PERIPHERAL NERVE-CONDUCTION BLOCK BY HIGH MUSCLE-COMPARTMENT PRESSURE

Using an experimental model developed to study the effects of increased tissue-fluid pressure on peroneal-nerve function within the anterolateral muscle compartment of the hind limbs of 22 dogs, nerve-conduction velocities and the amplitudes of the action potentials from the extensor digitorum brevis muscle were measured at normal (-3 ± 2 millimeters of mercury) and at elevated (ten to 120 millimeters of mercury) intracompartmental pressures. The pressures were elevated by the infusion of autologous plasma and were continuously monitored by two wick catheters. In the presence of severe intracompartmental edema, there was a gradual decline in the amplitude of the action potentials, followed by complete conduction block. The time required to produce the conduction block was inversely proportional to the intracompartmental fluid pressure. At pressures between eighty and 120 millimeters of mercury, nerve conduction was completely blocked in less than two hours. Complete block of conduction was obtained at a pressure as low as fifty millimeters of mercury. The conduction block was incomplete after six to eight hours of pressurization at forty and at thirty millimeters of mercury. At pressures of twenty millimeters of mercury or less for eight hours, conduction remained normal. The presence of a complete conduction block correlated with histopathological evidence of axonal degeneration observed three weeks after compartmental pressurization. The results in these experiments helped to identify a critical level (thirty millimeters of mercury) and duration (six to eight hours) of pressure at which fasciotomy should be performed in patients with a threatened compartment syndrome.