In a patient with warfarin-induced skin necrosis, which is the most likely etiologic factor?

In a patient with warfarin-induced skin necrosis, which is the most likely etiologic factor?

• A. Protein C deficiency
• B. Vitamin K deficiency
• C. Thrombocytopenia
• D. Heparin-induced thrombocytopenia

Answer: (A)

Warfarin initially creates a temporary procoagulant state because it reduces protein C, an anticoagulant with a short half-life, before enough procoagulant factors are suppressed. In someone with a protein C deficiency, this imbalance is amplified, leading to microvascular thrombosis and skin necrosis after starting warfarin. The other options don’t fit as well: vitamin K deficiency would worsen bleeding rather than cause necrosis, thrombocytopenia involves low platelets without the same microvascular clot pattern, and heparin-induced thrombocytopenia is a separate prothrombotic disorder related to heparin exposure, not the heightened early wartfarin effect driven by low protein C.

Warfarin initially creates a temporary procoagulant state because it reduces protein C, an anticoagulant with a short half-life, before enough procoagulant factors are suppressed. In someone with a protein C deficiency, this imbalance is amplified, leading to microvascular thrombosis and skin necrosis after starting warfarin. The other options don’t fit as well: vitamin K deficiency would worsen bleeding rather than cause necrosis, thrombocytopenia involves low platelets without the same microvascular clot pattern, and heparin-induced thrombocytopenia is a separate prothrombotic disorder related to heparin exposure, not the heightened early wartfarin effect driven by low protein C.