Peripheral nerve-conduction block by high muscle-compartment pressure.

Abstract

Using an experimental model 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 mm Hg) and at elevated (10-120 mm Hg) intracompartmental pressures. The pressures were elevated by the infusion of autologous plasma and were continuously monitored by 2 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 80-120 mm Hg, nerve conduction was completely blocked in < 2 h. Complete block of conduction was obtained at a pressure as low as 50 mm Hg. The conduction block was incomplete after 6-8 h of pressurization at 40 and 30 mm Hg. At pressures of 20 mm Hg or less for 8 h, conduction remained normal. The presence of a complete conduction block correlated with histopathological evidence of axonal degeneration observed 3 wk after compartmental pressurization. The results in these experiments helped to identify a critical level (30 mm Hg) and duration (6-8 h) of pressure at which fasciotomy should be performed in patients with a threatened compartment syndrome.