Medline ® Abstracts for References 15,46,47

Acute compartment syndrome is a potentially devastating condition in which the pressure within an osseofascial compartment rises to a level that decreases the perfusion gradient across tissue capillary beds, leading to cellular anoxia, muscle ischemia, and death. A variety of injuries and medical conditions may initiate acute compartment syndrome, including fractures, contusions, bleeding disorders, burns, trauma, postischemic swelling, and gunshot wounds. Diagnosis is primarily clinical, supplemented by compartment pressure measurements. Certain anesthetic techniques, such as nerve blocks and other forms of regional and epidural anesthesia, reportedly contribute to a delay in diagnosis. Basic science data suggest that the ischemic threshold of normal muscle is reached when pressure within the compartment is elevated to 20 mm Hg below the diastolic pressure or 30 mm Hg below the mean arterial blood pressure. On diagnosis of impending or true compartment syndrome, immediate measures must be taken. Complete fasciotomy of all compartments involved is required to reliably normalize compartment pressures and restore perfusion to the affected tissues. Recognizing compartment syndromes requires having and maintaining a high index of suspicion, performing serial examinations in patients at risk, and carefully documenting changes over time.

An experimental and clinical tehcnique of measuring tissue pressures within closed compartments demonstrates a normal tissue pressure is approximately zero mmHg, and increased markedly in compartmental syndromes. There is inadequate perfusion and relative ischemia when the tissue pressure within a closed compartment rises to within 10-30 mm Hg of the patient's diastolic blood pressure. Fasciotomy is usually indicated, therefore, when the tissue pressure rises to 40-45 mm Hg in a patient with a diastolic blood pressure of 70 mm Hg and any of the signs or symptoms of a compartmental syndrome. There is no effective tissue perfusion within a closed compartment when the tissue pressure equals or exceeds the patient's diastolic blood pressure. A fasciotomy is definitely indicated in this circumstance, although distal pulses may be present. The measurement of tissue pressure aids in the early diagnosis and appropriate treatment of compartmental syndromes.

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.