An algorithm to improve outcomes of radial forearm flap donor site.

Abstarct Background: Due to the high rate of donor site complications the Radial Forearm Flap (RFF) has lost ground in favor of the Antero-lateral tight flap (ALT) and other flaps. We have designed a reconstruction algorithm for reconstruction of its donor site. The goal of this study was to retrospectively evaluate the impact of this algorithm on RFF donor site complication rates. METHODS: The authors analyzed retrospectively 31 patients who underwent free radial forearm flap reconstruction between November 2009 and May 2013. Donor site complications were compared with data from patients treated before introdutction of the algorithm. Within the group were compared patients in which the flap was harvested suprafascial with those in which the flap was harvested as subfascial. RESULTS: Before application of the algorithm, there was a 23.3% complication rate at the RFF donor site, in our experience. After introduction of the algorithm, complication rate has dropped to 3.2%, consisting in a partial skin graft necrosis treated by local wound-care and healed without further intervention. CONCLUSIONS: Application of the algorithm described has led to a significant reduction in RFF donor site complication rates. This demonstrates that if flap donor sites are analyzed and tailor treated in the same way as primary defects are, instead of being given secondary importance and just grafted, outcomes improve.

Irreversible changes occurring in long-term denervated Schwann cells affect delayed nerve repair.

OBJECTIVE Multiple factors may affect functional recovery after peripheral nerve injury, among them the lesion site and the interval between the injury and the surgical repair. When the nerve segment distal to the lesion site undergoes chronic degeneration, the ensuing regeneration (when allowed) is often poor. The aims of the current study were as follows: 1) to examine the expression changes of the neuregulin 1/ErbB system during long-term nerve degeneration; and 2) to investigate whether a chronically denervated distal nerve stump can sustain nerve regeneration of freshly axotomized axons. METHODS This study used a rat surgical model of delayed nerve repair consisting of a cross suture between the chronically degenerated median nerve distal stump and the freshly axotomized ulnar proximal stump. Before the suture, a segment of long-term degenerated median nerve stump was harvested for analysis. Functional, morphological, morphometric, and biomolecular analyses were performed. RESULTS The results showed that neuregulin 1 is highly downregulated after chronic degeneration, as well as some Schwann cell markers, demonstrating that these cells undergo atrophy, which was also confirmed by ultrastructural analysis. After delayed nerve repair, it was observed that chronic degeneration of the distal nerve stump compromises nerve regeneration in terms of functional recovery, as well as the number and size of regenerated myelinated fibers. Moreover, neuregulin 1 is still downregulated after delayed regeneration. CONCLUSIONS The poor outcome after delayed nerve regeneration might be explained by Schwann cell impairment and the consequent ineffective support for nerve regeneration. Understanding the molecular and biological changes occurring both in the chronically degenerating nerve and in the delayed nerve repair may be useful to the development of new strategies to promote nerve regeneration. The results suggest that neuregulin 1 has an important role in Schwann cell activity after denervation, indicating that its manipulation might be a good strategy for improving outcome after delayed nerve repair.