Compartment Syndrome
Acute compartment syndrome (ACS) of the extremity is a diagnosis requiring emergent surgical intervention. It is characterized by sustained elevation of tissue pressure within an osseofascial or fascial compartment that exceeds tissue perfusion pressure. This results in local circulatory impairment, ischemia, cellular anoxia, and ultimately tissue death. ACS represents the acute phase of the injury during which time surgical intervention can reduce the extent of irreversible muscle injury. Timely diagnosis and treatment are critical in reducing the extent of permanent changes within muscle and nerve tissue. Even with emergent treatment, there may be permanent disability in the affected extremity and a subsequent need for additional surgery, including amputation. Volkmann ischemic contracture represents the late sequelae of compartment syndrome. This disorder has a spectrum of fixed muscle contractures and muscular and neurologic impairments. Numerous authors have contributed to our understanding and treatment of this condition. Table 51.1 summarizes some of the historical events in the recognition of this entity, its etiology, its pathologic findings, and its sequelae.
| Author and Year | Development |
|---|---|
| Volkmann, 1881 | First thorough description of this entity with attribution of the cause to muscle ischemia |
| Leser, 1884 | Animal investigations; concluded that the pathologic findings were a result of oxygen deprivation |
| Hildebrand, 1890 | First to use the term Volkmann’s contracture ; now sometimes referred to as Volkmann-Leser contracture |
| Bardenhauer, 1906 | Release of internal pressure through a forearm fasciotomy to treat an impending Volkmann contracture |
| Brooks, 1922, 1925 ; Jepson, 1926 | Animal model used to reproduce compartment syndrome through vascular occlusion; muscle necrosis could be prevented by surgical decompression of the muscle compartment |
| Griffiths, 1940 | Emphasized arterial injury and reflex spasm of the collateral vessels as the sole source of muscle ischemia; minimized the role of tight external dressings as the cause of muscle ischemia |
| Seddon, 1956 and 1964 | Described the pattern of muscle infarction common in compartment syndrome (ellipsoid infarct) and treatment with infarct excision; also highlighted the importance of ischemic injury to nerves |
| Holden, 1975, 1979 | Reestablished both intrinsic and extrinsic causes of muscle ischemia; distinguished two patterns of injury leading to muscle ischemia: Type 1: Arterial insult proximal to the site of ischemia Type 2: Elevated intrinsic pressure within the compartment from either internal or external sources |
| Matsen, 1975 | Unified concept of compartment syndrome |
| Whitesides, 1975 | Tissue pressures as a determinant of the need for fasciotomy |
Types of Compartment Syndromes
Acute Compartment Syndrome
Acute compartment syndrome (ACS) occurs when tissue pressures rise high enough within an osseofascial compartment to cause tissue ischemia. The resultant tissue injury can range from reversible muscle swelling to permanent tissue necrosis depending on the magnitude and duration of tissue pressure elevation. When pathologic tissue pressure elevation has been present for less than 4 hours, ACS is in the early stage ; when pathologic tissue pressure elevation has been present for more than 4 hours, ACS is in the late stage.
Impending Compartment Syndrome
Impending compartment syndrome represents a clinical setting in which a compartment syndrome is at risk of developing; however, tissue pressure is not yet sufficiently elevated to cause muscle ischemia. Clinical scenarios in which this may occur include limb reperfusion after prolonged ischemia, posttraumatic swelling of a limb, or high-energy injuries.
Exercise-Induced or Exertional Compartment Syndrome
Exercise-induced compartment syndrome is a reversible tissue ischemia due to a noncompliant fascial compartment that is unable to accommodate muscle expansion occurring during exercise. It has been described in both the upper and lower extremities and is different from ACS in that the symptoms are reversible after cessation of exercise. Emergent surgery is not usually indicated. Both traditional fasciotomy and endoscopically assisted fasciotomy have been used to treat exercise-induced compartment syndrome.
Crush Injury or Crush Syndrome
Crush injury is the external compression of an extremity, as might occur in a building collapse or construction injury or in an obtunded patient who lays on an extremity for a prolonged period. The compression of the extremity leads to muscle ischemia and reperfusion injury as the compression is relieved. This process of events can lead to compartment syndrome. Crush syndrome is a localized crush injury with systemic manifestations. Reperfusion of the affected extremity can rapidly release muscle breakdown products into the system, which can lead to renal failure or death.
Neonatal Compartment Syndrome and Neonatal Volkmann Contracture
Both neonatal compartment syndrome and neonatal Volkmann contracture have been reported. Awareness of this diagnosis is important because early recognition and treatment can improve the functional outcome and growth in neonatal compartment syndrome. In addition to swelling of the forearm, there is often a characteristic skin lesion on the proximal lateral arm, known as the sentinel lesion of neonatal compartment syndrome . Established neonatal Volkmann contracture cannot be improved by early intervention; however, awareness of this diagnosis can aid in counseling of the family and treatment of the patient ( Figure 51.1, A and B ).
Volkmann Ischemic Contracture
Volkmann ischemic contracture is the end result of prolonged ischemia, is associated with irreversible tissue necrosis, and has a spectrum of presentations.
Etiologic Findings and Incidence
Compartment syndrome in the upper extremity is most commonly associated with trauma. A variety of conditions and injuries can lead to ACS. These include fractures, penetrating trauma, closed soft tissue injuries, infection, animal and insect bites, extravasation injuries, ischemia-reperfusion injury, external compression by tight dressings or casts, burns, or crush injuries. Compartment syndrome in the absence of fracture should raise concern about an underlying bleeding disorder ( Figure 51.2 ).
