Compartment Syndromes and Volkmann Contracture

Definition and History

Compartment syndrome is a condition in which the circulation within a closed compartment is compromised by an increase in pressure within the compartment, causing necrosis of muscles, nerves, and eventually the skin because of excessive swelling. Volkmann ischemic contracture is a sequela of untreated or inadequately treated compartment syndrome in which necrotic muscle and nerve tissue have been replaced with fibrous tissue.

In the upper extremity, compartment syndrome is most common in the forearm. The intrinsic muscle compartments of the hand also may be involved, and compartment syndrome of the upper arm has been reported.

In 1881, Volkmann stated in his classic paper that the paralytic contractures that could develop only a few hours after injury were caused by arterial insufficiency or ischemia of the muscles. He suggested that tight bandages were the cause of vascular insufficiency. This concept of extrinsic pressure as the primary cause of paralytic contracture persisted for some time in the English literature. In 1909, Thomas studied 107 paralytic contractures and found that some developed following severe contusions of the forearm in the absence of fractures, splints, or bandages. The idea was established that extrinsic pressure was not the sole cause of the ischemia. In 1914, Murphy reported that hemorrhage and effusion into the muscles could cause internal pressures to increase within the unyielding deep fascial compartments of the forearm, with subsequent obstruction of the venous return. In 1928, Jones concluded that Volkmann contracture could be caused by pressure from within, from without, or from both. Eichler and Lipscomb outlined the early technique of fasciotomy as the primary surgical treatment.

Anatomy

Four interconnected compartments of the forearm are recognized ( Fig. 74.1 ): (1) the superficial volar compartment, (2) the deep volar compartment, (3) the dorsal compartment, and (4) the compartment containing the mobile wad of Henry (brachioradialis and extensor carpi radialis longus and brevis). The volar compartments are most commonly involved, but the dorsal and mobile wad compartments can be involved alone or in addition to the volar compartments. It is usually difficult to clinically differentiate between isolated or combined involvement of the deep and superficial volar compartments; however, the deep volar compartment (flexor digitorum profundus, flexor pollicis longus, and pronator quadratus) may be solely involved.

In the hand, three palmar and four dorsal interosseous muscles are each surrounded by a tough, investing fascial layer, creating individual compartments, as shown by the injection dissections of Halpern and Mochizuki. The adductor pollicis, thenar, and hypothenar muscles also form three separate compartments ( Fig. 74.2 ). The neurovascular bundles of each digit also are compartmentalized by fascial layers, making them vulnerable to excessive swelling ( Fig. 74.3 ).

Etiology

Numerous injuries have been shown to result in compartment syndrome, including crush injuries, prolonged external compression, internal bleeding (especially after injury in patients with hemophilia), fractures, excessive exercise, burns, snake bites, and intraarterial injections of drugs or sclerosing agents. Infections also have been noted to increase pressures within compartments.

Elliott and Johnstone found that 18% of forearm compartment syndromes were caused by fractures, and 23% were caused by soft-tissue injuries without fractures. Although isolated distal radial fractures rarely were associated with compartment syndrome (0.3%), an ipsilateral elbow injury resulted in forearm compartment syndrome in 15% of patients. Historically, supracondylar humeral fractures were most frequently associated with forearm compartment syndrome in children; however, Grottkau et al. found that forearm fractures were actually more commonly associated (74% vs. 15%). In children, supracondylar humeral fractures with an associated neurovascular or floating elbow injury significantly increase the risk of compartment syndrome.

Acute compartment syndrome of the intrinsic muscles of the hand, resulting in contracture or necrosis of the muscle bellies such as those in the larger muscles in the forearm, can occur after compression injuries of the hand without fracture. Compartment syndrome has been noted in neonates following intrauterine malposition or strangulation of the extremity by the umbilical cord.

Direct trauma, crushing of the upper arm, shoulder dislocation, avulsion of the triceps muscle, pneumatic tourniquet use, and arteriography have all been reported as causes of compartment syndrome. Intravenous regional anesthesia has also been implicated as a cause when hypertonic saline is used to dilute an anesthetic.

Although more common in the lower extremity, chronic exertional compartment syndrome (CECS) may also involve the upper extremity. CECS most commonly affects the volar forearm compartment and the first dorsal interosseous muscle in the hand. It is most frequently diagnosed in competitive off-road motorcyclists. It has also been reported in kayakers and elite rowers and may occur in adolescents after puberty.

Any situation that causes a decrease in compartment size, an increase in compartment pressure, or a decrease in soft-tissue compliance can initiate compartment syndrome. As the intracompartmental pressure increases, capillary blood perfusion is reduced to a level that cannot maintain tissue viability. The increase in interstitial pressure overcomes the intravascular pressure of the small vessels and capillaries, which causes the walls to collapse and impedes local blood flow. In a canine model, muscle necrosis was shown to occur with a rise in pressure to within 20 mm Hg below the diastolic pressure. Local tissue ischemia leads to local edema, which increases the intracompartmental pressure. This cycle of increasing muscle ischemia was depicted by Eaton and Green, as shown in Figure 74.4 .

