Chapter 60. Acute Compartment Syndrome of the Limb: Implications for Regional Anesthesia

Compartment syndrome is an orthopedic emergency. It is an acute condition of the limbs in which the pressure of isolated or groups of compartments increases dramatically and limits local soft tissue perfusion to the point of ischemic necrosis. Regional anesthesia may mask the signs and symptoms of compartment syndrome, so practitioners should be alert to patient risk factors, clinical presentation, and management of this potentially limb-threatening condition. The musculoskeletal structures of the limbs are enclosed within compartments created by investing, inelastic sheets of fascia that have a limited ability to expand. These compartments contain skeletal muscles that form the bulk of their contents, along with the neurovascular structures that pass through the compartment. If missed, compartment syndrome1 can be a life- and limb-threatening condition.

Compartment syndrome is most common in the lower leg and forearm, although it can also occur in the hand, foot, thigh, and upper arm. In theory, the upper leg muscles are at a lower risk for injury than are the smaller muscles of the lower leg, because the muscles of the thigh can dissipate the large forces of direct trauma, causing less muscle injury and resultant edema.2 Acute compartment syndrome occurs more commonly in one of the four smaller compartments of the lower leg.

Historically, the consequences of persistently elevated intracompartmental pressures was first described by Richard von Volkmann,3 who documented nerve injury and late muscle contracture from compartment syndrome after supracondylar fracture of the distal humerus. Jepson4 described ischemic contractures in dog hind legs, resulting from limb hypertension after experimentally induced venous obstruction. Only after almost 30 years (1970s) has the importance of measuring compartmental pressures become apparent.

Etiology

Any condition that can reduce the volume of the compartment or increase the size of the contents of the compartment can lead to an acute compartment syndrome. Examples of factors leading to these changes are presented in Table 60–1.

Pathophysiology

Compartment syndrome is essentially soft tissue ischemia; however, the exact mechanism of compartment syndrome is unclear. Because various osseofascial compartments have a relatively fixed volume, introduction of excess fluid or external constriction increases pressure within the compartment and decreases tissue perfusion (Figure 60–1). As the compartmental pressure increases, the tissue hypoperfusion results in tissue hypoxia impeding cellular metabolism. If prolonged, permanent myoneural tissue damage occurs.14–16 Under physiologic circumstances, the venous pressure exceeds that of the interstitial tissue pressure, sustaining venous outflow.14 However, as tissue pressure increases, extrinsic venous luminal pressure is exceeded, resulting in collapse of the vein. The pressure at which this occurs is not known; however, it is generally agreed that compartmental pressures greater than 30 mm Hg require emergent intervention because ischemia is imminent.

Hypoxic injury causes cells to release free radicals, which increases endothelial permeability. This, in turn, leads to a vicious cycle of continued fluid loss, further increasing tissue pressure and injury. Diminished blood flow to local nerves first manifests as sensory changes. Paresthesias develop within 30 minutes of onset of ischemia. Irreversible nerve damage begins after 12–24 hours of total ischemia.14 Irreversible changes in the muscles begin after only 4–8 hours, leading to muscle fiber death and late myocontracture.17

Compartment syndrome is a clinical diagnosis that must be based primarily on the patient's clinical signs and symptoms. Pain out of proportion to the injury, especially with passive stretch of the muscles in the suspicious compartment or limb, is one of the most reliable indicators. A palpably tense extremity compared with the uninjured limb is also an important finding. The classic other P's of pallor, pulselessness, and paresis are not useful. Pallor and pulselessness are rarely present in compartment syndrome and by the time paresis manifests, the damage is largely irreversible.

In the unresponsive, obtunded, or anesthetized patient, measurement of compartmental pressures with a needle and arterial line transducer or other pressure-measuring device is useful (Figures 60–2 and 60–3). An absolute value above 30 mm Hg in the normotensive patient is consistent with compartment syndrome. This value is diminished in the hypotensive patient as the lower arterial pressure renders the limbs even more susceptible to ischemic injury. Near infrared spectroscopy is another noninvasive method suggested for monitoring the oxygen saturation of hemoglobin and myoglobulin in the tissue at risk (Figure 60–4).

The Upper Limb

There are several compartments of the upper extremity that, when injured, may result in compartment syndrome requiring fasciotomy in the arm, forearm, or hand.

The arm has two compartments: anterior and posterior (Figure 60–5).

The forearm has three compartments: the volar and dorsal compartments and the compartment containing the muscles of the mobile wad. Mubarak et al.18 have demonstrated that these compartments are interconnected, unlike the compartments of the leg (Figures 60–6 and 60–7). Consequently, decompression of the volar compartment alone may decrease the pressure in the other two compartments. Regardless, dorsal compartment fasciotomy should still be performed if it remains tight after volar decompression.19 The muscles of the volar compartment of the forearm include the digital and wrist flexors and the forearm pronators. These muscles are tested by passive extension of the digits and wrist and by supination of the forearm.

The dorsal forearm compartment contains the thumb and finger metacarpophalangeal joint extensors, the ulnar wrist extensors, and the forearm supinators and is tested by passive finger, thumb, and wrist flexion and by forearm pronation. The mobile wad includes the brachioradialis and the two radial wrist extensors and is tested by passive wrist flexion.

There are 10 compartments in the hand, the most prominent ones being the dorsal and palmar interosseous compartments, of which there are four and three, respectively (Figure 60–8). The other compartments are the hypothenar, thenar, and adductor. The compartment containing the adductor muscle of the thumb is often overlooked when doing fasciotomies. Studies using renograffin dye had shown no connection between the dorsal interossei and the other compartments, showing that each compartment has to be decompressed separately.

