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CHAPTER 21 Allergic reactions
Debra G. Perina and Briana N. Tully
Introduction
Potential allergic reactions and their sequelae are common complaints encountered in the EMS system. Allergic reactions can be triggered by many agents, such as foods, medications, topical products, and limitless environmental exposures including arthropod stings. Severity can vary from local reactions and discomfort to life‐threatening systemic anaphylaxis. EMS physicians and other clinicians must be able to rapidly recognize the manifestations of allergic reactions and anaphylaxis and begin prehospital treatment that can be lifesaving.
Physiology of allergic reactions
Allergic reactions are hypersensitivity reactions resulting from the exposure to an allergen [1]. In milder forms they may result in localized edema and pruritus. Systemic reactions can also be mild, resulting in a more widespread rash that can be pruritic. In their most severe form, allergic reactions progress to anaphylaxis with multisystem and potentially life‐threatening manifestations that include respiratory failure, circulatory collapse, and shock.
There are four types of hypersensitivity reactions (Box 21.1). Type I accounts for most cases of anaphylaxis. Type II reactions are typically seen in the setting of blood transfusions, drug reactions, and cases of idiopathic thrombocytopenic purpura. Type III reactions are responsible for serum sickness, reactions to tetanus toxoid, and poststreptococcal glomerulonephritis. Type IV reactions are T‐cell–mediated and delayed hypersensitivity responses that do not cause anaphylaxis.
Urticaria, or hives, is an often‐encountered symptom and physical sign of an acute allergic reaction. Although the potential etiologies of urticaria are numerous, the temporal link to a likely allergen can often be made upon consideration of recent exposures. For example, the patient might have recently started a new medication, been stung by an insect, or eaten a certain food. Urticaria, itself, is not particularly concerning. However, its potential as an indicator of a reaction in the evolution of systemic effects toward anaphylaxis should not go unrecognized.
Box 21.1 Types of hypersensitivity reactions and anaphylaxis production
Type I immediate(IgE or IgG) – most common
Type II Cytotoxic complement cascade (IgG or IgM) –Yes
Type III Immune complex (IgG or IgM) – Yes
Type IV Delayed T‐cell – No anaphylaxis
Allergic reactions that present as urticaria can progress to angioedema, resulting in histamine‐mediated facial or tongue swelling. Subsequently, airway obstruction might develop precipitously with obvious consequences. Angioedema also occurs without other manifestations of an allergic reaction and is due to non–histamine (bradykinin)‐mediated edema, such as the type that can develop from angiotensin‐converting enzyme inhibitors. This type of edema does not respond to conventional therapy of epinephrine, corticosteroids, and antihistamines. The patient may have been taking the medication for some time before such a reaction occurs. This can be confusing, as some assume that such a reaction would have occurred earlier in the course of taking the medication if the patient was going to exhibit one. It is vital to be able to distinguish between histamine and non–histamine‐mediated angioedema. Studies have shown that pruritus, uticaria, and angioedema associated with abdominal symptoms are more typical of non–histamine‐mediated angioedema, and airway maintenance and protection should be a priority focus [2].
Hereditary angioedema, on the other hand, does not represent a response to a specific allergen. However, it deserves mention because of its similar presentation to allergic reactions and other forms of angioedema. Hereditary angioedema is an autosomal dominant genetic disorder caused by a defect in the complement pathway that results in either a low C1 esterase level or a high level of dysfunctional C1 esterase. Symptoms can include pruritus, urticaria, wheezing, facial and tongue swelling, dizziness, hypotension, syncope, and gastrointestinal distress [3].
Box 21.2 Definition of anaphylaxis
Acute onset cutaneous and/or mucosal involvement after antigen exposure, plus any of the following:
Respiratory compromise
Bronchospasm
Stridor
Hypoxia
Cardiovascular compromise
Hypotension
Collapse
Persistent gastrointestinal symptoms
Vomiting
Cramping abdominal pain
At the severe end of the allergic reaction spectrum is anaphylaxis. Anaphylaxis can be variable in presentation and is defined by rapid progression to multiple system involvement (Box 21.2). In general, the incidence of anaphylaxis is increasing. The most common triggers are insect stings and food ingestions, particularly nuts. Food ingestions are particularly concerning and often the most severe. The faster a reaction develops after exposure to an allergen, the more likely it is to be severe and life‐threatening.
Causative agents
Almost anything can be a potential allergen (Box 21.3). Common agents include medications, foods and food additives, latex, arthropod bites and stings, mold, radiographic contrast media, and certain marine envenomations [1] (see Chapter 38). Some insect bites or stings, such as those of millipedes, caterpillars, and centipedes, most often cause only pain and local skin reactions such as blistering [4, 5]. Certain species of caterpillars have venom‐filled hair and spines that can cause systemic reactions, including anaphylaxis,