Compartmental Syndromes.

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

Figure 1 - Tissue pressure monitoring

Figure 2 - Formal exercise tests

About compartmental syndromes

Summary

Compartmental syndromes challenge even the best clinicians. These syndromes occur when locally increased tissue pressure compromises local circulation and neuromuscular function. The incidence of compartmental syndromes is rising along with the frequency of their various etiologies: extremity trauma, limb ischemia, intensive use of muscles, extremity surgery, and drug and alcohol abuse. Despite this increase in frequency, the compartmental syndrome remains sufficiently uncommon in the experience of the average practitioner that he may be unfamiliar with its diagnosis and management. Because prompt treatment of compartmental syndromes is essential, the consequences of this unfamiliarity may be serious. Even to those most familiar with them, compartmental syndromes pose major problems in pathogenesis, diagnosis, and treatment. For example, the precise effect of increased tissue pressure on the microcirculation-the key to understanding compartmental syndromes-remains a matter of considerable conjecture.

The clinical diagnosis of a compartmental syndrome is frequently made difficult by the fact that other conditions may produce similar symptoms and signs. Although new diagnostic methods, such as tissue pressure measurement, have been described, they have failed to completely resolve these problems of differential diagnosis. This failure is a result of practical problems in the application of these techniques and in the interpretation of their results. Thus, the physician is called upon to synthesize all the available information in arriving at the correct diagnosis.

Adequate treatment of compartmental syndromes requires the wide opening of all potentially affected compartments. Unfortunately, the institution of this treatment is often delayed in the hope that the compartmental syndrome will resolve spontaneously. Even if prompt surgery is performed, the functional result may be compromised by an incomplete decompression carried out in the hope of a superior cosmetic result. Special problems may be presented by the surgical wound after decompression and by fractures that are associated with compartmental syndromes. Compartmental syndromes may give rise to significant complications that include infection and myoglobinuric renal failure.

Definition of the compartmental syndrome

There is a vital need for new organization of the literature on compartmental syndromes. Attempts to locate the relevant articles are frustrated by the lack of an appropriate indexing system. For example, the Index Medicus has entries only for "Volkmann's ischemia" and "anterior compartment syndrome"; thus, it is difficult to know where to locate information on compartmental syndromes in other locations. Furthermore, in the Journal of Bone and Joint Surgery Quinquennial Index (1973-1977), all compartmental syndromes are listed under "Volkmann's ischemia." Finally, Sheridan and Matsen's classic article "Fasciotomy in the treatment of the acute compartment syndrome"1 is listed under the following headings in the Medline system: acute disease, adolescents, adults, aged, child, fascia/ surgery, female, human, male, middle age, neuromuscular disease/ surgery, postoperative complications/etiology, syndrome, and time factors. Thus, this important article could not be located by a search that requests articles dealing with compartmental syndromes, tissue pressure, or even ischemia.

A further example of the confusion resulting from the lack of organized nomenclature may be found in the 1979 American Academy of Orthopaedic Surgeons Orthopaedic In-Training Examination (page 5, question T3). The question concerns the early signs of "impending Volkmann's ischemic contracture," and for the answer we are referred to an article on "anterior tibial compartment syndrome." These two terms bear little apparent relation to one another.

Use of the literature is confused even further by a plethora of other names used to refer to the compromise of local circulation by increased tissue pressure.

Being aware of the problems with the existing nomenclature, I proposed a system for referring to those conditions in which pressure-induced circulatory compromise plays a central role.2l This proposed nomenclature is based on the following definition: A compartmental syndrome is a condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space. This definition brings out the four requisites of a compartmental syndrome: a limiting envelope within which increased tissue pressure produces reduced tissue circulation that results in abnormalities of neuromuscular function.

My sole purpose in using the term "compartmental syndrome" rather than "compartment syndrome" is to indicate that I employ the foregoing definition as opposed to the multiple vague definitions associated with the term "compartment syndrome." The definition permits the development of a "unified concept," which is founded on the premise that increased tissue pressure produces similar circulatory and functional effects wherever the process is located and whatever the initiating cause may be. 2l For example, increased tissue pressure in the forearm from a fracture and increased tissue pressure in the leg from intensive use of muscles are seen to produce similar physiological effects and clinical manifestations. Furthermore, the treatment of these two compartmental syndromes is the same: restitution of local blood flow by decompression of the tissues within the compartment.

This unified concept permits us to discuss a wide variety of compartmental syndromes together as a family group, distinguishing among the members only as their individual peculiarities require. Specific etiologies may be indicated, e.g., "compartmental syndromes due to intensive use of muscles." Location may also be specified, e.g., "deep posterior compartmental syndromes of the leg." Thus, the definition of the compartmental syndrome and the unified concept provide an organized system of nomenclature for referring either to all of these conditions as a group or to any member of that group.

Pressure measurement techiques

Several methods have been described for the measurement of tissue pressure, only a few of which are clinically useful.

The infusion technique is a reliable method for continuously monitoring tissue pressure in the clinical situation.

The continuous infusion and wick techniques give similar pressure readings for intramuscular tissue pressures in animal and human model systems.

Tissue pressure within a limb may significantly exceed the pressure applied externally to the limb.

To be reliable and thus clinically useful, any tissue-pressure-measurement technique should be practiced in normal subjects before it is used for evaluation of a patient with a possible acute compartmental syndrome.

Movie

• Infusion technique (1.63 MB)

Definition of tissue pressure

By definition, increased tissue pressure is the primary pathophysiological factor in compartmental syndromes. We must therefore define tissue pressure and attempt to resolve some of the confusion that has resulted from previous usage of this term.

A nonhomogeneous and anisotropic material such as tissue cannot be thought of as having a pressure in the same sense as a liquid or gas. This ambiguity is resolved somewhat by considering the two contexts in which the term "tissue pressure" might be invoked. The first concerns the exchange of fluid across a capillary wall. 1 2 This fluid movement is related to:

K (PC - PT ( H) + R OT - R OC) [ 1 ]

where K is a constant, PC is the capillary blood pressure, PT ( H) is the hydrostatic pressure of tissue fluid, R is the capillary membrane reflection coefficient, OT is the oncotic pressure of tissue fluid, and OC is the oncotic pressure of blood plasma.

The second situation in which the concept of tissue pressure might be invoked is in the consideration of forces operating on a vessel wall. The law of Laplace has been applied to this situation:

PI - PO = T/R [ 2 ]

where PI is the pressure exerted on the inside of the vessel wall, PO is the net force per unit area exerted on the outside of the vessel wall, T is the tension in the vessel wall, and R is the vascular radius.

Neither PT (H) nor PO is simple. Because extracellular fluid may exist in a free form, in a gel, and perhaps in other forms, PT (H) should actually refer to the physical chemical activity of extracellular fluid. 4 By contrast, PO is the resultant of several different elements. A positive contribution to PO may result from interstitial fluids, gels, and matrices, as well as from fibers and cells under compression. A negative contribution to PO may arise from cells and fibers under tension. Thus, in the general case it cannot be assumed that the two "tissue pressures" [PT (H) from equation 1 and PO from equation 2] are equal. 5- 6 To appreciate how they may differ, we have only to consider the analogy of a beaker that contains water and ball bearings. The hydrostatic pressure of water at the bottom of the beaker [analogous to PT(H)] is equal to the height of water in the beaker (H). The net force per unit area on the beaker bottom (analogous to PO) is equal to the total weight in water of the ball bearings (W) divided by the surface area of the beaker bottom (A) plus the hydrostatic pressure: W/A + H.

In discussing the effects of increased tissue pressure on local blood flow, the "tissue pressure" of primary interest is PO, the net force per unit area exerted on the outside of a vessel wall. This is the force that affects the pressure in and the flow through collapsible vessels. The mechanisms by which increased tissue pressure compromises local blood flow will be discussed in greater detail in Chapter 3.

Tissue pressure measurement

Because tissue pressure plays a central role in compartmental syndromes, it is appropriate to review some of the described techniques for tissue pressure measurement.

The capsule method employs a porous capsule surgically implanted in the tissue to be studied. After several weeks the fluid in the capsule reaches equilibrium with the surrounding interstitial fluid. The pressure of the fluid within the capsule is then measured with a pressure transducer. 5- 7- 8 This method has the clinical disadvantages of requiring surgical implantation and a prolonged period for equilibration. Stromberg and Wiederhielm 8 have criticized the capsule method on the basis that the observed pressure is influenced by the osmotic gradient between the fluid inside and the fluid outside the capsule.

Collapsible segment methods measure the pressure inside a flaccid-walled structure located within the tissue. 9 10 These methods are based on equation 2: when the walls of a fluid-filled structure are flaccid (the tension of the walls [ T ] is zero), the pressure of the fluid inside (PI) is equal to the pressure outside (PO). ; Thus, the measuring of the fluid pressure inside this structure ; yields the tissue pressure. Although some of these methods have l the disadvantage of requiring surgical implantation, Ryder et al. 11 and Kjellmer l2 have described variations using an in situ vein as the collapsible segment. Although the method of Ryder et al may be clinically useful for measuring subcutaneous tissue pressure, it is impractical for the measurement of intramuscular pressure in a X traumatized limb because it would require the cannulation of a deep intramuscular vein and repeated raising and lowering of the limb relative to the heart.

A servonull technique with micropipettes has been described by Wiederhielm. 4 In this method no net fluid is injected into the tissue, yet a continuous fluid column between the transducer and the tissue is maintained by a servosystem. Although this method is highly accurate and responsive, it appears to be too delicate and complicated for routine clinical use.

