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Coumarin skin necrosis: a severe complication of oral anticoagulation
Marianne Brodmann, Gerald Seinost, Ernst Pilger
To cite this version:
Marianne Brodmann, Gerald Seinost, Ernst Pilger. Coumarin skin necrosis: a severe complica- tion of oral anticoagulation. Vascular Medicine, SAGE Publications, 2006, 11 (4), pp.273-273.
�10.1177/1358863x06072229�. �hal-00571393�
A 39-year-old white female with severe peripheral arte- rial 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 treat- ment, 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 interna- tional 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 ampu- tation, 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
© 2006 SAGE Publications 10.1177/1358863x06072229
Images in vascular medicine
Coumarin skin necrosis: a severe complication of oral anticoagulation
Marianne Brodmann, Gerald Seinost and Ernst Pilger Vascular Medicine 2006; 11: 273
Division of Angiology, Department of Internal Medicine, Medizinische Universität Graz, Graz, Austria
Address for correspondence: Marianne Brodmann, Division of Angiology, Department of Internal Medicine, Medizinische Universität Graz, Auenbruggerplatz 15, A-8036 Graz, Austria.
Tel: ⫹43 316 385 80286; Fax: ⫹43 316 385 3788; E-mail:
low molecular weight heparin was resumed. Laboratory work-up indicated normal levels of protein C, protein S, antithrombin III, lupus anticoagulant and antiphospho- lipid antibodies. Testing for the factor V Leiden mutation was negative, as was testing for G 20210A mutation.
Within a 3-week period, the necrotic areas fully resolved spontaneously.
References
1 Kyrle P, Brockmeier J, Weltermann A et al. Inhibition rather than enhancement of hemostatic system activation during ini- tiation of oral anticoagulant treatment. Thromb Haemost 1997;
77: 685–89.
2 Stewart AJ, Penman ID, Cook MK, Ludlam CA. Warfarin- induced skin necrosis. Postgrad Med J 1999; 75: 233–35.
Panel A Panel B
‘Images in vascular medicine’ is a regular feature of Vascular Medicine. Readers may submit original, unpublished images related to clinical vascular medicine to: Mark A Creager, Editor in Chief, Vascular Medicine, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA.