Anaphylaxis treatment: the details

Axel Ellrodt raises several questions regarding discharge therapy after anaphylaxis. The first relates to alternatives to diphenhydramine prophylaxis. Diphenhydramine has been established as an effective agent in the treatment and prevention of anaphylactic and anaphylactoid reactions, where its sedative properties are an advantage.1 Given orally at doses of 25 to 50 mg every 4 to 6 hours, it remains the antihistamine of choice to prevent and manage these episodes. A second-generation antihistamine could be substituted if sedation were a concern. However, because biphasic reactivity may be delayed for up to 24 hours, the patient should be advised to minimize activity (including driving) during this interval, and sedative effects may therefore be unimportant. After this interval, treatment with either diphenhydramine or a nonsedating antihistamine such as cetirizine (10 mg daily for 3 days, given orally) would be appropriate. Although H₂ receptors are involved to a limited extent in the pathophysiology of anaphylaxis, we rarely administer H₂ blockers in this capacity and consider their use optional. With respect to prophylactic corticosteroids, we usually begin with a single oral dose of 50 mg prednisone, followed by reduced doses of 40 mg on days 2 and 3, then 20 mg on days 4 and 5, then discontinuation. The medication is given in the morning to optimize effect and minimize adrenocortical suppression.

The questions surrounding cross-reactivity of penicillin and third-generation cephalosporins remain unresolved. Allergic reactivity to cephalosporins (of any type) is 4 to 8 times greater in patients with a history of allergy to penicillin than in those without,2^,3 and the rate of reactivity to cephalosporins is 4% to 7% in patients with previous reactivity to penicillin.3 Recent evidence suggests that variable side-chains on the β-lactam ring, rather than the β-lactam nucleus, induce this cross-reactivity.4^,5 Indeed, several patients with documented skin test reactivity to penicillin who were given doses of second- and third-generation cephalosporins had no reactivity.6 Nevertheless, caution is advised in the administration of cephalosporins to patients with known anaphylactic reactivity to penicillin.

We agree that the designation 1:1000 or 1:10 000 can be confusing, but this description facilitates rapid dosing and administration of epinephrine, which is essential in managing anaphylaxis.7 In addition, this presentation displays the dilution much more prominently than if the dose is given as milligrams per millilitre (mg/mL).

Patrick Potter raises the issue of empiric use of glucagon for treatment-resistant anaphylaxis. Epinephrine resistance in anaphylaxis does suggest concomitant β-blockade and hence an indication for glucagon administration. However, glucagon may be associated with nausea, vomiting, hyperglycemia and allergic reactivity, which precludes its general use in anaphylaxis. If repeat doses of epinephrine yield inadequate clinical response during an episode of anaphylaxis, especially when there is evidence of increasing systolic hypertension due to unopposed α-adrenergic activation and bradycardia signifying reflex vagotonic effect, further epinephrine is contraindicated and glucagon should be administered.

Anne K. Ellis James H. Day Division of Allergy Kingston General Hospital Kingston, Ont.