The incidence of upper extremity compartment syndrome is difficult to determine. The estimated incidence in pediatric upper extremity fractures is approximately 1%. In a large series of trauma patients, the incidence of fasciotomy associated with all upper extremity traumas was 0.41%. Branco and colleagues noted a decreasing incidence of the need for surgical fasciotomy over a 10-year period, despite stable injury severity scores, with the overall incidence for upper and lower extremity trauma decreasing from 3.2 to 0.7%. They suggested a possible explanation for the declining incidence as the diminished use of crystalloid for fluid resuscitation and the use of mannitol to decrease extracellular fluid volume. Fasciotomy rates associated with traumatic arterial injury ranged from 6.7 to 16%.
Historically, ACS of the upper extremity in the pediatric population was most commonly reported in association with supracondylar humerus fractures. Likely, this was related to the historical treatment methods of casting with the elbow in a position of hyperflexion. Currently, pediatric fracture patterns most associated with forearm compartment syndrome are both-bone forearm fractures and supracondylar humerus fractures associated with distal radius fractures (i.e., floating elbow injury). In adults, the most common upper extremity fractures associated with compartment syndrome are distal radius fractures and both-bone forearm fractures.
Compartment syndrome is more prevalent in males younger than 35 years of age, penetrating trauma, open fractures, elbow dislocations, and vascular injuries. The need for surgical fasciotomy increases dramatically when vascular injury is present. Compartment syndrome in the hand is most commonly associated with intravenous injections.
Pathophysiologic Findings
The pathophysiology of ACS is complex. Several theories and models have been developed. The common prerequisite is a soft tissue structure (usually fascia) that prevents muscle expansion when the muscle is exposed to increased fluid volume. In all cases, the final common pathway is cellular anoxia.
Matsen presented a “unified concept” of compartment syndrome that incorporates several mechanisms of vascular compromise all leading to cellular injury. Increased compartmental pressure occurring from either internal injury (edema, reperfusion, or bleeding) or external injury (tight cast or dressing, pressure garment) causes a decreased perfusion gradient between arteriole and venous pressures and a resultant decrease in local tissue perfusion. Decreased tissue perfusion results in further tissue insult, increased capillary leakage, and further increase in intracompartmental pressure. This causes a vicious cycle of increasing cellular ischemia leading to further capillary leakage and swelling and increasing compartment pressures ( Figure 51.3 ).
Ongoing ischemia eventually leads to cell death and lysis of the myocyte. Degradative enzymes are activated and released into the interstitial tissues, causing further tissue necrosis. The extent of muscle injury depends on the duration of ischemia and the metabolic rate of the tissue. Prolonged ischemia can ultimately lead to liquefactive necrosis of the muscle compartment.
Diagnosis
Diagnosis of Acute Compartment Syndrome
The diagnosis of ACS is principally based on clinical examination. Maintenance of a high index of suspicion, particularly in the setting of at-risk injuries and conditions, aids in the prompt recognition and treatment of this condition.
Although compartment syndrome is frequently associated with fractures, many other causes can also lead to ACS. Causes are commonly separated into intrinsic causes (typically, bleeding or swelling into a compartment) and extrinsic causes (applied external pressure preventing a compartment from expanding) ( Box 51.1 ). The physician must keep this in mind because ACS not associated with fracture frequently has a delayed diagnosis and worse clinical outcomes.
Intrinsic Injuries
High-energy fracture, usually in young male (open fractures more at risk than closed fractures)
Fracture in child
- •
Supracondylar fracture of humerus, especially one associated with distal radius fracture
- •
Both-bone forearm fractures (intramedullary nailing of pediatric both-bone and radial head fractures is associated with difficult reduction and prolonged tourniquet times )
Fracture in adult
- •
Distal radius fracture
- •
Upper extremity fractures associated with vascular injury
- •
Soft tissue trauma without fracture
- •
Blunt trauma without fracture or skin violation)
Penetrating trauma (usually from bleeding into otherwise closed compartment)
Vascular injury
- •
Trauma
- •
Iatrogenic procedures, such as venipuncture or arterial blood draw
- •
Reperfusion after prolonged ischemia
- •
Prophylactic fasciotomy should be considered after vascular repair
Burns
- •
Edema associated with burn injury
- •
Electrical burns associated with deep muscle damage and edema
- •
Systemic inflammation and fluid resuscitation
- •
Burn eschar causes an extrinsic compression
Animal and insect bites (e.g., Crotalidae [pit viper] snakebite)
- •
Treatment of impending compartment syndrome from snakebite should be with antivenin
- •
(Crofab [ovine]; Antivenin Crotalidae Polyvalent ACP [equine])
- •
Rarely requires surgical decompression
Intravenous fluid extravasation (hypertonic fluids such as intravenous contrast material)
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Intraoperative fluid extravasation, particularly in patients where the arm position does not allow easy visualization of the extremity, and when infusion pumps are used
Infection
Bleeding disorders
- •
Coagulation disorders (e.g., von Willebrand hemophilia)
- •
Anticoagulation therapy
- •
Spontaneous bleeding may occur with no trauma or minor trauma
Extrinsic Injuries
Compressive casts or dressings
Burn eschar (circumferential inelastic eschar)
- •
Important to release fingers with dermotomies if burn involves the hand
Crush injury
- •
In obtunded patient during drug or alcohol overdose
- •
Resulting from coma, seizure, or hypoglycemic episode
- •
Building collapse
- •
Intraoperative positioning (prone or lateral positioning with poorly positioned axillary or chest roll causing axillary artery occlusion; also seen in the lower extremity with prolonged lithotomy position)
The timing of presentation can vary from within the first few hours of injury to several days following injury.
