Acute Compartment Syndrome
By Andrew D. Perron, MD, FACEP, FACSM
Compartment syndrome is a serious limb- and life-threatening complication of extremity trauma. Fractures, crush injuries, burns, and arterial injuries all can result in an acute compartment syndrome. It develops when there is increased pressure within a closed tissue space, such as muscle compartments bound by dense fascial sheaths.1 This increased pressure compromises blood flow through vessels supplying the contained muscles and nerves. Compartments in the arm and leg are most vulnerable to this syndrome, but virtually any muscle group surrounded by fascia is at risk.
Frequently cited locations for compartment syndrome other than the lower leg include the hand, forearm, shoulder, back, buttocks, thigh, and foot.2-4 The incidence of compartment syndrome in the emergency department (ED) is unknown. Approximately three-quarters of cases are associated with fractures,5 and tibia fracture has the highest association.6-7 Early diagnosis and treatment is of the utmost importance; delay can lead to tissue necrosis, and ultimately severe, permanent disability, as with Volkmann’s ischemic contracture.
Compartment syndrome results when there is increased pressure within a closed tissue space that compromises blood flow to muscles and nerves. The increase in pressure can result from external compression of the compartment (e.g., circumferential cast or burn eschar) and/or volume increase within the compartment (e.g., hematoma or edema). The pathophysiology of compartment syndrome also can involve local hydrostatic and osmotic pressure conditions within the compartment. When the intracompartmental pressure increases above a specific level due to the above factors, perfusion is impaired, resulting in disruption of metabolic processes. Cell wall membrane integrity is compromised, leading to cytolysis and release of osmotically active cellular contents, drawing additional fluid into the interstitial space.8 The net effect is increased pressure and further impairment of perfusion to the compartment and distal structures in that vascular distribution. This ultimately can lead to a compromise of the circulation and/or nerve conduction as well as irreversible muscle injury, contractions, loss of limb, myoglobinuria, renal failure, and even death.9-10
Common fractures associated with compartment syndrome are tibial fractures, supracondylar and humeral shaft fractures, and forearm fractures. Crush injuries to the hand or foot, with or without associated fractures, are also at risk.
Clinical Presentation. A high suspicion remains the cornerstone of diagnosis. A traditional hallmark element in the history is pain disproportionate to the mechanism of injury in an awake, neurologically intact patient. Unfortunately, many patients at risk are injured severely or impaired, and cannot relate such symptoms.
The clinical signs of compartment syndrome often are remembered by using the mnemonic of the five Ps: pain, paresthesia, paresis, pallor, and pulses. Pain, especially disproportionate pain, often is the earliest sign, but the loss of normal neurological sensation is the most reliable sign.9,11 On physical examination, palpation of the compartment in question may or may not demonstrate swelling or a tense compartment. In the awake, intact patient, active or passive range of motion in the affected limb will elicit significant pain. Decrease or loss of two-point discrimination also can be an early finding of compartment syndrome.9,11 Clinical findings also can include shiny, erythematous skin overlying the involved compartment (described as a "woody" feeling), and excessive swelling. A thready or diminished pulse is not a reliable sign. Intracompartmental tissue pressure is usually lower than arterial blood pressure, making peripheral pulses and capillary refill poor indicators of blood flow. Patients with a low diastolic blood pressure are more susceptible to compartment syndrome.12 There are no distinguishing radiographic findings associated with compartment syndrome, but the fractures mentioned above (e.g., supracondylar and humeral shaft fractures, tibial fractures, and forearm fractures) should trigger consideration of this syndrome.
Determination of Compartment Pressures. The diagnosis of compartment syndrome is based primarily on determination of the intracompartmental pressure. There is some debate in the literature regarding what pressure level mandates fasciotomy. Some authors base recommendations on absolute compartment pressure,9,13,14 while others feel the pressure is meaningful only as it relates to the mean or diastolic blood pressure.15 Most literature, however, is based on absolute pressure within the compartment. Normal tissue pressure ranges between 0 and 10 mmHg. Capillary blood flow may be compromised at pressures greater than 20 mmHg. Muscle and nerve tissue is at risk for ischemic necrosis at pressures greater than 30 to 40 mmHg.
Several techniques are available for intracompartmental pressure determinations, each with advantages and disadvantages. They include the Stryker or Ace pressure monitors, the needle technique, the wick catheter, and the slit catheter. The Stryker and Ace monitors are used most frequently, and largely have replaced the other methods due to their ease of use and reproducible results. These monitors are self-contained, battery-powered pressure transducers. The other techniques have the advantage that they can be performed with items that are readily available in every ED. Descriptions of these techniques are beyond the scope of this article.
Regardless of the method used, the skin should be prepped with an antiseptic solution and infiltrated with local anesthesia at the prospective site. The site of pressure measurement is important. Heckman, et al16 reported that failure to measure tissue pressure within a few centimeters of the zone of peak pressure might result in serious underestimation of the maximum compartment pressure. Their results suggest that measurements should be taken at the level of the fracture as well as at locations proximal and distal to the fracture to determine reliably the locations of highest tissue pressure, and that the highest pressure be used in the decision-making process.
Pulse oximetry has been advocated falsely as a simple noninvasive indicator of vascular compromise. Mars et al found that at clinically significant pressures, the test had a sensitivity of approximately 40%. Hence, with a greater than 50% risk of a false-negative result, pulse oximetry is not recommended in the detection of elevated compartmental pressure.17
The goal of treatment is to decrease tissue pressure, restore blood flow, and minimize tissue damage and related functional loss. External pressure from casts or dressings should be alleviated immediately. It has been shown that if a cast is bivalved, the compartment pressures may decrease as much as 55%, and if completely removed, the pressure may decrease as much as 85%.6,12 The limb should be elevated to the level of the heart to promote arterial blood flow but not decrease venous return.
Acute compartment syndrome is a surgical emergency. Fasciotomy is the definitive therapy and should be performed as soon as possible. Delays of more than 24 hours can have devastating consequences, as outlined above. According to Mabee,1 absolute indications for fasciotomy are: 1) clinical signs of acute compartment syndrome, 2) raised tissue pressure greater than 30 mmHg in a patient with the clinical picture of compartment syndrome, and 3) interrupted arterial circulation to an extremity for greater than four hours. If performed within 12 hours of symptom onset, fasciotomy can prevent most ischemic myoneural deficits.18 Most studies report that between 1% and 10% of patients with acute compartment syndrome will develop Volkmann’s ischemic contracture.2
Dr. Perron, Residency Program Director, Department of Emergency Medicine, Maine Medical Center, Portland, ME, is on the Editorial Board of Emergency Medicine Alert.
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