Vigorous exercise results in increased muscle volume due to increased perfusion. This expansion of muscles can cause increased pressure within an unyieldingosteofascial compartment, particularly in the leg. In most people these elevated muscular pressures return to normal within seconds following rest.1 Some people experience prolonged elevation of intracompartmental pressures. When these abnormally high pressures are associated with pain or neurological symptoms, the condition has been described as an exercise-induced compartment syndrome.1-3

          Exercise-induced compartment syndrome is one of many causes of exercise related pain in the leg.4 Definitive diagnosis and distinction from other causes of exercise-induced leg pain can be difficult. It is the general consensus of most practitioners that the diagnosis must rest on measurement of abnormal resting and post-exercise intracompartmental pressures, but the threshold pressure values to define the condition and a rapid and reliable method to measure pressures have not been consistent. In addition, there are various techniques for performing intracompartmental pressure measurement tests before, during, and after exercise, and technique can have a substantial affect on recorded pressure. The difficulties associated with reliable diagnosis of the condition make it difficult to interpret data regarding treatment since patients from different series may not be comparable.

          We have been interested in chronic exercise-induced compartment syndromes for many years. This paper will discuss our work in the context of an overall review of the topic.

Anatomy

          The leg is commonly divided into four compartments on the basis of separate fascial envelopes: the anterior, lateral, superficial posterior, and deep posterior compartments. In the management of exercise-induced compartment syndrome, some have suggested that the tibialis posterior functions as if it were its own compartment (the so-called fifth compartment of the leg) and may be selectively vulnerable to exercise-induced compartment syndrome.5

          Each of the four major compartments contains a nerve with a sensory component. Increased pressure in the anterior compartment may cause diminished sensation in the dorsum of the first web space of the foot (deep peroneal nerve). Elevated pressure in the lateral compartment might cause sensory loss of the dorsum of the foot (superficial peroneal nerve). The sural nerve lies within the superficial posterior compartment and increased pressures may cause numbness over the lateral aspect of the leg and foot. The deep posterior compartment contains the tibial nerve and the sole of the foot may therefore become numb with increased pressures. Abnormalities of motor function, such as a transient foot drop, may also occur with exercise-induced compartment syndrome. We have found that this transient foot drop is present in nearly all patients with exercise compartment syndrome and have coined the term ÒSlap SignÓ to describe the onset of weakness during the course of running exercise.

          Transient pressure elevation within a compartment during exercise is not abnormal and reflects both transient increases in tissue perfusion and the pressure of muscle contraction, which may cause pressures upwards of 80 mm Hg in a normal muscle.6 The amount of stretch placed upon a muscle (i.e. the position of adjacent joints) also affects compartment pressures. These factors must be taken into account when interpreting pressure measurements.

          Muscle herniation through fascial defects has been identified in upwards of 40% of patients with chronic compartment syndromes, compared to only 5% of controls.2 The importance of this finding is not known.

Presentation

          The typical history associated with exercised-induced compartment syndrome was outlined by Detmer and colleagues.7 Most patients are avid runners who are completely asymptomatic in the off-season but gradually develop an aching pain in the lower leg as training progresses. The pain is initially present near the end of a run and disappears shortly thereafter. As symptoms progress, the pain may persist after the activity, even into the next day. Paresthesias may develop on the sole of the foot with a deep posterior compartment syndrome and on the dorsum of the foot in an anterior compartment syndrome. These two locations account for over 80% of all exercise-induced compartment syndromes in the leg.2, 5 The physical examination is usually normal. Athletes report a progression of the onset of symptoms with time and severe pain with their sport, combined with weakness and a positive Slap Sign.

Diagnosis

Differential Diagnosis
          Active young patients complaining of exercise-induced leg pain may suffer from medial tibial stress syndrome, stress fracture, nerve entrapment, or exercise-induced compartment syndrome.4 Bone scans and radiographs can usually identify the first two conditions. In medial tibial stress syndrome, the bone scan shows diffuse activity along the posteromedial cortex. Stress fractures cause a focal area of uptake. Radiologic investigations are normal with nerve entrapment conditions and, generally, negative in exercise-induced compartment syndrome, which may show areas of nucleotide uptake along the tibia by bone scan.

Intracompartmental Pressure Monitoring
          To test for an exercised-induced compartment syndrome, most authors have the patient perform running or isokinetic exercises until either pain or fatigue limit further activity. Measurements are taken pre and post-exercise. The position of the knee and ankle must be standardized since joint position can effect compartment pressure. The wick and slit catheter techniques have been popular instruments for obtaining pressure measurements. This abbreviated measurement method has several drawbacks, but does provide the practitioner with a crude measure of muscular pressures associated with exercise.