The hallmarks of diagnosis of ACS have classically been described as the six P s of compartment syndrome ( Table 51.2 ): pain, pressure, paresthesias, pallor, paresis, and pulselessness. Some authors have added or substituted poikilothermia of the extremity as one of the P s. This use of the term poikilothermia is not completely accurate but indicates that the affected extremity is cool relative to body temperature. In most series, pain has been the earliest and most reliable finding. However, pain peaks at 2 to 6 hours of ischemia and then gradually subsides as muscle necrosis progresses and nerve function becomes impaired. Therefore, patients with a late presentation of or late diagnosis of compartment syndrome have less pain than those with an earlier presentation.
| Sign or Symptom | Description |
|---|---|
| Pain | Described as deep, constant, often poorly localized pain that is disproportionate to the physical findings; often poorly responsive to analgesics Pain is accentuated with passive stretching of the involved compartment. Although this is the most consistent and reliable finding, cases of “silent” compartment syndrome of the lower extremity have been reported (Badhe) and likely also occur in the upper extremity. Pain usually peaks at around 2 to 6 hours of ischemia and then subsides. Patients who present late with acute compartment syndrome may not report as much pain. |
| Pressure | Affected compartment(s) are firm and noncompressible; often described as “rock hard” |
| Paresthesias | Numbness or “pins-and-needles” sensation in the cutaneous distribution of the nerves that traverse the affected compartment |
| Pallor | Usually pale, but the extremity may also appear blotchy and often cool (see poikilothermia) |
| Paralysis | Late and unreliable finding. Muscle paralysis may be pain related. When true paralysis is present, this is a poor prognosticator for recovery. |
| Pulseless | Also usually a late finding and poor prognosticator for recovery |
It has been suggested that in pediatric patients, “it’s the A s, not the P s” that signal ACS. These A s are an increasing requirement for analgesia, the presence of anxiety (or restlessness), and the presence of agitation (or crying). Children are unable to articulate the feeling of paresthesias, and sensibility testing is unreliable.
Certain conditions can make the clinical diagnosis of ACS challenging. Altered levels of consciousness as can occur in head trauma, a medically induced coma, or obtundation from other causes can obscure the normal pain response that is one of the early signs of compartment syndrome. Similarly, distracting pain from polytrauma, neurologic injury in the affected limb, and/or regional anesthetic blockade can mask the signs and symptoms of compartment syndrome. Diagnosis is also more difficult in children and infants who may have difficulty in cooperating with examination, are nonverbal, or are apprehensive and crying. Also, the thicker layer of subcutaneous fat in children may contribute to a false sense of a soft compartment on palpation, further complicating the diagnosis. Diagnosis or exclusion of compartment syndrome on clinical grounds alone is often impossible.
If the clinician is uncertain of the diagnosis based on equivocal physical findings, compartment pressure can be measured ( Figure 51.4 and Table 51.3 ). Several different methods can be used. Continuous pressure measurements can be obtained with a wick catheter or connection to a continuous pressure monitor. Typically, the newer digital devices are used to assess or monitor the compartment. These devices are sensitive to patient motion and should not supplant repeat clinical examinations. Although controversial, the thresholds/indications for fasciotomy are an absolute pressure greater than 30 to 40 mm Hg or pressures within 30 mm Hg of either the diastolic blood pressure or the mean arterial pressure.
| Aspect of Measurement | Considerations |
|---|---|
| Patient position |
|
| Needle | 18-g straight, side-port, slit catheter, or wick |
| Transducer |
|
| Needle placement |
|
| Threshold pressure |
|
| Contraindications to measuring compartmental pressure |
|
Although pulse oximetry of the affected extremity has not been found to be useful, near-infrared spectroscopy (NIRS) may prove to be useful in the early diagnosis and monitoring of an impending compartment syndrome. This technique was proposed as a method of monitoring for compartment syndrome as early as 2001, but it has not been widely adopted because of its cost and problems with availability of sensors and equipment. NIRS is noninvasive and capable of measuring the oxygenation state of at-risk tissues and may gain wider use in the future. NIRS is limited by the depth of tissue penetration (2 to 3 cm) and the presence of hematoma within the compartment.
In these questionable clinical situations, the safer intervention is to perform a fasciotomy. Bulging of the muscle compartment and clinical softening of the extremity at the time of fasciotomy confirms the diagnosis.
Diagnosis of Exertional Compartment Syndrome
Chronic exertional compartment syndrome of the upper extremity has been described in the flexor compartment of the forearm and in the anconeus muscle; in the hand, it has been described specifically in the adductor of the thumb. Patients with chronic exertional compartment syndrome typically complain of pain that starts as a dull ache within the first 30 minutes after starting an activity. Burning, cramping, or aching pain progresses as the activity is continued. The pain escalates to a level of discomfort where the patient can no longer continue or where it adversely affects the patient’s performance. Activities associated with exertional compartment syndrome of the upper extremity include sports such as rowing, bicycle riding, or motorcycle riding or repeated episodes of manual labor requiring a prolonged grip or pinch. The pain and tissue firmness resolve spontaneously with cessation of the activities. Diagnostic studies have principally involved measurement of compartment pressures before, during, and after exercise. More recently, magnetic resonance imaging has been used before and after exercise as a diagnostic tool. A signal change in T2 imaging in an isolated fascial compartment associated with activity supports the diagnosis of exercise-induced compartment syndrome.
