eMedicine Specialties > Orthopedic Surgery > Trauma

Compartment Syndrome, Upper Extremity

Author: Stephen Wallace, MD, Staff, Department of Emergency Medicine, Eastern Idaho Regional Medical Center
Coauthor(s): Douglas G Smith, MD, Associate Professor, Department of Orthopedic Surgery, University of Washington, Harborview Medical Center
Contributor Information and Disclosures

Updated: Feb 21, 2009

Introduction

Compartment syndrome (CS) occurs when the tissue pressure within a closed muscle compartment exceeds the perfusion pressure and results in muscle and nerve ischemia. The cycle of events leading to acute CS begins when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and lack of waste product removal result in pain and decreased peripheral sensation secondary to nerve irritation. Late manifestations of CS include the absence of a distal pulse, hypoesthesia, and extremity paresis because the cycle of elevating tissue pressure eventually compromises arterial blood flow. If left untreated, the muscles and nerve within the compartment undergo necrosis, and a limb contracture, called a Volkmann contracture (VC), results.

The compartments of the lower leg, foot, and volar forearm are particularly prone to developing CS. The intrinsic muscle compartments of the hand and, less commonly, the upper arm may also be affected. The most common etiology of an upper extremity CS is a displaced supracondylar humerus fracture. The diagnosis is made on the basis of clinical examination when the physician has a high index of suspicion; operative decompression is the definitive treatment. In the forearm, usually both volar and dorsal compartments are released.

Morbidity and mortality from CS stem from a delay in the treatment or diagnosis. After prolonged muscle ischemia, muscle necrosis results in scarring and contracture, named after Volkmann, who described the contracture in 1875.¹ Rhabdomyolysis and subsequent renal failure are among the most severe complications of CS; however, these conditions usually have a self-limited course if treated appropriately. This article summarizes the current understanding of acute and CCS in the upper extremity.

Related eMedicine topics:

Compartment Syndrome, Lower Extremity

Supracondylar Humerus Fractures

Volkmann Contracture

Rhabdomyolysis

Acute Renal Failure

History of the Procedure

Compartment syndrome (CS) was first described in 1872 in association with injuries that were sustained from surgical positioning.¹ In his classic paper of 1881, Volkmann described paralytic contractures of the forearm muscles in a patient after casting for closed reduction of an elbow fracture. He hypothesized that the contractures resulted from ischemic muscle necrosis caused by vascular insufficiency from tight casting. In 1909, Thomas published a paper in which he described paralytic contractures after severe muscle contusions, thus identifying an intrinsic etiology as well.²

In 1914, Murphy reported that hemorrhage into the muscles could cause pressure to rise within the deep fascial compartments of the forearm, with subsequent obstruction of the venous return.² Murphy suggested that fasciotomy might be of clinical benefit. In 1928, Sir Robert Jones concluded that Volkmann contracture was the result of a CS from elevated pressures that were intrinsic or extrinsic, or both, in origin.²

In 1926, Jepson was the first investigator to prove that paralysis and contracture could be prevented by prompt decompression.^2,3 In the early 1900s, surgically implanted capsule and balloon measuring devices were used to make the diagnosis of CS. In 1968, the wick-catheter technique was introduced; and in 1975, Whitesides et al developed an infusion technique that uses a slit-catheter.⁴ Concurrently, Matsen et al completed extensive research and published clinical guidelines detailing the indications for fasciotomy.^5,6 Currently, portable compartment-pressure monitoring devices have been marketed that are easy to use and that provide accurate results (available from the Stryker Corporation, Kalamazoo, Mich).

Chronic compartment syndrome (CCS), also known as chronic exertional CS, exertional CS, recurrent CS, and subacute CS, is a distinct entity from acute CS. First described in 1956, CCS was thought to be a form of shin splints in the lower extremity (anterior tibial enthesitis).⁴ However, with the increased popularity of endurance sports over the past few decades, additional research on exercise-induced leg and arm pain has demonstrated that CCS is a well-defined clinical entity.

Problem

The literature is somewhat confusing because of the interchangeable use of the terms compartment syndrome (CS); acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. CS is a condition in which increased tissue pressure within a closed osteofascial compartment compromises blood flow to the muscles and nerves within that compartment, which results in tissue and nerve damage. Crush syndrome is distinct from CS and occurs when primary muscle necrosis initiates the cycle of events that may lead to an acute CS. Volkmann ischemic contracture is a sequela of untreated or inadequately treated CS, in which necrotic muscle and nerve tissue have been replaced with fibrous tissue.

