Chronic Compartment Syndrome

Robert A. Pedowitz MD, PhD

Derek W. Weichel BS

Key Points

Compartment syndrome is a condition of elevated pressure within a space bounded by bone and/or fascia which results in decreased perfusion of tissues within the compartment.
Chronic compartment syndrome (CCS) is the chronic exertional form of compartment syndrome, found as a result of sports or exercise.
CCS is always associated with pain that occurs during exercise and with increased intracompartmental pressures.
Patients with CCS often do not present with a classic set of symptoms. Therefore a high index of suspicion is required for patients with exertional extremity pain. The clinical examination is more effective in ruling out other possibilities than it is for providing a definitive diagnosis of CCS.
Patients will almost always describe pain that is induced by exertion and resolves with rest. Elite athletes, as well as recreational athletes, involved in both running and nonrunning activities can suffer from CCS.
Direct measurement of intracompartmental pressure remains the hallmark of objective assessment of both CCS and acute compartmental syndrome (ACS).
During measurement of pressure, the physician should avoid injecting large amounts of anesthetic into the compartment. However, the skin, subcutaneous tissue, and fascia can be anesthetized without fear of raising intracompartmental pressure.
It is important that CCS patients reproduce their symptoms during diagnostic assessment. The patient needs to perform the specific exercise activity that causes the pain.
Activity modification, taping, stretching, nonsteroidal anti-inflammatory administration (NSAID), and the use of orthotics are included in nonsurgical management of CCS, but are rarely successful.
Fasciotomy is advised for patients who want to return to full unrestricted activities and can be effective even after a delayed diagnosis.

Compartment syndrome can occur, either acutely [acute compartment syndrome (ACS)] or in a chronic exertional form [chronic compartment syndrome (CCS)] in sports and exercise. CCS should be in the differential diagnosis of any patient who presents with exertional extremity pain (1,2,3,4). Mubarak and Hargens (5) define compartment syndrome as a condition of elevated pressure within a space bounded by bone and/or fascia that results in decreased perfusion of tissues within the compartment. There have been many reports of compartment syndrome in both the upper and lower extremities (6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24). The pathophysiology of CCS is not yet fully understood; however, it can be treated surgically in the majority of cases. This chapter will address the pathophysiology and diagnosis of CCS.

ANATOMY

The anatomical features that are relevant to a discussion of compartment syndrome have been described previously (25). Local osseofascial anatomy defines the compartments of the body and it is useful to think of each compartment as a closed space. Each compartment has its own pressure-volume relationship. Factors that cause an increase in intracompartmental volume, such as hemorrhage or interstitial swelling, may lead to significant increases in intracompartmental pressure, since bone and fascia have little elasticity.
Extrinsic compression, such as a cast or tight dressing, can also lead to increased pressure within the compartment. In ACS, increased intracompartmental pressure leads to decreased perfusion, tissue ischemia, and a persistent vicious cycle of further swelling, etc. If the ischemia is prolonged, Volkman’s ischemic contracture (25a) with myonecrosis, decreased extremity function, and permanent deformity may result.

Rarely, CCS will develop into ACS (26,27). Prolonged tissue ischemia is not typically associated with CCS. Intermittent elevation of compartment pressure is observed with exertion in CCS. CCS is always associated with pain that occurs during exercise and with increased intracompartmental pressures. However, the mechanism of pain production associated with CCS is still debated.

ACS or CCS can be seen in virtually any extremity or axial skeletal muscle; however, CCS is most commonly diagnosed in the four compartments of the leg. Anatomic dissections that revealed variable proximal and distal sub-compartments of the deep posterior compartment of the leg (28) support the claims made by some authors that the deep posterior compartment of the leg is subdivided into two or three sub-compartments (29,30). When making the diagnosis or considering surgical treatment, such variations in anatomy should be considered. The anterior, lateral, and superficial posterior compartments make up the remaining leg compartments.

The three compartments of the thigh are the anterior which includes the quadriceps, the posterior which includes the hamstrings, and the adductor groups. The upper arm also has three compartments which are the deltoid, the posterior which contains the triceps, and the anterior (biceps-brachialis). The volar and dorsal compartments make up the forearm; however, the mobile wad is considered to be functionally separate by some authors. The hand is made up of the interosseous groups, thenar, and hypothenar compartments. The carpal tunnel is typically considered to be a distinct compartment from both the forearm and the hand. The foot has lateral, medial, central, and intraosseous compartments.

The gluteal muscles are a functionally separate compartment. Remaining compartments include the paraspinal musculature and the muscles of the internal and external pelvis. The abdomen is also considered a functional compartment in which organ ischemia and severe morbidity may result from increased abdominal pressure (31,32). Improper placement of invasive intra-muscular pressure measurement devices can penetrate and damage neurovascular structures. Therefore, it is important to have a good understanding of the three dimensional anatomy of these muscular compartments.

