Compartment syndrome: a quantitative study of high-energy phosphorus compounds using 31P-magnetic resonance spectroscopy.

The purpose of this study was to quantitate the intracellular high-energy phosphate compounds during 6 hours of tissue ischemia in the anterior tibial compartment of beagles subjected to an induced traumatized compartment syndrome. The goal of this work was to provide clinicians with objective criteria to augment clinical judgment regarding surgical intervention in the impending compartment syndrome. A beagle model was utilized in which the Delta pressure (difference between the mean arterial pressure and compartment pressure) could be controlled. The model, in conjunction with 31P-magnetic resonance spectroscopy (MRS), allowed a measure of high-energy phosphate compounds and pH in the compartment at various Delta pressures. The extent of ischemic metabolic insult in the compartment was then quantitated. Our data suggest the following: 1) lower Delta pressures result in a proportionally greater drop in the intracellular phosphocreatine ratio and pH; 2) at lower Delta pressures, there is proportionally greater decline in the percentage recovery post-fasciotomy; 3) blood pressure is extremely important and periods of hypotension may result in increased muscle damage at lower compartment pressures.

The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy.

In an experimental ischemic compartment syndrome in dogs, phosphorus (31P) nuclear magnetic resonance (NMR) spectroscopy was used to determine the tissue pressure threshold at which resting skeletal muscle begins to use anaerobic energy sources due to insufficient cellular oxygen delivery. The interactive effects of systemic perfusion pressure and moderate muscle trauma on this anaerobic threshold were also evaluated. The severity of cell injury produced by various degrees of compartment pressurization over an eight-hour period was concomitantly studied using muscle biopsy and electron microscopy. Clinical correlation of a preliminary patient series studied using 31P-NMR demonstrated that the threshold for cellular metabolic derangement in skeletal muscle subjected to increased tissue pressure was more closely associated with the difference between mean arterial blood pressure (MABP) and compartment pressure than with the absolute compartment pressure alone. The difference is termed MABP-compartment pressure, or delta P. The lowest delta P at which a normal cellular metabolic state can be maintained is approximately 30 mmHg in normal muscle and 40 mmHg in moderately traumatized muscle. It is imperative to interpret compartment pressure measurements in light of the degree of soft tissue trauma sustained and the patient's blood pressure, as well as the clinical signs and symptoms.

Intramuscular pressure, muscle blood flow, and skeletal muscle metabolism in chronic anterior tibial compartment syndrome.

One hundred eight patients with lower leg pain of unknown cause underwent intramuscular pressure measurements by the wick technique. Fifteen patients (14%) were found to have a chronic anterior tibial compartment syndrome. In these patients the intramuscular pressure was significantly increased at rest and during and after exercise as compared with normal subjects. The pressure increase after exercise was long-lasting (40 minutes). Biopsies of the anterior tibial muscles showed increased water content, which may explain the elevated pressures. Muscle blood flow during exercise as measured by the xenon-133 clearance technique was decreased, and muscle lactate concentration was increased in the anterior tibial muscles. Fasciotomy relieved pain and normalized intramuscular pressure, muscle blood flow, and skeletal muscle metabolism.

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.