The injection technique measures the pressure necessary to inject a small quantity of fluid into the tissue through a f needle. l3-l7 Although this method has the advantage of using inexpensive equipment, it has a disadvantage in that a steady-state reading is not attained. Thus, it may be somewhat awkward in practice because a fluid manometer and an air-water meniscus must be observed simultaneously to detect the pressure at which fluid first begins to flow into the tissue. In an animal model where tissue pressure was elevated by fluid infusion at a known pressure, Hargens et al found that the injection technique overestimated low tissue pressures and underestimated high tissue pressures. Clayton et al 9 evaluated the injection technique by applying known pressures to the extremities of six rabbits with a pneumatic cuff. A good linear correlation was obtained with a slope of 1.03 (r = 0.99).

The wick technique employs strands of wettable material extending into the tissue from a fluid-filled catheter connected to a pressure transducer. 6,7, 20-22 The wick increases the surface area in contact with the tissue. To protect its fibers, the wick catheter is inserted through a larger cannula, which is then withdrawn. Clotting around the fibers is minimized by heparinization of the fluid within the catheter. Various materials have been used to make wick catheters; these include cotton and polyglycolic acid suture. The latter is most commonly used in the clinical situation. Zeluff 23 pointed out, however, that polyglycolic acid suture has a short shelf life after sterilization and suggested that Dacron (DuPont) may be a more suitable material.

Continuity of the fluid column between the tissue and the transducer is necessary for accurate pressure measurement. This continuity may be verified by observing a sharp increment in the observed pressure when the tissue overlying the catheter is pressed manually. If catheter patency cannot be assured, the catheter may be flushed with a small volume of heparinized saline. Mubarak et al 22 found that the wick catheter accurately reflected pressures applied by fluid infusion in dog limbs. We obtained reproducible results with the wick catheter when known increments of pressure were applied externally to rabbit and human limbs as long as the wick catheter remained patent. 24

In the continuous infusion technique, the patency of a hypodermic needle or intravenous catheter inserted into the tissue is maintained by the slow but continuous infusion of nonheparinized saline solution. The pressure of the fluid within the needle or catheter is continuously monitored with a standard blood pressure transducer. Since its original descriptions this technique has been improved through the use of noncompliant tubing, a simplified fluid path, and an ordinary needle or catheters

For continuous pressure monitoring, an infusion rate of 0.7 cc per day is used. Laboratory studies have demonstrated that the pressure measured is relatively independent of the rate of infusion: an acute 40-fold increase in the infusion rate from 0.7 to 29 cc per day produced only a 4-mm Hg increase in measured pressure. 25 It could be argued theoretically that even a rate of infusion as low as 0.7 cc per day could be hazardous to the patient. For example, Hargens et al 2 found that the acute infusion of 2 cc of plasma into a canine anterolateral compartment (volume of 40 cc) raised the intracompartmental pressure from 30 to 45 mm Hg. The pressure increment from saline infusion is unlikely to be a problem clinically, however, for two reasons: saline is absorbed three times more rapidly than plasma, 2 and three days of pressure monitoring would be necessary to infuse the volume of 2 cc. Furthermore, most human compartments are well over 10 times as large as the canine anterolateral compartment. The data obtained by Whitesides et al 7 from a limb amputated for sarcoma of the femur indicated that over the range of intracompartmental pressures from 10 to 50 mm Hg, the infusion of 1 cc of saline into the anterior compartment of the leg produced a 1-mm Hg increment in intracompartmental pressure. Thus, even assuming the worst possible case in which saline absorption is zero (i.e., a totally ischemic compartment), three days of continuous pressure monitoring with an infusion rate of 0.7 cc per day would give rise to an increment in tissue pressure of only 2 mm Hg.

We have demonstrated the accuracy and dependability of the continuous infusion technique in rabbit and human model systems where known increments of pressure were applied to living limbs.

Results of different tissue pressure measurement t

Earlier in this chapter we discussed the fact that there are at least two different "tissue pressures": the PO in the law of Laplace and the PT(H) in the capillary filtration equation. Because these two quantities cannot in the general case be expected to be identical, it would not be surprising if different tissue-pressure-measuring techniques yielded somewhat different values.

To determine whether or not the wick and continuous infusion techniques yielded significantly different results, we conducted side-by-side studies in rabbit and human model systems in which increments of external pressures were applied. We found that as long as wick catheter patency was closely monitored and any obstruction was cleared by flushing with a minimal volume of fluid, the two methods yielded virtually identical results in compressed rabbit and human muscle.

Even when no pressure was applied, our side-by-side comparison yielded similar pressure measurement values in human tibialis anterior muscle with the wick and the infusion techniques: 7+3 mm Hg and 9+3 mm Hg, respectively. 24 These values do not appear to be significantly different from those obtained with the wick technique by Mubarak et al 22 in normal forearm and leg muscle: 4 +4 mm Hg. Thus, in our hands, there is no practical difference between the results of the wick and the infusion techniques for intramuscular pressure measurement.

I prefer the continuous infusion technique for clinical tissue pressure measurement for the following reasons:

1. No specially prepared catheter is required; any needle or small intravenous catheter will serve. In compartments of the forearm and leg we routinely use a standard 22-gauge intravenous catheter with a 19-gauge inserting needle. This is considerably smaller than the 14- and 16-gauge placement units recommended for use with the wick catheters 22 We have used 25- and 27-gauge needles to measure pressure within the interosseous compartments of the hand.
2. Heparinization of the fluid within the catheter is not required; thus, the possibility of enhanced local bleeding is eliminated.
3. Catheter patency is continuously maintained by a volume-controlled infusion. As a result, catheter obstruction has not occurred in our clinical use of this monitoring method. Continuous pressure monitoring may be carried out for periods of at least 72 hours without the need for adjusting or manually flushing the system.
4. The pressure can be read at any time from the meter of the transducer monitor.
5. The equipment for the technique is available in most hospitals. Anesthesiologists are well acquainted with the calibration, zeroing, and operation of pressure transducers and can be of great assistance in setting up the system.
6. The results are accurate and reproducible.
7. On removal of the catheter or needle, there need be no concern about retained wick elements. 18

Like all other techniques for tissue pressure measurement, the continuous infusion method requires attention to detail and practice before proficiency and the necessary bedside efficiency are attained. Thus, I believe it is unwise to try to learn this or any other tissue pressure-measuring technique when confronted with a possible acute compartmental syndrome. The experience is likely to be frustrating, and the pressure reading obtained is unlikely to be reliable. An incorrect pressure reading is worse than none at all because it may distract from important clinical findings.

For those interested in being prepared to perform reliable pressure measurements, I would suggest practicing the technique on normal subjects until consistent readings in the normal range are obtained. If desired, one can apply a known pressure to the limb with an air splint to see if the measured pressure increases by the expected increment.

Relationship of applied and measured pressure

It has been generally assumed that the pressure applied to the outside of a limb is distributed essentially unaltered throughout the tissue. However, in our initial studies of the infusion technique, 25 we identified a phenomenon of "summation": the intramuscular pressure measured when an external pressure is applied to a limb is equal to the measured intramuscular pressure before pressure application plus the externally applied). More recent data 24 indicated an additional feature in the variance of applied and measured pressure: the increment in measured pressure within muscle exceeds the increment in applied pressure by a factor ranging from 1.02 to 1.3, depending upon the model system, as indicated by slopes of the plots of measured and applied pressure. This geometric augmentation of applied pressure is referred to as "amplification." 24 This phenomenon was found to be most striking in the anterior compartment of the rabbit leg, where the amplification factor obtained with both the wick and infusion techniques was 1.3 (i.e., the increment in measured pressure was 30% higher than the increment in externally applied pressure). At present we have not identified the mechanism of amplification. The fact ; that in the rabbit anterior compartment the amplification factor was dramatically diminished by fasciotomy suggests that the nonyielding fascia may have a significant effect on the pressure field induced by externally applied pressure.

Both summation and amplification can result in a significant difference between the pressure applied to an extremity and the pressure measured within it. This difference may be important in e interpreting experiments on the amount of pressure required to arrest blood flow, 33 in deciding the safe limits for air splints and pressure dressings, 34 and in interpreting the results of sphygmomanometry. 35 The magnitude of the apparent discrepancy is significant. The observed relationship of externally applied pressure.

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.

Tolerance of tissue for increased pressure

Increased tissue pressure compromises nerve and muscle function.

The time required to produce functional abnormalities is related to the severity of the pressure-induced circulatory compromise.

Nerve and muscle have a significant potential for recovery and reconstruction following ischemic injury.

Individuals differ with regard to the amount of pressure their limbs can tolerate before neuromuscular deficits are produced.

Hypotension, hemorrhage, arterial occlusion, and limb elevation all appear to reduce the tolerance of limbs for increased tissue pressure.

In Chapter 3 we saw that increased pressure compromises tissue blood flow, tissue oxygenation, and tissue function.. In dealing with clinical compartmental syndromes, the physician is concerned with the pressure tolerance of the tissue, i.e., how much pressure tissue can tolerate before its function becomes abnormal. Abnormal tissue function ensues when local blood flow is reduced to the point where it no longer meets the tissue's metabolic demands.

The pressure tolerance of tissue depends on several factors:

1. The specific effect of increased tissue pressure on local blood flow in the tissue under consideration.
2. The metabolic demands of the tissue.
3. The duration of increased tissue pressure.

Each of these factors may vary from one clinical situation to another. The specific relationship of tissue pressure and tissue blood flow is affected by the presence of hypotension, shock, arterial occlusion, and limb elevation. The metabolic demands of tissue are related to the presence and severity of local tissue injury. Finally, the duration of increased pressure depends on the rate of onset of the compartmental syndrome and the promptness with which it is treated. Thus, the tolerance of tissue for increased tissue pressure will vary considerably among patients. Because of this variability, one specific value for tissue pressure tolerance cannot be applied to the general population. With this perspective, let us review some of the specific data available on the tolerance of nerve and muscle for increased tissue pressure in animal and human model systems.

