Fluoroscopy-induced skin necrosis.

A 48-year-old obese man with a history of hypertension, coronary artery disease, and status post–quadruple bypass presentedwithan8-monthhistoryofpainfululcerationon therightmidback.The initial lesionwasdescribedasa4-cm square area of eroded eczematous dermatitis, which later developed 2 areas of ulceration that worsened despite various treatments, includingoral and intralesional corticosteroids, oral antibiotic agents (erythromycin and ciprofloxacin), dapsone, and a hydrocolloid dressing. Six months after onset, after initiation of high-dose prednisone therapy, examination revealed progression of the lesions into a large, necrotic ulcer measuring 4 4 3 cm, with copious amounts of expressible pus and foulsmelling discharge and muscle readily palpable on probing. Initial laboratory tests revealed a normal blood count, liver function, and serum protein electrophoresis. Wound culture revealed moderate Enterococcus species, diphtheroids, rare hemolytic streptococcus B, and -hemolytic Streptococcus species. On immediate hospital admission, it was first discovered that he had undergone a complicated single-vessel angioplasty lasting over 21⁄2 hours, during which he experienced angina and electrocardiogram changes, 1 month before his initial presentation to a dermatologist. Fluoroscopy-induced skin necrosis was likely the cause of his cutaneous ulceration. The wound was explored under general anesthesia, and debridement of the necrotic, infected material was performed. Histopathologically, there was extensive necrosis of the reticular dermis and subcutis, neutrophilic infiltrates, and numerous gram-positive cocci, occasionally in chains. Wound culture grew Enterococcus. Intravenous ampicillin sulbactam was administered, 3 g every 6 hours. A second surgical debridement was performed 1 week later and included a portion of fascia, which demonstrated serous exudation and inflammation. The depth of the wound was such that a latissimus dorsi musculocutaneous flap was necessary for closure.