Seen within the first few days of treatment with high doses of warfarin
Warfarin inhibits all vitamin K-dependent coagulation factors: anticoagulants protein C and protein S have a relatively short half-life and are depleted more quickly than procoagulants factors II, IX, and X → increased factor V and VIII activity → initial hypercoagulable state → formation of microthrombi → vascular occlusion, tissue infarction, and blood extravasation
Increased risk in patients with underlying hereditary protein C deficiency
Increased risk in patients with underlying hereditary protein C deficiency
Presentation:
- painful purpura, hemorrhagic blisters, and large areas of necrosis;
- mostly affects areas with significant subcutaneous adipose tissue (thighs, abdomen)
Immediate management:
- discontinue warfarin,
- administer IV vitamin K,
- unfractionated heparin, and
- source of protein C (protein C concentrate, FFP);
- surgical debridement and grafting in therapy-refractory cases
Prevention:
temporary bridging anticoagulation with heparin until warfarin has started to act and the initial hypercoagulable state has been bridged
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