Compartmental Syndromes.

Edited By: Frederick A. Matsen III, M.D., Winston J. Warme, MD
Last updated Thursday, February 10, 2005

Pathophysiology

Reduction in tissue blood flow

Sequential increases in tissue pressure produce increasingly more severe reductions in tissue blood flow and tissue oxygenation. No evidence has been found to support the concept of a "critical pressure" above which the circulation is suddenly compromised.

Increased tissue pressure results in an increase in local venous pressure, which produces a diminished local arteriovenous gradient. When increased tissue pressure reduces the local arteriovenous gradient and local blood flow to the point where the metabolic demands of the tissue are no longer met, loss of tissue function, and thus a compartmental syndrome, ensue.

Movie

• Pathophysiology of compartmental syndromes (0.43 MB)

Pathophysiology of increased tissue pressure

The normal function of tissue is maintained by circulation that is sufficient to meet the tissue's metabolic needs. In a compartmental syndrome, increased tissue pressure compromises local circulation to the point where the tissue's metabolic needs are no longer met and functional abnormalities ensue. This chapter will first review the data demonstrating that increased tissue pressure compromises tissue circulation, oxygenation, and function and then proceed to a discussion of the mechanisms by which this pressure-induced circulatory compromise may be produced.

The fact that increased tissue pressure compromises local circulation has been demonstrated by the plethysmographic studies of Ashton. 1 A similar effect has been demonstrated by others who observed the washout rates of various indicators. Rorabeck and Clarke 2 and Rorabeck and MacNab 3 used technetium and xenon, Dahn et al 4 used xenon, Sheridan et al 5 used rubidium, and we 6 have more recently used argon. Taken together these studies indicate that pressure as low as 20 mm Hg applied to a limb can significantly reduce local blood flow. This reduction in blood flow becomes increasingly severe at higher pressures. In none of these studies was there evidence for a "critical" pressure above which tissue blood flow suddenly became compromised.

One of the most important functions of the local circulation is to deliver oxygen to the tissue. The Teflon (Du Pont) membrane catheter-mass spectrometer system is useful for continuously monitoring muscle PO2, which is in turn a reflection of the balance between tissue oxygen delivery and tissue oxygen consumption. 5-9 We conducted studies in rabbit and human model systems correlating anterior tibial muscle PO2 with externally applied and measured tissue pressures. The results were very similar to those of the blood flow studies; that is, higher tissue pressures resulted in lower muscle PO2 values 6 8 l0. In the human subjects muscle PO2 was significantly reduced by an applied pressure of 20 mm Hg. Muscle PO2 values decreased essentially linearly as the applied pressure was increased. Thus, again no critical pressure was observed, but rather a greater compromise of muscle PO2 at higher tissue pressures.

Increased tissue pressure also compromises neuromuscular function. Sheridan et al 5 evaluated the effect of inflation of an intracompartmental latex balloon on the response of nerve and muscle to direct electrical stimulation in a rabbit model system. Higher pressures and longer periods of pressure application produced more frequent functional losses. In another rabbit model system, we arrested nerve conduction by applying external pressure to the hindlimb 6. Rorabeck and Clark 2 and Hargens et al 11 slowed nerve conduction velocity by the pressure-controlled infusion of blood or plasma into the anterior compartment of the legs of dogs. We were able to produce similar decrements in human nerve conduction velocity through the external application of pressure to the leg 12.

In theory these pressure-induced functional deficits could be due either to a direct mechanical effect of increased tissue pressure or to reduced tissue circulation. We may argue strongly for the second alternative because the amount of pressure a limb can tolerate before functional abnormalities are produced is altered by factors affecting local blood flow: limb elevation, arterial occlusion, hypotension, and hemorrhaged 13 If the effect of pressure on nerve and muscle were purely mechanical, these factors would not be expected to change the pressure tolerance. The concept of tissue pressure tolerance will be discussed in greater detail in Chapter 4.

This review of the physiological effects of increased tissue pressure indicates that tissue circulation is compromised by applied pressures as low as 20 mm Hg and that tissue circulation is increasingly reduced as applied pressure is raised from this value. Any theory concerning the mechanism by which increased pressure affects local circulation must be consistent with these observations. In this light let us review several of the proposed mechanisms of pressure-induced circulatory compromise.

Benjamin, 14 Eaton and Green, 15 Foisie, 13 and Gardner 17 suggested that increased tissue pressure induces arterial spasm, which, in turn, produces intracompartmental ischemia. Although there is some clinical and laboratory evidence to support this mechanism, l4' 15 the commonly observed preservation of pulses distal to the affected compartment would tend to refute it. 19-20 Furthermore, arteriograms performed on patients with compartmental syndromes usually do not show arterial spasm, but rather gradual tapering of the vessels as they course through the affected compartment.