The tolerance of tissue to prolonged ischemia varies according to the type of tissue. Functional impairment in muscles has been demonstrated after 2 to 4 hours of ischemia, and irreversible functional loss occurs after 4 to 12 hours. Nerve tissue shows abnormal function after 30 minutes of ischemia, with irreversible functional loss after 12 to 24 hours.

Diagnosis

A crush injury or fracture of the forearm or elbow, especially in the supracondylar area of the humerus, should raise suspicion that a forearm compartment syndrome may develop. Early diagnosis of impending ischemia is essential because irreversible damage can occur quickly. Commonly described characteristics of compartment syndrome in adults include the five “P’s”: pain with passive stretch of the involved compartment (or pain out of proportion to examination), paresthesias, pallor, paralysis, and pulselessness. Increasing pain that is out of proportion to the injury and worsens with passive stretching of the involved muscles is an early indication that a compartment syndrome is developing. The volar and/or dorsal forearm is tender and tense with swelling, and sensibility of the fingertips may be diminished. Two-point discrimination and 256-cycle vibratory testing can be helpful in determining nerve ischemia. Paralysis of involved muscle function and loss of the radial and/or ulnar pulse present as late findings unless there is direct arterial injury.

Diagnosis of compartment syndrome in an individual interosseous muscle can be difficult. The hand is swollen and tense, and the fingers are held almost rigid in a partially flexed position with the wrist in neutral. Any passive movement of the fingers that causes metacarpophalangeal joint extension usually causes considerable pain. The adductor compartment of the thumb can be tested by pulling the thumb into palmar abduction and stretching the adductor muscle. The thenar muscles rarely are involved. Diagnosis in obtunded and pediatric patients is more difficult. In children, the five “P’s” are considered less reliable. Bae et al. advocated using the three “A’s” (increasing analgesic requirements, unremitting agitation, and anxiety) as more reliable indicators of developing pediatric compartment syndrome. Compartment syndrome in a neonate may manifest as a sentinel bullous or ulcerative skin lesion, usually over the dorsum of the forearm, wrist, or hand. Unilateral aplasia cutis congenita also must be considered in this setting.

When compartment syndrome is suspected and the necessary equipment is available, compartment pressures should be obtained to confirm the diagnosis. Compartment pressures over 30 mm Hg or within 30 mm Hg of the diastolic pressure (delta P) are indicative of compartment syndrome. The delta P value compares the compartment pressure to the diastolic blood pressure and thus controls for variation in a patient’s blood pressure. All involved compartments should be measured, and the results should be interpreted with regard to the overall clinical picture. Forearm measurements can be obtained from the superficial and deep volar compartments, and the mobile wad and dorsal compartments. The location for pressure monitoring using a needle manometer is commonly the middle third of the forearm for both flexor compartments and for the dorsal extensor compartment. The deep flexor compartment is measured just anterior to the ulna. The mobile wad of Henry may be entered in the midline of its bulk. Hand measurements may be obtained from the thenar, hypothenar, adductor pollicis, and interosseous muscles. Digital pressures are not routinely obtained.

In 1975, Whitesides et al. described a technique for measuring compartment pressures using an 18-gauge needle, saline syringe, three-way stopcock, and a mercury manometer; however, a handheld pressure monitoring device or an arterial line monitoring system, connected to either a straight needle, a side-port needle, or slit catheter, is currently preferred. Boody and Wongworawat compared the intracompartmentalpressure monitoring system, an arterial line manometer, and the Whitesides apparatus, each with a straight needle, a side-port needle, and a slit catheter, and found that the arterial line manometer with a slit catheter was the most accurate technique. The handheld pressure monitoring system also was found to be accurate. Side-port needles and slit catheters were more accurate, whereas straight needles tended to overestimate the pressure. We most commonly use the Stryker handheld pressure monitoring device to determine intracompartmental pressures. The arterial line monitoring system is useful if continuous monitoring is desired.

To use the handheld pressure monitoring device (Stryker), the needle is placed firmly onto the chamber stem, a prefilled syringe is placed into the remaining chamber stem, and the chamber is firmly seated into the device. The needle is held at 45 degrees from horizontal and the system is purged of excess air. When the unit is turned on, the display should read 0 to 9 mm Hg. To calibrate the system, the zero button should be pressed and the display should read 00. The needle is then inserted into the desired compartment, and no more than 0.3 mL of solution is injected. The device then displays the pressure of the compartment. In an experimental model, Doro et al. showed that measurement of intramuscular glucose levels can identify compartment syndrome with high sensitivity and specificity.

