Nerve injuries associated with inversion sprains of the ankle have been mentioned in the literature on a case presentation basis only. Sixty-six consecutive patients with Grade II (30) and Grade III (36) ankle sprains were examined by electromyography 2 weeks after injury to determine the presence and distribution of nerve injuries. Ankle active range of motion (AROM) and the number of weeks postinjury when the patient could heel/toe walk and return to full activity were also noted. Five patients (17%) with Grade II sprains had mild peroneal nerve injury and three (10%) injured the tibial nerve. Clinical measurements were normal by the end of the second week. Thirty-one patients (86%) with Grade III sprains injured their peroneal nerve, while 30 (83%) incurred posterior tibial nerve injury. Ankle AROM was impaired, and heel/toe walking (5.1 weeks) and return to full activity (5.3 weeks) were markedly prolonged. The likely cause of this injury is considered to be a mild nerve traction or a hematoma in the epineural sheath at the bifurcation of the sciatic nerve into peroneal and posterior tibial branches. This report indicates that a consistently high percentage of patients with Grade III ankle sprains sustain a significant injury to both motor nerves in the leg and that rehabilitation time is markedly prolonged.

A pattern of variability was noted in the rehabilitative progress of patients undergoing knee surgery. Forty-eight patients who underwent routine medial or lateral meniscectomy were studied in a controlled, randomized, prospective investigation designed to identify electromyographic (EMG) and functional deficits associated with using a pneumatic tourniquet in knee surgery. The control group (24 individuals) underwent knee surgery without te use of a tourniquet. Six weeks postoperatively all patients were studied by EMG and functionally by determining the single leg vertical leap of the affected leg and expressing this as a percentage of that accomplished by th sound leg. The results were: (1) 17 of 24 (71%) of the tourniquet group had EMG evidence of denervation and a functional capacity of 39% of the normal leg. (2) 7 of 24 (29%) of the tourniquet group had no evidence of denervation and a 71% functional capacity. (3) The control group had no evidence of denervation and a functional capacity of 79%. Of the patients on whom a tourniquet was used, total tourniquet time and pressure did not vary significantly between those patients who demonstrated EMG findings and those who did not. Arthrotomy in the absence of a tourniquet required more attention to hemostasis, but did not present overwhelming difficulty. Operative time was slightly prolonged. This investigation suggests that the ideal of early return to functional activity after knee surgery can best be accomplished by avoiding use of a pneumatic tourniquet.

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In a recent study (Nitz et al., Exp Neurol 94:264-279, 1986) the validity of a rat animal model to examine effects of tourniquet compression and vascular occlusion on limb motor function, leg girth, and electrophysiologic changes was established. Here we report observations on sciatic nerve morphologic and morphometric alterations of these same animals. The hindlimbs of 90 rats were compressed by a pneumatic tourniquet at clinically relevant pressures (200 to 400 mm Hg) for 1 to 3 hours, and the sciatic nerve was assessed by light and electron microscopy at 1, 3, and 6 weeks post compression. The nerves were also examined from five additional animals at each of these time intervals following arterial ligation and sciatic nerve epineurectomy (30 rats). Percentage of degenerating myelinated nerve fibers and volume fraction of mast cells and fibroblasts were quantified morphometrically. The percentage of degenerating myelinated nerve fibers after moderate to severe tourniquet compression and vascular manipulation was similar and ranged from 15% to 45%. Tourniquet compression, but not vascular occlusion, resulted in an increase of mast cells and fibroblasts and disruption of endothelial cells of endoneurial vessels. The results suggest that clinically relevant tourniquet compression causes a secondary increase in vascular permeability, intraneural edema, and subsequent prolonged tissue ischemia, resulting in nerve degeneration.

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