Exertional Compartment Syndrome of the Leg: Steps for Expedient Return to Activity
Peter Edwards, MD; Mark S. Myerson, MDTHE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 4 - APRIL 96
In Brief: The pain and swelling associated with exertional compartment syndrome is caused by raised intracompartmental pressures possibly induced by muscle swelling or increased osmotic pressure. Although either the acute or chronic form of exertional compartment syndrome may occur, chronic is more common. Patients typically experience pain and swelling and may also have sensory deficits or paresthesias, and motor loss or weakness. Diagnosis is confirmed by intracompartmental pressure measurements before and after exercise. Although activity modification may alleviate symptoms, fasciotomy may be required.
Exertional compartment syndrome (ECS) of the leg—whether acute or chronic—is characterized by exercise-induced pain and swelling that is relieved by rest. Weakness and paresthesia may accompany the pain; these are related to ischemic changes within the compartment. Reneman (1) in 1975 defined the clinical manifestations of this condition and identified increased intracompartmental pressure as the cause. Although ECS has been described in the forearm, thigh, and gluteal regions, the leg remains the most common site of involvement.
The leg contains four osseofascial compartments, each surrounded by a relatively inelastic fascial covering (2,3). Each compartment contains a major nerve: the deep peroneal in the anterior compartment, the superficial peroneal in the lateral compartment, the saphenous in the superficial posterior compartment, and the tibial in the deep posterior compartment (figure 1: not shown).
Swelling in the lateral or the anterior compartment can compress both the deep and the superficial peroneal nerves against the neck of the fibula. The superficial peroneal nerve usually lies in the interval between the two peroneal muscles for a short distance and then emerges anterior to the peroneus brevis (2). It pierces the lateral compartment fascia at the junction of the midthird and distal third of the leg. Fascial hernias commonly occur at the superficial peroneal nerve's point of exit and can cause compression neuropathy.
The anatomy of the two posterior compartments can vary, but both, particularly the deep compartment, are frequently involved in ECS (4-8). The deep posterior compartment has a thin investing fascia that covers the entire compartment as it runs beneath the soleus muscle belly. In addition, a thickened band of fascia lies distal to the medial edge of the soleus muscle where the anterior and posterior fascial layers of the soleus combine. This "soleus bridge" then crosses over the distal deep posterior compartment to insert on the posteromedial distal tibia.
The importance of the soleus bridge is threefold. Irritation at its tibial insertion has been implicated in medial tibial stress syndrome, which is commonly confused with ECS (6). Also, failure to release the soleus bridge during deep posterior compartment fasciotomy may result in recurrent ECS symptoms. Finally, the soleus bridge is substantially tightened by pronation of the foot. Patients with ECS related to soleus bridge compression will therefore benefit from orthotic support that controls rapid pronation of the midfoot in the stance phase of gait.
Chronic ECS is far more common than the acute form (2). The clinical presentation of chronic and acute ECS differs only in severity; the pathogenesis of the elevated pressures in both is similar. The only other difference between acute and chronic ECS is onset and acuteness of symptoms. ECS is associated with increased pressure while muscles are relaxed. Skeletal muscle is perfused only during muscle relaxation, and relaxation pressure that exceeds 35 to 45 mm Hg results in decreased blood flow and acute myoneural ischemia typical of an acute compartment syndrome.
The etiology of increased relaxation pressure in ECS is unclear, although two theories have been proposed. Normal compartmental volume can increase 20% with exercise because of fiber swelling and increased intracompartmental blood volume. In the conditioned athlete, muscles may hypertrophy, and these anatomic changes alone may raise the local pressure enough to cause decreased perfusion pressure and resultant myoneural ischemia. This, however, is clearly not a sufficient explanation, because not all athletes with hypertrophy develop increased compartmental pressure.
Alternatively, the mechanical damage theory proposes that eccentric exercise results in myofiber damage and release of protein-bound ions. Repetitive eccentric contraction, such as occurs in the anterior compartment of runners, results in an increased release of ions and increased osmotic pressure within the compartment. The resultant osmotic pressure gradient increases capillary relaxation pressure and consequently decreases blood flow.
Acute ECS generally occurs in relatively sedentary people who undertake markedly strenuous exercise. Acute ECS produces severe muscle swelling due to increased interstitial edema, resulting in increased intracompartmental volume and perfusion deficits severe enough to cause irreversible myoneural ischemia within the compartment. Such severe findings may not be proportional to the intensity of the exercise.
Chronic ECS usually occurs in well-conditioned athletes younger than 40. Athletes with chronic ECS who markedly increase their training are also at risk of developing acute ECS.
