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What causes anaphylactic shock in children?
Last reviewed: 04.07.2025
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The antigen can enter the body in any way:
- parenterally when administering medications - most often penicillin (1 case per 6 million penicillin administrations), vitamin B6, polypeptide hormones (ACTH, parathyroid hormone, insulin), novocaine, lysozyme, etc.; anti-tetanus and other serums; preventive vaccinations;
- orally - food allergens (especially nuts, oysters, crabs), preservatives added to food products (methyl bisulfate, glutamate, aspartate, etc.), spices, poor quality artificial fats, etc.;
- inhalation;
- locally - insect and snake bites.
Repeated intermittent courses of treatment and long intervals between drug administrations increase the risk of developing anaphylaxis.
The possibility of anaphylactic shock cannot be ruled out when conducting food provocation tests after elimination of the product; skin scarification tests with exogenous allergens; when conducting specific hyposensitization, especially if it is carried out under conditions of increased exposure to allergens in natural conditions.
Latex anaphylaxis (sensitization to residual proteins of the rubber tree) may occur in a child when catheters are used to treat severe genitourinary diseases.
An anaphylactoid reaction may occur after sudden cooling, intense physical exertion, exposure to iodine-containing radiographic contrast agents (in 0.1% of patients), dextran, vancomycin, vitamin B6, D-tubocurarine, captopril, acetylsalicylic acid. In recent years, there has been an increase in the number of cases of idiopathic anaphylaxis.
Pathogenesis of anaphylactic shock
The consequence of an immediate-type allergic reaction with a massive release of biologically active substances (not only histamine, but also synthesized prostaglandins and leukotrienes) is a pathophysiological reaction of microcirculation disorders, a drop in systemic arterial pressure, blood deposition in the portal system, bronchospasm, and the development of laryngeal, pulmonary, and cerebral edema. As with any type of shock, disseminated intravascular coagulation naturally develops.
Pseudoallergic anaphylaxis develops without the participation of reagins due to the activation of basophils and mast cells by anaphylotoxins C3a and C5a (the classical pathway of complement activation), which also leads to the release of allergy mediators and clinical manifestations of acute vascular collapse.