The paper is devoted to the analysis of anaphylaxis – a life-threatening allergic reaction characterized by several symptoms, such as swelling or nausea, and physical manifestations including bronchospasms, vasodilation, and hypotension. The main chemical mediators of an anaphylactic reaction are IgE, histamine, and tryptase, and the presence of these chemical agents in blood serves as the major indicators of anaphylaxis. It is important to commence treatment of symptoms without delay because severe health problems, i.e. cardiovascular collapse or respiratory failure, may develop within minutes.
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Anaphylaxis is an acute allergic life-threatening systematic reaction of hypersensitivity. It occurs as a result of immune processes mediated by immunoglobulin E (IgE) which provokes a release of histamine, heparin, tryptase, chymase, etc. from activated mast cells and basophils (Mustafa & Kaliner, 2016). Activation of histamine through H1-H4 receptors leads to vasoconstriction and heart failure (H1-receptors), tachycardia (H2-receptors), chemotaxis, and release of multiple inflammatory mediators (H4-receptors) (Galli & Tsai, 2012).
Heparin contributes to the activation of bradykinin, fibrinolysis, and complement system processes while platelet-activating factor reduces coronary flow and myocardial contractility, increases activation of neutrophils, and eosinophils cause local and systemic platelet aggregation, as well as peripheral vasodilation and hypotension (Galli & Tsai, 2012). Physiological changes induced by anaphylactic reaction provoke compensatory mechanisms including renin-angiotensin-aldosterone system, increased norepinephrine secretion from the local sympathetic nerve endings, and it can cause heart arrhythmias and other conditions of the cardiovascular system (Galli & Tsai, 2012).
The explicit symptoms of acute anaphylaxis are swelling and redness on the part of the body exposed to Hymenoptera venom (due to a bee sting), a sharp decrease in blood pressure, larynx swelling, and bronchial spasms which result in severe respiratory distress (Stritzke & Eng, 2013). The patient with an anaphylactic reaction looks pale and may lose consciousness (Takase & Kosut, 2013). Other symptoms include abdomen pain, nausea, vomiting, or diarrhea.
The diagnostics should start with the assessment of the overall patient’s condition, evaluation of symptoms, and anamnesis. The key factors defining the diagnosis of anaphylaxis are sudden onset of symptoms, multisystem symptoms, and their rapid progression (Barnett, Kort, & Campasano, 2003).
Due to the involvement of different organs and systems in the pathological process, no laboratory parameter would provide complete accuracy and sensitivity in the identification of anaphylaxis. However, within the first hours of anaphylactic reaction’s progression, the levels of histamine and tryptase in the patient’s blood increase. Tryptase level reaches its peak in 60-90 minutes after the onset of anaphylactic symptoms, and it remains elevated for up to 3 hours while a high concentration of histamine is observed within one hour (Barnett et al., 2003).
Increased serum level of tryptase often confirms the clinical diagnosis of anaphylaxis due to insect sting or injection of drugs in patients with suddenly developed hypotension. When the symptoms are reduced, it is recommended to conduct a test aimed to identify the presence of IgE in blood. The data accumulated through the test is used to find potentially dangerous allergen which is perceived by the immune system as an alien substance and which causes the allergic reaction.
The major method of treatment for anaphylaxis is epinephrine injection. However, for children, it is suggested to administer antihistamines first because they frequently demonstrate dermal symptoms (Takase & Kosut, 2013). The intramuscular injection of epinephrine should comprise a max of 0.5 mg per dose (Takase & Kosut, 2013). It is also suggested to dose the drug by 0.5 ml of 1:1000 IM – two doses per 15 minutes (and every 4 hours if required) (Takase & Kosut, 2013). While epinephrine administration may be regarded as the major method of acute symptoms’ treatment, antihistamines primarily serve as an additional treatment.
At the beginning of the reaction’s development, it can be difficult to predict the ultimate severity of the condition, and death can occur within minutes. Each clinical scenario is of individual character – every similar episode of anaphylaxis may vary in different patients. Therefore, treatment should be administered immediately, without any delay.
Barnett, B., Kort, D., & Campasano, V. J. (2003). The approach to the patient with anaphylaxis. Primary Care Update For OB/GYNS,10(5), 205. Web.
Galli, S. J., & Tsai, M. (2012). IgE and mast cells in allergic disease. Nature Medicine, 18(5), 693-704. Web.
Mustafa, S., & Kaliner, M. (2016). Anaphylaxis. Web.
Stritzke, A. I., & Eng, P. A. (2013). Age-dependent sting recurrence and outcome in immunotherapy-treated children with anaphylaxis to Hymenoptera venom. Clinical & Experimental Allergy, 43(8), 950-955. Web.
Takase, B., & Kosut, J. (2013). Chapter V.2. Anaphylaxis and other acute allergic reactions. Web.