The finger is enclosed in a tight investing fascia and is compartmentalized by the fascia and the volar skin at the flexor crease. Although no muscle bellies are distal from the metacarpophalangeal joints, ischemia and engorgement can lead to tissue loss (Figure 60–9).

The Lower Limb

Thigh

The thigh muscles are divided into three compartments invested by thick fascia: the anterior, medial, and posterior (Figures 60–10 and 60–11). Because thigh compartment syndrome is uncommon, it may go unrecognized. A history of anticoagulant use is common in patients with thigh compartment syndrome. Signs and symptoms include a history of thigh swelling and/or hematoma and pain after a minor injury in a patient who is anticoagulated.20,21 Although rare, the thigh syndrome can also occur in patients after joint replacement surgery. The combination of minor trauma and anticoagulation produces bleeding into muscle and tissue spaces, leading to increased compartment pressure. Pain ranges from mild to severe and may be elicited only when the hip and knee are flexed and extended. Other findings of vascular occlusion—loss of pulse, pallor, paresthesias, and paralysis—are frequently absent.

Lower Leg

The lower leg contains four compartments, each invested by inelastic fascia (Figures 60–12 and 60–13). Each compartment contains a major nerve: the deep peroneal in the anterior compartment, the superficial peroneal in the lateral compartment, the saphenous in the superficial posterior compartment, and the tibial in the deep posterior compartment. Swelling in the lateral or the anterior compartment can compress both the deep and superficial peroneal nerves against the neck of the fibula. The superficial peroneal nerve usually lies in the interval between the two peroneal muscles for a short distance and then emerges anterior to the peroneus brevis. It pierces the lateral compartment fascia at the junction of the middle and distal third of the leg. The anatomy of the superficial and deep posterior compartments is somewhat variable, but both compartments, and especially the deep compartment, are frequently involved in compartment syndrome.

The Foot

The foot has numerous rigidly bound compartments, and even mild bleeding into these spaces can elevate the pressures dramatically (Figure 60–14). According to Manoli and Weber,22 there are nine compartments in the foot. Three compartments run the entire length of the foot (medial, lateral, and superficial). Five compartments are contained within the forefoot (adductor and four interossei). The calcaneal compartment is confined to the hind foot, but communicates with the posterior compartment of the leg. This compartment contains the quadratus muscle and the lateral plantar neurovascular bundle. The clinically most relevant compartments are the medial, central, lateral, and interossei.23,24

A wide spectrum of injuries can result in compartment syndrome of the foot; the most likely ones are crush injuries, especially those associated with multiple metatarsal fractures. Often, the only reliable method of diagnosis is by clinical suspicion and measurement of the intracompartmental pressures. Loss of posterior tibial or dorsalis pedis pulse is notoriously unreliable in the early diagnosis of the compartment syndrome. The earliest clinical findings are muscle and nerve ischemia and pain. Although this pain might be confused with that of pain from the injury itself, it may be exacerbated by gentle, passive dorsiflexion of the toes, which stretches the intrinsic muscles of the foot. Lack of sensation is generally accepted as an important sign of nerve ischemia, but it is less reliable when compared with a two-point discrimination and light touch over the plantar aspect of the foot and toes.

Compartment pressure measurements are the only objective and accurate tests to diagnose and record compartment syndrome, particularly because the changes in the compartment pressures can precede the clinical signs of the compartment syndrome.

The central compartment can be measured by passing the needle between the metatarsal and abductor hallucis muscle at the base of the first metatarsal. The interossei compartment is measured in two positions by introducing the needle through the intermetatarsal spaces, preferably between the second and forth web spaces to avoid punctures to the dorsalis pedis within the first intermetatarsal region.

The calcaneal or quadratus compartment is measured by inserting the needle 5 cm distal and 2 cm inferior to the medial malleolus and advancing through the abductor muscle.

Emergency fasciotomy remains the definitive treatment for a diagnosis of compartment syndrome because of its well-documented, limb-saving results. It is universally accepted as being the best chance for complete recovery and for prevention of further tissue necrosis. Treatment is based primarily on the clinical picture together with corroborative compartmental pressure measurements (Figure 60–15). The surgeon should proceed emergently with a decompression fasciotomy when clinically indicated because the exact pressure at which fasciotomy should be performed remains controversial. Most studies have shown that fasciotomy is indicated when the compartment pressure reaches 30 mm Hg.24–26 Fasciotomy is also recommended when the compartmental pressure is within 30 mm Hg of the patient's diastolic pressure.26

After a complete fasciotomy, there is rarely a need for additional releases. The fasciotomy incisions are always left open with wound closure delayed for a minimum of 5 days. The patient is followed up clinically unless anesthetized or obtunded, in which case regular compartment pressure measurements should be made.

Because regional anesthesia may mask pain in compartment syndrome, regional blocks should be performed in consultation with the surgical team, and shorter-acting local anesthetics should be used in uncertain circumstances.

Prolonged surgery, especially in patients undergoing procedures in the Trendelenburg or lateral decubitus positions, poses a risk of compartment syndrome. The Trendelenburg position requires that the legs are strapped at a higher level than the heart. This can be avoided by repositioning and redraping the legs, or if this is not possible, the head-down tilt position should be reversed every 2 hours so that reperfusion of the lower limbs can occur. In the lateral decubitus position, the down arm and the down leg must be well padded to avoid excessive compression.

Patients on anticoagulation medication tend to have a higher risk of thigh compartment syndrome, even with relatively minor trauma or surgical interventions. This clinical scenario must be approached with a high index of suspicion.