How To Detect And Treat Chronic Compartment Syndrome

Certainly, one of the greatest challenges practitioners face is properly evaluating exercise-induced leg pain. All too commonly pigeonholed under the term shin splints, chronic (or exertional) compartment syndrome (ECS) is a unique disorder whose term specifies its clinical and pathological features. Those who treat the condition recognize the list of differentials can be exhausting and an accurate diagnosis is essential to providing proper treatment. Compartment syndromes are either acute or chronic. The acute form first described by Volkman in 1881, is irreversible and may be initiated by trauma such as fracture, muscle contusion and, rarely, strenuous exercise. With acute compartment syndrome, rapid intracompartmental pressure develops to such a degree and duration (> than 30mm/Hg for > eight hours) that ischemic muscle necrosis and permanent neurological damage occurs if immediate fascial decompression is not performed. This is in contrast to the chronic form which, by definition, is reversible and has symptoms that are only transient in nature. ECS is a condition in which exercise induces high pressure within a closed space bounded by bone and fascia. The symptoms will present as pain with or without dysesthesia and muscle weakness secondary to an increase in compartmental intramuscular pressure. Why The Etiology Of ECS Remains An Enigma The etiology behind this syndrome continues to be a hotly contested issue. Unlike the acute form, which can be recreated by artificially raising the compartment volume or pressure, a good experimental model for ECS does not exist, leaving investigators much room for conjecture. The various mechanisms hypothesized are subsequently based on observation of normal muscle response. Generally, four factors are believed to contribute to an increase in compartment pressures in ECS. These include inelasticity of the fascial sheath; an increase in volume of skeletal muscle secondary to blood volume and edema; muscle hypertrophy in response to exercise; and dynamic contraction factors due to demands in the gait cycle. Volume increases are consistent and measured at levels above 20 percent. Recently, the supplement creatine has been implicated as a cause of ECS in athletes due to its effect on fluid retention and increase in muscle size. Nevertheless, some of these proposed factors continue to be challenged. For instance, biopsy studies have been largely unable to uncover abnormal changes in the fibroelastic tissue of the deep fascia. Muscle tissue biopsy reveals normal histology and essentially normal EMG studies. However, the broad concept of ischemia remains. What Role Does Ischemia Play In ECS? Elevated postexertional serum lactate levels in ECS are consistent with muscle under stress and presumed to be analogous to that found in ischemia. The levels have been noted to return to normal after decompression fasciotomy. Proponents of the ischemia theory generally believe in three possible mechanisms for tissue ischemia in ECS: arterial spasm causing inflow obstruction; obstruction of microcirculation; and, more recently, articles have embraced the concept of venous obstruction. Specifically, this concept states that an increase in venous pressure results in a decrease in arteriovenous gradient and ultimately a reduction in blood flow. Still, some investigators question whether ischemia is the true etiology of pain related to ECS. They point to a few studies as evidence. Using 31 NMR spectroscopy, a technique regarded as a reliable and sensitive measure of muscle metabolism, a lack of evidence failed to support the ischemia theory. With a radiopharmaceutical tracer to enhance imaging of tissue metabolism, MRI investigation of ECS was consistent with findings in NMR spectroscopy. This led investigators to argue that even though elevated intracompartmental pressure is a consistent feature of this condition, there are no studies illustrating a direct link between compartment pressure and ischemic pain. In fact, pressures as high as 160mm/Hg are needed to impose arterial occlusion and these levels are considered rare to nonexistent in the syndrome. As debates continue, additional explanations for the symptoms related to ECS emerge. Some have speculated that claudicant-type symptoms may possibly be related to sensory receptor stimulation in the fascia or periosteum, or perhaps even biochemical factors released as a result of aberrant blood flow. Performing a fasciotomy may therefore allow mechanical release of tension or alter biochemical reactions rather than reverse ischemia. In any event, you must be careful not to draw conclusions from these contradictory observations since most, if not all, experimental constructs are hindered by their own set of limitations. Essential Diagnostic Pointers To have a good understanding of ECS, its diagnosis and surgical approaches, a strong grasp of the cross-section boundaries of the leg is essential (see “A Review Of Compartment Anatomy”). Be aware that the differential diagnosis for exercise induced leg pain can have referred or local etiologies. Referred causes include spinal-related pathology presenting as radiculopathy or various vasculopathies that encompass claudication type syndromes, popliteal artery entrapment