Diagnosis

It has been stated that the greatest difficulty in managing compartment syndrome is determining when a fasciotomy is indicated.9 In North America, failure to correctly diagnose compartment syndrome is one of the most common causes of litigation against the medical profession.10 A 1993 study of the malpractice costs found that an average indemnity of nearly $280,000 was awarded in cases of missed compartment syndrome.10 A later study reported on 19 closed claims regarding compartment syndrome.11 These claims were associated with a total liability of $3.8 million ($200,000 per claim). Ten of the claims (53%) were resolved in favor of the physician, but required an average of 5.5 years to resolve. Three claims went to trial and resulted in a verdict for the physician. Poor physician–patient communication was found in six cases, all of which resulted in an indemnity payment (p < 0.01). Increasing time from the onset of symptoms to the fasciotomy was linearly associated with an increased indemnity payment (p < 0.05). In contrast, a fasciotomy performed within 8 hours of presentation of symptoms was always associated with a successful defense.11

The key to making a timely diagnosis of compartment syndrome is considering it in the first place. Hope and Mc-Queen12 evaluated a series of 164 cases of compartment syndrome and found that cases occurring after a fracture were diagnosed sooner and were associated with less tissue necrosis at the time of fasciotomy than the cases that occurred without a fracture.12 This suggests that the presence of a fracture heightens one′s awareness of compartment syndrome. It is critical to consider that any patient with a swollen, painful limb might have compartment syndrome, even without obvious skeletal trauma. Therefore, one must be aware of circumstances in which compartment syndrome is possible. In large series of patients with tibia fractures, the overall incidence of compartment syndrome is low. McQueen et al13 reported an incidence of 1.5% in 67 tibia fractures, and found that there were no differences in pressures between low- and high-energy fractures, open or closed fractures, or those treated before or after 24 hours from the time of injury. Later work from the same institution has shown that compartment syndromes are more common in young men with tibial shaft or forearm fractures.14 Although the leg is most frequently involved (80%), compartment syndromes have been reported in virtually every muscle compartment in the upper extremities, lower extremities, and trunk. Table 4.1 lists specific fracture types that are at increased risk of acute compartment syndrome.

It is important to note that compartment syndrome occurs in children as well. A recent paper reviewed 42 cases of acute compartment syndrome in children15; 83% were associated with fractures of the tibia and fibula that occurred in a motor vehicle accident. Despite a long period from injury to fasciotomy (the mean time was 20 hours in this series), the children had no infectious complications and very good outcomes. Only two cases had any functional sequelae, and both of these had fasciotomy more than 80 hours postinjury. The authors note that acute compartment syndrome may present later in children and may be more difficult to diagnose, and they suggest that fasciotomy should be done in the acute swelling period. Compartment syndrome may also be seen following fractures of the forearm in children; in one study the incidence was greater following intramedullary fixation than following closed reduction and casting.16 Finally, one must not forget that compartment syndrome may also occur in open fractures, with a reported incidence of 2.7%17 to 33.3%.18

The classic symptoms for the diagnosis of compartment syndrome are referred to as the five P′s: pain, pallor, pulselessness, paresthesia, and paralysis. However, these criteria are subjective, are not uniformly present, and are often difficult to assess, and when they present they are indicative of an advanced stage of injury that may be irreversible. The most reliable symptom of acute compartment syndrome is pain out of proportion to the injury, and pain with passive stretching of the involved muscles. The use of regional anesthetic blockade should be avoided in patients with compartment syndrome, and even the use of standard patient-controlled anesthesia can completely mask the increases in pain that occurs with compartment syndrome.19 The involved compartment is usually quite tense when palpated. Because of the sensitivity of peripheral nerves to ischemia, dysesthesias in a specific nerve located in the involved compartment are a very sensitive early finding (Table 4.2).20,21 Gross neural dysfunction manifested by complete sensory loss represents a later finding, and when present is indicative of an advanced degree of pathology. Certain subsets of patients, such as schizophrenic patients,22 patients receiving parenteral narcotics or regional anesthesia, and those who are obtunded or intoxicated might not demonstrate significant pain despite compartment syndrome.

The inconsistency and variability in signs and symptoms make the diagnosis of compartment syndrome largely one of clinical judgment. Although acute compartment syndrome is related to elevated intramuscular pressure, there is no specific and reproducible test that reliably confirms the diagnosis.23–32 Ulmer30 reviewed the literature regarding compartment syndromes of the lower leg, and found that the sensitivity of clinical findings for diagnosing compartment syndrome was very low (13 to 19%). Similarly, the positive predictive value of the clinical findings was only 11 to 15%. In contrast, the specificity and negative predictive value were each 97 to 98%. Thus, the clinical findings associated with compartment syndrome of the lower leg are more useful in excluding the diagnosis by their absence than they are in confirming the diagnosis by their presence.30 Given these problems with ascertaining when compartment syndrome is present, a high index of suspicion must be maintained for patients at risk, and the surgeon must err on the side of performing too many fasciotomies in order not to miss one. The subjective nature and lack of consensus regarding the diagnosis of acute compartment syndrome leads to significant variation in the practice of fasciotomy.33

