Warfarin-induced skin necrosis was initially reported by Flood et al1 in 1943. The condition usually occurs within 10 days of the initiation of warfarin therapy. The lesions are initially erythematous, purpuric, and sharply demarcated. They may resolve spontaneously or progress to form hemorrhagic bullae with eventual necrosis. Eighty percent of lesions occur in the lower half of the body in areas with abundant adipose tissues, such as the thighs, breasts, abdomen, and buttocks. In our patient, necrotic lesions uncharacteristically affected the medial canthal region of the eyelids as well as the trunk and arm. The mechanism for the development of warfarin-induced skin necrosis involves an early decline in vitamin K–dependent coagulation factors with short half-lives, such as proteins C and S and factor VII, leading to a transient hypercoagulable state.2 The risk factors include high loading doses of warfarin, prior deficiencies of proteins C and/or S and antithrombin III, and mutations in the methylenetetrahydrofolate reductase gene.3 Histopathologic studies have demonstrated thrombosis of the subcutaneous and dermal vessels with a relative lack of inflammation.4 Small lesions heal by secondary intention, whereas large lesions require surgical intervention.