Studies (2,5) have shown that transient increases in compartmental pressure during exercise are tolerated and don't cause symptoms in initially asymptomatic people. These pressures normalize quickly after exercise, usually within 5 minutes. In chronic ECS, intracompartmental exercise pressures may remain abnormally high for 20 minutes or longer after exercise before returning to normal.
As chronic ECS worsens, the periods of pressure elevation after exercise lengthen. If pressures remain elevated long enough, a potentially irreversible cycle of swelling and ischemia can occur, leading to acute ECS. In this situation, tissue metabolic demands are not met, leading to more swelling, which further restricts local blood flow. Acute ECS is relieved by rest, but a fasciotomy is warranted if pressure is significantly high. Superficial peroneal nerve paresthesias may be secondary to ischemic change in the lateral compartment as well as local compression from fascial hernias in either the lateral or anterior compartments.
The anterior compartment is most commonly involved in chronic ECS (45% of cases), followed closely by the deep posterior compartment (40%) (5). The lateral compartment is affected 10% of the time, and the superficial posterior compartment 5%.
Typical Clinical Presentation
Acute ECS causes agonizing pain, tense swelling, and pain on passive stretch of the involved muscles. Patients may also have sensory deficits—such as paresthesia or anesthesia to light touch—in the distribution of the involved nerves, and may have motor loss, including foot drop in severe cases.
People who experience chronic ECS report a gradual onset of aching leg pain and a feeling of fullness, both over the involved compartments. Activity-related pain begins at a predictable time after starting exercise or after reaching a certain intensity level. About 50% to 70% of patients will have bilateral involvement, with one side being somewhat worse. The pain is always fully relieved by rest, usually within 20 minutes of exercise completion, only to recur on resuming exercise. Patients occasionally report paresthesia in the leg and dorsum of the foot during exercise. Many patients who experience symptoms of anterior compartment pain will have demonstrable fascial defects or hernias, usually in the distal third of the leg over the intramuscular septum.
Physical examination in chronic ECS is usually normal unless the patient has recently exercised. Therefore, performing the physical exam after the patient has exercised strenuously enough to reproduce symptoms is recommended. Such exercise will produce swelling and tension in the involved compartments and increased leg girth. The leg will be tender over the involved muscles, and, with severe ECS, the patient will exhibit muscle weakness and paresthesia to light touch.
Tenderness, if present, is located proximal to the posterior medial tibial cortex in the midthird of the leg, although typically patients with ECS have no focal pain. Furthermore, they have no pain with vibratory testing of the tibia or circumferential bony tenderness, as seen with stress fractures. Accessory muscles or identifiable bone abnormalities are not usually present; figure 2 shows an unusual presentation. Tinel's sign over the common or superficial peroneal nerve is usually negative, as are other provocative tests for neural irritability. In addition, patients who have ECS show no evidence of vascular abnormality with resisted ankle plantar flexion, as seen with anomalous gastrocnemius compression of the popliteal artery.
Finally, patients with ECS do not have tenderness over the posterior medial tibial cortex in the distal leg, which contrasts with medial tibial stress syndrome, in which tenderness is quite specific and located in this area. In medial tibial stress syndrome, local inflammation of the periosteum results in activity-related pain early in a bout of exercise, but the pain tends to abate as exercise continues or with enhanced conditioning. However, pain may persist for hours or even days after exercise and may progress to involve other activities.
Key Diagnostic Tools
Anteroposterior, lateral, and oblique radiographs of the leg are warranted but are usually normal. A bone scan is rarely positive for ECS but should be obtained to rule out stress fracture and periostitis. The bone scan will show a transverse linear pattern for stress fracture and a longitudinal linear uptake in the cortex for medial tibial stress syndrome.
Atypical neurologic symptoms or signs may occasionally necessitate electromyography and nerve conduction studies, although these are not routinely necessary. If the patient has a foot drop, electrophysiologic testing is quite helpful in documenting the extent of motor loss. Compression neuropathy of the superficial peroneal nerve is the most common finding, although the saphenous nerve may also be involved. Finally, magnetic resonance imaging (MRI) may help evaluate intracompartmental contents for muscle abnormalities (figures 2c and 2d). MRI, however, is not recommended unless symptoms are accompanied by a visible or palpable mass in the leg.
To confirm the diagnosis of ECS, intracompartmental pressure must be measured. This is done most easily with a wick or slit-catheter technique. The needle tip location and depth of penetration, as well as knee and ankle position, are controlled to obtain reliable measurements. Our patients are tested supine with the knee extended and the ankle in neutral dorsiflexion. We use an 18-gauge needle and a hand-held compartment measurement device (Compartment Pressure Monitor, Stryker Instrument, Kalamazoo, Michigan).