Pertinent Anatomy
The compartments of the upper extremity are listed in Table 51.4 . Any of these anatomic spaces can be affected by tissue pressure elevation. Although elevated tissue pressures are most commonly seen in osseofascial spaces, other tissue structures provide a rigid barrier that does not expand sufficiently to accommodate swelling. In the upper extremity, the fascial components and the skin can act as barriers that require decompression at the time of surgery.
| Compartments | Contents | ||
|---|---|---|---|
| Arm | Anterior | Biceps and brachialis muscles, brachial artery, and median nerve | |
| Posterior | Triceps muscle and ulnar and radial nerves | ||
| Deltoid | Not technically a separate compartment but has a thick epimysium that may require decompression | ||
| Forearm | Volar | Superficial | Flexor carpi radialis, palmaris longus, pronator teres, flexor carpi ulnaris, and flexor digitorum superficialis muscles |
| Deep | Flexor digitorum profundus, flexor pollicis longus, pronator quadratus muscles, * and anterior interosseous nerve and artery | ||
| Dorsal | Mobile wad | Brachioradialis, extensor carpi radialis longus, and extensor carpi radialis brevis muscles | |
| Extensor | Extensor digitorum communis, extensor carpi ulnaris, extensor pollicis longus, abductor pollicis longus, extensor pollicis brevis, and supinator muscles, † and posterior interosseous nerve | ||
| Anconeus * | Anconeus | ||
| Hand | Thenar | Abductor pollicis brevis, opponens pollicis, and flexor pollicis brevis muscles | |
| Hypothenar | Abductor digiti minimi, flexor digiti minimi, and opponens digiti minimi muscles | ||
| Adductor pollicis | Adductor pollicis muscle (two heads) | ||
| Dorsal interossei (4) | Each is a separate compartment | ||
| Volar interossei (3) | Each is a separate compartment | ||
| Fingers ‡ | |||
* Reported isolated involvement in exertional compartment syndrome.
† The supinator muscle is not typically a component of the extensor compartment, but decompression can be done through the brachioradialis/extensor carpi radialis longus interval.
‡ Compression of the neurovascular structures by rigid Cleland and Grayson ligaments can lead to skin necrosis and/or loss of the finger.
Treatment
The goal of treatment is to prevent tissue necrosis, avert neurovascular compromise, and avoid permanent functional deficits. These devastating complications can be minimized or avoided with early recognition and prompt intervention.
The first step in treatment is to remove all possible extrinsic causes of pressure, including circumferential dressings, cast padding, and casts. Casts have been shown to restrict compartment expansion by 40%. Release of a cast and subsequent spreading reduces pressure elevation by 40 to 60% depending on the presence of dry or wet blood on the cast padding. The limb should be elevated only to heart level. Although limb elevation may decrease swelling, it can also reduce perfusion to the affected limb, risking exacerbation of tissue ischemia.
A history of bleeding disorders or use of anticoagulation therapy should be obtained from the patient or family member. Laboratory analysis should include a complete blood count, prothrombin time, and partial thromboplastin time. If there is a suspicion of a bleeding disorder, a hematologist should be involved in the evaluation and treatment of the patient. Urinalysis for myoglobin, serum electrolytes, creatinine, and myoglobin should be obtained in the setting of prolonged ischemia, crush injury, or ischemia-reperfusion injury. Medical management of shock, hypoxia, metabolic acidosis, and electrolyte imbalance should be addressed immediately. Supportive care with vigorous hydration, correction of metabolic function, and treatment of hyperkalemia is necessary to prevent sequelae such as renal failure, shock, hypothermia, cardiac arrhythmias, or cardiac failure. Supportive care should be initiated in the emergency room but should not delay surgical treatment.
Hypertonic mannitol has been used to lower intracranial pressure. The use of mannitol in decreasing extremity swelling has been described in animal models and limited case studies. It has not gained widespread use for treatment of impending or acute compartment syndrome. Nonetheless, it has been hypothesized that the use of mannitol may have played a role in the decreased incidence of compartment syndrome in trauma patients at a single medical center over a 10-year time period. Hypertonic mannitol has been found to decrease endothelial swelling and may help reduce muscle necrosis in its function as an oxygen-free radical scavenger. In one clinical report, patients were given a 100-mL bolus of 20% mannitol, followed by an infusion of 10 g/hour for 6 to 24 hours.
Emergent surgical decompression (fasciotomy, or release of the fascia overlying the affected compartments) performed as quickly and safely as possible is needed for ACS. Fasciotomy within the first 8 hours after diagnosis is associated with a lower risk of permanent functional impairment. Release of the epimysium surrounding the muscle may also be necessary. Necrotic tissue should be excised because it may become a nidus for infection or lead to subsequent fibrosis and contracture. Questionable tissue should be left in place for a second look at a later date. Late fibrosis of necrotic muscle can lead to compression of the adjacent nerves and further impair extremity function. Other concomitant procedures may be indicated based on the cause of the compartment syndrome, including fracture reduction and stabilization, vascular repair, and nerve exploration if indicated. Nerve repair or grafting should be performed at the time of definitive wound closure.