Tolerance of nerve for increased tissue pressure

Several recent studies have investigated the effects of different tissue pressures on nerve function. Sheridan et all inflated a latex balloon within the anterior compartment of rabbits to investigate the effects of different pressures on the response of nerve and muscle to direct electrical stimulation. Only one of the four rabbits receiving a pressure of 40 mm Hg for six hours demonstrated a loss of response to the electrical stimulus. An applied pressure of 60 mm Hg for six hours produced more consistent functional losses. Each rabbit receiving a pressure of 100 mm Hg for 8 or 12 hours lost all discernible response to nerve or muscle stimulation.

In a different rabbit model system in which external pneumatic pressure was applied, we investigated the effects of different pressures on the conduction velocity of the tibial nerves. Each pressure tested was applied for a period of five hours. Conduction ceased completely in nine animals: seven of the eight that received 80 mm Hg, one that received 70 mm Hg, and one that received 60 mm Hg. An average of 2.2+1.6 hours intervened between the application of pressure and the cessation of conduction in these nine animals (range: eight minutes to four hours).

Rorabeck and Clarke 3 investigated the effect of a pressure-controlled infusion of autologous blood into the anterior compartments of dogs. They found that a pressure of 40 mm Hg reduced peroneal nerve conduction velocity from 40 to 30 m/sec over 2.5 hours. A pressure of 80 mm Hg arrested peroneal nerve conduction after four hours.

Hargens et al 4 investigated a model compartmental syndrome in which tissue pressure was elevated by the pressure-controlled infusion of autologous plasma. They found no changes in peroneal nerve conduction velocity when 10 mm Hg was applied for eight hours. Although there was some slowing of nerve conduction when a pressure of 30 mm Hg was applied for 8 hours and when 40 mm Hg was applied for 14 hours, neither of these conditions was sufficient to arrest nerve conduction. A pressure of 50 mm Hg exerted for 330 minutes did arrest conduction. Less time was required to arrest nerve conduction at higher tissue pressures: nerve conduction ceased after only 50 minutes when a pressure of 120 mm Hg was applied.

In a human model systems we investigated the effect of different externally applied pressures on the nerve conduction velocity and clinical neurological examinations of three normal subjects. Pressures were applied for a maximum of 80 minutes. Each subject demonstrated a different tolerance for increased tissue pressure. Subject 1 maintained essentially normal function until the tissue pressure (as measured by the continuous infusion technique) exceed 65 mm Hg. Subject 2 tolerated pressures up to 75 mm Hg, and subject 3 tolerated pressures only as high as 55 mm Hg. This variability in pressure tolerance could not be attributed to differences in systemic blood pressure. When the pressure tolerance for each subject was exceeded, clinical and electrophysiologic changes occurred in a reproducible sequence.

Tolerance of muscle for increased tissue pressure

It is more difficult to quantify the effect of increased tissue pressure on muscle function than on nerve function. For example, we have been unable to develop a good model for the measurement of the strength of muscle contraction in a limb with increased tissue pressure. The only studies of muscle function found in the literature are those of Sheridan et all in which the response of muscle to direct electrical stimulation was observed.

Other investigators have correlated the amount and duration of pressure application with evidence of muscle damage. In their model compartmental syndrome, Rorabeck and Clarke 3 found increased femoral vein creatinine phosphokinase activity when a pressure of 40 mm Hg was applied to the anterior compartments of dogs. However, the absolute value of this enzyme could not be correlated with the amount of pressure applied. Similar findings were noted for lactic dehydrogenase. Hargens et al 7 investigated the effects of increased pressure in their model system using technetium-99m stannous pyrophosphate. They found that in the dog, intracompartmental pressures in excess of 20 mm Hg produced a significant uptake of the label when maintained for eight hours. From this point the amount of uptake increased dramatically as higher pressures were applied.

Recovery of nerve and muscle

Both nerve and muscle have the capacity for recovery after a significant ischemic insult. Rorabeck and Clarke 3 studied the recovery of canine nerve function for six hours after surgical treatment of model compartmental syndromes. In these short-term studies they found that if surgical decompression was performed within four hours after the initiation of a compartmental syndrome, nerve conduction velocity always returned to normal regardless of the amount or duration of pressure application. If surgical decompression was performed 12 hours after a pressure of 40 mm Hg or more was introduced, the nerve conduction velocity did not return to normal within the six-hour period of observation. In his studies of tourniquet palsy in rabbits, Lundborg 3 demonstrated that the extent and rapidity of nerve recovery depend on the duration of the ischemic insult. All 10 animals with two hours of nerve ischemia recovered after two weeks. Out of 12 animals with six hours of nerve ischemia, only 5 had recovered six weeks later.

Sanderson et al 9 and Vracko and Bendittl indicated that as long as the basal lamina remained intact, muscle had a significant potential for reconstruction after an ischemic insult.

Because nerve and muscle have the potential to recover after an ischemic insult, caution should be used in applying the term "irreversible" to ischemic damage. For the same reason, debridement of potentially viable muscle and nerve at the time of surgical decompression should be kept at an absolute minimum.

Clinical data on pressure tolerance

To help elucidate pressure tolerance in the clinical situation, we investigated 42 patients at risk for compartmental syndromes. These patients were frequently examined for clinical evidence of a compartmental syndrome. Tissue pressure in the compartment at greatest risk was continuously monitored with the infusion technique. No patient whose peak pressure was 45 mm Hg or less developed a clinical compartmental syndrome, whereas all of those with peak pressures of 60 mm Hg or more did develop a clinical compartmental syndrome. Five of the seven with pressures between 45 and 60 mm Hg developed compartmental syndromes, while two did not. Thus, these patients varied significantly with regard to their pressure tolerance.

The variability in pressure tolerance among individuals is of particular interest for two reasons:

1. It indicates that there is no "critical pressure" that can serve as a general criterion for diagnosis and treatment of a compartmental syndrome.
2. It prompts us to investigate the factors responsible for this variability in pressure tolerance to gain a better understanding of the compartmental syndrome.

Factors affecting the pressure tolerance of tissue

The arteriovenous gradient theory for the pathogenesis of a compartmental syndrome (see Chapter 3) enables us to predict that any cause of lowered local arterial pressure will diminish the pressure tolerance of tissue. We have investigated the effects on pressure tolerance of four clinically common causes of reduced local arterial pressure: anesthetic-induced hypotension, hemorrhagic shock, arterial occlusion, and limb elevation. In a rabbit model system we investigated the effect of hypotension induced by halothane anesthetic on muscle blood flow and muscle PO2. 2 A pressure of 60 mm Hg was applied to a hindlimb in two groups of animals: one in which the halothane anesthetic used for preparation was discontinued immediately after preparation, and a second in which the halothane anesthetic was continued throughout the entire five-hour period of pressure application. The circulatory effect of 60 mm Hg was much more profound in the hypotensive animals.

In a second study we investigated the effect of hemorrhagic shock in a rabbit model systems This condition is particularly important clinically because individuals sustaining compartmental syndromes from trauma may also sustain hemorrhagic shock. We investigated the effects on the pressure tolerance of rabbit hindlimbs of an acute 20% hemorrhage produced by the removal of 12 cc of whole blood per kilogram. This 20% hemorrhage reduced mean arterial blood pressure from a mean value of 88_12 to 75_1 1 mm Hg. An applied pressure of 40 mm Hg led to significantly greater reductions in muscle nitrogen washout, muscle oxygenation, and muscle action potential amplitude in the hemorrhage group as compared with the nonhemorrhage group. 11

Zweifach et al 12 investigated the effect of hemorrhage on the uptake of technetium-99m after the application of different intracompartmental pressures in dogs. In this study some animals were bled until mean arterial pressure reached 65 mm Hg. An applied pressure of 25 mm Hg produced the same effect in the hypotensive animal that a pressure of 40 to 50 mm Hg produced in a normotensive animal.

We carried out a study of the effect of superficial femoral arterial ligation on the response of rabbit muscle to an applied pressure of 40 mm Hg l3. Although arterial ligation alone produced significant decrements in muscle nitrogen washout, PO2, and action potential amplitude, all of these parameters fell to zero when the external pressure of 40 mm Hg was applied.

We also manipulated the pressure tolerance of normal human limbs. Instead of inducing systemic hypotension by hemorrhage or anesthetic, we induced local arterial hypotension by elevating the limbs above the level of the heart. Limb elevation reduced local arterial pressure by an amount equal to the pressure produced by the column of blood from the limb to the heart. This hydrostatic column pressure may be calculated by dividing the amount of limb elevation above the heart in centimeters by 1.3 cm of whole blood per millimeter of mercury l3-14.

Elevation of a limb from the dependent position may lower local venous pressure; however, elevation cannot lower local venous pressure below the level of local tissue pressure. Thus, for any given tissue pressure, elevation of a limb above the supine position reduces the local arteriovenous gradient. The diminished pressure tolerance of elevated limbs was apparent in our series of experiments in which anterior compartment muscle PO2 was measured in normal subjects l5. A pressure of 20 mm Hg applied to a limb elevated 54 cm above the heart reduced muscle PO2 by the same amount as a pressure of 60 mm Hg applied to the limb level with the heart.

We demonstrated the functional significance of this lowering of pressure tolerance by limb elevation in another series of experiments. 5 Here, nerve conduction velocity was measured in level and elevated limbs receiving different applied pressures. Once more the tolerance of the limbs for increased tissue pressure was diminished by an amount equal to the hydrostatic column pressure produced by the limb elevation.

