Key result
Restarting warfarin post-sepsis may trigger fatal skin necrosis via transient protein C and S deficiency.
Case Report (n=1)
Sepsis should be recognized as a potential cause of acquired protein C deficiency that can precipitate warfarin-induced skin necrosis.
Answers are grounded in this paper and cite their sources.
Sepsis may warrant caution before warfarin re-challenge due to acquired protein C/S deficiency; single case leaves open need for validation.
Warfarin Induced Skin Necrosis is a well-known and dreaded complication in patients who is being started on warfarin without adequate bridging with other anticoagulants. The mechanism is thought to be due to protein C deficiency acquired after initial exposure to warfarin. We present a rather unusual cause of protein C deficiency due to sepsis resulting in warfarin induced skin necrosis. 43 year old lady who has been on chronic warfarin therapy secondary to anti phospholipid syndrome was admitted to the hospital for acute ischemic cerebellar stroke. Warfarin was held due to acute thrombocytopenia. She was discharged after restarting the warfarin. She presented back with septic shock due to pneumonia. She was found to have multiple necrotic areas consistent with skin necrosis. Unfortunately, patient died due to multi organ failure despite goal directed therapy. This case demonstrates the importance of recognizing the sepsis as an acquired cause of protein C deficiency.
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Kannan et al. (2014) conducted a case report in Warfarin-induced skin necrosis and acquired Protein C/S deficiency (n=1). Warfarin and Sepsis was evaluated on Warfarin-induced skin necrosis. Sepsis can cause transient acquired protein C and S deficiency, leading to fatal warfarin-induced skin necrosis upon reintroduction of warfarin therapy.
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