Late or delayed diagnosis increases the risk for severe complications, including infection, neurologic injury, need for amputation, and death. In the past, concerns about an increased risk of infection have led some authors to recommend not performing a fasciotomy after 24 hours has elapsed since the onset of symptoms. We do not feel this risk outweighs potential benefits and no longer consider this a contraindication for surgery. Currently, there are more options for wound management and antibiotic therapy. Removal of necrotic muscle can decrease the severity of subsequent muscle fibrosis and joint contracture. Débridement of nonviable muscle improves the environment for the neurovascular structures and may allow early functional reconstruction of the lost muscle(s) by means of tendon transfers or free functional muscle transfers (FFMTs).
In addition, the length of time that elevated pressure sufficient to cause tissue necrosis has been present is often unclear, and some muscle preservation may be facilitated with late fasciotomy. In some cases, good results in children have been reported following fasciotomy as late as 72 hours after the injury (within the acute swelling phase). Dramatic, essentially full, recovery has been reported following compartment syndrome of the lower leg in children after delayed presentation.
Surgical Procedure
Indications.
The indications for surgical fasciotomy are described previously. Our preference is to manage questionable cases of impending compartment syndrome with surgical decompression, provided the patient is stable enough for the procedure. Prophylactic fasciotomies should be performed following vascular repair/reconstruction where ischemia time exceeds 3 hours. Shorter periods of ischemia do not eliminate the risk of developing compartment syndrome, and careful monitoring is necessary after vascular surgery.
Contraindications.
Contraindications to fasciotomy are few. Coagulopathy should be corrected prior to surgical intervention. Plasma, factor, or platelet transfusion may be necessary to optimize the patient for surgery. Intubated patients who are not stable for surgery should be considered for a bedside fasciotomy using local anesthesia and sedation.
Author’s Preferred Method of Treatment
The surgical incision for the upper extremity is extensile from the brachium to the carpal tunnel. The extent of the release performed is tailored to the clinical and intraoperative findings. Release of the dorsal forearm and compartments of the hand requires separate incisions when indicated. A separate incision for a dermotomy of each of the fingers may also be added to prevent skin necrosis and loss of the fingers.
Release of the Compartments of the Arm.
The anterior and posterior compartments of the arm can be decompressed through a single medial incision. This allows access to the neurovascular structures of the arm, the medial fascia of the biceps and brachialis in the anterior compartment, and the fascia of the triceps. Excision of the medial intermuscular septum will provide additional decompression of both compartments ( Figure 51.5 ). The incision can be easily extended to the elbow crease and incorporated with the incision for decompression of the forearm. This also allows release of the lacertus fibrosus and access to the brachial artery. When there is no anticipated need to evaluate the brachial artery or to decompress the forearm compartments, fasciotomies can be performed through separate anterior and posterior midline incisions to decompress the flexor and extensor compartments, respectively.
Release of the Compartments of the Forearm.
Several skin incisions have been described for the forearm. Because the surgical incisions are long and extensile, almost any incision can be used to decompress the forearm compartments ( Figure 51.6 ). Because the incisions are left open, we prefer an incision that minimizes exposure of neurovascular structures and can be extended in a proximal direction into the medial arm and in a distal direction into the carpal tunnel (see Figure 51.6, A and B ). Once the skin incision has been made, the antebrachial fascia is incised longitudinally from the lacertus fibrosus to the wrist flexion crease. This decompresses the superficial flexor compartment. The deep flexor compartment is most easily and safely exposed through the ulnar side of the forearm. We begin at the mid to distal forearm and identify the interval between the flexor carpi ulnaris and flexor digitorum superficialis. The flexor digitorum profundus and flexor pollicis longus fascias are exposed and released through this interval ( Figure 51.7 ). This is the most important component of this procedure because the deep flexor compartment is usually the one first and most affected by increased compartmental pressure. Through the same interval, the fascia overlying the pronator quadratus is released.
During the dissection, if the muscles appear pale after release of the fascia, additional release of the epimysium of the pale muscle should be performed. For these muscles, if the epimysium is not released, reperfusion injury will lead to additional swelling within the muscle and further muscle damage.
Clinical evaluation of the remaining tension in the dorsal forearm compartment and/or hand should be done to determine whether additional release of the extensor and hand compartments should be added.
The extensor compartments are released through a midline longitudinal dorsal incision extending from the lateral epicondyle to the distal radioulnar joint. This will allow release of the mobile wad and the extensor compartment ( Figure 51.8 and see Figure 51.6, C and D ).
Release of the Compartments of the Hand.
The hand has 10 separate compartments. It is rarely necessary to release all 10 compartments, and intraoperative assessment and/or measurement of compartment pressures should be used to determine the extent of release needed ( Figures 51.9 and 51.10 ).
Volar Release.
Decompression should start with an extended carpal tunnel release. Carpal tunnel release will usually adequately release the Guyon canal without division of the volar carpal ligament (roof of the Guyon canal) and directly decompress the ulnar neurovascular structures. The carpal tunnel incision can be extended to the second volar web space. In the distal portion of the incision, the volar fascia of the adductor pollicis muscle can be released. Also, the fascia extending from the long finger metacarpal to the palmar fascia (separating the deep radial and ulnar midpalmar spaces) can be released. This will help decompress the volar interosseous muscles. The thenar and hypothenar muscles are decompressed through separate incisions as needed.
