Abstract

Cutaneous necrosis is a relatively rare complication of systemic drugs and can be mediated by various pathogenetic mechanisms. Anticoagulants such as warfarin and heparin are the leading cause of drug-induced cutaneous necrosis. Warfarin induces a transient protein C deficiency, prior to reductions in the procoagulant factors. The resultant transient imbalance in the anticoagulant and procoagulant pathways leads to an initial paradoxical hypercoagulable state resulting in microvascular thrombosis and cutaneous necrosis. Heparin-induced cutaneous necrosis is a rare but serious complication of administration of low molecular weight heparin or unfractionated heparin. Drugs such as vasopressin can cause drug-induced vasculopathic reactions that may manifest as cutaneous necrosis. Various drugs have been implicated in the causation of purpura fulminans that can manifest as cutaneous necrosis. Drug-induced vasculitis and drugs inducing factitial dermatitis can also cause necrosis of the skin. Management of conditions causing cutaneous necrosis requires a multipronged approach. The primary aim should be to identify the culprit drug in cases of drug-induced cutaneous necrosis. Early diagnosis can allow for early treatment and can decrease the chance of morbidity and mortality.

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