Pathophysiology of Compartment Syndromes

It is understood that a common characteristic associated with compartment syndrome is elevated pressure within the osseofascial compartment which in the case of ACS causes ischemia and possible necrosis. However, the basic pathophysiology of this syndrome is still not completely understood. Capillary perfusion is required for healthy tissue. The Starling equation defines the balance of extravascular and intravascular fluid dynamics that affect transcapillary flow (33). Permeability factors (capillary surface area and water conductivity), colloid osmotic factors (plasma and interstitial colloid osmotic pressures), and hydrostatic factors (intravascular and interstitial fluid pressures) are all included in the Starling equation (33). Because normotensive humans have a capillary blood pressure between 20 to 30 mm Hg, interstitial fluid pressures that rise much above 30 mm Hg may lead to a slow decrease in capillary perfusion. This is the point at which hypoperfusion starts but it may not be the threshold for overt compartmental necrosis. A clinician’s clinical concern for compartment syndrome should be increased when interstitial pressure reaches 30 mm Hg in a normotensive individual. In a state of systemic hypoperfusion, the driving force for local perfusion is decreased which leads to decreased critical compartment pressure thresholds for tissue liability. This theory is supported by Arbabi et al. (34) who demonstrated that the neuromuscular abnormalities associated with compartment syndrome occur at lower compartment pressures when the compartment is also subjected to hypotension and hypoxia, suggesting that the signs and symptoms of compartment syndrome are related not only to the compartment pressures, but also to the compartment perfusion pressure.

The specific anatomic basis of microvascular dysfunction in compartment syndrome is not well understood. Early reports (35) suggested that increased intracompartmental pressure causes reflex arterial spasm with consequent tissue ischemia. However, Vollmar et al. (36) found that blood flow ceased in arterioles with increasing pressure on the vessel without any sign of spasm or collapse.

Other descriptions look at the effects of increased compartment pressure on the microvasculature. The theory which suggests that microvasculature occlusion occurs when the tissue pressure is greater than the arterial or transmural pressure was proposed by Burton (37) and Eaton et al. (38). These authors suggest that increased tissue pressure or decreased systemic blood pressure would lead to occlusion of the microvasculature.

It was proposed by Hargens et al. (39) that collapse and occlusion of the thin walled capillary vessels is caused by increased compartmental pressure. Normotensive dogs had intracapillary pressures between 20 to 30 mm Hg which correlates well with a compartmental pressure threshold of 30 mm Hg for observation of early ischemic changes associated with compartment syndrome. This concept has been challenged by Vollmar et al. (36) who found that capillaries did not collapse at high pressures even after they demonstrated cessation of blood flow.

The critical driving force for blood flow across the capillary bed is the arterial venous (A-V) pressure gradient. One theory is that a drop in the A-V gradient is caused by increased venous pressure due to the increased intracompartmental pressure (40). Birtles et al. (41) support the theory that the signs and symptoms associated with CCS are at
least partially due to venous obstruction caused by the increased intracompartmental pressure. They found that healthy patients demonstrated increased muscle fatigability, pain, and size in the anterior tibialis muscle when fitted with a sphygmomanometer cuff just below the knee that was inflated to a pressure of 81 mm Hg to occlude venous outflow. These findings are supported by Zhang et al. (42) who demonstrated that the anterior compartment of the leg had decreased blood flow and perfusion pressure with thigh tourniquet induced venous stasis. The work by Vollmar et al. (36) also supports these findings as they observed venular vessels collapse, regardless of diameter, at much lower pressures than those needed to collapse arteriolar vessels. Upon venular collapse and cessation of venular outflow, there was still perfusion of the arteriolar segments of the vasculature. Similarly, as pressure on the vessel was slowly decreased from levels at which both arteriolar and venular blood flow had ceased, arteriolar blood flow resumed before venous drainage was evident. Vollmar et al. (36) concluded that impaired venous drainage with impaired capillary stasis, but not arteriolar ischemia, could be the main physiological component of compartment syndrome.

Researchers cannot agree on one common etiology of CCS. It is understood that intermittent elevation of tissue pressure occurs during exertion and reverses at rest in patients with CCS. Intramuscular pressures greater than 500 mm Hg have been measured during normal vigorous skeletal muscle contractions (43,44). Therefore, tissue perfusion must occur between muscle contractions. However, the intramuscular pressures between contractions are elevated with CCS, thereby preventing effective tissue perfusion.

Styf and Korner (45) suggested that occlusion of large vessels by local muscle herniation as they transverse the interosseous membrane causes CCS of the anterior leg (46). Martens and Moeyersoons (47) believe that the fascia in CCS patients is not as compliant as normal fascia and that it is not able to accommodate the increased muscle volume that normally occurs during exercise. According to Raether and Lutten (19), vigorous exercise may result in an intracompartmental volume increase up to 20% over the baseline. Detmer et al. (2) observed increased fascial thickness in 25 of 26 samples taken from legs of CCS patients. Similar results were reported by Garcia-Mata et al. (7) who found that the fascia of adolescent patients with CCS was thicker, enlarged, and harder than that of normal patients. It is not known if these abnormalities are the cause or the effect of chronically increased intramuscular pressures. Deirder et al. (6) observed similar changes in muscle size during exercise between control subjects and subjects with CCS suggesting that tight fascia may not be the cause of pain in these patients. Others (18,48,49,50) have observed a variety of anatomic abnormalities that could put an individual at risk for CCS. However, no unifying theme has emerged in these observations.

