• Takashi Suzuki, Masateru Shindo, Yuichi Kataoka, Isao Kobayashi, Hiroshi Nishimaki, Shinichiro Yamamoto, Masataka Uchino, Naonobu Takahira, Kazuhiko Yokoyama, and Kazui Soma.
• Emergency Medicine and Critical Care Center, Kitasato University School of Medicine, Sagamihara, Japan. taku@mars.dti.ne.jp
• Arch Orthop Trauma Surg. 2005 Sep 1;125(7):448-52.

BackgroundTranscatheter arterial embolization (TAE) can cause gluteal skin and muscle necrosis. However, the ultimate and typical signs of gluteal necrosis resulting from TAE have not yet thoroughly been investigated.MethodsFrom January 1995 to December 2003, 165 pelvic fractures were managed with TAE to control retroperitoneal bleeding at our level 1 trauma center. From these, 12 patients suffered gluteal muscle and skin necrosis. We reviewed the medical records of these 12 patients for age, gender, fracture type, embolic sites, computed tomography (CT) findings, serum creatine kinase level, site of skin necrosis, time from injury to skin necrosis, treatment, and outcome.ResultsAll 12 patients underwent TAE of the bilateral internal iliac arteries with gelatin sponge slurries. One patient suffered from an infection of the gluteal muscle from an open fracture site. Five patients presented with signs of gluteal soft tissue injuries on admission. Of these, four had skin abrasions and three revealed fluid or air collection under the gluteal skin on CT. The remaining six patients showed no evidence of soft tissue injuries on admission, and the lesions appeared between 2 days and 7 days after their admission. In these six patients, low-density areas (LDAs) of gluteal muscle with a clear border on the CT were observed following the appearance of skin lesion. The skin necrosis was located in the center of either or both buttocks, and signs of ischemia were clearly demarcated from the adjacent normal tissue. Four of 12 patients died from sepsis, three of whom suffered from uncontrollable gluteal infections that had been pointed out as LDAs on the CT.ConclusionsIn every patient with gluteal necrosis associated with pelvic fracture following TAE, initial traumatic contusion cannot be ruled out as contributing to the development of the necrosis. However, for patients who undergo TAE of the bilateral internal iliac artery and who show clear-border LDAs on CT, skin necrosis centered on the buttock, and the delayed appearance of a skin lesion, careful attention must be given in the event of an arterial obstruction due to TAE.

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