Cutaneous necrosis is an infrequent but well-documented complication of oral anticoagulants. In the pathogenesis of cutaneous necrosis induced by oral anticoagulants recent hypotheses favour the combined role of local factors and a transient unbalance of coagulation mechanisms leading to an hypercoagulable state. There exists a genetic factor that determines a decreased level of two vitamin-K dependent glycoproteins, namely protein C and protein S. We present the case of an obese woman that developed an extensive cutaneous necrosis while receiving acenocoumarol for a deep venous thrombosis. She had an heterozygous deficit for protein C. The histopathologic findings of vessel thrombi and red blood cell extravasation were consistent with the clinical picture. A biopsy specimen taken from an initial lesion disclosed images of leucocytoclastic vasculitis. We reviewed the literature focusing on the pathogenesis and the histopathology of the disease.