LAUSR

© Author(s) (or their employer(s)) 2021. No commercial reuse. See rights and permissions. Published by BMJ. Warfarin, a double sword not only helps in anticoagulation by inhibition of vitamin K dependent clotting factors but also prevents clot lysis by inhibiting protein C and protein S. The halflife of protein C and S is shorter than vitamin K dependent clotting factors hence its plasma concentration falls faster. If started alone the patient is at risk of developing warfarin induced skin necrosis, a potentially disastrous although a rare complication (0.01%–0.1%) usually occurring 2–5 days after initiation of warfarin therapy. A 63yearold man recently diagnosed rheumatic heart disease with severe mitral stenosis presented with a 2day history of decreased urine output. He was started on tablet warfarin 5 mg once a day and tablet furosemide 20 mg two times a day 2 weeks ago. Physical examination showed pulse rate of 98 bpm, blood pressure of 140/88 mm Hg, respiratory rate of 26 breaths/min. Cardiac auscultation showed irregular rhythm. Respiratory and abdominal examinations were normal. Local examination revealed oedema of both lower limbs with discoloration and ulceration which started 5 days after his medications(figure 1). He was admitted in intensive care unit and routine blood investigations, cardiac enzymes, arterial blood gases and ECG was done. Patient was put on noninvasive ventilation and tablet furosemide 10 mg two times a day was started. Dermatology opinion was sought for the leg ulcers and biopsy were taken which showed features of necrotising dermatoses with leucocytoclastic vasculitis and bulla formation (figure 2). Surgical debridement of necrotic areas was done and intravenous clindamycin was given. Warfarin was stopped and the patient was started on subcutaneous enoxaparin. The ulcers later showed signs of healing.