A pedicled muscle flap based solely on a neural pedicle.

We tested the hypothesis that the intrinsic vascular plexus of the motor nerve could support viability in a rat hindlimb muscle flap. In a preliminary study, we examined the course and vascularity of the sciatic nerve, the peroneal nerve, and the peroneous longus muscle in the rat hindlimb via anatomic dissection, microangiography, and histologic study (n = 10 animals). On the basis of this examination, the peroneous longus muscle was chosen as our experimental model in this study. In 12 animals, the peroneus longus was acutely elevated, which severed all tendinous and vascular structures, this left the muscle pedicled on the motor nerve only (Group I). Animals in Group II underwent a staged elevation of the flap with division of the vascular pedicle, the tendon of insertion, and the tendon of origin during separate procedures that were 5 days apart (n = 12). Muscle viability was evaluated by gross inspection, measurement of muscle weight and length, nitroblue tetrazlium (NBT) staining, microangiography, and histology. NBT staining demonstrated that immediate elevation of the peroneus longus muscle flaps led to an average necrotic area of 80.6% +/- 9.8% (Group I). A significant improvement in viability was observed for muscle flaps of animals in Group II, with peroneus longus muscle necrosis averaging 25.6% +/- 9.3%. Microangiography demonstrated that the intrinsic vascularity of nerve was increased dramatically in Group II. These data support the hypothesis that the intrinsic vascular plexus of the motor nerve of a skeletal muscle can support at least partial viability of a muscle flap. However, this vascular axis is inadequate to support complete viability of a muscle flap if the flap is elevated immediately. If a staged elevation affects a surgical delay, the viability of a muscle flap elevated on a neural pedicle can be increased significantly. With adjustments in the delay procedure, this strategy may allow transfer of muscle flaps when maintenance or reconstitution of the primary vascular axis is not possible.