How To Detect And Treat Chronic Compartment Syndrome

By Michael M. Cohen, DPM

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.

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