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Multiple Choice

Warfarin-induced skin necrosis typically occurs when?

Warfarin-induced skin necrosis most often appears in the first few days after starting therapy, especially when a large loading dose is given without heparin bridging. The reason is that warfarin quickly lowers protein C, a natural anticoagulant with a short half-life, creating a transient hypercoagulable state. This promotes microthrombosis in skin vessels, particularly in fatty areas, leading to painful necrotic lesions. The risk is higher in patients with protein C or S deficiency. Clinically, lesions develop about 3–6 days after initiation. Management involves stopping warfarin, starting appropriate anticoagulation (often with heparin) and reversing with vitamin K as needed, with careful reconsideration of future anticoagulation and bridging strategies.

Warfarin-induced skin necrosis most often appears in the first few days after starting therapy, especially when a large loading dose is given without heparin bridging. The reason is that warfarin quickly lowers protein C, a natural anticoagulant with a short half-life, creating a transient hypercoagulable state. This promotes microthrombosis in skin vessels, particularly in fatty areas, leading to painful necrotic lesions. The risk is higher in patients with protein C or S deficiency. Clinically, lesions develop about 3–6 days after initiation. Management involves stopping warfarin, starting appropriate anticoagulation (often with heparin) and reversing with vitamin K as needed, with careful reconsideration of future anticoagulation and bridging strategies.