and rarely, popliteal aneurysm. Local causes of exercise-induced leg pain are far more common and numerous. They include stress fractures, periostitis or tibial fasciitis (also known as medial tibial stress syndrome), various tendinopathies, space-occupying lesions, local neurological compression syndromes in the leg (i.e. the common peroneal, superficial peroneal and tibial nerves), infection, fascial hernia and of course, ECS. This long list of differentials underscores the fact that a thorough history is paramount in making a proper diagnosis. Therefore, the decision to pursue the diagnosis of ECS is supported only by strong clinical suspicion. When Should You Be Suspicious Of ECS? The vast majority of patients with ECS are runners who range from the occasional jogger to the elite runner. In contrast, I have also treated athletes (usually unconditioned) who developed the symptoms after beginning an exercise program. Occasionally, you will recognize the disorder in cyclists as well. Patients with ECS will complain of cramping, burning, tightness and weakness of the ankle with exercise. Some will develop numbness in the foot and describe a foot slap during running. The most characteristic feature of ECS is that it is exercise-induced and never at rest. Patients will typically note its onset at a fixed point ranging from five to 30 minutes into an activity. The symptoms are reproducible with exertion and should be recreated in the office setting with an exercise challenge such as running on a treadmill or stair climbing. Specific motor and sensory testing after exertion will aid in confirming the diagnosis and specifying the compartment location. You will note that directly following activity, the compartment may feel tense or tender to deep palpation and passive stretch. Other remarkable findings include the variable presence of a fascial (or muscle) hernia located in the distal to middle third of the anterolateral leg. As stated previously, the defect represents the superficial peroneal (SPN) nerve conduit to the superficial fascia and is thought to be reflective of elevated intracompartmental pressure. The herniation will be particularly palpable and tender after exertion, produce dysesthesia along the route of the SPN and in rare cases, may present with a positive Tinel’s sign. The physical examination is otherwise generally unremarkable. This contrasts with a periostitis or tibial/fibular stress fracture, which presents with palpable tenderness over the tibial or fibular border regardless of preexertion. Be aware of combined etiologies which may cloud the clinical picture. Regardless, a proper diagnosis is essential in preventing frustration and lost time, an issue particularly valuable to the high level athlete. What About Imaging And Diagnostic Studies? In some cases, the diagnosis of ECS may be exclusionary. Radiographs, bone scanning, CT and MRI will aid in distinguishing stress fractures, periosteal reactions, tumors or lower back pathology. Interestingly, arterial and neurological studies are essentially of no value even when used after an exertional challenge, although you may use them to exclude other diagnoses as well. Recently, NMR and MRI have been found useful in diagnosing ECS. The techniques have been proposed as noninvasive alternatives to needle compartment testing. A correlation appears to exist between intracompartmental pressure and proton relaxation time when examining MRI results of patients with ECS. However, intracompartment pressure measurements clearly remain the gold standard in diagnosing ECS. Many different pressure limits have been proposed but at this time, the most acceptable and predictive values for diagnosing ECS are based upon specific criteria published by Pedowitz, et. al., who performed slit catheter measurements on 210 anterior muscle compartments. According to their findings, ECS is considered diagnostic if one or more of the following criteria are met: a pre-exercise pressure of 15mm/Hg or more; a one-minute post-exercise pressure of 30mm/Hg or more; or a five-minute post-exercise pressure of 20mm/Hg or more. Be aware that anterior compartment pressures tend to be higher than lateral and posterior compartment pressures, particularly at one to 10 minutes after exercise. Also keep in mind that positive pressure measurements should never replace a thorough history and physical examination in the diagnosis of ECS. Key Tips On Compartment Pressure Testing Several techniques are used for static and dynamic testing of compartment pressures. These include the wick catheter, slit catheter, continuous infusion and solid state transducer catheter. There are advantages and disadvantages to each of these techniques but most are time consuming and require a certain degree of skill. I prefer the Stryker Intracompartmental Pressure Monitor (Stryker Corporation, Kalamazoo, Mich.). The device’s readings have been found to be accurate and consistently reproducible. It is particularly user-friendly and quite easy to prepare in a clinical setting. You can use static quick pressure readings or a dynamic display using indwelling slit catheter measurements. Both have their advantages but I favor the static measurements due to standardized technique, measurements and ease of application. For static