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Large, full-thickness scalp defects represent a reconstructive challenge that has benefitted greatly from the introduction of microsurgical techniques. The authors review their experience with 16 patients with acquired defects of the scalp for which local or regional reconstructive options were unavailable. The mean age at the time of operation was 44.8 years. Nine patients underwent resection of malignant scalp lesions, followed immediately by free-flap coverage. Six patients required revision procedures for unstable scar as a result of prior trauma (2), old scalp avulsions (2), and multiple intracranial procedures (2). The remaining patient underwent replantation of an acutely avulsed scalp. The free-flap donor sites utilized included latissimus (6), scapular (3), radial forearm (2), rectus abdomnis (2), and omentum (2). Vein grafts were required in four cases. All flaps survived, although one required anastomotic revision and skin grafting for superficial loss. Additional complications were limited to seromas at two latissimus donor sites. Tumor control rates were poor, with all malignancy-associated defects having persistent disease or recurring soon after surgery. All patients eventually achieved full defect coverage. The authors conclude that microsurgical reconstruction is a reliable option for providing stable coverage of large, complex, scalp defects.

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The authors have demonstrated previously that pretreatment with deferoxamine, an iron chelator and antioxidant, at the time of release in acute nerve compression, provided protection against ischemia/reperfusion (I/R) injury. In the present study, they evaluated whether therapeutic intervention with hydroxyethyl-starch-bound deferoxamine (HES-DFO) at the time of release of the chronically-compressed peripheral nerve protects the nerve from I/R injury. The sciatic nerves of 43 male Sprague-Dawley rats, weighing 325 to 350 g, were subjected to 8 weeks of compression with Silastic tubing. The treatment group received intravenous HES-DFO (70 mg/kg) at the time of decompression, while the control group received an equal volume of intravenous hetastarch vehicle at the same time schedule and route. Nerve-tissue samples from the compression site, as well as contralateral noncompressed nerves, were assayed for malondialdehyde (MDA), a marker of I/R injury. The control group exhibited MDA levels up to five times normal, and did not return to normal for 21 days. In contrast, the HES-DFO group had MDA levels that were not statistically significantly different from normal levels. The results confirm that pretreatment with HES-DFO prior to the surgical decompression of chronically-compressed nerve provides marked protection against I/R injury.