Although testing has been recommended before, during, and after exercise, we do not recommend measuring during exercise because it is technically difficult and measurements are less reliable. An effective technique is to inject small amounts of local anesthetic into the skin alone and measure the pressures before exercise and at 1 and 5 minutes after exercise; however, we consider values obtained after exercise to be far more reliable for confirming the diagnosis. In fact, we rely solely on postexercise pressures, which we believe avoids repeatedly injecting the patient unnecessarily. The measurements obtained after exercise, however, are valid only if the exercise reproduces the patient's symptoms. We rarely obtain bilateral measurements because they are unnecessarily uncomfortable for the patient. However, comparison may be important if the results of pressure measurements are equivocal, or if both legs are symptomatic.
Rorabeck and coauthors (7,9,10), Fronek et al (11), and Pedowitz and Toutounghi (12) have proposed that elevated resting pressures above 10 to 15 mm Hg and 5-minute postexercise pressures above 15 to 25 mm Hg are diagnostic of ECS. Although any of their proposed criteria are useful, we use the guidelines proposed by Pedowitz et al (13): Preexercise and postexercise pressures above 15 mm Hg and 20 mm Hg, respectively, are diagnostic. The compartmental pressure measurements are rarely equivocal. If they are, measurements are repeated at a later date. In patients whose measurements are equivocal (ie, preexercise level of 10 to 15 mm Hg), increasing pressures in successive postexercise measurements are also considered diagnostic. In such patients, the rate of pressure decrease can be helpful: Pressure that remains elevated 10 to 15 minutes after exercise can be considered significant.
Acute ECS associated with high compartment pressure requires fasciotomy immediately after diagnosis. A two-incision technique is used, with generous medial and lateral incisions to completely release all surrounding compartments. Skin incisions are left open to keep intracompartmental pressure low, and delayed closure is performed 48 to 72 hours later.
When a patient first reports chronic ECS, we almost always begin nonoperative treatment and address extrinsic and intrinsic contributing factors. Extrinsic factors include training surface, shoe design, and training intensity, all of which can be modified. Intrinsic factors, such as muscle imbalance, flexibility, and limb alignments (especially hindfoot pronation), are treated with strengthening and stretching exercises and orthoses. These modifications are not always successful, although orthoses do decrease hyperpronation and thereby decrease compression of the deep posterior compartment by the soleus bridge.
Once a patient presents with chronic ECS, however, it is difficult to modify all these factors. Athletes routinely remain symptomatic unless they abstain from symptom-producing activities. These poor results from nonoperative treatment were highlighted by Fronek et al (11), who reported that five of seven patients were unable to return to sports after a conservative program.
If symptoms persist for 3 months, fasciotomy is recommended for chronic ECS and, unlike fasciotomy for acute ECS, may be limited to complete release of the involved compartments. Fasciotomies are performed through lateral, medial, or combination incisions (figures 3 and 4: not shown), depending on compartmental involvement as documented by pressure measurements. The results of anterior and lateral compartment releases are superior to those of posterior releases in most studies.
Postoperatively, patients are treated with immediate passive and active range-of-motion exercises to prevent fascial scarring. Weight bearing is begun within the first week. Athletes begin exercise on a stationary bicycle at 2 weeks and gentle isokinetic strengthening exercises at 3 to 4 weeks postoperatively. They begin running at 5 to 6 weeks, with speed and agility drills at 8 weeks.
Fronek et al (11) and Styf and coworkers (14-16) have shown normalization of resting pressures and decreased postexercise pressures in postfasciotomy patients. Thus, fasciotomy appears to decrease the inelasticity (or increase the compliance) of the involved compartments. If symptoms recur after fasciotomy, they can usually be traced to the deep posterior compartment, particularly if this compartment was not adequately released. Although some patients have recurrent symptoms related to inadequate release, a soleus bridge, scarring over of the fasciotomy defect, or entrapment of the saphenous nerve in the scar, in some patients the cause of these symptoms remains unclear. If fasciotomy fails, the diagnosis of ECS should be fully reevaluated.
Generally, we are able to return athletes to full sports participation by 8 to 12 weeks, when symmetric strength has returned as determined by instrument testing. Numerous researchers (5,11,14-17) have reported rates of 90% good-to-excellent results. Generally, athletes are able to return to sports without pain or with greatly diminished symptoms.
Dr Edwards is a fellow and Dr Myerson is the director of foot and ankle services in the Department of Orthopaedic Surgery at The Union Memorial Hospital in Baltimore. Address correspondence to Mark S. Myerson, MD, c/o Elaine P. Bulson, Editor, Union Memorial Orthopaedics, The Johnston Professional Bldg, Suite 400, 3333 N Calvert St, Baltimore, MD 21218.