Intramuscular Pressure Measurement

To make the diagnosis of compartment syndrome less subjective and to relate the diagnosis to the underlying patho-physiology, techniques to measure intramuscular pressure have been developed and utilized clinically.13,34–36 Both a commercially available device for measuring intramuscular pressure (Stryker Quick Pressure Monitor, Stryker Surgical, Kalamazoo, MI) and an intravenous manometric pump (Alaris Medical Systems, San Diego, CA) have been shown to be accurate and to provide reproducible measurements.34 However, controversy exists regarding what pressure criteria support the diagnosis of compartment syndrome,27,37 and the level of tissue pressure at which fasciotomy is recommended varies considerably among authors. Fasciotomy has been recommended if pressures are above 45 mmHg,38 above 30 mmHg,39 or within 30 mmHg of the patients’ diastolic blood pressure.26,40,41 Although intramuscular pressure is readily measured, the significance of a given pressure for a given patient is not certain.38,42 It has been shown that pressures vary within a single compartment, with statistically significant differences at distances as close as 5 cm from the site at which the highest pressure was recorded.43 Intramuscular pressures have been shown to vary depending on the position of the adjacent joints.44 Multiple intramuscular pressure measurements taken at different locations may be necessary, but there is no certainty as to which measurement is most predictive of the underlying pathophysiology. Janzing and Broos37 examined several different putative definitions of compartment syndrome based on either absolute intramuscular pressures or perfusion pressures, and found that a consistent pressure threshold for compartment syndrome does not seem to exist. Presently, a differential pressure (diastolic or mean arterial pressure minus compartment pressure) of less than 30 to 40 mmHg is considered more specific than an absolute pressure for the diagnosis of compartment syndrome.41 The use of intramuscular pressure greater than 30 mmHg as a fixed, absolute definition of compartment syndrome led to a 29% incidence of fasciotomy in one series.27 This is higher than the expected rate, and indicates that this definition is not specific enough, although one is not likely to miss a compartment syndrome with this definition.

Because of the problems with the clinical diagnosis of compartment syndrome as well as the inconvenience of performing multiple intramuscular pressure measurements, some investigators advocate continuous intramuscular pressure monitoring.13,40 McQueen et al40 have demonstrated that the continuous monitoring of a cohort of patients with tibia fractures led to a marked reduction in the incidence of fasciotomy without any apparently missed compartment syndromes. Moreover, when compartment syndrome occurred, it was diagnosed earlier, and those patients who underwent continuous monitoring also had improved clinical outcomes with fewer healing complications. However, Ulmer30 found that even intramuscular pressure measurements are not completely reliable for the diagnosis of compartment syndrome. There are several possible reasons why even measurement of intramuscular pressure may be misleading for diagnosing compartment syndrome. Most importantly, intramuscular pressure is really a surrogate outcome and does not directly measure muscle or nerve ischemia. The development of muscle ischemia is dependent on both magnitude and duration of elevated pressure.45,46 The tolerance of muscle to ischemia varies among patients because of shock, compensating hypertension, altered tone in vessel resistance, and degree of preexisting muscle injury.25,47 Furthermore, inherent inconsistencies and inaccuracies of pressure measurement systems and techniques lead to diagnostic uncertainties, and measured pressures vary considerably at different sites within the same compartment.43

Measurement of Intramuscular Pressure: Technique

There are many methods of measuring intramuscular pressure. Whitesides et al35 initially presented a technique that utilizes a needle manometer and saline injection; the method is cumbersome and there are better alternatives today.

There are several commercially available devices that are designed specifically for the purpose of measuring intramuscular pressure (Fig. 4.1). The devices are handheld, have a digital display, and utilize specially designed side-port needles or slit catheters for continuous monitoring.

The following steps relate to the Stryker Quick Pressure Monitor device (Stryker Surgical). The device is assembled according to the manufacturer′s directions. This requires the attachment of a small syringe filled with sterile saline. A side-port needle is attached to the opposite end of the device, and the system is flushed with saline to establish a fluid column. The needle is held at the level of the compartment to be measured and is zeroed. The needle is inserted into the compartment of interest and 0.3 mL of fluid is injected. This is enough to cause a transient increase in the intramuscular pressure, which then decreases to a steady-state value in 30 to 60 seconds. Repeated measurements are taken, both within and among the different compartments. The anterior compartment should be measured by inserting the needle 1 cm lateral to the anterior crest of the tibia; the lateral compartment is measured 1 cm anterior to the posterior border of the fibula; the deep posterior compartment is accessed by inserting the needle 1 cm behind the posteromedial border of the tibia. In nontraumatized limbs, palpation of bony landmarks is as accurate as ultrasound-guided needle insertion for the deep and superficial posterior compartments.48

For continuous monitoring, a slit catheter is recommended.13 It may be attached to the same handheld unit described, or attached to a blood pressure transducer.

