Further investigations on the pathophysiology of the compartmental syndrome.

A model compartmental syndrome is described in rabbits in which the intracompartmental pressure may be accurately controlled to investigate the pathophysiologic changes resulting from increased intracompartmental pressure. Oxygenation in the tibialis anterior muscle was measured using a medical mass spectrometer. The Po2 declined with increasing intracompartmental pressure from a control value of 10.8 mmHg to a minumum of 2.8 mmHg at a pressure of 90 mmHg. The functional integrity of the peroneal nerve and compartmental muscle was tested by direct electrical stimulation. Functional deficits were first noted when an intracompartmental pressure of 40 mmHg was exerted for 6 hours. The incidence of functional losses increased with increasing pressures and durations of pressure application. All animals subjected to 100 mmHg for eight or more hours lost both nerve and muscle function. These investigations demonstrate that increased intracompartmental pressure alone, without other associated vascular injury, may produce muscle hypoxia and loss of neuromuscular function. The continuous monitoring of intracompartmental pressures may, therefore, be a useful clinical adjunct in the management of patients at risk for a compartmental syndrome.