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Warfarin-induced skin necrosis.
Hospital Pharmacy 2014 December
BACKGROUND: Warfarin is a frequently used oral anticoagulant in the treatment and prevention of various medical conditions. One uncommon adverse effect that can occur following the initiation of therapy is warfarin-induced skin necrosis. Because it is a rare effect with an undetermined pathophysiology of disease, the treatment is not well established.
CASE: A 52-year-old female was prescribed warfarin and enoxaparin for a newly diagnosed deep vein thrombosis (DVT) in the left lower extremity. On day 4 of therapy, the patient had a supra-therapeutic international normalized ratio (INR), prompting the discontinuation of enoxaparin and a decrease in the warfarin dose. The patient returned to the emergency department on day 7 of treatment with a purple, cold, and extremely painful right foot with punctate areas of necrosis and petechiae proximal to the discoloration. The patient's INR was found to be 10.64. Following the diagnosis of warfarin-induced skin necrosis, the patient was administered vitamin K intravenously and fresh frozen plasma (FFP) to reverse the effects of warfarin and promote protein C and S synthesis. Once the patient's INR was no longer supratherapeutic, subcutaneous enoxaparin was re-started as treatment for the known recent DVT. The patient's necrotic foot began to improve and she was discharged home with an anticipated full recovery.
CONCLUSIONS: Based on the proposed pathophysiology of disease, adequate bridge therapy may decrease the likelihood of developing this life-threatening condition. Early recognition and treatment with intravenous vitamin K, FFP or 4-factor prothrombin complex concentrate, and continued wound care are essential to prevent further complications.
CASE: A 52-year-old female was prescribed warfarin and enoxaparin for a newly diagnosed deep vein thrombosis (DVT) in the left lower extremity. On day 4 of therapy, the patient had a supra-therapeutic international normalized ratio (INR), prompting the discontinuation of enoxaparin and a decrease in the warfarin dose. The patient returned to the emergency department on day 7 of treatment with a purple, cold, and extremely painful right foot with punctate areas of necrosis and petechiae proximal to the discoloration. The patient's INR was found to be 10.64. Following the diagnosis of warfarin-induced skin necrosis, the patient was administered vitamin K intravenously and fresh frozen plasma (FFP) to reverse the effects of warfarin and promote protein C and S synthesis. Once the patient's INR was no longer supratherapeutic, subcutaneous enoxaparin was re-started as treatment for the known recent DVT. The patient's necrotic foot began to improve and she was discharged home with an anticipated full recovery.
CONCLUSIONS: Based on the proposed pathophysiology of disease, adequate bridge therapy may decrease the likelihood of developing this life-threatening condition. Early recognition and treatment with intravenous vitamin K, FFP or 4-factor prothrombin complex concentrate, and continued wound care are essential to prevent further complications.
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