These investigations of elevated limbs are clinically important in that they suggest that limbs with compartments showing signs of inadequate blood flow should not be elevated. In this situation, elevation will lower local arterial pressure but will not affect local venous pressure. Thus, the arteriovenous gradient will be further diminished when blood flow is already inadequate. These findings have proved clinically useful: on several occasions the symptoms and signs of compartmental syndromes have resolved upon lowering the affected limbs from an elevated position. Unnecessary surgical decompression has thereby been avoided.

Etiologies of compartmental syndromes

A compartmental syndrome may occur whenever tissue pressure within a limited space rises to the point that it compromises local circulation and function.

The two prerequisites for a compartmental syndrome are (a) a limiting envelope surrounding tissue and (b) a cause of increased tissue pressure within that envelope.

A wide variety of etiologies may produce a sufficient increase in local tissue pressure to cause a compartmental syndrome.

The relative frequency of the different etiologies may differ dramatically in different patient populations.

Postischemic swelling is a particularly sinister cause of a compartmental syndrome.

By definition, a compartmental syndrome is produced when the tissue pressure within a limited space rises to the point where the circulation and function of the tissues within that space are compromised.

There are therefore two prerequisites for the production of a compartmental syndrome: (a) an envelope limiting the available space and (b) a cause of increased pressure within that envelope.

The first prerequisite, a limiting envelope, may be any structure of limited compliance that surrounds tissue. Several different materials may compose these limiting envelopes. Envelopes may consist of fascia and bone, as in the anterior compartment of the leg, or may consist of fascia alone, as in the gluteal compartment. l The skin may serve as a limiting envelope in burned extremities or in cases in which the skin has been closed after surgical opening of the fascia. 2-7 Even the connective tissue layer that surrounds each muscle, the epimysium, may serve as the limiting envelope in a compartmental syndrome. 8- 9 Limiting envelopes may also be produced by the physician in the form of tight external dressings or casts. In 1881, Volkmann provided one of the first written descriptions of circulatory compromise from tight dressings. His identifications of externally applied pressure as a cause of muscle ischemia is important, even though he incorrectly attributed the ischemia to arterial occlusion. Edgar Bick's translation of this description is reproduced below: 10

For many years I have noted on occasion, following the use of bandages too tightly applied, the occurrence of paralysis and contraction of the limb, not, as has been previously assumed, due to paralysis of the nerve by pressure, but as a quick and massive disintegration of the contractile substance and the effect of the ensuing reaction and degeneration. The paralysis and contracture are to be understood as purely myogenic.

A series of new experiences has merely confirmed the correctness of this assertion, and also produced certain views about the character of the process here in question. Accordingly, I might summarize my views in the following sentences:

1. The paralyses and contractures appearing after too tight bandaging of the forearm and hand, less frequently in the lower extremity, are to be considered ischemic. They are caused by prolonged blocking of arterial blood. The almost simultaneous occurrence of massive venous stasis manifests itself at the beginning of the paralysis only to accelerate its progress.
2. The paralysis is based upon the fact that the muscle bundles, too long deprived of their acids become necrotic. The contractile substance coagulates, disintegrates into clumps and will be resolved later. The ensuing contracture is thereby to be understood above all as simply rigor mortis and shows the paralyzed and contracted limb-if as usual the entire musculature of a limb or part of a limb is affected-always in the same position which we find in the limbs of rigor mortis.
3. Characteristically, the paralysis and contracture appear simultaneously or follow immediately after one or the other, while in paralysis of nerve origin in the extremity the contracture develops gradually, and often much later; months and years pass before a deformity develops that cannot be overcome by immediate passive hand-power.
4. On the contrary, ischemic contracture shows its nature from the first moment by the great resistance it opposes to straightening the limb. The affected muscles have already completely and immediately lost their elasticity as in rigor mortis and are completely stiff.
5. The reactive and regenerating processes, always very imperfect in man, following the disintegration of the contractile substance, make the diseased muscles even more unyielding and further increase the contracture by cicatrization.
6. Ischemic paralysis and contraction of similar character also occur after application of any tight bandage, too long continuation of an Esmarch constriction of the limbs, and also after lacerations and contusions of large vessels, and perhaps also after long periods of severe cold.

The second prerequisite for a compartmental syndrome, a cause of increased pressure within the envelope, may be a decrease in the volume of the envelope, an increase in the content within the envelope, or the application of pressure to the outside of the envelope. Whitesides et al 11 and Hargens et al 12 sequentially increased the content of a dog's anterior compartment while observing the resulting changes in intracompartmental pressure. The initial increases in compartmental content produced only small increments in intracompartmental pressure; thus lax fascia appears to have a significant compliance. With increasing compartmental content, intracompartmental pressure rose more steeply, that is, the fascial compliance progressively diminished. This pressure content relationship is further emphasized by data of Whitesides et al 11 from an amputated human leg: a 30% increase in the content of the anterior compartment from 110% to 140% of normal raised the intracompartmental pressure only 20 mm Hg (from 10 to 30 mm Hg), whereas a 30% increase in content from 150% to 180% of normal caused the intracompartmental pressure to rise 75 mm Hg (from 45 to 120 mm Hg).

Any cause of locally increased tissue pressure is a potential cause for a compartmental syndrome:

Decreased compartmental volume:

• closure of fascial defects
• application of excessive traction to fractured limbs.

Increased compartmental content:

• bleeding
• vascular injury
• bleeding disorder
• anticoagulants
• increased capillary filtration
• increased capillary permeability
• post ischemic reperfusion
• trauma
• intensive use of muscles
• burns
• intraarterial drugs
• cold
• surgery
• snakebites
• increased capillary pressure
• venous obstruction
• diminished serum osmolarilty
• nephrotic syndrome
• infiltrated infusions
• muscle hypertrophy
• popliteal cysts

Externally applied pressure:

• tight casts, dressings
• air splints
• lying on limb

The relative frequency of these different etiologies may vary markedly from one geographical location to another. For example, in our series from the University of Washington affiliated hospitals, l3 extremity trauma was the etiology in 24 of 44 cases. By contrast, in the series from the University of California in San Diego, limb compression in association with drug overdose accounted for 5 of 11 cases, l4 an etiology not seen in our series.

Whereas the mechanism by which most of the etiologies produce increased tissue pressure is apparent, postischemic swelling deserves some additional discussion. Like other tissues, capillary endothelium is damaged by prolonged ischemia. This damage is reflected by an increase in capillary permeability. If the circulation is restored through ischemically damaged capillaries, the increased capillary permeability results in extravasation of fluid with an increase in extracellular volume. Cell volume may also be increased because ischemia may deprive cells of their normal membrane integrity and ionic pump functions. This postischemic swelling has been demonstrated by two laboratory investigations. Fuhrman and Crismon 83 measured the water content of rabbit muscle two hours after different periods of tourniquet ischemia. They found that three hours of ischemia gave rise to postischemic swelling of 30 to 60%. Whitesides et al 11 measured tissue pressures in the compartments of dog hindlimbs after a period of tourniquet ischemia. The postischemic increment in pressure was higher the longer the tourniquet had been applied. Whereas only a few of the animals with four hours of ischemia showed a significant increase in tissue pressure, most of the six-hour and all of the eight-hour animals showed significant pressure increases after the release of the tourniquet.

Compartmental syndromes resulting from postischemic swelling can present a diagnostic challenge. Because the tissue is injured by the initial period of ischemia, neuromuscular function may already be abnormal. Thus, the detection of additional deficits from a superimposed compartmental syndrome requires very close observation of the patient's nerve and muscle function.

Where do compartmental syndromes occur?

A compartmental syndrome may occur wherever tissue is surrounded by a limiting envelope.

Certain factors may favor the development of a compartmental syndrome in a specific location. Examples include relatively noncompliant fascia, exposure to trauma or ischemia, and vigorous use of the compartmental musculature.

The frequency with which the different compartments are involved may vary from one geographical area to another.

Movie

• Common sites for compartmental syndromes (0.41 MB)

Anatomical locations of compartmental syndromes

A compartmental syndrome may potentially occur wherever a limiting envelope surrounds neuromuscular tissue. Certain anatomical locations are particularly predisposed to the development of a compartmental syndrome. This predisposition may result from the limited compliance of the compartment. Whitesides et also found the human anterior compartment of the leg to be significantly less compliant than the superficial or deep posterior compartments of the leg. A high susceptibility to trauma may be another predisposing factor. For example, the anterior compartment of the leg is vulnerable to contusion and is frequently injured in fractures of the tibia. The four compartments of the leg are often affected by ischemic conditions of the lower extremity, a situation that places them at risk for compartmental syndromes resulting from postischemic swelling. The muscles of the leg and forearm are often exercised vigorously; thus, their compartments are potential sites of compartmental syndromes from intensive use of muscles. Additionally, other factors predispose the compartments of the upper and lower extremities to the development of compartmental syndromes, including their accessibility for drug injection and their vulnerability to burns.

The relative frequency of involvement of different compartments may vary from one geographical area to another. The high incidence of the anterior compartmental syndrome of the leg in the University of Washington series is a reflection of the large number of trauma cases seen in our hospital system. The relatively high incidence of involvement of the gluteal, quadriceps, biceps, and deltoid compartments in the series from the University of California at San Diego is related to the frequency with which drug overdosage with limb compression is seen there.

Each of most commonly involved compartments is surrounded by relatively unyielding fascia and is in a location where it is predisposed to trauma and other causes of tissue swelling that could give rise to a compartmental syndrome.

How are compartmental syndromes diagnosed?

Most compartmental syndromes may be diagnosed on the basis of clinical symptoms and signs alone. These include:

1. pain out of proportion to what is anticipated from the clinical situation,
2. weakness of the muscles in the compartment,
3. pain on passive stretch of the muscles of the compartment,
4. hypesthesia in the distribution of the nerves coursing through the compartment, and
5. tenseness of the compartmental envelope.

