ANAPHYLAXIS, ACUTE ALLERGIC REACTIONS, AND ANGIOEDEMA

Allergic reactions range from mild cutaneous symptoms to life-threatening anaphylaxis.

Common exposures are medications, insect stings, and foods. Many cases are idiopathic.

Half of the fatalities from anaphylaxis occur within the first hour.

PATHOPHYSIOLOGY

Mast cell activation caused by histamine, prostaglan-din D2, leukotrienes, and other mediators play a role in the progression to anaphylaxis.

Anaphylactoid reactions, unlike IgE-mediated allergic responses, do not require a previous sensitizing exposure, but both reactions may ultimately progress to anaphylaxis.

Concurrent use of β-blockers is a risk factor for severe, prolonged anaphylaxis.

CLINICAL FEATURES

Anaphylaxis describes an acute progression of organ system involvement that may lead to cardiovascular collapse.

Reactions may occur in seconds or may be delayed an hour or more after exposure.

Up to 20% of reactions are “biphasic,” with further mediator release peaking 4 to 8 hours after exposure.

Symptoms can include dermatologic (flushing, urticaria, angioedema), respiratory (wheezing, cough, dyspnea, stridor), cardiovascular (dysrhythmia, collapse), gastrointestinal (vomiting, diarrhea), and eye (tearing, redness, pruritus) complaints.

DIAGNOSIS AND DIFFERENTIAL

The diagnosis is clinical. Consider the diagnosis in any rapidly progressing multisystem illness.

An exposure to an allergen can confirm the diagnosis, but the exposure will not always be identified.

Work-up should focus on excluding other diagnoses while stabilizing the patient.

The differential depends on which organ systems are involved. Considerations may include vasovagal reaction, asthma, acute coronary syndrome, epiglottitis or airway foreign body, carcinoid, mastocytosis, and hereditary angioedema.

EMERGENCY DEPARTMENT CARE AND DISPOSITION

Patients should have intravenous access and be placed on a cardiac monitor with pulse oximetry.

Angioedema or respiratory distress should prompt early consideration for intubation. Preparations should be made for “rescue” transtracheal jet insufflation or cricothyroidotomy.

Eliminate the exposure. This may be as simple as stopping a drug or removing a stinger.

First-line therapy for anaphylaxis is epinephrine. In patients without cardiovascular collapse, administer 0.3–3.0 milligrams (0.3–3.0 mL of 1:1000; pediatric dose, 0.01 milligrams/kg to a maximum of 0.5 milligrams) intramuscularly in the thigh; repeat every 5 minutes as needed.

Patients who are refractory to IM dosing or in significant shock should receive intravenous epinephrine. A bolus of 100 micrograms of 1:100,000 dilution (place 0.1 mL of 1:1000 in 10 mL normal saline) can be given over 5–10 minutes followed by an infusion of 1–4 micrograms/min.

Hypotensive patients require aggressive fluid resuscitation with normal saline 1–2 L (pediatric dose, 10–20 mL/kg).

Steroids are indicated in all cases of anaphylaxis. Severe cases can be treated with methylprednisolone 125 milligrams IV (pediatric dose, 2 milligrams/kg). Mild allergic reactions can be treated with oral pred-nisone 60 milligrams (pediatric dose, 2 milligrams/kg).

Administer diphenhydramine 50 milligrams IV (pediatric dose, 1 milligram/kg). In addition, an H₂ blocker such as ranitidine 50 milligrams IV (pediatric dose, 0.5 milligrams/kg) may be helpful.

Bronchospasm is treated with nebulized β-agonists such as albuterol 2.5 milligrams. If refractory, consider an inhaled anticholinergic, ipratropium bromide 250 micrograms, and intravenous magnesium 2 grams (25–50 milligrams/kg in children) over 20 to 30 minutes.

For patients on β-blockers with refractory hypotension, use glucagon 1 milligram IV every 5 minutes. An infusion of 5 to 15 micrograms/min should be started once blood pressure improves.

Angiotensin-converting enzyme inhibitors are a common trigger for nonallergic angioedema, which can rapidly lead to airway compromise. Treatment is supportive; epinephrine, steroids, and antihistamines are often given, although benefit has not been proven.

Patients with hereditary angioedema do not respond to treatment for anaphylaxis and should be treated with C1 esterase inhibitor replacement. Treatment with fresh frozen plasma has been reported as an alternative when C1 esterase inhibitor replacement is not available.

Unstable or refractory patients merit admission to the intensive care unit.

Patients with moderate to severe symptoms should be admitted for observation.

Patients with mild allergic reactions should be observed in the ED and may be sent home if symptoms are stable or improving.

Patients who received epinephrine are generally felt to be safe for discharge after 4 hours without symptoms.

Consider observing patients with a history of severe reactions and patients on β-blockers for a longer period.

Discharge patients on an antihistamine and a short course of prednisone. Counsel all patients about the possibility of a late recurrence of symptoms and about avoiding future exposures to the allergen.

All patients who have experienced severe allergic reactions should have and know how to use an epinephrine autoinjector. Consider Medic-Alert bracelets and referral to an allergist in these patients.