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Dermatology · Drug reactions
Sample itemOn the fourth day after starting warfarin for a deep vein thrombosis without heparin cover, an obese woman develops painful red-purple patches on her breasts and thighs that progress to haemorrhagic necrosis. What is the mechanism, and what is the immediate management?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Transient hypercoagulable state from early fall in protein C, with warfarin stopped and heparin and vitamin K given
Warfarin-induced skin necrosis usually occurs on days three to five, when protein C (half-life about six hours) falls before the longer-lived procoagulant factors, leaving a transient prothrombotic state. It occurs in fatty areas, and is more frequent in protein C deficiency. Warfarin is stopped, vitamin K and heparin are given, and protein C concentrate may be used.
Option by option
A. Heparin-induced thrombocytopenia, with heparin stopped
HIT arises after exposure to heparin, and here no heparin was given.
B. Transient hypercoagulable state from early fall in protein C, with warfarin stopped and heparin and vitamin K given (correct)
Correct. An early drop in protein C causes microvascular thrombosis.
C. Antiphospholipid syndrome, with warfarin dose increased
Increasing warfarin would worsen the problem.
D. Direct warfarin toxicity to dermal fibroblasts, with topical steroids
The mechanism is thrombotic, not a fibroblast toxicity, and steroids do not help.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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