Anaphylaxis: Office Management and Prevention
Section snippets
Clinical manifestations of anaphylaxis
Signs and symptoms of anaphylaxis vary, but cutaneous features (urticaria and/or angioedema) are the most common overall [2]. Clinically, anaphylaxis is considered likely to be present if any one of three criteria is satisfied within minutes to hours:
Acute onset of illness with involvement of skin, mucosal surface, or both, and at least one of the following: respiratory compromise, hypotension, or end-organ dysfunction
Two or more of the following occur rapidly after exposure to a likely
Biphasic and protracted anaphylaxis
Biphasic anaphylaxis occurs in 1% to 20% of anaphylaxis cases [14]. Signs and symptoms experienced during the recurrent phase may be equivalent to or worse than those observed in the initial reaction and may occur 1 to 72 hours (most occur within 8 hr) after apparent remission. Data are inconclusive, but some investigators have suggested that risk factors might include relatively large doses of epinephrine administered during the initial phase [15], lower doses of epinephrine and
Diagnosis of anaphylaxis
Anaphylaxis remains a clinical diagnosis based on probability and pattern recognition (see Box 1). No evaluation can prove causation of anaphylaxis conclusively without directly challenging the patient with the suspected agent, a course of action that generally is contraindicated because of ethical and safety concerns. Cause-and-effect often is confirmed historically in patients who experience objective findings of anaphylaxis upon inadvertent re-exposure to the offending agent.
Diagnostic
Differential diagnosis of anaphylaxis
Several systemic disorders share clinical features with anaphylaxis. The vasodepressor (vaso–vagal) reaction probably is the most common. In vasodepressor reactions, however, urticaria and dyspnea are absent; the blood pressure is usually normal or elevated, and the skin is typically cool and pale. Although tachycardia is the rule, bradycardia also may occur in anaphylaxis. Thus, bradycardia may not be as helpful to differentiate between the two syndromes as traditionally thought. Brown and
Management of anaphylaxis
Practice parameters [22] and consensus emergency management guidelines [23], [24], [25], [26] concerning anaphylaxis and its management have been published. Similar to asthma and other diseases for which there are published guidelines, however, providers may not apply them. In a standardized clinical scenario of anaphylaxis as defined by United Kingdom Resuscitation Council guidelines, in the judgment of investigators, 5% of 78 senior house officers beginning emergency department
Epinephrine
Epinephrine is the treatment of choice for anaphylaxis [22], [23], [24], [34]. Again, the authors' rule is “sooner better than later.” Fatalities in anaphylaxis usually result from delayed or inadequate administration of epinephrine and from severe respiratory and/or cardiovascular complications [8], [22]. There is no absolute contraindication to epinephrine administration in anaphylaxis [22]. All subsequent therapeutic interventions depend on the initial response to epinephrine. Development of
Oxygen and airway adjuncts
All patients who have anaphylaxis should receive oxygen at 6 to 8 L/min. Oxygen administration is especially important in patients who have a history of cardiac or respiratory disease, inhaled β2-agonist use, and who have required multiple doses of epinephrine [22]. Continuous pulse oximetry or arterial blood gas determination (where available) should guide oxygen therapy if the potential development of hypoxemia is a concern.
Because adequate oxygenation also depends on ventilation, it may be
Special considerations for β-adrenergic blockade
Patients taking β-adrenergic blockers may be more likely to experience severe anaphylactic reactions characterized by severe bronchospasm, paradoxical bradycardia, and profound hypotension. Use of selective β1 blockers does not reduce the risk of anaphylaxis, because both β1 and β2 blockers may inhibit the β-adrenergic receptor [41], [42], [43]. In such situations, intravenous glucagon potentially may reverse hypotension and bronchospasm, because it bypasses the β receptor and directly
The role of antihistamines, inhaled adrenergic agonists, and corticosteroids
H1 and H2 antihistamines are used commonly as additional agents. Antihistamines, however, act much slower than epinephrine, have minimal effect on blood pressure, and should not be administered alone as treatment for anaphylaxis [22]. Inhaled β2 agonists (eg, albuterol) are helpful when bronchospasm resists epinephrine injections alone. Systemic corticosteroids traditionally have been used in anaphylaxis, but controlled trials have not evaluated their effect. They might help to prevent biphasic
Follow-up and observation after anaphylaxis
Observation after anaphylaxis should be individualized and based on such factors as comorbid conditions and distance from treatment facilities, particularly because there are no reliable predictors for biphasic anaphylaxis [14], [22]. For example, patients who have severe anaphylaxis should be admitted, and others who experience anaphylaxis in the office setting probably should be discharged home only if they stay for the next 72 hours where they have adequate supervision and, if symptoms
Prevention of anaphylaxis
Optimizing prevention (Box 3) is crucial, because future anaphylaxis may be fatal despite appropriate management. An allergist–immunologist can provide comprehensive professional advice on these matters and should be consulted if he/she is not already involved in the anaphylaxis plan of care. All patients at risk for future anaphylaxis should carry at least one epinephrine syringe and know how to administer it. An EpiPen (Dey Laboratories, Napa, California) is a spring-loaded,
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