Burton 21-22 and later Ashton 1 observed that as progressively higher external pressures were applied to a limb, blood flow ceased before the difference between mean arterial and applied pressure became zero. These observations have given rise to the critical closure theory. According to this theory, a significant transmural pressure (mean arteriolar pressure minus tissue pressure) is required to maintain arteriolar patency. This transmural pressure is necessary because of the high tension in the walls of arterioles which is actively produced by smooth muscle contraction. When tissue pressure is elevated to the point that transmural pressure is insufficient, the arterioles actively close and blood flow ceases. Support for critical closure is gained from the studies of Ashton 1 on the effect of limb temperature. She demonstrated that the transmural pressure at which circulation ceased varied with limb temperature in a manner consistent with the critical closure theory: a greater transmural pressure was required to maintain blood flow when the tone of arteriolar wall smooth muscle was increased by local cooling. Although critical closure may occur over the short term, I doubt that this mechanism could produce prolonged compartmental ischemia because ischemia is a strong local stimulus for vasodilatation. Furthermore, in the presence of ischemia there is a diminishing energy supply available for the maintenance of active smooth muscle contraction. l, 23

Dahn et al 4 proposed the "tidal wave" theory. They suggested that unless tissue pressure is significantly below arterial diastolic pressure, the microcirculation will not remain open long enough to perfuse the capillaries, but will rather ebb and flow on the arteriolar side of the microcirculation. While this is a picturesque theory, there is, as yet, insufficient evidence to support it.

Hargens et al 24- 25 made direct measurements of normal capillary pressure and found it to be between 20 and 33 mm Hg. They postulated that when tissue pressure exceeds these values, capillary blood flow is reduced by microvascular occlusion. Unfortunately, no measurements of capillary pressure have been made in the presence of increased tissue pressure. If one assumes that capillary pressure remains approximately 30 mm Hg when tissue pressure is increased, it would seem reasonable to expect these vessels to become occluded if tissue pressure exceeded this level. However, venous pressure rises in the presence of increased tissue pressure. 28-23 If venous pressure rises, capillary pressure must also rise; thus, the 30 mm Hg value for capillary pressure does not appear to be relevant to the situation in which tissue pressure is elevated.

Several investigators, including Kjellmer, 29 Reneman, 30 and Matsen et al, 27 31 have proposed what might be referred to as the arteriovenous gradient theory. According to this theory, increases in tissue pressure reduce the local arteriovenous gradient and thereby local blood flow. When blood flow is reduced to the point where it no longer meets the metabolic demands of the tissue (but not necessarily to zero), functional abnormalities, and thus a compartmental syndrome, result.

The relationship between arteriovenous gradient and local blood flow is as follows:

LBF = (PA - PV)/R

where LBF is local blood flow, PA is local arterial pressure, PV is local venous pressure, and R is the local vascular resistance. Because veins are collapsible tubes, the pressure inside them (PV) cannot be less than local tissue pressure (PT). Thus, when tissue pressure rises, the pressure in the local veins must also rise. This increased local venous pressure reduces the local arteriovenous gradient. This phenomenon has been confirmed by the direct measurement of local venous pressure 27-29.

Some reduction in local arteriovenous gradient can be compensated for by changes in local vascular resistance. This process, known as autoregulation, 33 maintains local blood flow over a range of arteriovenous gradients. However, when the arteriovenous gradient is significantly reduced, autoregulation becomes relatively ineffective. 23 At this point the local blood flow is determined primarily by the local arteriovenous gradient. With further increases in tissue pressure, local blood flow is reduced to the point where it no longer meets the metabolic demands of the tissue, functional abnormalities ensue, and a compartmental syndrome results.

The arteriovenous gradient theory is consistent with the observed reduction in tissue blood flow accompanying even a small increase in tissue pressure and with the greater reductions in tissue blood flow observed as tissue pressure is further increased. It emphasizes the interrelationships of tissue pressure, local venous pressure, local blood flow, and the metabolic demands of the tissue.

Clinically it is useful because it predicts that a reduction in local arterial pressure (for example, from elevation of the limb above the heart) will exaggerate the circulatory effect of any given tissue pressure increase. It further predicts that lowering local venous pressure by decompressing the tissue (lowering local tissue pressure) is an effective method for restoring circulation if a compartmental syndrome ensues. Finally, this theory predicts the preservation of pulses and distal circulation frequently seen in a compartmental syndrome. The pulses and distal circulation may remain intact for two reasons. First, the increases in tissue pressure usually observed in compartmental syndromes have a minimal effect on arterial flow. Second, the venous pressure in the digits distal to the compartment is usually normal; thus, a normal digital arteriovenous gradient and normal digital blood flow result.

Surgery for Compartmental Syndromes at the University of Washington

How useful was this page or article? This article is rated out of 5 stars (374 ratings). Not useful at all Not very useful Useful Very useful Extremely useful