Contents
Warfarin-induced skin necrosis or, anticoagulant-induced skin necrosis is a condition in which skin and subcutaneous tissue necrosis occurs due to acquired protein C deficiency following treatment with anti-vitamin K anticoagulants (4-hydroxycoumarins, such as warfarin).
- Drug eruption usually occurs within 3-10 days of start of therapy (with warfarin derivatives)
Clinical features
- Pain & redness in affected area → Sharp bordered lesions → Petechial lesions → Hard and purpuric lesions → Resolve or progress to form large, irregular, bloody bullae with eventual necrosis and slow-healing eschar formation
- Common sites:
- Subcutaneous fat: Breasts, thighs, buttocks and penis
- Fascia and muscle (rare)
Differential diagnosis:
- Pyoderma gangrenosum
- Necrotizing fasciitis
- Purple toe syndrome
- Usually occurs three to eight weeks after the start of anticoagulation therapy
Management
Vitamin K1
Reverse the effects of warfarin
Heparin or LMW-heparin
Act by a different mechanism than warfarin, so these drugs can also be used to prevent clotting during the first few days of warfarin therapy and thus prevent warfarin necrosis (this is called ‘bridging’)
Low levels of protein C:
- Fresh frozen plasma
- Pure activated protein C
Advanced cases:
- Debridement
- Skin grafting