The role of muscle ischemia in CCS has been a surprisingly controversial subject. Amendola et al. reported that MR imaging did not reveal consistent ischemic changes in patients with CCS. Similarly, nuclear magnetic resonance spectroscopy did not show ischemic changes in the majority of patients studied by Balduini et al. (51); however, a number of articles do support the theory that muscle ischemia is a significant factor in CCS. Takebayashi et al. (52) observed decreased Thallium201 distribution in muscle affected by CCS using SPECT imaging. In addition, Mohler et al. (53) observed greater relative deoxygenation, as well as delayed re-oxygenation, after exercise in patients with CCS using near infrared spectroscopy (NIRS). Van den Brand et al. (54) also noted greater relative deoxgenation during exercise in patients with CCS compared with normal subjects when measured with NIRS. Ota et al. (55) reported delayed muscular re-oxygenation in a patient with chronic exertional compartment syndrome following exercise. Breit et al. (56) observed oxygen levels in muscles subjected to exercise and external compression progressively decreased while it remained fairly constant in subjects with no compression. During recovery, it also took longer for the tissue oxygenation levels to return to baseline in subjects with external compression. Abraham et al. (57) observed limited maximal blood flow immediately after exercise which seemed to be caused by increased intracompartmental pressure in CCS patients; however, a delayed peak in hyperemia following exercise coincided with pain relief. New diagnostic methods may facilitate better understanding of the underlying etiology and pathophysiology of CCS.

Birtles et al. (58) observed greater delayed onset muscle soreness in patients who have CCS and suggested that this may be due to damage and inflammation of the connective tissue. However, Kalchmair et al. (59) observed several biological changes in the plasma during reperfusion following a period of ischemia which could also be related to this finding. They found increased histamine release immediately upon reperfusion which is kept in check by diamine oxidase (DO) for the first 60 minutes after which the DO is no longer able to metabolize all the histamine. The plasma monomine oxidase levels also remain consistently high throughout the reperfusion period.

Differential Diagnosis of CCS

The differential diagnosis of CCS has been described previously (25). The signs and symptoms associated with CCS are very similar to those of other etiologies of exertional leg pain. According to the classification established by Detmer et al. (2), a stress fracture (Type I), medial tibial periostalgia (Type II), and CCS (Type III) are the most common diagnoses to consider in patients with exertional leg pain. Venous stasis, vascular or neurogenic claudication, tendonitis, nerve entrapment disorders, occult infection, metabolic bone disease, or neoplastic process are other possible diagnoses. Turnipseed (60) observed that 93% of cases of atypical claudication in adolescents and young adults were caused by CCS.

Some types of vascular abnormalities could be misdiagnosed as CCS. Intermittent distal ischemia can be caused by popliteal entrapment syndrome (61) or by constriction of the superficial femoral artery in the adductor canal (62). A subject with a popliteal artery aneurysm was originally misdiagnosed and treated with a fasciotomy for CCS in a case reported by Knight et al. (63). Studies including bone scintigraphy, magnetic resonance imaging, angiography, or electromyography may be needed to rule out other disorders in the process of making the correct diagnosis. Definitive diagnosis of CCS often requires the use of objective diagnostic methods.

Clinical Presentation of CCS

Patients with CCS often do not present with a classic set of symptoms and therefore a high index of suspicion is required for patients with exertional extremity pain. Although some of the described clinical presentations will be found in both upper and lower extremity CCS, most of the published information pertains to the lower leg.

Patients will almost always describe pain that is induced by exertion and resolves with rest. Elite athletes as well as recreational athletes involved in both running and nonrunning activities can suffer from CCS. Some reports state that the sex distribution is equal (2,3); others claim that it is more prevalent in males (47,64). More recent reports, however, observed a higher prevalence in females (65,66). Although CCS has been diagnosed in elderly patients and adolescents (3,7), it is usually seen in active, young adults.

Any patient who may have CCS should be carefully questioned about their pain which they may describe as cramping, muscle tightness, swelling, or a feeling of weakness or numbness. The symptoms may be achy, sharp, dull, or diffuse. Neuromuscular disorders such as slap foot or abnormal distal sensation during exercise may be described. A recent report found that 68% of patients with CCS had it bilaterally (66). The pain caused by CCS could be brought on with relatively light exertion or heavy exercise; however, each athlete usually has a consistent pattern of pain production in terms of duration of exercise. Their symptoms will also normally resolve over a consistent time period which may be minutes, hours, or rarely days after exertion. The clinical presentation may be complicated if other forms of exercise-induced extremity pain are also present. CCS has been described in the intra-osseous compartments of the hand, dorsal, and volar forearm compartments, lumbar paraspinal muscles, the feet, and the thigh (6,8,9,10,11,16,18,19,20,21,22,23,24,48,67); however, it is most common in the leg.

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