In certain instances adjunctive diagnostic techniques such as tissue pressure measurement and direct nerve stimulation may be useful in the diagnosis of compartmental syndromes.

The period of risk for compartmental syndromes appears to extend at least to three, and possibly to six, days after the initial cause of compartmental swelling.

Arterial occlusion and primary nerve injury may produce a clinical picture similar to that of a compartmental syndrome; yet the differential diagnosis can usually be made by careful clinical examination with occasional recourse to ancillary diagnostic techniques.

Movies

• Anterior compartment of the leg (0.33 MB)
• Deep posterior compartment of the leg (0.28 MB)
• Tissue pressure measurement (1.63 MB)
• Diagnosis of a compartmental syndrome (somewhat lengthy) (1.30 MB)

Clinical diagnosis

The essential elements in diagnosing a compartmental syndrome are revealed in its definition: a compartmental syndrome is a condition in which increased pressure within a limited space compromises the circulation and function of the contents of that space. Thus, to make a rigorous diagnosis of this condition, the physician should have evidence for increased tissue pressure, inadequate tissue perfusion, and loss of tissue function.. When all of these are present, the diagnosis of a compartmental syndrome may be made with assurance; when one or more of these factors is absent, the diagnosis is less secure.

Evidence for increased tissue pressure may include the patient's complaints of tightness or pressure in the involved area. The physician may perceive tenseness of the compartmental envelope by palpation. Or he may detect significantly increased tissue pressure by direct pressure measurement.

Evidence for inadequate perfusion of local tissue may include the symptom of pain out of proportion to what would be anticipated from the clinical situation. For example, one would not anticipate a progressive increase in pain from a properly splinted fracture. Requests by the patient for more analgesic medication are often discounted by nurses and physicians, but may actually provide a vital clue to the onset of locally insufficient blood flow. Pain on stretch of the intracompartmental muscles is a useful indication of inadequate local perfusion, particularly if these muscles have not been otherwise injured.

Although muscle blood flow may be quantitated in the laboratory with various measurement techniques these techniques are as yet difficult to apply to the clinical situation. Even if such quantification were practical, the results would only be useful if the circulatory requirements of the tissue in question were known.

Peripheral pulses are frequently normal in compartmental syndromes because intracompartmental pressures are usually insufficient to affect arterial flow. Thus, whereas diminished pulses suggest reduced arterial flow from some cause or other, the presence of distal pulses provides no information about the adequacy of compartmental perfusion. A similar statement may be made about the presence of Doppler signals distal to the compartments In our investigations of a model compartmental syndrome in humans, we found that an excellent Doppler signal could be detected in the presence of severely compromised compartmental function.

One may reasonably ask whether compromised tissue perfusion may be determined from tissue pressure measurements alone. Whereas intramuscular pressures in excess of 20 mm Hg are abnormal and have been shown to reduce tissue blood flow and oxygenation, 5, 6 they do not necessarily indicate inadequate tissue perfusion. The local circulatory effect of a given tissue pressure depends upon the pressure tolerance of the tissue (see Chapter 4). However, a rough guideline may be derived from our past experience with clinical tissue pressure monitoring: significantly compromised tissue perfusion is likely when tissue pressure exceeds 45 mm Hg.

Evidence for abnormal tissue function includes weakness of the intracompartmental muscles and hypesthesia in the distribution of nerves coursing through the involved compartment. Because both nerve and muscle function may be altered by direct injury, evidence of progressive functional losses after an initial injury is a particularly important sign of a compartmental syndrome. Detection of this progression is obviously dependent upon good neuromuscular examinations repeated frequently and documented adequately.

The function of muscles at risk is graded on a zero to five scale (where zero indicates no function and five indicates normal function). Toe extension must be specifically examined because a patient without any anterior compartment function can "wiggle his toes" quite well by using his toe flexors and then allowing his toes to spring back to the neutral position. Sensation is a bit more difficult to quantitate, but most observers could agree on definitions of normal, slightly diminished, significantly diminished, and absent.

It is important to record the time and results of these examinations so that changes in the patient's condition may be easily determined. A shorthand notation is useful.

In most cases, the diagnosis of a compartmental syndrome can be made from the clinical evaluation alone. The symptoms and signs usually associated with a compartmental syndrome may be summarized as follows:

1. Pain out of proportion to what is anticipated from the clinical situation.
2. Weakness of the muscles in the compartment.
3. Pain on passive stretch of the muscles in the compartment.
4. Hypesthesia in the distribution of the nerves coursing through the compartment.
5. Tenseness of the compartmental envelope.

Adjunctive diagnostic techniques

Although the clinical examination is the cornerstone of the diagnosis of compartmental syndromes, it has two distinct disadvantages: (a) it is partially subjective, and (b) it requires cooperation from the patient. Furthermore, in certain situations the clinical evaluation may be insufficient to allow the examiner to distinguish among several possible causes of neuromuscular deficit. In these instances, quantitative, objective techniques such as tissue pressure measurement and direct nerve stimulation may be useful adjuncts.

Tissue Pressure Measurement

Tissue pressure measurement may be of great value in the diagnosis of compartmental syndromes because it quantitates the physical factor responsible for the syndrome. A tissue pressure in excess of 45 mm Hg is usually associated with a compartmental syndrome, and a tissue pressure of 60 mm Hg or higher consistently gives rise to this condition. Because the tolerance of tissue for increased pressure may be reduced by such factors as shock, arterial occlusion, and limb elevation, compartmental syndromes may occur at significantly lower tissue pressures (see Chapter 4).

Tissue pressure measurement is most often useful where the diagnosis of a compartmental syndrome cannot be established or excluded on the basis of symptoms and signs alone. The clinical presentation is likely to be ambiguous in a patient who has more proximal neurologic lesions involving peripheral nerves or the central nervous system, a patient with other causes of compartmental ischemia, or a patient with such anxiety that the usual tests for compartmental function are unreliable. (Even in these situations, however, the clever clinician is sometimes able to make use of withdrawal reflexes or Babinski signs to evaluate compartmental function.)

Another application of pressure monitoring is in the early detection of compartmental syndromes in patients at risk for this condition. The pressure is continuously monitored in the compartment judged to be at highest risk (the one that is clinically tightest, the one that has received the most direct trauma, or the one known to be most predisposed to the development of compartmental syndromes). Pressure monitoring is continued until the question of a compartmental syndrome is resolved-a period that usually does not extend beyond three days. The infusion technique is of particular value in this application because it allows continuous pressure monitoring for extended periods.

A typical example of the usefulness of continuous pressure monitoring is the case of a 22-year-old man whose leg had been pinned for five hours beneath a heavy sign. Continuous monitoring of the pressure within the anterior compartment indicated a rise in tissue pressure from 20 to 50 mm Hg in the first two hours after the patient's admission to the hospital. This rapid pressure increase heralded the onset of a compartmental syndrome, which was successfully treated by prompt surgical decompression.

The use of tissue pressure measurement in the diagnosis of compartmental syndromes assumes that the measured pressure accurately reflects the pressure within the compartment. There is always a danger, particularly in inexperienced hands, that the pressure reading is erroneous, due to such factors as an occluded catheter, a leaky connector, bubbles in the system, an inaccurately zeroed or calibrated transducer, incorrect catheter or needle placement, or misreading of the transducer monitor. Bleeding from the catheter insertion may falsely elevate local tissue pressure, particularly if a heparinized saline solution is used to flush the catheter. Finally, it must be remembered that tissue pressure cannot be measured in all parts of all compartments at risk. Thus, a sampling problem may exist: the maximum tissue pressure may be at some point other than where the tissue pressure is being measured. These potential sources of measurement error, along with the observation that pressure tolerance varies among individuals, indicate that the diagnosis of a compartmental syndrome cannot be based on pressure measurements alone.

Direct Nerve Stimulation

Time at risk

In considering patients at risk for a compartmental syndrome, one may appropriately ask, How long must the vigil be maintained? In our review of patients having surgical decompression for compartmental syndromes the interval between the etiological event (e.g., contusion or fracture) and the onset of the compartmental syndromes (that is, the earliest evidence of functional deficits related to the compartmental syndrome) averaged 15 hours. In our series of patients with deep posterior compartmental syndromes of the leg, l2 this interval ranged from two hours to six days, with mean and median values of approximately 1% days. In the latter series, the most rapid onset of a compartmental syndrome occurred in a 20-year-old male who sustained a severe contusion of his leg that was followed two hours later by deep and superficial posterior compartmental syndromes. The longest interval between the etiological event and the onset of a compartmental syndrome was six days. This occurred when anterior and deep posterior compartmental syndromes resulted from a compound fracture of the distal tibia and fibula.

In an unpublished study, Veith l3 prospectively monitored the anterior compartmental pressures in eight patients with displaced closed fractures of the tibial shaft. In each case he found that maximum pressure occurred 21 to 36 hours after the tibial fracture. None of these patients developed compartmental syndromes.

Because the time at risk for a compartmental syndrome extends to three, and possibly six, days after a significant extremity injury, the physician cannot relax his watch until the intracompartmental swelling has shown definite signs of resolution.

Differential diagnosis

Acute arterial occlusion, whether from arterial embolization or thrombosis, may mimic a compartmental syndrome by producing signs of compartmental ischemia and loss of neuromuscular function. In the case of isolated arterial occlusion, local tissue and venous pressures are normal. If increased tissue pressure additionally compromises compartmental blood flow, the patient has a superimposed compartmental syndrome. In this case the patient will benefit from surgical decompression. This procedure will improve the local arteriovenous gradient by lowering tissue pressure and local venous pressure.

When faced with a compartmental syndrome and a possible coexistent arterial injury, it is usually prudent to perform a surgical decompression immediately. Then if a significant arterial injury cannot be excluded, an arteriogram can be performed while the patient is still on the operating table so that prompt vascular repair may be carried out if needed. Arteriography performed before the patient is taken to the operating room may excessively delay surgical decompression.