Acute CS typically occurs subsequent to a traumatic event, most commonly fractures.⁴ Chronic CS (CCS) is a recurrent syndrome that occurs with exercise or work. CCS characterized by pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed. Although more common in the anterior compartment of the lower leg, CCS has been described in the forearm of motocross racers and other athletes.^7,8,9

Pedowitz et al proposed criteria for the diagnosis of CCS, which requires one or more of the following¹⁰ :

• A resting compartment pressure of 15 mm Hg or higher
• A 1-minute postexercise compartment pressure of 30 mm Hg or higher
• A 5-minute postexercise compartment pressure of 20 mm Hg or higher (95% confidence level)

Frequency

In isolated humerus fractures or isolated forearm fractures, the incidence of compartment syndrome (CS) has been reported to be 0.6-2%. Patients with combined ipsilateral humerus and forearm fractures, however, have an incidence as high as 30%.¹¹ Overall, the prevalence of CS is much higher in cases in which there is an associated vascular injury. In a report by Abouezzi et al, fasciotomy was performed for 29.5% of isolated arterial injuries, 15.2% of isolated venous injuries, and 31.6% of combined arterial and venous injuries; and it was not related to venous repair or ligation.¹² Feliciano et al similarly reported that overall, 19% of patients with a vascular injury required fasciotomy.¹³

Etiology

Elevated intracompartmental pressure within the forearm is most common in the volar compartment or in the combined volar and dorsal compartments. Although rare, compartment syndrome (CS) may occur in the dorsal compartment alone.

CS may be the result of externally applied or internally expanding forces. It is most frequently associated with supracondylar fractures of the humerus, and it has been reported in conjunction with fractures of the radial or ulnar diaphysis, with surgical neck fractures of the humerus, and following Colles fractures.

Although trauma is the most common etiology, CS has been shown to occur in neonates from intrauterine malposition or strangulation of the extremity by the umbilical cord. It has also been recognized in association with crush injuries, vascular disruption, burns, infections, heroin intoxication, carbon monoxide intoxication, triceps contusions in football players, and avulsion of the triceps origin; following tourniquet or blood pressure (BP) cuff use; and even after minor trauma.

In addition, CS may be seen as a result of iatrogenic injury that is secondary to intraosseous infusion, the use of devices for pressurized intravenous (IV) infusion of parenteral hypertonic contrast agents, attempts at cannulating veins and arteries of the arm in patients on systemic anticoagulants or patients treated with thrombolytic drugs, the intraoperative use of a pressurized pulsatile irrigation system, and the use of a pump for infusion of fluids into the joint during an arthroscopic procedure. Chemotherapy drugs can produce true CS or mimic the pain and swelling of CS due to extravasation. Swaringen et al reported a rare case of multiple compartment involvement in a 10-year-old boy with influenza-induced myositis.¹⁴

CS that follows operations for orthopedic fixation (eg, open reduction and internal fixation [ORIF]) in the forearm is usually due to postoperative hematoma, muscle edema, or tight closure of the deep fascia. These risks can usually be minimized by releasing the tourniquet before wound closure to ensure that hemostasis is adequate and by closing only the subcutaneous tissue and skin.

A summary of CS etiologies is as follows:

• External restriction of the muscle compartment
  • Military antishock trousers (MAST) (CS in the lower extremity)
  • Tight splints, casts, dressings
  • Burns¹⁵
  • Tight fascial closure during ORIF (open reduction and internal fixation)
  • Lithotomy position (CS in the lower extremity)
  • Malfunctioning sequential compression devices (SCDs)
  • Tight ski boots (CS in the lower extremity)
  • Localized external pressure
• Internal increase in compartment volume/content
  • Hemorrhage (due to trauma, warfarin [Coumadin], tissue plasminogen activator [t-PA])^16,17
  • Hemophilia
  • Postischemic swelling
  • Fractures⁹
  • Postoperative hematoma/muscle edema
  • Gunshot wounds to the thigh (CS in the lower extremity)
  • Massive hypertonic IV fluid infusion
  • Drug/alcohol abuse and coma
  • Compartment fluid injection¹⁸
  • Snake envenomation
  • Nephrotic syndrome
  • Crush injuries, burns
  • Rhabdomyolysis¹⁹
  • Gastrocnemius or peroneus muscle tear (CS in the lower extremity)
  • Weight lifting, overuse of weights, exercise
  • Androgen abuse/muscle hypertrophy
  • Knee arthroscopy (CS in the lower extremity)
  • Ruptured Baker cyst
  • Influenza myositis
  • Seizure and eclampsia
  • Autoimmune vasculitis²⁰

