et al. Anaphylaxis in America: the prevalence and characteristics of anaphylaxis in the United States. J Allergy Clin Immunol. 2014;133(2):461-467. PubMed ↩