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Research Article Open access CC BY 4.0

Extensive Vitamin K Antagonist-induced Skin Necrosis Leading to Fatal Septic Shock: A Case Report

Asmaa Elfathi, Imane Chadbellah, Salma Nafidi, Sana Nehame, Abdelkarim AIT YAHYA, Mustapha El Hattaoui

Cardiology and Angiology: An International Journal · pp. 109–119 · Published 28 Apr 2026

10.9734/ca/2026/v15i2541

Abstract

Background: Vitamin K antagonist (VKA)-induced skin necrosis is a rare but life-threatening complication, typically occurring during the initiation phase of anticoagulation therapy. Its disseminated presentation is exceptional and poses a major diagnostic and therapeutic challenge. Despite its rarity, mortality rates remain high, particularly when complicated by secondary infection and multi-organ failure. The coexistence of leukocytoclastic vasculitis on biopsy adds further complexity to an already difficult clinical picture. Case Presentation: We report the case of a 46-year-old woman with known moderate mitral stenosis in sinus rhythm, who developed extensive necrotic skin lesions involving the upper and lower limbs, face, and trunk, fifteen days after initiation of acenocoumarol therapy for a new-onset episode of atrial fibrillation. Laboratory findings revealed a supratherapeutic INR of 6.12, associated cardiac decompensation, severe inflammatory syndrome, and acute kidney injury. Protein C and Protein S deficiency were excluded. Despite intensive care management, the patient rapidly progressed to septic shock secondary to Pseudomonas aeruginosa superinfection. Skin biopsy unexpectedly revealed leukocytoclastic vasculitis, raising a complex differential diagnosis. Discussion: This case illustrates the diagnostic complexity surrounding severe VKA-induced skin reactions. The clinical timeline strongly suggested coumarin-induced thrombotic necrosis; however, histological evidence of leukocytoclastic vasculitis introduced the possibility of drug-induced vasculitis or septic purpura as contributing or alternative etiologies. The absence of heparin bridging at the time of VKA initiation likely represents the pivotal preventable factor in this fatal outcome. Conclusion: This exceptional case underscores the importance of rigorous INR monitoring during VKA initiation, the necessity of systematic heparin bridging, and the need to consider multiple competing diagnoses when facing severe cutaneous complications of anticoagulation therapy. Early skin biopsy and prompt dermatological assessment are essential to guide management in such cases.

Skin necrosis acenocoumarol leukocytoclastic vasculitis septic shock anticoagulation heparin bridging atrial fibrillation protein C deficiency

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