Merle A. Carter

Background

Though recognized as a clinical syndrome in the mid-19th century, the pathophysiology of ischemia in extremities was not fully described until more than a century later. Postischemic myoneural dysfunction and its associated contractures were first described in the 1870s by the German surgeon Richard von Volkmann, who recognized the effects of increased pressure causing vascular compromise of the limb.⁴

Various needles and equipment have been developed to measure compartment pressure (Fig. 54-2).^5–11 The wick catheter, originally developed to measure subcutaneous and brain tissue pressure, was modified during the mid-1970s to provide continuous compartment pressure measurements. This catheter is rarely used today because of the fear of catheter breakdown leading to errors in measurement and retained foreign bodies. This prompted development of the slit catheter in 1980.^10,11 This catheter has slits at its distal end that prevent the catheter from clogging. The proximal end of the catheter is connected to a transducer and infusion system, which permits continuous monitoring. Both the wick and slit catheters have been shown to offer similar accuracy and reproducibility as long as patency of the catheter is ensured.^11–13 A newer approach to predicting the onset of compartment syndrome involves measuring compartment pH as a marker of compromised circulation and decreased tissue perfusion.¹⁴ A rise in lactic acid from ischemic tissue lowers the pH of the compartment and has promise as an early predictor of compartment syndrome.

The Stryker Intracompartmental Compartment Pressure Monitoring System (Kalamazoo, MI) has become the most commonly used commercially available device to measure compartment pressure in the emergency department (see Review Box 54-1). This device uses a fluid-filled pressure measurement catheter, a pressure monitor, and a fluid infusion mechanism that maintains catheter patency and ensures accurate measurement. In contrast to earlier devices in which relatively large volumes of fluid were injected into the compartment to measure pressure, the Stryker system uses a minimal amount of saline (<0.3 mL). This helps ensure accurate measurements while reducing the chance of further increases in compartment pressure. The Stryker system also has the ability to record a single measurement or provide continuous compartment pressure recordings when required.

Noninfusion systems such as the transducer-tipped fiberoptic system offer a distinct advantage over conventional fluid-filled systems in that they do not produce hydrostatic pressure artifacts or require the injection of fluid for long-term or continuous measurements. However, the fiberoptic transducer is relatively large, must be attached to a sheath approximately 2.0 mm in diameter, and is likely to cause pain during measurements.¹⁵ In recent years, noninvasive, less painful methods of measuring compartment pressure have been studied in patients with both acute and chronic exertional compartment syndrome. Investigations using magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), myotonometry, electromyography, ultrasound, near-infrared spectroscopy, and microwave tomography have provided encouraging results in the evaluation of compartment syndrome.^16–33 In addition, externally applied devices that measure muscle tissue “hardness” are under investigation as an economic alternative to these modalities, although support of their use has been mixed.^34–36

Though promising, these evolving noninvasive methods have not yet replaced needle-driven techniques as the standard for measuring intracompartmental pressure. The remainder of this chapter describes the most commonly used devices and techniques for measuring compartment pressure in the acute setting. Each method provides rapid measurements with reasonable accuracy. The method chosen will depend on the availability of the supplies and equipment necessary for a particular procedure and the experience of the operator.

Pathophysiology

Several theories have been proposed to account for the tissue ischemia associated with compartment syndrome, including the “arteriovenous (AV) gradient” theory, which suggests that reduced AV pressure-perfusion gradients prevent adequate blood supply³⁷; the “critical closure” theory, in which blood flow is arrested well before the AV perfusion gradient declines to zero^38,39; and the “venous occlusion” theory,⁴⁰ which states that externally applied pressure, thrombotic events, and reperfusion contribute to the increased compartment pressure and, ultimately, tissue ischemia. Although the exact mechanism has not been agreed on, inherent in each of these theories is a decrease in blood flow to levels below those required to meet the metabolic demands of the tissue. Hence, the final common pathway is cellular hypoxia and muscle necrosis.

Adequate blood flow to tissues is a function of AV gradients across capillary beds. Once blood flow falls below a critical level, delivery of oxygen to these structures is impaired and aerobic cellular metabolism is no longer possible. Anaerobic metabolism then ensues until energy stores become depleted. Muscles become ischemic, and a reduction in venous and lymphatic drainage creates increased pressure within this confined space. It is important to note that ischemia and necrosis of the musculature can occur despite an arterial pressure high enough to produce pulses, so merely assessing distal pulses is insufficient.⁴¹

A drop in blood pressure, an increase in compartment pressure, or a combination of the two can reduce AV gradients and lead to insufficient blood flow to tissues. Hypotension can occur in a variety of settings, including hypovolemia, acute blood loss, cardiac disease states (e.g., ischemia), and sepsis. An increase in the contents of a compartment, a decrease in its volume capacity, and external constriction of a compartment can all lead to increases in compartment pressure. Thus, the relationship between intracompartmental pressure and the circulatory status of the extremity is an important factor in the development of compartment syndrome.⁴² Compartment syndrome may also develop in an extremity in the absence of direct trauma. This is most often due to prolonged ischemia associated with acute arterial occlusion by thrombi or proximal arterial injury.

