Key result
Rapid phenprocoumon loading triggers severe skin necrosis secondary to acute protein C depletion.
Case Report (n=1)
Illustrates a severe case of coumarin-induced skin necrosis associated with rapid protein C depletion (<5%) and premature discontinuation of heparin bridging during high-dose phenprocoumon initiation.
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Premature heparin stop during phenprocoumon loading may precipitate severe skin necrosis; case report leaves open optimal bridging protocols.
A 39-year-old white female with severe peripheral arterial disease, due to fibromuscular dysplasia, developed coumarin-induced skin necrosis. Owing to recurrent arterial thromboses, including one episode which resulted in left above-knee amputation, phenprocoumon therapy was initiated, at doses of 15, 9 and 3 mg on the first, second and third days of treatment, respectively. This treatment overlapped with a continuous intravenous infusion of heparin that was adjusted to aPTT levels of 1.5 to 2.5 times the normal range. On the third day of treatment she had an international ratio (INR) 4.5 (normal therapeutic range 2–4.5); the protein C level was below 5%. Heparin therapy was then stopped. Twenty-four hours later she developed severe pain of the left thigh, above the site of the amputation, associated with extensive erythema. Another 24 hours later, petechial hemorrhages had developed (Panel A) and were rapidly followed by necrosis (Panel B). Oral anticoagulation was discontinued and
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Brodmann et al. (2006) conducted a case report in Severe peripheral arterial disease due to fibromuscular dysplasia with recurrent arterial thromboses (n=1). Phenprocoumon was evaluated on Coumarin-induced skin necrosis. Phenprocoumon therapy (15, 9, and 3 mg over 3 days) led to an INR of 4.5, protein C <5%, and severe coumarin-induced skin necrosis 48 hours after stopping heparin.
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