Dorsal Release.
The dorsal interosseous muscles (and volar interosseous muscles) are decompressed through dorsal incisions between the second and third metacarpals and fourth and fifth metacarpals. The first dorsal interosseous muscle is decompressed through an incision placed in the first dorsal web space. The dorsal fascia of the adductor pollicis can also be released through this incision (see Figure 51.9 ).
Release of the Fingers.
Tense swollen fingers can result in skin and subcutaneous tissue necrosis. The tight fibers of Cleland and Grayson ligaments can compress and obstruct the digital arteries. Dermotomy of all involved fingers reduces the risk of necrosis of the skin and possible loss of a digit. Dermotomies should be done in the midaxial plane to prevent subsequent contracture. When possible, the dermotomy should be performed on the side that will cause the least amount of scar irritation. The preferred locations for finger and thumb dermotomies are shown in Figure 51.9, A and B .
See Case Study 51.1 and for further information on compartment release of the arm, forearm, and hand.
Diagnosis
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Diagnosis is usually a clinical one
- •
Pain is out of proportion to clinical findings
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Pain with passive motion
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Firm, “rock hard” compartment
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Objective findings include elevated compartment pressures and 30 to 40 mm Hg or within 30 mm of diastolic blood pressure or mean arterial pressure
Management
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Correct any underlying coagulopathy
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Perform emergent fasciotomy
- •
Perform vascular repair or reconstruction when indicated
- •
Treat associated injuries
- •
Repeat surgical débridement
- •
Close the wound with delayed primary closure, split-thickness skin graft, or flap
- •
Perform early reconstruction when indicated with tendon transfer or functional muscle transfer
Arm Management
- •
Anterior and posterior compartments
- •
Medial incision to decompress both compartments
- •
Deltoid may require epimysiotomy
Forearm Management
- •
Deep volar, superficial volar, and extensor compartments
- •
Deep compartment must be released
- •
Best decompressed through the interval between the flexor carpi ulnaris and the ulnar side of the flexor digitorum superficialis
- •
Extensor compartment may soften with release of volar compartments but requires separate assessment and release if indicated
Hand Management
- •
Ten separate compartments
- •
Start with extended carpal tunnel release
- •
Release additional compartments as necessary
Finger Management
- •
Tense, swollen fingers can result in digital necrosis
- •
Midlateral dermotomies are performed dorsal to the neurovascular bundles
Pitfalls
- •
Failure to diagnose in a timely manner
- •
Failure to adequately release compartments
- •
Inadequate excision of necrotic tissue leading to scarring and fibrosis around nerves
Surgical Approach to Treatment
All or portions of this approach can be used, depending on the clinical setting. The approach is extensile from the arm to the distal forearm, and separate incisions are required to release the extensor compartment (when indicated). Multiple incisions are used to release the compartments of the hand.
Fasciotomy of the Upper Extremity
Incisions are designed to provide the most coverage of neurovascular structures (at the time of later closure). Linear incisions across flexion creases are avoided. After the skin incision, the antebrachial fascia is released, allowing assessment of the superficial flexor compartment. The interval between the flexor digitorum superficialis and flexor carpi ulnaris is opened to provide access to the deep flexor compartment of the forearm.
After release of the flexor compartments, muscles are inspected and epimysiotomies are performed for tense or dysvascular muscles. Once the flexor compartments are released, the extensor compartment is assessed. If tense, this is released through a dorsal midline incision.
Release at the elbow requires division of the lacertus fibrosus with exploration of the median nerve and brachial artery. Fasciotomies in the hand are performed through a carpal tunnel release, release of the thenar and hypothenar eminences, and dorsal incisions for the release of the interosseous muscles.
Decompression of the fingers may be necessary to prevent digital loss. This is performed through midlateral incisions, avoiding pinching surfaces, including the radial border of the thumb, ulnar borders of the index and long fingers, and radial borders of the ring and small fingers.
The Cleland ligaments are released when necessary to decompress the digital arteries (see ).
Postoperative Management
All surgical incisions are left open. We prefer not to use retention sutures. Even if there is minimal swelling of the muscle(s) during the primary release, muscle swelling will usually increase after perfusion has improved. If nerves and arteries are not exposed, a negative-pressure wound dressing (e.g., VAC, Kinetic Concepts, Inc., San Antonio, TX) can be used. We use lower pressures for the negative pressure dressing than in other wounds, usually just enough to maintain good seal on the dressing. If nerves or arteries are exposed, we prefer to use a moist gauze dressing. Dressing changes should be done in the operating room at 24 to 48 hours. Partial delayed primary wound closure can be performed at that time if swelling has decreased and/or to provide coverage over open neurovascular structures. Definitive delayed primary wound closure should be performed only after swelling has decreased. Some cases will require repeat débridement of necrotic tissue. Split-thickness skin grafting for closure is necessary in many patients. Younger patients with high-energy or crush injuries are more likely to require split-thickness skin grafting at 48 hours. In our practice, we prefer to manage the wound until swelling decreases sufficiently to allow delayed primary wound closure if possible, which may require 7 to 10 days. In the hand, only the incision for the carpal tunnel release should be considered for delayed primary wound closure. The other palmar and dorsal incisions as well as the dermotomy incisions will heal quickly by secondary intention. If the skin cannot be closed without tension, split-thickness skin grafting with or without dermal substitutes such as Integra (Integra, Plainsboro, NJ) should be used.