          Diagnostic criteria for exercise induced compartment syndrome vary. Rorabeck and co-workers required both a resting pre-exercise pressure of 10 mm Hg and a 15 minute post-exercise pressure greater than 15 mm Hg for diagnosis.3 Pedowitz and colleagues accepted any one of the following as diagnostic: 1) pre-exercise pressure greater than 15 mm Hg; 2) a one-minute post-exercise pressure greater than 30 mm Hg; or 3) a five-minute post-exercise pressure greater than 20 mm Hg.2
Our initial studies focused on the development of a miniaturized fluid pressure monitor for office use, which was found to be practical, accurate and rapid.1 Our current technique involves pressure measurements of symptomatic compartments in the office setting using a hand-held digital monitor (Stryker Corporation, Kalamazoo, MI). In an effort to provide complete and sophisticated pressure data, each compartment is monitored continuously starting at rest, during the course of four minutes of in-office exercise, and after exercise for five minutes.

           Most recently, this test has been adapted from a four-minute outdoor running test (which proved to be inconsistent) to our present use of a four-minute provocative supine exercise test. During the test the patient performs a vigorous isometric muscle contraction against the force of the examiner during pressure measurement. This brief office-based testing program consistently reproduces the patientÕs symptoms and provokes pressure elevation.

Our parameters for the diagnosis of chronic exercise-induced compartment syndrome include:

1. Elevated resting muscular compartment pressures (>12 mmHg);
   
   
2. Elevated relaxed muscle pressures during exercise (>60 mmHg),
   
   
3. Post-exercise pressure elevated above rest pressure at 5 minutes, and
   
   
4. The onset of characteristic pain during the four minute study.

          All four criteria were required for diagnosis. Those patients with compartment syndrome were found to consistently have resting pressures in the low twenties, exercise pressures of 90-110 and elevated post-exercise pressures.

          We have also developed a noninvasive four-minute standing exercise test. In a review of 33 patients, we found that this test accurately distinguished patients with exercise-induced compartment syndrome from those with medial tibial stress syndrome.(unpublished data) Patients with exercise-induced compartment syndrome consistently reproduced their characteristic disabling pain and all had a significantly diminished increase in calf circumference with exercise compared to normal subjects.

Treatment

           Patients with exercise-induced compartment syndrome do not require surgery if they are willing to curtail inciting sports activities. In our experience, 95% of patients desire to remain active in exercise and sport. Nonoperative treatment has not been effective. Patients that want to remain active in their sport usually require operative treatment. Operative treatment requires fascial release of the involved compartments. Many surgeons attempt to do this through a limited incision.8 Our experience with the operative treatment of exercise-induced compartment syndrome suggests that limited skin incisions with extensive subcutaneous release of involved compartments are preferable.

          Among patients requiring operative release of an exercise-induced compartment syndrome under our care 55% involved the anterolateral compartments, 24% the posterior compartments, and in 21% both areas. Both legs were involved in 82% of patients. We performed two-incision fasciotomy, with the subcutanous fascial incisions extended from ankle to knee. As a gauge of complete fasciotomy, compartment pressures were measured before and after release. Pre-operative pressure measurements recorded in the operating room matched those measured at rest in the office setting. In 32% of patients, post-fasciotomy pressure measurements were found to be greater than 15 mm Hg. Exploration of the release identified numerous fibrous bands overlying the fascia in each case. When these additional bands were released, the final resting pressure was below 9 mm Hg in each case. Overall, the resting pressure had decreased from an average of 23 mm Hg pre-op to an average of 7 mm Hg post-op. Nearly all of the patients had satisfactory relief of pain with return to full sports activities.

Conclusions

           We have attempted to simplify the office diagnosis of exercise-induced compartment syndrome of the leg and have developed methods for measurement. Measurement of muscle pressures during the described exercise test differentiates exercise compartment syndrome from other disorders causing exercise pain. Although conservative treatment methods have failed, the results of operative fascial release have been highly successful. We recommend extensive subcutaneous fascial release of each involved compartment and intraoperative pressure monitoring. With careful diagnosis and treatment, the results of operative treatment can be rewarding.

Brian J. Awbrey, MD is an Attending Surgeon at Massachusetts General Hospital and Clinical Instructor of Orthopaedic Surgery at Harvard Medical School

Shingo Tanabe, MD, PhD was a visitor from the Departments of Physiology and Sports Medicine at the The University of Tokushima School of Medicine and The Kanzaki Central Hospital, Tokushima, Japan

Address Correspondence to:
Brian J. Awbrey, M.D.; Department of Orthopaedic Surgery; Massachusetts General Hospital; 151 Merrimac Street, Suite 202; Boston, MA 02114