Anaphylaxis

Diagnosis

Anaphylaxis is a severe, multisystem allergic reaction that occurs suddenly after contact with an allergen. The classic presentation includes urticaria or angioedema, hypotension, and bronchospasm. However, anaphylaxis can often be difficult to diagnose, with up to 20% of anaphylactic reactions lacking any cutaneous manifestations or signs of vasomotor instability.2 Diagnostic criteria were established by a multidisciplinary task force in 2005 to aid in the recognition of atypical presentations of anaphylaxis.2

In cases of anaphylaxis, laboratory tests might show transient elevation of tryptase and histamine levels, but these are not useful diagnostically in the acute setting.3

Pathophysiology

Anaphylaxis is the result of immunoglobulin E–mediated mast cell degranulation, which releases inflammatory immune mediators. These mediators cause increased vascular permeability, peripheral vasodilation, increased mucus production, and bronchial smooth muscle contraction.4 Anaphylactoid reactions do not require a previous exposure to an allergen, but the clinical course and treatment are identical to those of anaphylaxis.

Causes

The primary precipitants of anaphylactic reactions are foods (eg, milk, soy, eggs, nuts, and shellfish), medications (eg, antibiotics [penicillin], nonsteroidal anti-inflammatory drugs, anesthetics), venom (Hymenoptera stings), intravenous contrast materials, and latex. Up to 20% of anaphylactic reactions are idiopathic.

Mortality

The primary cause of mortality in anaphylaxis is airway compromise or cardiovascular collapse. The median time interval between onset of symptoms and cardiopulmonary arrest in one study was less than 30 minutes.5 Fatal anaphylactic reactions are more common in asthmatic patients.5

Treatment

Treatment of anaphylaxis begins with removal of the offending agent, preparation for impending airway obstruction, and correction of vasomotor instability. The 2 most common errors associated with mortality in severe anaphylaxis are delays in intubation and delays in administration of epinephrine.

Airway edema can be rapid and dramatic. In patients with stridor, tongue swelling, or hoarseness, immediate airway protection is imperative. Rapid sequence intubation can be used, but rescue airway methods must be readily available at the bedside.

The treatment of choice for anaphylaxis is epinephrine. The recommended dose of epinephrine in anaphylaxis is 0.3 to 0.5 mg (concentration of 1:1000) intramuscularly (IM) every 5 to 10 minutes for adults (Table 1). Intramuscular injection in the anterolateral thigh is the preferred route regardless of age, as faster and higher plasma concentrations are obtained.6 Intravenous epinephrine is reserved for cases of cardiovascular collapse that are unresponsive to IM therapy.2

Safety of epinephrine

Epinephrine is a lifesaving medication; however, because it is available in different doses, concentrations, and routes of administration (Table 1), there is frequent confusion in its use. Inadvertent overdose can cause coronary artery dissection, acute myocardial infarction, cardiomyopathy, arrhythmias, and death.7 The error rate of epinephrine administration causing potentially fatal adverse reactions in one study was reported to be 2.4%.8 One study suggested that prefilled syringes of 0.3 mg of 1:1000 epinephrine clearly labeled to be given IM for anaphylaxis would decrease the incidence of dosing errors.8

Fluid resuscitation

Anaphylaxis is a distributive form of shock. Patients with severe reactions require aggressive fluid resuscitation, frequently with up to 5 to 7 L of normal saline.5

Treatment adjuncts

Other treatments of anaphylaxis classically taught include histamine (H₁ or H₂) blockers and steroids. A systematic review of the literature has failed to demonstrate the effectiveness of any of these medications in the treatment of anaphylaxis.5 They have not been shown to relieve upper or lower airway obstruction, gastrointestinal symptoms, or shock.5

Steroids are unlikely to be helpful in the treatment of acute anaphylaxis. They have a delayed onset of 4 to 6 hours. Steroids are thought to play a role in preventing rebound anaphylaxis; however, this has never been proven.5

Bronchodilators might be used in patients with refractory wheeze, but they do not relieve bronchial smooth muscle contraction or decrease mucus production.

One study showed that patients suffering from anaphylaxis received both antihistamines and corticosteroids more frequently than epinephrine despite the lack of evidence for their use as first-line agents in anaphylaxis.9

Rebound anaphylaxis

Patients with severe anaphylactic reactions, particularly of rapid onset, are at risk of biphasic or rebound anaphylaxis. The recurrence rate is up to 20%.3 Most biphasic responses occur during the first 8 hours, but it might be delayed up to 72 hours.5 There is no consensus on the optimal period of observation for a patient who has been treated for anaphylaxis.4 In patients with moderate or severe anaphylaxis, consider admission. For patients whose symptoms resolve promptly and completely, it is recommended that they be observed for 4 to 8 hours. All patients being sent home from the emergency department should have immediate access to epinephrine injectors.

Once you have ascertained that there is no evidence of biphasic anaphylaxis, it is recommended that you do a SAFE (Support; Allergen; Follow-up; Epinephrine injector) discharge (Table 29).

Conclusion

Yes, this patient is suffering from an anaphylactic reaction. She is successfully treated with 2 doses of 0.3 mg of epinephrine IM and steroids. She stays in the emergency department overnight and is safely discharged in the morning with a prescription for epinephrine.