Therapy should be started immediately following surgery to promote maximum active and passive range of motion of the fingers. Splinting should be done for soft tissue stabilization and/or for treatment of other associated injuries. Cessation of therapy during healing of skin grafts may be necessary, but therapy should be resumed as soon as tissue healing allows. Once the soft tissues are adequately healed, nighttime splinting is continued to prevent contractures of the wrist and fingers. Splinting is continued until scars and soft tissues are mature and supple.
Outcomes and Expectations
Outcomes following fasciotomy depend on the duration and severity of the compartment pressure elevation and the resultant extent of muscle necrosis. Early prompt fasciotomy within the first 4 hours usually results in minimal sequelae. Delayed management results in muscle fibrosis and contracture that varies with the extent of muscle necrosis and nerve involvement. Secondary surgery is usually necessary to improve the outcome of these delayed cases.
Outcomes following fasciotomy for chronic exertional compartment syndrome are good. Preoperative symptoms of pain related to activity resolve, and 90% of patients are able to return to sports or other activities.
Complications of compartment syndrome and its treatment are common. In a metaanalysis, Kalyani and colleagues reported a complication rate of 42% (18 of 43 patients). Duckworth and associates reported a complication rate of 32% (29 of 99 patients). The most common complication was a neurologic deficit. Other complications included contracture, reflex sympathetic dystrophy, gangrene, muscle weakness, fracture nonunion, and soft tissue tethering associated with skin grafting.
Volkmann Contracture
Volkmann ischemic contracture is the end result of prolonged ischemia and associated with irreversible tissue necrosis. Established Volkmann contracture has a much different presentation than ACS. It has a broad clinical spectrum, based on the extent of muscle necrosis and degree of nerve injury. Unlike ACS, patients with an ischemic contracture do not have pain but rather have deformity and dysfunction resulting from the ischemic event and subsequent muscle scarring and fibrosis. Nerve dysfunction can occur either from the initial trauma or subsequent ischemic insult or secondary to the fibrosis around the nerves. The muscle fibrosis and neurologic deficits lead to deformity of the joints distal to the site of ischemia. The deformity is progressive over the ensuing weeks to months. In children, an untreated deformity will progress until skeletal maturity because the ischemic muscles are unable to elongate during limb growth. Even when the contractures are treated, the affected extremity is shortened due to the tethering across the physis.
Classification
Several classification systems have been described for Volkmann contracture of the forearm. Most are based on the extent of muscle involvement and the severity of the clinical disability. The classification systems can be useful in guiding treatment plans for functional reconstruction. Most authors recognize the tremendous variability of the clinical presentations and the subsequent limitations of the classification systems.
The most commonly used, and our preferred, classification system is that proposed by Tsuge. Established Volkmann contracture was divided into mild, moderate, and severe types, according to the extent of muscle involvement ( Figures 51.11 through 51.13 and Table 51.5 ). Tsuge’s category of severe contractures included cases of moderate tissue necrosis that were exacerbated by fixed joint contractures, a scarred soft tissue envelope, or failed surgeries.
| Type | Findings | Treatment Options |
|---|---|---|
| Mild |
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| Moderate |
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| Severe |
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Within each classification type, there is a broad range of clinical presentations. The heterogeneity of presentation makes it difficult to apply a specific treatment based solely on the classification system. The variability also confounds meaningful outcome and comparison studies.
Treatment
There is a limited role for the nonoperative treatment of established contracture. There may be some benefit from therapy to stretch and splint mild contractures. In children, splinting is continued until skeletal maturity. Moderate and severe contractures are usually recalcitrant to therapy.
Operative Treatment
A variety of surgical techniques have been proposed, including bony and soft tissue management ( Table 51.6 ).
| LATE MANAGEMENT OF COMPARTMENT SYNDROME; SURGICAL OPTIONS FOR THE FOREARM | |||
|---|---|---|---|
| Operation | Authors | Advantages | Disadvantages |
| Bone | |||
| Proximal row carpectomy | Zancolli, 1979 Goldner, 1975 | Addresses wrist flexion contracture without causing additional scarring in the forearm | (1) Nonselective shortening of both extensors and flexors (2) Limb is already shortened from ischemic insult |
| Diaphyseal shortening | Rolands, 1905 Domanasiewicz, 2008 Pavanini, 1975 | Satisfactory correction of contracture Does not preclude other procedures | (1) Nonselective shortening of both extensors and flexors (2) Limb is already shortened from ischemic insult (3) High nonunion and refracture rate reported |
| Arthrodesis | Botte, 1998 Goldner, 1975 | Wrist: Maintains wrist in physiologic position; if additional tendon transfers are needed, if wrist is fused, one less donor muscle is needed and wrist extensor muscles are available as donors for finger function PIP: Fingers maintained in a more functional position; may be only option to correct intrinsic imbalance | Wrist: (1) Loss of tenodesis effect of wrist position (2) Decreased grip strength (3) Loss of motion PIP: (1) Loss of finger flexion (2) Resultant loss of grip strength |
| Soft Tissue | |||
| Fractional or tendon “Z”-lengthening | Goldner, 1975 | Straightforward surgical release of flexion contracture | (1) Loss of active flexion (2) More disruption of muscle resting length and loss of flexion strength |
| Infarct excision with tendon reconstruction/transfer | Seddon, 1964, Seddon, 1956 Tsuge, 1975 | Tsuge advocated infarct excision for mild contractures with involvement of only one or two fingers | (1) Late infarct excision creates more scarring around nerves (2) Deficit created from scar excision is replaced with more scar tissue later |
| Flexor-pronator slide | Page, 1923 Scaglietti, 1957 Gosset, 1956 Sharma, 2012 | Allows greatest correction of flexion contracture with least impact on muscle resting length | (1) Will not fully correct finger flexion contracture that is not passively correctable in maximal wrist flexion (2) Wide surgical dissection with potential injury to CIA/PIA |
| Functional free muscle transfer | Zuker, 1989, Zuker, 2007 Manktelow, 1978 Manktelow, 1989 Doi, 1993 | Only procedure that can restore function for severe contracture according to Tsuge classification | (1) Difficult microsurgical procedure requiring an experienced team (2) Failure can only be remedied with a second functional free muscle transfer |
Bone Procedures.
