The effects of limb elevation and dependency on local arteriovenous gradients in normal human limbs with particular reference to limbs with increased tissue pressure.

Although clinically useful for the control of extremity swelling, the combination of compression and elevation may significantly reduce the local arteriovenous gradient.

Transcutaneous oxygen tension measurement in peripheral vascular disease.

To date, results of laboratory and clinical investigations suggest that transcutaneous pO2 measurements hold considerable promise as a technique for evaluating the adequacy of cutaneous circulation. The advantages of this technique are that it is simple to use, noninvasive and does not require the use of radioactive isotopes. Since the available data are, as yet, insufficient to confirm the reliability of this technique, a prospective study of segmental transcutaneous pO2 values in patients with peripheral vascular disease is being continued. These values are then being correlated with the subsequent clinical course.

Diagnosis and management of compartmental syndromes.

Patients at risk for compartmental syndromes challenge both the diagnostic and the therapeutic abilities of the physician. Suboptimum results may be due to delays in diagnosis and treatment, to incomplete surgical decompression, and to difficulties in the management of the limb after decompression. Although careful clinical assessment permits the diagnosis of a compartmental syndrome in most patients, we have found measurement of tissue pressure and direct nerve stimulation to be helpful for resolving ambiguous or equivocal cases. In our experience, the four-compartment parafibular approach to the leg and the ulnar approach to the volar compartments of the forearm provide efficient and complete decompression of potentially involved compartments. The skeletal stabilization of fractures associated with compartmental syndromes may facilitate management of the limb after surgical decompression.

Nicolas Andry Award. Increased tissue pressure and its effects on muscle oxygenation in level and elevated human limbs.

Increased tissue pressure is an important cause of local circulatory compromise. In both rabbit and human model systems known external pressures were applied to otherwise normal limbs. Side-by-side comparison of the wick and the infusion techniques revealed that both methods of pressure measurement yielded essentially identical results when tissue pressure was elevated. Measured tissue pressure significantly exceeded the external pressure applied to the limb. Using a mass spectrometer-Teflon membrane catheter system, we monitored muscle PO2 and PCO2 at different applied pressures. Muscle PO2 decreased progressively with increasing tissue pressure but did not approach zero until tissue pressure exceeded local arterial pressure. Comparison of results with level and elevated limbs indicated that elevation of an extremity dramatically lowered its tolerance for increased tissue pressure. Although they may be clinically useful modalities, these are conditions in which compression and elevation have a significant potential for compromising local circulation.

Physiological effects of increased tissue pressure.

The physiological effects of increased tissue pressure were studied using a model system in which known pressures were applied uniformly to the hindlimbs of rabbits for a period of 5 h. Muscle blood flow was monitored using a new argon washout technique. Muscle pO2, pCO2, and pAr were measured using a Teflon membrane catheter-mass spectrometer system. The myoneural conduction velocity served as a measure of the functional status of the limb. Higher tissue pressures led to successively greater compromise of muscle blood flow and pO2. Myoneural conduction velocity decreased significantly only when a pressure of 80 mm of mercury was applied, at which time muscle blood flow and pO2 were zero. These observations suggest that abnormalities of neuromuscular function are relatively late manifestations of a pressureinduced circulatory deficiency.

Compartmental syndromes.

Because the compartmental syndrome occurs under such a wide variety of circumstances and because early diagnosis is vital, it is essential that all physicians be familiar with this condition. Results of relatively simple clinical tests permit the diagnosis in most instances. Ancillary diagnostic techniques may prove helpful in questionable instances. Prompt, complete decompression of the affected compartments can preserve function and minimize complications.

A model compartmental syndrome in man with particular reference to the quantification of nerve function.

A human model system was used to investigate the effect of increased tissue pressure on different parameters of the function of the nerves and muscles in the anterior compartment of the leg. Abnormalities of sensation, strength, motor nerve-conduction velocity, and compound muscle-action-potential amplitude occurred in a parallel fashion when the intracompartmental pressure exceeded a threshold value. This threshold was significantly lowered by elevation of the extremity. Grossly abnormal functional parameters were consistently elicited when the peripheral pulse remained intact. The motor nerve-conduction velocity and compound muscle-action-potential amplitude appear to be reliable, non-invasive, and quantitative parameters of the physiological status of the neuromuscular tissue within the compartment.

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.

Monitoring of intramuscular pressure.

Increased pressure within an osteofascial compartment may produce a compartmental syndrome, one of the principal causes of local circulatory compromise in traumatized extremities. In certain instances, monitoring of intracompartmental pressure may be a valuable adjunct in the clinical evaluation of patients at risk for this syndrome.