1. ABSTRACT Warfarin Induced Skin Necrosis (WISN) is a rare but serious complication of anticoagulant therapy. Its prevalence is reported to be only 0.1-0.01% among patients on oral Warfarin theraphy 1. Its cutaneous findings include petechiae that progress to echymoses and hemorrhagic bullae. Characteristic dermatopathological findings are diffuse painful lesions with red cell extravasation with progression to full thickness Coagulative Necrosis. The lesions of WISN may be difficult to differentiate from mimickers, but skin biopsy in conjunction with careful consideration of the clinical history, including time of onset, cutaneous distribution of the lesions, and laboratory findings, are essential for prompt diagnosis. WISN is also known as Caumarin induced skin necrosis, coumarin-congener-associated skin necrosis, and warfarin dermal gangrene. Affected age goup ranges from 16 to 93 years. Female:Male ratio is 9:1. Classically, the lesions appear in the breast, buttock, abdomen, or thigh where significant underlying subcutaneous fat tissue is present. Several theories have been suggested related to the pathogenesis of WISN, although the exact etiology is obscure. It is proposed that warfarin had a direct toxic effect (toxic vasculitis) at the junction of the precapillary and arterial capillary of the dermovascular loop 2. The damaged capillaries dilate and rupture, and petechiae are developed. Veins distal to the injured capillaries get thrombosed, creating stasis of blood and tissue necrosis. Another proposed theory gaining acceptance is related to acquired or congenital coagulopathies. Protein C and Protein S deficiencies and inadequate Antithrombin III have been reported in a large percentage of WISN-affected patients 3. Differential diagnosis is a challenge, as CISN may mimic multiple other conditions like purpura fulminans, necrotizing fasciitis, microembolization, pressure ulcers, breast cancer, calciphylaxis, pyoderma gangrenosum, venous gangrene, purple toe syndrome, heparin-induced skin necrosis, and cryofibrinogenemia. DISCUSSION CASE REPORT We report a case of 52 year old female who was diagnosed with bilateral lower limb DVT and started on oral Warfarin therapy. After few days she developed painful ulcerative skin lesion on both thighs and buttocks. In presence of risk factors like CKD, female gender, perimenopausal age, uncontrolled DM initially suspected to be Calciphylaxis. Appearance of lesions typically after initiation warfarin therapy, showing improvement after discontinuation and history of Warfarinisation with large doses without concomittent heparinisation were the clues in clinical history suggesting it to be WISN. REFERENCES 1.Chan YC, Valenti D, et al: Warfarin induced skin necrosis. Br J Surg 87:266e272, 2000 2.Janice M. Beitz, WOUNDS. 2002;14(6):217-220. 3.Despoina D. Kakagia, Nikolaos Papanas et al. Ann Dermatol Vol. 26, No. 1, 2014:96. WARFARIN INDUCED SKIN NECROSIS Dr Parag Waghmode, Dr D. G. Bhosle, Dept. of Medicine, Bharati Vidyapeeth Deemed University Medical College, Pune LEARNING POINTS 1.Concomittent Heparinisation is very important during initiation of anticoagulation therapy. 2.Large swings in INR with high doses of warfarin should be avoided during initiaton of anticoagulation 3.Early diagnosis of WISN reduces the risk of permanent tissue damage