Anaphylaxis and Acute Allergic Reactions

Allergic reactions can range from trivial-appearing urticaria to full-blown anaphylaxis with cardiovascular collapse and respiratory compromise. The most common etiologies include intravenous penicillin and hymenoptera stings. Although most acute allergic reactions are type I, where an antigen interacts with IgE on mast cells and basophils, other hypersensitivity reactions include type II antigen interacting with IgG and IgM antibodies (e.g., blood transfusion reaction, idiopathic thrombocytopenic purpura); type III, deposition of antigen-antibody complexes (e.g., serum sickness, poststreptococcal glomerulonephritis); and type IV, delayed hypersensitivity reaction from T lymphocytes (e.g., poison ivy, skin test for tuberculosis).

Clinical Features
Anaphylaxis can occur within seconds, but can be delayed an hour, after a sensitized individual is exposed to such things as (a) drugs (e.g., penicillin and trimethoprim-sulfamethoxazole), (b) foods (e.g., shellfish, nuts, eggs, and preservatives such as sulfites and tetrazine dyes), and (c) stings (especially hymenoptera). In addition, such things as dextran, codeine, and radiocontrast material can cause an anaphylactoid reaction, which is non-IgE-mediated and requires no sensitizing exposure. Both anaphylaxis and anaphylactoid reactions have the same final common pathway, through mast-cell degranulation. Finally, aspirin and other nonsteroidal anti-inflmmatory drugs can cause anaphylactic symptoms through modulation of the cycloxygenase-arachidonic acid pathway.
Anaphylactic reactions range from local organ involvement to serious multisystem effects. Dermatologic features include pruritis, urticaria, erythema multiforme, and angioedema. The latter can be seen as an isolated response to angiotensin-converting enzyme (ACE) inhibitors. By definition, anaphylaxis includes either respiratory compromise or cardiovascular collapse. Respiratory features may include tracheal swelling, stridor, wheezing, and respiratory arrest. Gastrointestinal (GI) features include nausea, cramps, vomiting, and diarrhea. Untreated, anaphylaxis leads to shock with tachycardia and hypotension. Cardiac patients are susceptible to myocardial ischemia as well as an exaggerated allergic response if on b blockers. If patients survive the initial insult, a second phase of mediator release can occur at 4 to 8 h in up to 20 percent of cases.

Diagnosis and Differential
Diagnosis will be based on symptoms seen in any particular patient. Usually history will confirm exposure to a potential allergen, such as a new drug, food, or insect sting. There is no specific test available in the emergency department to confirm the diagnosis. Workup, however, may include a complete blood cell count, glucose, electrolyte levels, urinalysis, and arterial blood gas analysis, depending on presenting symptoms. The differential includes myocardial infarction, asthma, carcinoid, hereditary angioedema, and vasovagal reactions.

Emergency Department Care and Disposition
The airway is the primary concern in the treatment of any allergic reaction. Patients with respiratory symptoms or abnormal vital signs should be placed on pulse oximetry and cardiac monitor with intravenous access. The combination of oxygen and epinephrine can usually reverse any impending respiratory compromise.

1. High-flow oxygen should be administered by face-mask, if necessary, to maintain adequate oxygenation. Endotracheal intubation, if required, can be difficult because of angioedema or laryngeal spasm; therefore, preparation should be made for transtracheal jet insufflation or cricothyroidotomy.
2. Any patient with airway symptoms or hypotension should receive epinephrine. This can be given subcutaneously 0.3 to 0.5 mg (0.3 to 0.5 mL) of 1:1000 (pediatric dose 0.01 mL/kg). In the presence of shock or respiratory arrest, a bolus of 100 µg of intravenous epinephrine as a 1:100,000 dilution (0.1 mL of 1:1000 in 10 mL normal saline) can be given over 5 to 10 min.
3. Attention must be made to termination of further exposure. This may be as simple as stopping an intravenous line of drug or removing a stinger.
4. Most patients, especially if hypotensive, will require large volumes of crystalloid fluids. If after 1 to 2 L, patients are still hypotensive, then intravenous epinephrine (1:10,000) should be administered at 1 to 4 µg/min (pediatric dose, 0.1 to 1 µg/kg/min).
5. Every patient with allergic symptoms requires antihistamines. Diphenhydramine can be given 25 to 50 mg (pediatric dose 1 mg/kg), intravenously in serious cases. In addition, an H2 blocker such as ranitidine 50 mg intravenously (pediatric dose 0.5 mg/kg) can be helpful.
6. After treatment with epinephrine, any persistent bronchospasm can be treated with nebulized b agonists, such as albuterol 0.5 mL of 5% in 3 mL saline.
7. Steroids are useful in controlling persistent or delayed allergic reactions. Severe cases can be treated with methylprednisolone 125 mg (pediatric dose 1 to 2 mg/kg) intravenously. Milder reactions can be treated with oral prednisone, 60 mg to start.
8. If patients are taking b blockers, glucagon (1 to 2 mg every 5 min) can be used for hypotension refractory to epinephrine and fluids.

In mild reactions, patients may be observed several hours prior to discharge. Severe cases, with any evidence of hypotension or respiratory compromise, deserve prolonged observation (> 6 h) with repeated doses of antihistamines and steroids as needed. Patients can be discharged on an antihistamine and prednisone for 4 days. Remember, all serious cases deserve preventive therapy upon discharge. This includes a self-administration epinephrine kit, as well as referral to an allergist for desensitization therapy. The recurrence rate for anaphylaxis from insect stings is 40 to 60 percent.