Pathophysiology

Compartment syndrome (CS) occurs when an elevated intrafascial compartment pressure results in ischemia of muscle and nerve tissue. Although the inciting pathogenic factor in CS is increased tissue pressure, 3 theories have been proposed to explain the development of tissue ischemia, as follows:

• A critical closing pressure of the arterioles is reached, similar to the West zones in the lung, and the arterioles snap shut.²¹  
• Arterial spasm occurs from inflammatory mediators, from a nitric oxide pathway, or from elevated pressure alone.²²
• Thin-walled veins close when compartment pressure rises, but the veins reopen if blood continues to flow from the capillaries and elevates local venous pressure. The resulting narrowed arterial-venous perfusion gradient progresses until, eventually, muscle ischemia occurs.

Ashton examined the effect of increased compartment pressure on regional blood flow and concluded that at least 2 mechanisms were involved, as follows²² :

• Active closure of the arterioles when the transmural pressure is lowered, either by a decrease in intravascular pressure or by a rise in tissue pressure
• Collapse of soft-walled capillaries when tissue pressure rises

Skeletal muscle responds to ischemia by releasing histaminelike substances that increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood as the blood flows inward. One milliosmole is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment can attract sufficient fluid to cause a further rise in intramuscular pressure. With diminished blood flow, muscle ischemia and subsequent cell edema worsens. This vicious cycle of worsening tissue perfusion continues until eventual compartment tamponade occurs. The transmural pressure at which blood flow ceases depends on adrenergic tone, volume status, and other factors.

Within 6-10 hours, muscle infarction and nerve injury result. Muscle has considerable ability to regenerate by forming new muscle cells; therefore, it is extremely important to decompress ischemic muscle as early as possible. Cellular destruction and alterations in vascular membrane permeability lead to the release of myoglobin into the circulation. Advanced CS may result in rhabdomyolysis, or rhabdomyolysis may result in CS. For uncertain reasons, CS that is associated with surgical positioning may present later, with a mean time to presentation of 15-24 hours or longer postoperatively.²³

Reneman described the pathogenesis of chronic CS (CCS) in the leg.²⁴ Muscle bulk increases 20% during exercise and contributes to the transient increase in intracompartmental pressure. As the intracompartmental pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping.

Presentation

The patient afflicted by compartment syndrome (CS) may experience crescendo pain that is out of proportion to the original injury. The pain is deep and aching in nature and is worsened by passive stretching of the fingers. The patient may also describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of CS. The forearm is often tender and tense, and the sensibility/sensitivity of the fingertips may be diminished.

Paraesthesia, or numbness, is an unreliable early complaint of CS⁵ ; however, decreased 2-point discrimination is a more reliable early test and can be helpful to make the diagnosis. Botte and Gelberman reported that 4 of 9 awake patients with compartment pressures higher than 30 mm Hg had median nerve 2-point discrimination of more than 1 cm.²⁵ Correlation has also been reported between diminished vibration sense (256 cycles/s) and increasing compartment pressure.

On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of an evolving CS. Comparison of the affected limb to the unaffected limb is useful. Pulselessness is a late and unreliable finding, and the presence of a radial pulse does not exclude the possibility of a CS. The most important diagnostic physical finding is a firm, wooden feeling on deep palpation. Bullae may also be seen; however, so-called fracture blisters are common in the absence of CS. As the pressure increases, pallor and loss of pulses are late findings. If objective evidence of a motor deficit is found, the CS is far advanced. Laboratory testing that reveals a creatine kinase (CK) of 1000-5000 U/mL or greater or the presence of myoglobinuria can suggest CS.

CS in the hand most often occurs following iatrogenic injury in a patient who is obtunded in an intensive care unit. Symptoms may be nonspecific compared with those in other CS cases. Early recognition of this complication is based on physical examination and a high index of suspicion. Unlike elsewhere, CS in the hand lacks abnormalities in the sensory nerves, as no nerves are found within the compartments.

Consider the diagnosis when nonspecific aching of the hand, increased pain, loss of digital motion, and continued swelling are present. A tight, swollen hand in an intrinsic minus position—with the digits in metacarpophalangeal (MCP) extension and proximal interphalangeal (PIP) flexion—is highly indicative. Intrinsic tightness becomes evident on examination because motion of the PIP joint becomes dependent on the position of the MCP joint (more PIP motion is possible with MCP flexion than with MCP extension).