At rest, normal adult compartment pressure is typically below 10 mm Hg. However, deviations of 2 to 6 mm Hg have been reported.1,8–10,12 Recent data suggest that normal compartment pressures in the lower extremity at rest are higher in children.⁴³ The perfusion pressure of a compartment, also known as the compartment delta pressure (ΔP), is defined as the difference between diastolic blood pressure and intracompartmental pressure.⁴⁴ A model using legs of normal volunteers has shown that a progression of neuromuscular deficits occurs when intracompartmental pressure rises to within 35 to 40 mm Hg of diastolic blood pressure.⁴⁵ Above this level, tissue perfusion is interrupted. Studies of neuromuscular tissue ischemia have demonstrated that inflammatory necrosis can occur at pressures between 40 and 60 mm Hg.^46,47

Whitesides and colleagues demonstrated that when tissue pressure within a closed compartment rises to within 10 to 30 mm Hg of the patient’s diastolic blood pressure, inadequate perfusion ensues and results in relative ischemia of the involved limb.⁶ Heppenstall and associates further clarified this relationship by demonstrating that the difference (ΔP) between mean arterial pressure (MAP) and the measured compartment pressure is directly related to blood flow to the tissue.⁴⁸ They noted that as compartment pressure approaches MAP, ΔP decreases. Once ΔP falls below 30 mm Hg, tissue ischemia becomes more likely. In normal musculature, a ΔP of less than 30 mm Hg results in loss of normal aerobic cellular metabolism.⁴⁸ In traumatized muscle, a ΔP of less than 40 mm Hg is associated with abnormal cellular function, thus highlighting the importance of maintaining adequate systemic blood pressure in the setting of neuromuscular injury.⁴⁸

For years, conventional wisdom maintained that immediate reperfusion of traumatized tissue would provide improved motor and neurologic function after injury. In the last decade, research suggests that muscle tissue may remain viable even after prolonged periods of ischemia and that a substantial proportion of the injury is generated on reperfusion.49,50 Tissue acidosis, intracellular and extracellular edema, free radical–mediated injury, loss of adenine nucleotide precursors, and interruption of mitochondrial oxidative rephosphorylation by increased intracellular calcium have been implicated in the development of reperfusion-associated compartment syndrome.^49–54 A recent study has identified the potential role of N-acetylcysteine in the attenuation of tissue injury in compartment syndrome.⁵⁵ Even in the absence of local trauma, ischemia followed by reperfusion has been shown to increase compartment pressure in canine models of hypovolemic shock.⁵⁶

Evidence also suggests that elevated compartment pressure itself (in addition to causing ischemia) plays a role in the cellular deterioration seen with compartment syndrome.⁵⁷ In a study by Heppenstall and associates,⁵⁷ muscle ischemia caused by placement of a tourniquet was compared with an experimentally derived high-pressure compartment syndrome. The authors found no difference in the degree to which phosphocreatine levels fell between groups. However, levels of adenosine triphosphate (ATP) diminished rapidly in the compartment syndrome group in comparison to the tourniquet group. Moreover, phosphocreatine levels, ATP, and tissue pH normalized within 15 minutes of releasing the tourniquet. In the group with compartment syndrome, these levels remained low even after fasciotomy. These results suggest that elevated tissue pressure plays a synergistic role with ischemia in cellular deterioration.

Clinical Features

Any compartment limited by fascial planes is potentially at risk for compartment syndrome. However, because of their propensity for injury and the presence of several low-volume compartments, the lower extremities are most commonly affected. In the leg, the anterior compartment is involved most often,⁵⁸ whereas the posterior compartment is a site frequently missed. The hands, feet, forearms, upper part of the arms, thighs, abdomen, gluteal musculature, and back are other locations where compartment syndrome is known to occur.¹ Increased compartment pressure may be caused by a variety of conditions (see Box 54-1). Risk factors for the development of compartment syndrome include recent trauma to an extremity (including acupuncture, venipuncture, intravenous infusions, or intravenous drug use), bleeding within a compartment, a restrictive cast or splint, a crush or compression injury, a prolonged lithotomy position, placement of a tourniquet during an operative procedure, and circumferential burns.^59–63

Long-bone fractures account for about 75% of traumatic compartment syndromes, and the absence of a fracture in a traumatized extremity is a factor in delayed diagnosis. The tibia is most often involved, followed by bones of the forearm. Supracondylar fractures in children are at risk for compartment syndrome. Comminuted fractures increase the risk. Closed fractures are of greatest concern, but an open fracture does not necessarily decompress elevated compartment pressure. Treatment of fractures, by both open and closed reduction, can increase compartment pressure. Compartment pressure may peak immediately after reduction. In addition, some evidence suggests that compartment syndrome may occur in the setting of chronic exertion and muscle overuse.64,65 Although the exact etiology remains elusive, studies have demonstrated elevated lactate and water levels in the tibialis anterior muscle after exercise with a reduction in these levels after fasciotomy.^66,67 Increases in muscle mass (related to a rise in blood volume during exertion) and hypertrophy of muscle and fascia with chronic use and exertion have also been reported.^68–72