Management

Acute compartment syndrome of the forearm

Impending tissue ischemia may be considered when the tissue pressure reaches between 30 and 20 mm Hg below the diastolic blood pressure. A higher pressure is a strong indication that fasciotomy should be recommended. In a hypotensive patient, the acceptable pressure is lower. Fasciotomy should be performed in (1) normotensive patients with positive clinical findings and compartment pressures of greater than 30 mm Hg, and when the duration of the increased pressure is unknown or thought to be longer than 8 hours; (2) uncooperative or unconscious patients with compartment pressures of greater than 30 mm Hg; (3) patients with low blood pressure and compartment pressures of greater than 20 mm Hg; and (4) patients with a delta P value of less than 30 mm Hg. As a general rule, when in doubt, the compartment should be released. If it proves later to have been unnecessary, only a scar will result. However, if a fasciotomy should have been done but was not, loss of muscle and nerve tissue carries a high risk for a poor functional outcome. In one study, a delay in diagnosis was the most important determining factor for poor outcome. Compartment pressure should be monitored in young patients with injury to the forearm diaphysis or distal radius, or in patients with significant soft-tissue injury and a bleeding diathesis. Normal function was regained in 68% of patients in one study when fasciotomy was performed within 12 hours of the onset of compartment syndrome. When performing a volar fasciotomy, a volar curvilinear incision is used; this allows release of the lacertus fibrosus proximally and the carpal tunnel distally. The interval between the flexor carpi ulnaris and the flexor digitorum sublimis is used for release of deep and superficial compartments. The dorsal forearm fascia is released through the interval between the extensor carpi radialis brevis and the extensor digitorum communis. The mobile wad of Henry can be released through this same incision.

Forearm Fasciotomy and Arterial Exploration

Technique 74.2

• For the volar fasciotomy ( Fig. 74.5B ), make an anterior curvilinear skin incision medial to the biceps tendon, crossing the elbow flexion crease at an angle. Carry the incision distally and radially over the brachioradialis, then distally and ulnarward, eventually coursing medial to the palmaris longus. Cross the wrist flexion crease at an angle and continue in the midline of the palm to allow for a carpal tunnel release. Curving the incision at the wrist ulnarly will decrease the risk of injury to the palmar cutaneous branch of the median nerve. The underlying subcutaneous tissues should be spread longitudinally, protecting the lateral and medial antebrachial cutaneous nerves and the palmar cutaneous branch of the median nerve.

  

• Divide the lacertus fibrosus proximally and evacuate any hematoma.

• In patients with suspected brachial artery injury, expose the brachial artery and determine if there is free blood flow. If the flow is unsatisfactory, remove the adventitia to expose any underlying clot, spasm, or intimal tear. Resect the adventitia, if necessary, and anastomose or graft the artery.

• Release the superficial volar compartment throughout its length with open scissors, freeing the fascia over the superficial compartment muscles.

• Identify the flexor carpi ulnaris and retract it with its underlying ulnar neurovascular bundle medially, and then retract the flexor digitorum superficialis and median nerve laterally to expose the flexor digitorum profundus in its deep compartment. Check to see if the overlying fascia or epimysium is tight and incise it longitudinally.

• If the muscle is gray or dusky, the prognosis for recovery may be poor; however, the muscle may still be viable and should be allowed to perfuse.

• Continue the dissection distally by incising the transverse carpal ligament along the ulnar border of the palmaris longus tendon and median nerve.

• In cases of median nerve palsy or paresthesia, observe the median nerve along the entire zone of injury to ensure that it is not severed, contused, or entrapped between the ulnar and humeral heads of the pronator teres. If it is, a partial pronator tenotomy is necessary.

• In a patient with a supracondylar fracture, reduce the fracture, pin it with Kirschner wires, and control the bleeding.

• Do not close the skin at this time; anticipate secondary closure later.

• If the median nerve is exposed within the distal forearm, suture the distal, radial-based forearm flap loosely over the nerve.

• Check the dorsal compartments clinically or repeat the pressure measurements. Usually, the volar fasciotomy decompresses the dorsal musculature sufficiently, but if involvement of the dorsal compartments is still suspected, release them also.

• Make the incision distal to the lateral epicondyle between the extensor digitorum communis and extensor carpi radialis brevis, extending approximately 10 cm distally. Gently undermine the subcutaneous tissue and release the fascia overlying the mobile wad of Henry and the extensor retinaculum.

• Apply a sterile moist dressing and a long-arm splint. The elbow should not be allowed to flex beyond 90 degrees.

Postoperative Care

The arm is elevated for 24-48 hours after surgery. If closure is not possible within 5 days, a split-thickness skin graft should be applied. Alternatively, closure of fasciotomy wounds can be accomplished gradually, using vessel loops that are progressively tightened postoperatively during dressing changes. Wound closure using this method usually can be accomplished in 2 weeks ( Fig. 74.6 ). A vacuum-assisted wound closure system may be used to assist in wound management. The splint is worn until the sutures are removed, or as determined by fracture care requirements.

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