Chronic CS (CCS) is clinically distinct from the acute CS; it often occurs bilaterally, and pain may be reproducible at a specific workload or time interval. Most athletes cannot play through the severe pain, but symptoms tend to resolve within an hour of terminating the activity. Bilateral CCS should be suspected in patients who complain of bilateral exercise-induced pain in the anconeus muscle, the forearms, the thenar and hypothenar regions, and the first dorsal interosseous muscle. The symptoms are usually minimal during normal daily activities.

Indications

In the setting of the classic compartment syndrome (CS) presentation and physical examination findings, no further diagnostic studies are needed. No uniform consensus exists on the minimum pressure for which fasciotomy should be performed. Whitesides et al noted that fasciotomy should be performed when the compartment pressure rises to within 10-30 mm Hg of the patient's diastolic blood pressure (the so-called delta-P).⁴ Since then, many surgeons have used 30 mm Hg as a cutoff for fasciotomy. Mubarak and Hargens recommended that fasciotomy be performed for the following patients²⁶ : (1) those who are normotensive with positive clinical findings, who have compartment pressures of greater than 30 mm Hg, and whose duration of increased pressure is unknown or thought to be longer than 8 hours; (2) those who are uncooperative or unconscious, with a compartment pressure of greater than 30 mm Hg; and (3) those with low blood pressure and a compartment pressureof greater than 20 mm Hg.

The tolerance of tissue to prolonged ischemia varies depending on the type of tissue that is involved. Matsen showed that muscles have functional impairment after 2-4 hours of ischemia and irreversible functional loss after 4-12 hours.⁵ Nerve tissue shows abnormal function after 30 minutes of ischemia, with irreversible functional loss after 12-24 hours. Additional experimental data, however, have shown significant changes in somatosensory potentials as early as 45 minutes after compartmental pressure increases up to 30 mm Hg. If the compartment pressure is greater than 40 mm Hg, a fasciotomy is usually performed emergently, and fasciotomy is indicated if the pressure remains 30-40 mm Hg for longer than 4 hours. As a rule, when in doubt, the compartment should be released.

In the hand, surgeons should have a lower threshold for decompression; a compartmental pressure of greater than 15-20 mm Hg is a relative indication for release.

Relevant Anatomy

Four interconnected compartments of the forearm are recognized, as follows:

• Superficial volar (flexor) compartment
• Deep volar (flexor digitorum profundus, flexor pollicis longus, and pronator quadratus muscles and tendons) compartment
• Dorsal (extensor) compartment
• Compartment containing the mobile wad of Henry (brachioradialis, extensor carpi radialis brevis [ECRB], and extensor carpi radialis longus muscles and tendons)

Elevated pressures most commonly affect the volar compartments, but the dorsal and mobile wad compartments may also be involved, alone or in addition to the volar compartments. It is usually difficult to clinically differentiate isolated or combined involvement of the deep and superficial volar compartments.

In the wrist, most of the soft tissues are bound within rigid compartments. The volar wrist tendons, for the most part, are tightly constrained within the carpal tunnel (thumb and finger long flexor tendons), except for the flexor carpi radialis, flexor carpi ulnaris, and palmaris longus tendons, which are in separate compartments. Consideration of a carpal tunnel release is warranted when performing a volar release. Mostly, the dorsal compartments are channels for tendons and rarely are afflicted by CS.

The dorsal extensor tendons pass under an extensor retinaculum and are divided into 6 compartments, as follows:

• Radial wrist abductor (abductor pollicis longus tendon) and thumb extensor (extensor pollicis brevis tendon) dorsal to the trapezium bone
• Radial wrist extensors (extensor carpi radialis longus and ECRB tendons) dorsal and radial to the trapezoid bone
• Extensor pollicis longus tendon
• Common finger extensors (extensor digitorum communis [EDC] tendon) dorsal to the capitotrapezoid articulation
• Extensor digiti minimi tendon to the fifth digit
• Ulnar wrist extensor (extensor carpi ulnaris tendon) in a groove adjacent to the ulnar styloid

The hand has 10 compartments, as follows:

• Dorsal interossei (4 compartments)
• Palmar interossei (3 compartments)
• Adductor pollicis compartment
• Thenar compartment
• Hypothenar compartment

Contraindications

If compartment syndrome (CS) is diagnosed late, fasciotomy is of no benefit. In fact, fasciotomy probably is contraindicated after the third or fourth day following the onset of CS. When fasciotomy is performed late, severe infection usually develops in the necrotic muscle. However, if the necrotic muscle is left alone and the compartment is not open, it can heal with scar tissue. This may result in a more functional extremity with fewer complications. However, in the setting of an unclear syndrome duration, the surgeon should elect to decompress the indicated compartments.

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