Chronic Exertional Compartment Syndrome

Chronic exertional compartment syndrome (CECS) is a condition in athletes that can occur from repetitive loading or exertional activities. CECS is usually observed in competitive or collegiate athletes; long-distance runners, basketball players, skiers, and soccer players. Although it is most common in the lower legs, CECS can occur in any compartment of the extremities; for example, it has been described in the forearms of motocross racers and other athletes. ^{[1, 2, 3]}  The estimated incidence is about 1 in 2000 persons each year. ^[4]

CECS is characterized by exercise-induced pain that is relieved by rest. In some cases, weakness and paresthesia may accompany the pain. Onset of symptoms typically occurs at a specific exercise distance or time interval or intensity level (eg, within 15 min of initiating a run). Symptoms tend to subside with rest and are minimal during normal daily activities but return when activity is resumed.

Unlike acute compartment syndrome, which usually results from trauma, the pathophysiology of CECS is not well understood. CECS may result from ischemic changes within the compartment; however, multiple theories and mechanisms have been suggested (see Pathophysiology and Etiology).

Although physicians have been aware of CECS symptoms since the early part of the 20th century, it was not until the late 1950s that the first reports on CECS were documented. Mavor was the first to describe the entity in 1956 in a patient who experienced recurrent anterior leg pain with exertion that was associated with herniation of the muscle and numbness of the affected extremity. ^[5] In 1975, Reneman defined the clinical manifestations of CECS and identified increased intracompartmental pressure as the cause.

CECS was initially thought to be a form of shin splints (anterior tibial enthesitis). ^{[6, 7]} However, with the advent of the fitness boom and the increased popularity of endurance sports, additional research on exercise-induced leg pain has demonstrated that CECS is a well-defined clinical entity.

The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Compartment syndrome is a condition in which increased tissue pressure within a closed osteofascial compartment compromises blood flow to the muscles and nerves within that compartment, resulting in the potential for tissue and nerve damage (acute compartment syndrome), as well as in symptoms/disability (CECS).

Crush syndrome is distinct from compartment syndrome and occurs when primary muscle necrosis initiates the cycle of events that may lead to an acute compartment syndrome. Volkmann ischemic contracture is a sequela of untreated or inadequately treated compartment syndrome, in which necrotic muscle and nerve tissue have been replaced with fibrous tissue.

Compartment pressure readings with and without exercise are the gold standard for the diagnosis of CECS. ^{[8, 9, 10]} A trial of conservative treatment may be undertaken for CECS, but symptoms generally recur when the patient returns to exercise. ^[11] If conservative treatment is unsuccessful, the patient should be referred to an orthopedic surgeon for consideration of fasciotomy.

For patient education information, see the Sports Injury Center.

A firm grasp of lower extremity anatomy is central to understanding the pathophysiology, diagnosis, and treatment of CECS. The lower leg is divided into 4 compartments: anterior, lateral, superficial posterior, and deep posterior. A fifth compartment, the tibialis posterior, has been documented, but its clinical significance has yet to be established.

The anterior compartment consists of the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius. The borders of this compartment are the tibia, fibula, interosseous membrane, and anterior intermuscular septum. Typically, the anterior compartment of the leg is the most frequently affected compartment in cases of CECS.

The lateral compartment includes the peroneus longus and brevis. Within the compartment lie the common peroneal nerve and its superficial and deep branches. This compartment is bordered by the anterior intermuscular septum, the fibula, the posterior intermuscular septum, and the deep fascia.

The superficial posterior compartment is surrounded by the deep fascia of the leg and contains the gastrocnemius, soleus, and plantaris.

The deep posterior compartment lies between the tibia, fibula, deep transverse fascia, and interosseous membrane. The muscles within the deep posterior compartment are the flexor digitorum longus, flexor hallucis longus, popliteus, and tibialis posterior. Also within this compartment lie the posterior tibial artery and vein and the tibial nerve.

The tibialis posterior compartment (a subdivision of the deep posterior compartment) is more recently described. It consists of the tibialis posterior, which has recently been shown to have its own fascial layer.

The pathology of CECS is not well established and is still debated; a general discussion follows.

CECS is associated with increased pressure in muscles at rest. Transient increases in compartmental pressure have been demonstrated experimentally as a normal response to exercise. Repetitive muscle contraction alone can increase intramuscular pressure to levels that may cause transient ischemia.

Elevated pressures usually normalize within 5 minutes after cessation of exercise. In CECS, however, the pressure between successive contractions remains high and impedes blood flow. As the pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping. ^[12] Pressures may remain elevated for 30 minutes or longer in persons with CECS.

Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure. This is also stated by the following formula:

LBF = (PA - PV)/R

In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance.

Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg. ^[13]

When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

With myocyte necrosis, myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood. One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure.

When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate. Changes in local vascular resistance (autoregulation) can compensate for some reduction in the local AV gradient. However, compartment tamponade occurs as arterial blood flow is occluded.

Shrier and Magder questioned this traditional hypothesis for the pathophysiology of CS and postulated that a critical closing pressure exists within muscle compartments (similar to West zone II in lung physiology). ^[14] These authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow.

The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures that exceed 30 mm Hg and persist for 6-10 hours result in muscle infarction, tissue necrosis, and nerve injury. For unclear reasons, compartment syndrome that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively. ^{[15, 16]}

Pressure-induced functional deficits are likely due to decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion.

In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis (acute compartment syndrome); conversely, rhabdomyolysis may result in compartment syndrome. ^{[17, 18]}

CECS usually results from repetitive microtrauma (overexertion). It is typically observed in long-distance runners, basketball players, skiers, and soccer players.

The pain in CECS has been thought to derive from the same pathologic processes that cause pain in acute compartment syndrome—that is, compromise of the vascular supply, which leads to myoneural ischemia.

Various mechanisms have been suggested as to the cause of this tissue ischemia, including arterial spasm, capillary obstruction, arteriovenous collapse, or venous outflow obstruction. However, a magnetic resonance imaging (MRI) study conducted by Amendola et al showed that significant tissue ischemia does not develop. ^[19]

Other theories suggest that muscle hypertrophy and/or fascial inflexibility is the origin of pain in patients with this CECS. However, not all athletes with muscle hypertrophy develop compartment syndrome.

Another theory, the mechanical damage theory, posits that exercise results in myofibril damage and release of protein-bound ions. Frequent damage, such as that occurring in the anterior compartment of runners, results in an increased release of ions, increased osmotic pressure, and decreased blood flow within the compartment.

Despite these various explanations for the cause of pain in CECS, no single theory has been overwhelmingly accepted. Further investigation is needed, including that regarding the relationship between pain and compartment metabolites.