measurements, use the monitor with a sterile packet that contains a syringe filled with 3cc of sterile normal saline, a diaphragm chamber and an 18-gauge needle. After assembling the unit, anesthetize the skin over the compartment in question subcutaneously with Marcine 0.25% or lidocaine 1% plain. Avoid delivering the anesthetic into the compartment. To easily identify the target site, I will occasionally circle the injected area with a pen. Prep the skin with Betadine. Positioning of the knee, leg and foot should be standardized for all readings. Zero the monitor at a 90-degree angle off the skin and penetrate the skin at a 45-degree angle through the fascia until you feel a sharp “pop,” representing entry into the deep fascia. Slowly inject 0.3 to 0.5 ccs of saline into the compartment to allow equilibration with the interstitial fluids and then read the compartment pressure. I always check the anterior and lateral compartments when assessing anterior ECS and measure both the deep and superficial posterior compartments when evaluating posterior ECS. The entry point for the anterior compartment is anterolaterally, midtibia and over the anterior tibialis muscle belly. The lateral compartment is lateral and posterior to the septum directly over the peroneal muscle bellies. Penetrating the deep posterior compartment safely is more difficult, requiring a solid knowledge of leg anatomy. My entry point is in the lower to middle third of the leg medially, directly behind the posterior edge of the tibia, anterior to the neurovascular bundle. The needle hugs the posterior tibia (direct anterolateral) and is advanced through the flexor digitorum muscle belly and into the tibialis posterior muscle belly. The tibia is triangular and the posterior edge deviates anteriorly. Following the bony contour allows you to enter the deep compartment safely. How To Use The Slit Catheter After following the anesthesia and prep previously described, remove the needle from the monitor. Attach the slit catheter snugly to the tapered chamber stem. Push the catheter through the breakaway needle until it peaks out of the end without protruding. Insert the needle into the compartment at a 45-degree angle and thread the catheter through the needle. Pull the needle back out of the leg as you advance the catheter into the compartment. Remove the breakaway needle by splitting it into two using the attached green fins. Inject approximately 0.3 to 0.5 ccs of saline into the compartment until you achieve equilibration. Read the monitor at intended intervals. The advantages of using the slit method include the ability to obtain continuous readings without the need for repeated sticks and the ability to acquire dynamic measurements if you have a treadmill in the office. You can accomplish this by taping the catheter to the leg but you may only measure one compartment at a time during dynamic testing. Otherwise, insert multiple catheters in different compartments and tape them into place to allow static readings without repeated sticks. Surgical Insights For The Anterior And Posterior Compartments Although debate exists with regard to the pathology behind ECS, few would argue the available treatment modalities. Once you make the diagnosis, there are generally three conservative options available to the athlete: reduce mileage, reduce intensity or abandon the sport. Stretching and various types of orthotics fail to provide any substantial benefits. A recently published running injury text touts a vacuum suctioning device that you apply externally to stretch the fascia and allow volume expansion. This technique is presumably for anterior ECS but results are anecdotal and absent in scientific literature. Many techniques are available for fascial release of the anterior compartment. These include a two-incision technique described by Rorabeck, a recently proposed endoscopically guided release and the single incisional release advocated by Mubarak, which I prefer. With either technique, experience dictates a complete release is essential to obtaining an acceptable outcome. When performing an anterior release, you would routinely release both the anterior and lateral compartments. After anesthetic induction and prep, inflate a thigh tourniquet. In the absence of a fascial hernia, make a 4 to 6 cm incision at the midpoint of the leg between the shaft of the fibula and the tibial crest. Often, the anterolateral intermuscular septum is visible subcutaneously in this area. Undermine the wound proximally and distally to allow full exposure of the compartment fascia. Identify the septum and note the location of the SPN within the lateral compartment. With right angle retraction, penetrate the anterior fascia with a longitudinal incision and use 12-inch Metzenbaum scissors to split the fascia longitudinally by capturing the edge of the fascia between its jaws. Push the scissors distally toward the direction of the great toe and proximally toward the patella. Make a 90-degree fascial transverse incision through the previous incision to preclude reapproximation of the tissue. Enter the lateral compartment in line with the fibular shaft. Identify and protect the SPN. Using the same technique, split the fascia towards the lateral malleolus distally (to avoid the SPN) and fibular head