Are free radical scavengers beneficial in the treatment of compartment syndrome after acute arterial ischemia?

Because it is postulated that compartment syndrome developing secondary to an acute arterial occlusion may be due to reperfusion injury, oxygen-derived free radicals have been implicated in its genesis. To assess the possible beneficial effect of free radical scavengers in this setting, we used a previously established in vivo canine model of compartment syndrome to compare four groups: group I, no treatment; group II, prophylactic fasciotomy; group III, intravenous albumin conjugated superoxide dismutase (SOD); group IV, intravenous mannitol (hydroxyl radical scavenger). Both hind limbs were completely devascularized at the popliteal level except for an isolated pedicle to the anterior compartment. The right limb served as the nonischemic control, whereas the left underwent 8 hours of ischemia followed by reperfusion. Continuous monitoring of transfascial oxygen tension (tfPO2) demonstrated severe ischemia during occlusion (tfPO2 5.7 +/- 5.1 mm Hg) and restoration of blood flow with reperfusion (mean tfPO2 50 to 60 mm Hg). Measurements of compartment pressure were significantly higher after reperfusion in groups I, III, and IV when compared with those of group II (p less than 0.001, groups I and II; p less than 0.01, group IV). Extent of muscle necrosis assessed by technetium pyrophosphate scanning and expressed as a ratio of left to right legs was as follows: group I, 8.9 +/- 5.0; group II, 2.6 +/- 0.5; group III, 2.8 +/- 0.8; group IV, 1.8 +/- 0.6. Muscle contraction studies 16 hours after reperfusion indicated abnormal findings in all but group II. In conclusion, administration of free radical scavengers did not preserve normal neuromuscular function despite a significant reduction in muscle damage.(ABSTRACT TRUNCATED AT 250 WORDS)