Clinical hallmarks of compartment syndrome include pallor of the extremity, a pulse deficit with respect to the opposite limb, paresis or paralysis of the involved extremity, paresthesias in the distribution of the involved nerves, and pain on passive stretch of the involved musculature (the “5 P’s” of compartment syndrome). Paresthesias are secondary to ischemic nerve dysfunction. These signs and symptoms may be unreliable in pediatric populations.73,74 In addition, though commonly seen, pain and paralysis are late findings. Early, more subtle signs of compartment syndrome include a burning sensation over the involved compartment, nonspecific sensory deficits, or poorly localized deep muscular pain. Pain that seems out of proportion to the apparent injury and clinical examination and pain that intensifies when the musculature is passively stretched are common features.

The period between the injury and the onset of symptoms can be as short as 2 hours and as long as 6 days.⁷⁵ The peak interval appears to be 15 to 30 hours. Frequently, the first symptom described by patients is pain greater than expected given the clinical scenario. Although pain out of proportion to the visible injury may raise the question of drug-seeking behavior, a focused evaluation for the possibility of limb-threatening disorders must precede this diagnosis of exclusion. Physical examination may reveal muscles that are weak and tense with hypoesthesia in the distribution of the involved nerves. Sensory deficits, including loss of two-point discrimination and decreased vibratory sensation, are frequently present.^76–78 The presence or absence of a palpable arterial pulse is not an accurate indicator of relative tissue pressure or the risk for compartment syndrome. Pulses may be present in a severely compromised extremity.⁷⁹ Table 54-1 lists the signs and symptoms of compartment syndrome specific to each compartment.

Diagnosis

Even experienced clinicians find it difficult to evaluate a potential compartment syndrome, and no specific standard of care exists with regard to a time interval from injury to definitive treatment. In an unconscious patient or in those with other life-threatening conditions that mandate other priorities, the clinical scenario simply does not allow a diagnosis to be made in timely fashion. In cases without trauma or in patients who are unable to voice pain or cooperate with an examination, compartment syndrome is often not considered and the diagnosis is delayed. Regional nerve blocks or epidural anesthesia may also obscure the signs and symptoms of increased compartment pressure and cause further delays in diagnosis.

The difficulty in diagnosing acute compartment syndrome was highlighted in a report by Vaillancourt and coworkers.⁸⁰ In a retrospective review of 76 patients who underwent fasciotomy at major university trauma centers or teaching hospitals, the interval from initial patient assessment to diagnosis of compartment syndrome was up to 8 hours. Delay in diagnosis was most common in nontraumatic cases. The interval from the precipitating event to definitive surgery was up to 35 hours, thus reflecting the difficulty in suspecting this diagnosis and instituting definitive therapy in clinical practice. Such statistics describe actual care, which may be less than ideal when compared with theoretical benchmarks.

Notwithstanding the difficulty just described, the diagnosis of compartment syndrome is primarily a clinical one that may be supplemented by direct measurement of compartment pressure. In a study evaluating the utility of clinical findings in making the diagnosis of compartment syndrome, Ulmer noted that the sensitivity and positive predictive value of clinical findings are low whereas the specificity and negative predictive value of these findings are high.⁸¹ Nevertheless, the study found that although the sensitivity of an individual clinical finding may be low, the probability of compartment syndrome rises considerably when more than one clinical hallmark is present.⁸¹ However, other studies have suggested that the absence of clinical evidence is more useful in excluding compartment syndrome than its presence is in confirming the diagnosis.^82–84 All things considered, compartment syndrome remains largely a clinical diagnosis, and a high index of suspicion is paramount.

The differential diagnosis of compartment syndrome is extensive and includes primary vascular, nerve, and muscle injuries that produce similar findings. Acute arterial occlusion, cellulitis, osteomyelitis, neurapraxia, reflex sympathetic dystrophy, synovitis, tenosynovitis, stress fractures, envenomations, necrotizing fasciitis, deep vein thrombosis, and thrombophlebitis are additional diseases that should be considered. Differentiating compartment syndrome from these and other orthopedic disorders requires a detailed history and thorough physical examination, often supplemented by measurement of compartment pressure (Table 54-2).

Ancillary Studies

In general, laboratory and radiographic studies are not helpful in confirming the diagnosis of compartment syndrome. However, they might be useful in identifying other diagnoses, associated conditions, and complications. Box 54-2 lists useful studies for patients in whom compartment syndrome is suspected.

Invasive Compartment Pressure Monitoring

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