Skeletal shortening or fusions are frequently performed in conjunction with some of the soft tissue procedures listed in Table 51.6 . Shortening procedures include shortening osteotomy of the radius and ulna and proximal row carpectomy. These procedures have been used to match the skeletal length to the shortened fibrotic muscle. One concern with bone procedures is that the principal contracture is within the flexor compartment. Shortening the forearm indiscriminately lengthens the muscle resting length of both the flexor and extensor muscles, neglecting the predominant involvement of the contracture within the flexor compartment muscles. Shortening procedures raise additional concerns in children because the forearm is already shortened by the initial ischemic insult to the bone and growth plates.
Bony reconstructive procedures are useful for residual problems related to nerve dysfunction or for long-standing contractures not amenable to additional soft tissue release. Options include wrist fusion, trapeziometacarpal joint fusion, or thumb metacarpophalangeal joint fusion. Severe progressive finger deformities can also be managed with arthrodesis in a more functional position. These procedures are ideally done after skeletal maturity but may need to be performed earlier if there is progressive deformity. In these cases, we attempt to fuse the joint and preserve the growth plate (i.e., chondrodesis).
Soft Tissue Procedures.
Soft tissue procedures include excision of the infarcted muscle, fractional or “Z”-lengthening of the affected muscles, muscle sliding operations (flexor origin muscle slide), neurolysis, tendon transfers, and functional free-tissue transfers, as well as combinations of these procedures. Excision of scarred fibrotic nerves without distal function followed by nerve grafting has been described to try and establish some protective sensation in the hand. Fixed contractures of the joints can be addressed with soft tissue release, including capsulectomy and collateral ligament recession or excision, depending on the joints involved.
Authors’ Preferred Methods of Treatment
Our preferred methods of treatment depend on the general classification of severity of contracture, individualized to the patient presentation.
Mild (Localized) Type (Deep Flexor Compartment Without Neurologic Deficit).
For mild contractures that have failed to respond to nonsurgical management, our preferred treatment is a muscle sliding operation initially described by Page and subsequently endorsed by several others. We have found this procedure effective as long as good active finger flexion is present. We do not combine this procedure with infarct excision, nor have we found it necessary to release the distal insertion of the pronator teres to correct pronation contracture.
A limited flexor slide may be done for mild deformity, affecting only a portion of the flexor digitorum profundus. Because the flexor digitorum profundus originates solely from the ulna, the flexor pronator mass does not have to be released from the medial epicondyle and the ulnar nerve does not have to be transposed. This limited approach reduces potential scarring and vascular compromise to the remaining muscles and nerves in the flexor compartment.
Moderate Type (Deep and Superficial Flexor Compartment With Neurologic Deficit).
For moderate deformity, we prefer a flexor muscle origin slide to correct the tightness of the flexors, provided that there is still adequate remaining strength in the flexors. Because neurologic impairment is characteristic of the moderate injury, we combine the flexor slide with neurolysis of both the median and ulnar nerves. A separate incision to release the carpal tunnel may also be needed. Depending on the functional deficits, tendon transfer can be combined with flexor origin slide, either as a staged or simultaneous procedure.
Reconstruction of Thumb Function.
Our preferred transfer for thumb flexion is to transfer the brachioradialis or extensor carpi radialis longus to the flexor pollicis longus. The extensor indicis proprius can be used for thumb opposition at a later date.
Reconstruction of Finger Flexion.
When the finger flexors are very weak or absent, an FFMT may produce a better functional result than a tendon transfer. However, if an FFMT is not an option, tendon transfers may be considered depending on the availability of donors. The best option is transfer of the extensor carpi radialis longus to the flexor digitorum profundus because this transfer is synergistic and easy to relearn. Other lesser options include the biceps brachii elongated with graft, the brachioradialis, the extensor carpi ulnaris, and the extensor indicis proprius. Many of these secondary options do not have sufficient excursion to match the flexor muscles, but in the absence of other options, they can provide some improvement in grasp. Lastly, if there is minimal involvement of the flexor digitorum superficialis muscle, this muscle can be used as a donor to the flexor digitorum profundus
Nerve Reconstruction.
When sensory impairment is severe and there has been no recovery, the nerve should be carefully evaluated at surgery. A densely scarred atrophic nerve or avascular nerve requires resection back to fascicles that appear healthy followed by sural nerve grafting to restore protective sensation to the hand ( Figure 51.14 ).
