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The new guidelines for the practical approach to management of pulmonary embolism (PE) are clearly welcome to help all clinicians dealing with such patients.1 I would, however, like to take issue with the statement advising the administration of hydrocortisone in conjunction with streptokinase to reduce the risk of allergic complications.
Allergic reactions are a well recognised adverse effect of intravenous streptokinase treatment and are probably due to immediate hypersensitivity reactions mediated by IgE antibodies to streptokinase.2 The incidence of allergic reactions is low (1.7–18%)2 and was only seen in 3.6% of patients entered into the Third International Study of Infarct Survival (ISIS-3) trial.3 Indeed, only 0.3% of patients in ISIS-3 had allergic reactions causing “persistent symptoms”.3
Patients at risk of allergic and anaphylactic reactions can be identified rapidly by intradermal streptokinase skin testing, which correlates with elevated levels of IgE to streptokinase.2This test will give results in approximately 15 minutes but is not widely utilised. At risk patients include those who have received prior streptokinase treatment, including those who have had previous intradermal streptokinase skin tests. The intradermal skin test will not, however, detect patients with IgG antibodies to streptokinase who are at risk of delayed reactions and may not have effective thrombolysis due to IgG neutralising antibodies.
Antihistamines and hydrocortisone may help to reduce the effects of immediate hypersensitivity reactions, but steroids are not routinely administered in the major cardiovascular thrombolytic trials or in most UK coronary care units. As patients with pulmonary embolism are at no greater risk for allergic reactions to streptokinase, there does not seem to be good evidence for the statement in the guidelines. It may be more appropriate to consider alternative thrombolysis if there is genuine concern regarding allergic reactions in individual patients.
authors’ reply Although indeed unusual, an allergic reaction to streptokinase in a patient with massive pulmonary embolism who, by definition, is already critically ill and hypotensive (unlike most myocardial infarction patients) could be disastrous, which is our reason for advocating the routine addition of hydrocortisone. This is not a problem with other thrombolytics; some hospitals, including mine, have already agreed that this advantage of alteplase in massive pulmonary embolism justifies its much greater cost. Our third suggestion, urokinase, is both safe and cheap, but although many pharmacies stock it for unblocking central venous catheters, few have the much higher dose formulation required for acute pulmonary embolism.