Heckman et al43 found that tissue pressures are highest within 5 cm of the fracture in patients with tibia fractures. It is probably best to take multiple measurements of tissue pressure both near the fracture and further away from it. However, it is impractical to make multiple measurements of all compartments in a given extremity. Because the anterior compartment of the leg and the volar compartment of the forearm are typically the compartments with the highest pressures and are always involved when compartment syndrome occurs, they may considered to be “sentinel” compartments and should be the compartments most closely monitored.

Imaging

Traditional imaging has only a minor role in the management of compartment syndrome; it is used primarily to diagnose the primary injury and assess possible fracture or dislocation. However, it has been recently demonstrated that magnetic resonance imaging (MRI) may have a role in the management of acute compartment syndrome. Rominger et al49 performed serial MRI in 15 patients (10 established, five “imminent”) with compartment syndrome. It demonstrated swollen compartments with loss of normal muscle architecture. T2-weighted spin-echo and magnetization transfer images showed bright areas that enhanced after intravenous injection of gadolinium. Early follow-up images demonstrated changes in enhancement patterns, whereas late follow-up images showed fibrosis and cystic and fatty degenerations of the affected compartments. These authors conclude that MRI can assist in the diagnosis of compartment syndrome in clinically ambiguous cases, can indicate the affected compartments, and can enable the surgeon to selectively split the fascial spaces.

Pearl

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  The diagnosis of compartment syndrome depends on a high degree of suspicion and careful, repeated, documented clinical examination. Decreased sensation in the first web space is often the earliest sign of compartment syndrome in the leg, indicating dysfunction of the deep peroneal nerve due to elevated pressure in the anterior compartment. However, pain is the most obvious symptom of compartment syndrome. Because pain is not easily assessed in the sedated, intoxicated, or head-injured patient, routine pressure monitoring is indicated in these conditions. The safest “threshold” for diagnosing compartment syndrome based on intramuscular pressures seems to be the perfusion pressure, calculated as follows: DP = diastolic blood pressure minus intramuscular pressure. Using this definition, fasciotomy should be considered whenever DP < 30 mm Hg.

There are several new, less invasive techniques that are currently being assessed for their efficacy in diagnosing compartment syndrome. These include measurements of the surface hardness of the compartment,50 transcutaneous oxygen measurements, measurement of mechanical impedance,51 near-infrared spectroscopy,52 and thallium stress testing.53 These are mostly research methods, and none have proven useful to diagnose acute compartment syndrome. In a comparative study, Dickson et al54 found that the specificity of the noninvasive measurement of hardness compared with traditional invasive pressure measurement (0.82 vs 0.96) was too poor to support the use of the hardness monitor in the diagnosis of compartment syndrome. Improved methods for the accurate diagnosis of acute compartment syndrome are needed.

Nonoperative Treatment

Several nonsurgical techniques for the treatment of compartment syndrome have been studied, but none is routinely successful, and the recommended treatment for acute compartment syndrome is surgical fasciotomy. Successful nonoperative management of compartment syndrome following rattlesnake envenomation has been reported; this indication in particular may be one of the few circumstances in which nonoperative treatment of recognized compartment syndrome may be initially considered.56

Nonsurgical treatment strategies typically rely on either reducing pressure or reducing tissue injury secondary to inflammatory-mediated cellular damage. Pressure can be reduced by intravenous or intramuscular injection of a hypertonic solution, or by removal of tissue fluid. Hutton et al57 demonstrated in dogs that compartment pressures returned to zero after 2 hours of treatment with intravenous hypertonic mannitol. Gershuni et al58 used intramuscular injections of hyaluronidase to decrease intracompartmental pressures in a canine model. Christenson et al59 demonstrated that diuretics seem to lower anterior leg compartment pressures after injury or surgery. Pneumatic foot compression stockings may have some utility in preventing compartment syndrome in high-risk patients.60 In an animal model, Odland et al61 were able to use tissue ultrafiltration to reduce intramuscular pressure; the removed tissue fluid had dramatically elevated levels of creatine phosphokinase and lactate dehydrogenase, suggesting that measurement of muscle enzymes may have diagnostic implications.

With respect to tissue preservation therapies, hyperbaric oxygen may have a role in the treatment of compartment syndrome by maintaining cellular adenosine triphosphate (ATP) levels.62 Antioxidants such as vitamin C and N-acetylcysteine have demonstrated efficacy in animal models in maintaining muscle viability.63,64 Anti-inflammatory medication using indomethacin has also been shown to reduce muscle injury and preserve perfusion in rodent models.65,66 All of the above nonsurgical therapies offer some promise in the future treatment of acute compartment syndrome, but none replaces the role of emergent surgical fasciotomy.