Drug-induced angioedema without urticaria - Incidence, prevention and management

Angioedema without urticaria is a clinical syndrome characterised by self-l imiting local swellings involving the deeper cutaneous and mucosa tissue la yers. Most occurrences of angioedema respond to treatment with a histamine H-1 receptor blocker (antihistamine) because they are an allergic or parall ergic reaction. A small number of cases do not respond to antihistamine tre atment. Such cases tend to occur in patients with deficiency or dysfunction of the inhibitor of the first component of the complement (Cl-INH), but mo re rarely can occur in patients with other conditions and as an adverse dru g reaction. Angioedema is well documented in patients taking ACE inhibitors. Considerin g that 35 to 40 million patients are treated worldwide with ACE inhibitors, this drug class could account for several hundred deaths per year from lar yngeal oedema. ACE inhibitors certainly do not mediate angioedema through a n allergic or idiosyncratic reaction. For this reason the relationship with this drug is often missed and consequently quite underestimated. Rare inst ances of angioedema have also been reported with angiotensin II receptor an tagonists. This adverse effect seems to occur less frequently with angioten sin II receptor antagonists than with ACE inhibitors. However, we do not kn ow whether this adverse effect has the same mechanism with the 2 classes of medications. Some cases of severe angioedema have been recently reported a fter treatment with fibrinolytic agents. Scattered reports suggest the poss ibility of angioedema associated with the use of estrogens, antihypertensiv e drugs other than ACE inhibitors, and psychotropic drugs. Angioedema can a lso occur with nonsteroidal anti-inflammatory drugs. Prevention of angioedema relies first on the patient history. Estrogen and ACE inhibitors should be avoided in a patient with congenital or acquired C l-INH deficiency. In the case of ACE inhibitors, the appearance of angioede ma following long term treatment does not lessen the probability that such an agent could be the cause. The most important action to take in a patient with suspected drug-induced angioedema is to discontinue the pharmacologic al agent. Epinephrine (adrenaline), diphenydramine and intravenous methylpr ednisolone have been proposed for the medical management of airway obstruct ion, but so far no controlled studies have demonstrated their efficacy. If the acute airway obstruction leads to life-threatening respiratory compromi se an emergency cricothyroidotomy must be performed.