INTRODUCTION:
We report a series of cocaine-induced full-thickness skin necrosis of 10-20% total body surface area. Wound management included aggressive serial debridement and split-thickness skin grafting.
METHODS:
A retrospective review was performed of patients presenting with cocaine- induced skin necrosis. IRB approval was obtained to review patient demographics and medical history. Skin histology, serum immunology and clinical course were analyzed.
RESULTS:
Three patients (age 37-50) with cocaine-induced skin necrosis were identified between December 2010 and February 2011. All patients admitted to recent cocaine use followed by a prodrome of purpura, progressing to full thickness necrosis of 10-20% TBSA within 4-6 weeks. Areas involved included the ears, face, trunk and extremities. All patients exhibited autoantibodies, including ANA, P-ANCA, lupus anticoagulant and rheumatoid factor. Histopathology consistently revealed cutaneous and deep thromboses in the absence of inflammation. One patient eviscerated through her necrosis and her wounds were closed primarily. Management of the other patients included debridement, temporary xenografting, and definitive split-thickness skin grafting.
CONCLUSIONS:
Cocaine has been used as a recreational drug for over 100 years. However, skin necrosis secondary to cocaine abuse has not been reported. The implicated cause is not cocaine itself, but rather the adulterant levamisole, which is added to increase the volume of the powder. Levamisole is now detected in 70% of cocaine transported into the US. Historically used to treat nephrotic syndrome in children, levamisole is no longer used due to side effects including agranulocytosis and purpura of the auricular helices. In recent reports, levamisole has been linked to life-threatening agranulocytosis and purpura. In all cases, lesions resolved completely with abstinence from cocaine.
All of our patients presented outside the window for levamisole detection. Toxicology for cocaine was positive and histopathology revealed thromboses in the absence of inflammation. These findings are identical to the histology seen in recent case reports of purpura. In these patients, levamisole exposure caused thromboses of dermal vessels with a paucity of inflammatory cells or a true vasculitis. This series represents the first report of cocaine exposure causing full thickness skin loss requiring surgical debridement and reconstruction.
As reconstructive surgeons, we must have a heightened awareness of this new disease process to aid in prompt diagnosis and treatment of cocaine-induced full thickness skin necrosis.