Primary nerve injury may also present a problem in differential diagnosis. Nerve injury is expected to produce deficits in neuromuscular function, but these should not be progressive after the initial injury. Furthermore, signs and symptoms of ischemia and increased tissue pressure should be absent. Direct nerve stimulation as described above and standard nerve conduction velocity measurements may be useful diagnostic adjuncts. Electromyography is not likely to be helpful because several weeks are required before signs of denervation manifest themselves.

Other differential diagnostic possibilities include osteomyelitis, synovitis, tenosynovitis, and deep vein thrombosis, each of which may produce significant local swelling. A compartmental syndrome may be excluded if neuromuscular function is normal. However, it must be remembered that any condition that produces significant intracompartmental swelling may produce a compartmental syndrome.

The most challenging differential diagnostic problems occur when several potential causes of functional loss exist. An example is the loss of anterior compartmental function after an osteotomy of the tibial shaft to correct a valgus deformity. This functional loss could result from (a) a compartmental syndrome, (b) a traction injury to the peroneal nerve, or (c) a traction injury to the anterior tibial artery. l4.

Details about treatment

The objective of treatment of a compartmental syndrome is to minimize deficits in neurological function by promptly restoring local blood flow, usually by surgical decompression.

Certain nonoperative measures may be effective, such as eliminating external envelopes and maintaining local arterial pressure.

Vasodilator drugs or sympathetic blocks appear to be ineffective in the treatment of compartmental syndromes, probably because in this condition maximal local vasodilatation is already present.

Surgical decompression of all limiting envelopes is usually indicated in the presence of (a) a characteristic clinical picture of a compartmental syndrome, or (b) an ambiguous clinical picture in the presence of a measured tissue pressure in excess of 40 mm Hg, provided the patient has a normal pressure tolerance.

Only obviously nonviable tissue is debrided at the time of surgical decompression.

The skin is left open after surgical decompression to prevent it from becoming a limiting envelope during the anticipated period of postischemic swelling.

Skin closure may usually be accomplished three to five days after surgical decompression by direct suture or meshed skin graft. The skin may also be progressively closed over the ensuing 10 to 14 days with suture or sterile paper tape.

Skeletal fixation is a useful adjunct to management of the limb when a compartmental syndrome is associated with an unstable fracture.

Increased tissue pressure is the pathogenic factor in the compartmental syndrome. Thus, the primary goal in treating this condition is the prompt lowering of tissue pressure to normal levels. A definitive reduction in tissue pressure is accomplished by the complete opening of all envelopes surrounding the affected tissue. This opening must not only decompress the contents of the compartment, but also accommodate any postischemic swelling occurring after the decompression procedure. If significant postischemic swelling occurs within incompletely opened envelopes, a "rebound" compartmental syndrome may occur.

Movies

• Treatment of anterior compartmental syndrome (rather lengthy) (4.46 MB)
• Results of that treatment (0.84 MB)

Opening external envelopes

Maintaining local arterial pressure

Before operative methods for reducing tissue pressure are discussed, the importance of maintaining local arterial pressure should be considered. Local arterial hypotension reduces the tissue's pressure tolerance and increases the adverse effects of a given tissue pressure (see Chapter 4). This is true whether the local arterial pressure has been reduced by shock, peripheral vascular disease, or elevation of the limb above the heart. Thus, treatment of systemic hypotension and avoidance of limb elevation are important for the maintenance of local arterial pressure and in the management of compartmental syndromes.

Although it may seem that vasodilator drugs or sympathetic blocks might also be of benefit in improving local circulation, the ineffectiveness of these treatments has been revealed by clinical experience Apparently, the local circulatory insufficiency in a compartmental syndrome is such a potent stimulus for vasodilatation that the elimination of sympathetic tone does not additionally augment local blood flow.

Indications for surgical decompression

If the release of all external envelopes and optimization of local arterial pressure fail to eliminate the compartmental syndrome, prompt surgical decompression must be considered. Rigid indications for surgical decompression are difficult to establish; each patient and each compartmental syndrome has an individuality that affects the way in which they are managed. In general, however, surgical decompression is indicated in the presence of:

1. Significant deficits in neuromuscular function related to increased tissue pressure. The term "significant deficits" refers to any functional losses that would not be acceptable in the end result. The presence of increased tissue pressure may be detected by palpation of the compartment or by measurement of intracompartmental pressure.
2. An ambiguous clinical picture with a tissue pressure above 40 mm Hg in a patient expected to have a normal pressure tolerance. Forty millimeters of mercury is an empirically derived figure based on our experience with prospective monitoring of tissue pressure in patients at risk for compartmental syndromes (see Chapter 4). This value is not proposed as a "critical" pressure applicable to all patients. Patients with peripheral vascular disease, patients in shock, and patients with elevated limbs are expected to have a diminished pressure tolerance and may require surgical decompression at lower tissue pressures. In arriving at the appropriate therapeutic decision, we use pressure measurement data as an adjunct to whatever clinical information is available: the greatest weight is given to the presence, severity, and time-course of deficits in the function of intracompartmental nerves and muscles.

When indicated, surgical decompression is an emergency because delay increases the damage inflicted on intracompartmental tissue as well as the incidence of complications (see Chapter 9).

Techniques of surgical decompression

Decompression of the Leg

When a compartment of the leg is involved with an acute compartmental syndrome, it is usually preferable to open all four compartments through a single lateral incision without removing the fibula. 11 Because all four compartments are usually exposed to the same etiological events, involvement of one compartment may be associated with impending involvement of the others. I have seen two cases in which decompression of only the anterior compartment left the patient with sequelae of an untreated deep posterior compartmental syndrome.

Decompression of the Volar Forearm

Care After Surgical Decompression

Skeletal fixation of associated fractures

Increased tissue pressure within the fascial compartments may splint a fractured limb by an action resembling that of an air splint. When surgical decompression is carried out, this splinting effect is lost and the fracture may become considerably less stable.

If a stable and satisfactory reduction cannot be accomplished, consideration should be given to skeletal fixation of unstable fractures associated with compartmental syndromes. External pin fixation, plates, and intramedullary nails have been used in this applications 11 If employed, the stabilization is performed immediately after surgical decompression. The management of wound, limb, and fracture is thus greatly facilitated.

Sequelae of compartmental syndromes

Sequelae of compartmental syndromes may include persistent hypesthesia and dysesthesia, persistent motor weakness, infection, myoglobinuric renal failure, contractures, amputation, and death.

These sequelae are the direct result of nerve and muscle injury and death, and thus their frequency and severity are minimized by prompt diagnosis and treatment of compartmental syndromes.

The potential sequelae of a compartmental syndrome include persistent hypesthesia and dysesthesia, persistent motor weakness, infections of bone and soft tissue, renal failure, contractures, amputation, and death. Early treatment of compartmental syndromes is the best method for preventing these sequelae. This point is well demonstrated by our retrospective review of 46 extremities in 44 patients having surgical decompression of compartments afflicted with compartmental syndromes. 1 Only 7 of the 22 extremities decompressed within 12 hours of the appearance of the compartmental syndrome showed residual deficits at the time of follow-up examination; only 1 had a significant complication. In four of these cases, compartmental syndromes developed after intra-arterial drug injection, a situation in which microembolization also compromises local circulation. 2-4 If these four cases are excluded, residual deficits occurred in only 3 of the remaining 18 extremities that received early decompression. By contrast, 22 of the 24 extremities having late decompression showed residual functional losses (none of these compartmental syndromes resulted from intra-arterial drug injection). In the late decompression group 13 of the 24 extremities had complications, 5 of which required amputation.

It is important to realize that in this study the duration of the compartmental syndrome before surgical decompression was determined retrospectively from the time that the earliest evidence of functional deficits appeared, not the time at which the syndrome was diagnosed by the physician caring for the patient. In many cases, much of the apparent 12-hour "grace period" had elapsed before the diagnosis of a compartmental syndrome was made.

Motor deficits resulting from a compartmental syndrome are initially treated with appropriate orthotic devices, e.g., a drop foot brace when the anterior compartment of the leg is affected. If function does not return in about one year, tendon transfer and other forms of reconstructive surgery may be considered. Hypesthesia and painful dysesthesia can also result from a compartmental syndrome. These may resolve slowly with time. Diphenylhydantoin (Dilantin, Parke-Davis) and carbamazepine (Tegretol, Ciba-Geigy) may be of some value in making the patient more comfortable.

Infection can be a serious complication of a compartmental syndrome. In our retrospective reviews 11 of 24 extremities having late surgical decompression developed infections. Five, or almost one-half, of these infections led to an amputation. One case of osteomyelitis occurred in a patient with an initially closed tibial fracture who underwent fasciotomy and primary closure 28 hours after the onset of the compartmental syndrome. Infection appears to be most frequent in the presence of devitalized muscle, particularly if skin closure has been attempted. Infected compartments are treated by wide opening of dressings, skin, and fascia, thorough lavage of all affected areas, and debridement of infected tissue. The wound is treated open with damp dressings until it is sufficiently clean for closure or skin grafting. In some cases of refractory osteomyelitis associated with severe functional losses, amputation may present the only reasonable treatment.