proximally. If a fascial hernia is present, center the incision over the hernia so you can fully explore the area and perform a full release of the nerve. A complete release may require using ancillary proximal incisions, particularly if the leg is long. After release, close the incision using running subcuticular sutures. My familiarity with the deep posterior release resulted from decompressing compartment abscesses in the diabetic foot that extended directly into the flexor compartment of the leg. The deep posterior release is demanding and requires a thorough knowledge of leg anatomy. This is not a procedure you should attempt alone for the first time and in certain instances (such as a recurrent deep posterior compartment syndrome in which anatomy is scarified), you may wish to seek a vascular surgeon’s assistance. Recurrent cases require a complete release with exposure of the vascular bundle proximally along the soleal bridge. My approach is a midtibial single incisional technique. Make a 6 to 8 cm incision paralleling the posteriomedial border of the tibia. Identify the saphenous nerve and vein, and retract them anteriorly. Release the deep fascia along with the soleal insertion on the posterior tibia. In this area, you often encounter multiple perforating vessels which require ligation. If you desire release of the posterior tibial muscle compartment, identify the flexor digitorum longus (fdl) muscle and bluntly retract it posteriorly, bringing the posterior tibial muscle into view. Blunt retraction of the fdl will protect the vascular bundle. Incise the posterior tibial compartment sheath longitudinally along the length of the tibia. Release the superficial compartment by incising the sheath surrounding the gastroc muscle belly using the technique described above. Drop the tourniquet and check the wound for bleeders. Because the deep posterior release has a tendency to bleed, close the wound in layers over a hemovac drain. What Can You Expect During Rehabilitation? In my experience, patients undergoing a two-compartment anterior/lateral release rehabilitate much quicker than those who have had a posterior release. Given this, I won’t hesitate to perform bilateral anterior compartment releases. Give the patient a pair of crutches postoperatively and allow weightbearing to toleration. Encourage aggressive rehabilitation after suture removal, including cycling and range of motion exercises. Allow patients to return to running at weeks eight to 12. Athletes should be aware there will be a visible muscle hernia after a release. Patients undergoing a posterior release tend to have more swelling and pain postoperatively. The rehabilitation period is longer and there is a longer period of dependency for crutch assistance. If I’ve performed four compartment releases, I will usually admit the patient for a 23-hour stay. If there is excessive bleeding or significant dissection, I’ll initiate a short course of Lovenox. You can allow weightbearing to toleration in posterior release cases. Be aware though that a consistent finding of posterior releases includes the patient’s inability to bear weight on the heel and the tendency to hold the ankle in equinus for two weeks or even greater. Like the anterior compartment, aggressive physical therapy begins at suture removal and a return to sport usually occurs at weeks eight to 12. Calf stretches are essential during the rehab process and a heel lift may be required for a short period of time. A Few Words About Surgical Results Decompression fasciotomy has proven to be a successful treatment for ECS. Success rates in the anterior compartment have been reported to range from 85 to 96 percent in the short term. Notably, however, different criteria have been used in various studies to measure success rates. Furthermore, recent reports question standards used to evaluate long term success rates. Without question, anterior compartment releases have a much better prognosis leading to dissention among surgeons of whether posterior compartment syndrome is a true entity. The success rate for the deep posterior compartment after fasciotomy is reported to be only 65 percent. Recurrent cases of ECS often require more aggressive dissection and fasciectomy. Complication rates are about 10 percent and include hemorrhage, wound breakdown, pain and anesthetic problems. Final Thoughts When treating exercise-induced leg pain, keep in mind the diagnosis of ECS. Pay close attention to distinct clues in the patient’s history and physical findings. Supplement a strong clinical suspicion with compartment pressure readings. Although discrepancies exist regarding the pathophysiology of ECS, there is no argument that surgical release is the treatment of choice in those who wish to continue to pursue their sport. Hopefully, as advances are made, a better understanding of the pathophysiology surrounding the syndrome will evolve, making nonsurgical treatment options available. Dr. Cohen is Chief of the Podiatry Section and Director of the Podiatric Primary Medicine and Surgical residency programs at the Veterans Affairs Medical Center in Miami. He is a Diplomate of the American Board of Podiatric Surgery and is Fellow of the American College of Foot and Ankle Surgeons.
 

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