Myoglobinuric renal failure is another serious and potentially fatal complication of compartmental syndromes. 5-l0 Myoglobin is released from damaged muscle cells in amounts related to the severity of the muscle damage. If the damaged muscle is perfused, myoglobin enters the circulating blood and is filtered by the kidney. Muscle ischemia of 4 hours gives rise to significant myoglobinuria, which reaches a maximum approximately 3 hours after the circulation is restored, but which persists for as long as 12 hours. Significant myoglobinuria produces myoglobinuric renal failure, which may be due to a direct toxic effect of myoglobin, to renal vasoconstriction, to precipitation of myoglobin in the renal tubules, or to a combination of these factors. Most hospitals have sensitive and specific assays for urinary myoglobin. If these are not available, dark urine may usually be attributed to myoglobinuria if the benzidine or hemastix tests are positive in the absence of pink serum and microscopic hematuria. If myoglobinuria is suspected, one should endeavor to maintain a high urinary output to dilute the effect of myoglobin on the kidney. Because myoglobin is less soluble in acid urine, precipitation may be minimized by the maintenance of an alkaline urine through the administration of lactate or bicarbonate. If renal failure ensues, prompt institution of dialysis may be required. Whereas myoglobinuric renal failure may complicate any compartmental syndrome, it appears to be most common after compartmental syndromes produced by prolonged limb compression in a drug-overdosed patient.

Contractures not infrequently complicate compartment syndromes. l 4,11-15 They appear to result from the shortening of ischemically damaged muscle and from associated nerve damage. Contractures appear to be most common after volar compartmental syndromes of the forearm and deep posterior compartmental syndromes of the leg. In both locations the long flexor muscles of the digits and the nerve supply to the intrinsic muscles are affected. Curiously, the muscles of the commonly involved anterior compartment of the leg rarely undergo postischemic contracture.

Contracture from compartmental syndromes is minimized by early compartmental decompression and by appropriate splinting of the limb during the postoperative period. Passive stretching exercises may help maintain muscle length and the range of motion of the joints. If contractures become established, some combination of muscle-releasing procedures, tendon lengthenings, muscle debridement, neurolysis, tendon transfers, and bony procedures may be necessary.

Death has been known to result from compartmental syndromes. In the series reported by Sheridan and Matsen, 1 a patient with brittle diabetes died from overwhelming sepsis after delayed surgical decompression. Coupland 16 reported a case of sudden death after surgical decompression and attributed this to the sudden release of a large quantity of acidotic, hyperkalemic blood that apparently produced a fatal arrhythmia. When the patient's life is threatened by infection, myoglobinuria, or other systemic effects of a compartmental syndrome, emergency amputation may be life saving.

Minimizing morbidity

The following approach is proposed to help minimize the morbidity from compartmental syndromes.

• Prevent compartmental syndromes whenever possible. Effective measures may include prophylactic fasciotomy, minimization of soft tissue trauma and ischemia, and avoidance of tight circumferential dressings.


• Identify patients at risk. All patients with the potential for significantly increased intracompartmental pressure should be considered to be at risk for a compartmental syndrome. The common causes of increased intracompartmental pressure are listed in Chapter 5. Patients with these conditions require close observation for early evidence of a compartmental syndrome.


• Perform a thorough initial examination and document it well. The initial examination may serve two functions: (a) it helps with the diagnosis or exclusion of a compartmental syndrome at the time this examination is made, and (b) it establishes the base line for determining subsequent changes in the patient's condition. For example, any deterioration of neuromuscular function after the initial examination would strongly suggest a compartmental syndrome rather than nerve or muscle damage occurring at the time of the initial injury. The patient's chart should reflect the date, time, and name of the examiner as well as the following information about the compartments at risk: (a) the patient's complaints of pain, (b) the strength of the muscles in the compartment, (c) the patient's response to passive stretch of the muscles in the compartment, (d) the sensation in the distribution of nerves coursing through the compartment, and (e) the tenseness of the compartmental envelope.


• Admit patients at significant risk for compartmental syndromes. The frequent examinations that are necessary to permit early diagnosis and treatment are only possible when the patient has been admitted to the hospital. Care should be taken to assure that those observing the patient understand the proper techniques for examination. Uninstructed, inexperienced examiners may fail to test specifically for toe extension and fall into the "wiggle your toes" trap (see Chapter 7). They may also be unaware of the important sensory area of the deep peroneal nerve in the first web space and overlook the presence of hypesthesia in that location. When the responsibility of the examination is passed from one individual to another, for example, at the nurses' change of shift, it is very useful for the person coming on duty and the person leaving to perform an examination together; this joint effort eliminates any confusion about the current status of the patient or the technique of the examination.


• Remove circumferential dressings early. The appearance of pain out of proportion to what is expected from the clinical situation, deficits in motor or sensory function, or pain on passive muscle stretch may well be evidence of a compartmental syndrome. To assure that increased tissue pressure is not resulting from tight circumferential dressings, casts should be bivalved (see Chapter 8); one-half of the cast is removed, and all soft dressings are split to the skin. Frequently, simply splitting the cast does not provide adequate decompression. The consequences of loss of fracture position are insignificant compared with those of a compartmental syndrome.


• Maximize local arterial pressure, especially if there is evidence of compartmental ischemia. Systemic hypotension should be treated; local hypotension should be minimized by placing the limb at the level of the heart.


• Utilize tissue pressure measurement, particularly if the clinical evaluation is incomplete or confusing. Tissue pressure measurement is a useful adjunct to the clinical evaluation of patients at risk for compartmental syndromes.


• If surgical decompression is indicated, promptly and completely open all potentially limiting envelopes. The use of limited skin incisions, primary closure of the skin, or failure to open all four compartments of the leg may permit the recurrence of compartmental syndromes after surgical decompression.


• Minimize operative debridement. The potential of nerve and muscle for repair or reconstruction after an ischemic insult indicates that only obviously nonviable tissues should be removed at the time of surgical decompression.


• Consider skeletal fixation of unstable fractures associated with compartmental syndromes.


• Delay skin closure until three to five days after surgical decompression. At this time, delayed primary closure, the application of meshed skin grafts, or progressive wound edge approximation may usually be safely instituted. If questionably viable tissue is present, closure should be further delayed.


• Minimize contractures by appropriate splinting and range of motion exercises.


• Look for myoglobinuria and other systemic consequences of muscle necrosis. If myoglobinuria is suspected, maintain a high urinary output to lessen the nephrotoxic effect.

Syndromes due to exercise

Recurrent leg pain with exercise is a commonly observed symptom. A relatively small number of patients with this symptom have recurrent compartmental syndromes due to intensive use of muscles.

Recurrent compartmental syndromes often produce pain, muscle tightness, and weakness that require the patient to slow down or cease exercising altogether.

These syndromes may be diagnosed by examination of the patient during and after exercise as well as at rest. Tissue pressure monitoring during a standard exercise test is helpful.

Careful evaluation is required to differentiate this condition from tendinitis, shin splints, and fatigue fractures.

Patients with well-documented recurrent compartmental syndromes due to intensive use of muscles benefit from decompression of the affected compartment.

Intensive muscular work increases muscle volume and thus can lead to increased intracompartmental pressure. Although increased intramuscular pressure from exercise may resolve without producing any symptoms, it may also give rise to two varieties of compartmental syndromes: an acute form and a recurrent form. The acute compartmental syndrome from intensive use of muscles is diagnosed and treated as other compartmental syndromes along the lines presented in the foregoing chapters. Recurrent compartmental syndromes from exercise produce a somewhat different clinical picture and thus deserve a separate discussion. The term "recurrent" is preferred over the more familiar term "chronic" because the patient does not have chronic disability, but rather is asymptomatic between recurrences. l-6

Pathophysiology

Diagnosis

Clinically, recurrent compartmental syndromes differ from the acute variety in that symptoms are brought on by excessive exercise of the affected compartment and dissipate with a period of rest, generally in the order of minutes. Whereas a high degree of exertion is often required to precipitate the symptoms, a slower pace of exercise may allow these symptoms to resolve. In many cases symptoms recur predictably with approximately the same amount of exercise.

Recurrent compartmental syndromes of the leg are usually found in athletes and military recruits. The patient typically notes a painful, tight sensation in the affected compartment along with weakness of the muscles in that compartment. For example, a patient with a recurrent anterior compartmental syndrome of the leg may develop a foot-slap on heel strike due to weakness of the tibialis anterior muscle. Occasionally, paresthesias are experienced in the distribution of the nerves running through the affected compartment. Recurrent compartmental syndromes are encountered most frequently in the anterior and lateral compartments of the leg. 5 The deep and superficial posterior compartments of the leg may also be involved.

The physical examination of the nonexercising patient with a recurrent compartmental syndrome is often unremarkable. However, Reneman 5 noted fascial hernias in the majority of his patients with this condition. Garfin et al 11 pointed out that these fascial defects tend to occur at the site of emergence of the superficial peroneal nerve. Thus, symptoms may arise from the compartmental syndrome, from herniation of muscle through the defect, or from local compression of the nerve.

Because this syndrome is produced by exercise, it is most useful to examine the compartment during and after vigorous exertion of the muscles in the compartment. The compartment may be most conveniently exercised by asking the patient to repeatedly contract the compartmental muscles against manual resistance until characteristic symptoms are produced. At this point the compartment may be palpated for tenseness and the muscles examined for weakness. When involvement is unilateral, the opposite side is used for comparison. The patient may also be asked to perform exactly the exercise that causes his symptoms with the physician running or biking at his side. This type of "on the scene" evaluation gives the physician the most accurate idea of what is occurring in the patient's extremities. Pain that occurs with the first few steps, but that can be "run through," cannot be attributed to a recurrent compartmental syndrome. Pain that comes on after a more or less predictable amount of exercise and that requires the patient to slow his pace or stop exercising is much more typical, particularly if associated with a tight compartment and weakness of the intracompartmental muscles.

Reneman 5 provided good evidence that increased tissue pressure is important in recurrent compartmental syndromes. With the use of an injection technique, he measured tissue pressures in the anterior compartment of the leg before exercise and at zero, three, and six minutes after a standard exercise test (repeated dorsiflexion of the foot against resistance). This test was carried out in normal volunteers and in a group of male patients in whom the need for surgical decompression had been determined on clinical grounds. Resting pressures were only slightly elevated in the patients requiring surgical decompression. However, the tissue pressure six minutes after exercise was significantly increased in all 34 of these patients.

We have used the continuous infusion technique (see Chapter 2) in a similar exercise test to evaluate patients for recurrent compartmental syndromes. In this application an 18-gauge catheter and an infusion rate of 0.1 cc per hour provide a better dynamic response than the smaller catheter and slower infusion rate used in monitoring limbs at risk for acute compartmental syndromes. Use of the infusion technique provides continuous pressure monitoring during and immediately after exercise. With the catheter in the muscle of the compartment, base-line readings are obtained. The compartmental muscles are then contracted against resistance at a rate of one per second for three minutes. Particular notice is taken if the patient's symptoms are reproduced during the exercise test. In the examination of the anterior compartment of the leg, resistance to foot dorsiflexion may be applied manually or with the use of a hinged footboard connected through a pulley to a 6-kg weight.

We studied seven anterior compartments of the leg in five patients believed to have recurrent compartmental syndromes because of their clinical findings. We also studied a control group consisting of six male and six female volunteers (age range- 12 to 61 years; average age, 28 years). The results are quite interesting. In our patient group, resting anterior compartment pressure averaged 16+2 mm Hg compared with 11+2 mm Hg in our control group (mean +SD). The postexercise pressure curve in the patient group deviated dramatically from that of the control group. For the patients, the postexercise pressures were higher and did not return to pre-exercise levels within six minutes. These results are identical to those of Reneman. 5

Differential diagnosis

The common diagnoses requiring differentiation from recurrent compartmental syndromes include tendinitis, fatigue fractures, and the poorly understood entity known as shin splints. These conditions are probably more common causes of exercise-related leg pain than are recurrent compartmental syndromes. Although they may produce leg symptoms similar to those of recurrent compartmental syndromes, these conditions are not accompanied by indications of increased intracompartmental pressure. In addition, whereas many patients can run through symptoms due to these conditions, such is not the case with compartmental syndromes.

Symptoms of tendinitis usually persist after the exercise has been stopped; pain is often reproduced by passively stretching the affected tendon. In fatigue fractures, a sharply defined area of bone tenderness usually extends Mom one side of the bone to the other. Radiographic evidence of periosteal new bone formation may be present in long-standing cases. Bone scans frequently indicate locally increased bone turnover. In shin splints, pain is usually located just behind the medial tibial crest, often at the junction of the middle and distal thirds of the tibia. The area of tenderness is often 10 cm or more in length. While roentgenograms remain normal, the bone scan may show increased bone turnover along the area of tenderness. In our experience, patients with shin splints do not demonstrate increased tissue pressure at rest or after exercise. Therefore, we cannot recommend surgical decompression of the deep posterior compartment in the treatment of this condition as suggested by Puranen. 12

Treatment

Many patients with recurrent compartmental syndromes due to intensive use of muscles are relieved to gain an understanding of their condition and are willing to modify their exercise program to avoid the resulting symptoms. Some serious athletes, however, are unable to modify their exercise program and request surgical decompression.

In recurrent compartmental syndromes due to intensive use of muscles, the surgical procedure is quite different from that used for treating acute compartmental syndromes. First, the procedure is not an emergency. Second, one compartment can usually be clearly identified as being responsible for the patient's symptoms. Third, postischemic swelling is not anticipated after the operative procedure; thus, subcutaneous fasciotomy is appropriate. The fascial incision is made through two small skin incisions and runs the entire length of the compartment, leaving no fascial bridges. Care is required to avoid injuring the branches of the superficial peroneal nerve in decompressing the anterior compartment of the leg, as pointed out by Garfin et al. 11 At the end of the procedure, the skin is closed with a cosmetic suture. The patient is warned that the extremity may swell with dependency for a few days up to a few weeks after the procedure. A progressive exercise program is instituted one week after surgery.

To date we have operated on five anterior compartments of the leg in four patients. These have included a runner, a race walker, an ice skater, and a professional soccer referee. All had significant improvement after their surgical procedure and returned to their activities. Reneman 5 6 also noted excellent results from his treatment of patients with this condition. Thirty-six of 40 patients who submitted to surgery were able to resume physical activities that had been prohibited by symptoms before surgery. One patient did not experience improvement, and three were lost to follow-up.

The following case report presents an instructive example of a recurrent compartmental syndrome due to intensive use of muscles:

A 32-year-old white male world class race walker had a 15-year history of painful tightness in both anterior compartments during exercise. His symptoms would typically appear in the first three or four miles of race walking at a competitive speed, although they could be avoided if he walked at a somewhat slower pace. The pain was accompanied by weakness of foot dorsiflexion noted as a foot-slap on heel strike. The patient also observed a vague numbness over the dorsum of his foot after the onset of pain. Although he was able to complete longer races and marathons, his speed was retarded by his symptoms.

Routine physical examination was unremarkable. No fascial hernias were detected. Upon repeated dorsiflexion of his foot against resistance, his anterior compartments became tense and his symptoms were reproduced. Formal exercise tests were conducted while anterior compartmental pressures were monitored using the continuous infusion technique. Resting anterior compartment pressures measured 15 mm Hg on the left and 14 mm Hg on the right. Postexercise pressures were markedly elevated and showed a retarded return toward the pre-exercise level.

Subcutaneous fasciotomies of both anterior compartments were performed. Six weeks after operation the patient was asymptomatic. A repeat pressure test during exercise at this time revealed a normal response. The patient returned to full training and competition. He placed in the top five in the Pan American games six months after surgery and at this writing is a strong candidate for the United States Olympic race walking team.

Challenges in diagnosis and treatment

Seven cases

Having reviewed most of the available information on compartmental syndromes, the reader may now find it interesting to study some cases that demonstrate problems in the diagnosis and management of this condition. Seven such cases are presented below. These cases have been arranged to challenge the reader to apply his knowledge in selecting the appropriate laboratory evaluation and treatment without being biased by what actually occurred. Thus, the history and clinical evaluation are presented separately from the subsequent course.

In the first three cases, earlier diagnosis and treatment as well as a better end result might have been possible had the physician originally treating the patient been more familiar with compartmental syndromes. The last four cases demonstrate that careful clinical evaluation and adjunctive diagnostic tests can help resolve some very challenging diagnostic problems.

Case 1

History and clinical evaluation

A 47-year-old male truck driver was in good health until he noticed the acute onset of anterior chest pain radiating down both arms while he performed push-ups. He came to the hospital in acute distress where a dissecting aneurysm of the ascending aorta was diagnosed. An emergency surgical repair was performed. This procedure was difficult and required 5 hours and 12 minutes of cardiopulmonary bypass using the right femoral artery. Cannulation of this artery in a retrograde manner produced a relative occlusion of the femoral artery.

After operation the patient was in serious condition in the intensive care unit. The neuromuscular function of his right leg was not checked until a consulting physician examined him approximately 14 hours after the conclusion of the original operation. This examination revealed a tense right leg from the knee to the ankle. The patient was unable to move his toes and had no sensation in his foot. There was pain on passive stretch in both the anterior and deep posterior compartments. His distal pulses were intact.

Laboratory evaluation, treatment, and result

The presence of a tense leg with severe neuromuscular deficits was deemed sufficient to establish the diagnosis of a compartmental syndrome and to justify immediate surgical decompression; no additional time was taken for diagnostic procedures. A four-compartment parafibular decompression was performed. The contents of all compartments bulged markedly. The muscle of the anterior compartment was quite dusky. This patient's subsequent clinical course was complicated by myoglobinuric renal failure that responded to hemodialysis. His wound was treated open with daily dressing changes for 13 days, at which time he was taken to the operating room for inspection of the wound and skin grafting. The anterior compartment appeared to be pale, and the extensor digitorum longus muscle was necrotic and required excision. Minimal debridement of the tibialis anterior and extensor hallucis longus muscles was performed. The rest of the leg muscles appeared healthy. A meshed split-thickness graft was applied. Eighty-five percent of the graft took primarily. The remainder of the wound was allowed to heal by granulation and epithelialization.

One year after surgery the patient had grade four strength of the muscles of the lateral, superficial posterior, and deep posterior compartments. The tibialis anterior muscles, which had apparently been functionless for over six months, had recovered grade three strength, and the patient no longer needed a drop foot brace. The patient's heart, aortic, renal, and cerebral function were all normal.

Comment

This case was made difficult by the patient's critical condition and by the intensive medical and surgical treatment required to save his life. In retrospect, prophylactic fasciotomy may have been indicated in view of the massive postischemic swelling expected after the release of prolonged occlusion of the femoral artery. The muscle of the anterior compartment obviously sustained a double ischemic insult, first from the arterial occlusion and then from the compartmental syndrome. It is ironic that although the function of his anterior compartment seemed insignificant while the patient was critically ill, the loss of this function is now his major disability. It is also instructive to note the delayed functional return of sufficient anterior compartmental function to make him brace free.

Case 2

History and clinical evaluation

A l6 year-old boy had surgical correction of a 20-degree valgus deformity of the right tibia. The osteotomy was performed just distal to the tibial tubercle along with a proximal fibular osteotomy. On awaking from anesthesia, the patient was unable to extend his toes or dorsiflex his foot. Hypesthesia was present in the distribution of the deep and superficial peroneal nerves. Twenty-four hours after operation, the patient complained of increasing pain in the leg, which responded incompletely to removal of the circumferential dressings. A consulting physician examined the patient two days later and noted anesthesia in the distribution of the deep peroneal nerve. Strength of toe flexion was four out of five; strength of toe extension was zero out of five. The leg was moderately tight on palpation, particularly in the proximal as