You are in: eMedicine Specialties > Orthopedic Surgery > TRAUMA Compartment Syndrome, Upper ExtremityArticle Last Updated: Jul 27, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Stephen Wallace, MD, Staff, Department of Emergency Medicine, Eastern Idaho Regional Medical Center Stephen Wallace is a member of the following medical societies: American Academy of Emergency Medicine Coauthor(s): Douglas G Smith, MD, Associate Professor, Department of Orthopedic Surgery, University of Washington, Harborview Medical Center Editors: Jeffrey L Visotsky, MD, Assistant Professor, Department of Clinical Orthopedic Surgery, Northwestern University; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Samuel Agnew, MD, FACS, Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma, University of Florida at Jacksonville; Consulting Surgeon, Department of Orthopedic Surgery, McLeod Regional Medical Center; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Mary Ann E Keenan, MD, Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania Author and Editor Disclosure Synonyms and related keywords: CS, acute compartment syndrome, subacute compartment syndrome, subacute CS, chronic compartment syndrome, CCS, chronic exertional compartment syndrome, exertional CS, recurrent compartment syndrome, recurrent CS, crush syndrome, crush injury syndrome, Volkmann ischemia, Volkmann contracture, VC, Volkmann ischemic contracture, ischemic contractures, fasciotomy, compartment release INTRODUCTIONSection 2 of 12
  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. 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 the 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 based on 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. Compartment pressure measurements (see Image 1) are usually reserved for diagnosing chronic compartment syndrome (CCS), for evaluating comatose or anesthetized patients, or for situations in which the clinical examination findings are equivocal and the possibility of nonoperative management is likely. Some authors suggest documentation of compartment pressures in all cases, regardless of the clinical examination findings, yet others do not advocate measurement of compartment pressures when the findings on clinical examination are clear and the patient is selected for surgery. 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 von 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. History of the ProcedureThe first suggestion of a CS was made in 1872 in association with injuries that were sustained from surgical positioning.1 In his classic paper of 1881, von Volkmann described paralytic contractures of the forearm muscles after a patient was casted for closed reduction of an elbow fracture. He hypothesized that the contractures resulted from ischemic muscle necrosis, which resulted from vascular insufficiency that was caused by the tight casting. Thomas published a paper in 1909 in which he discussed 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 VC was the result of a CS that occurred from elevated pressures from intrinsic, extrinsic, or both sources.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 used 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). CCS, also known as chronic exertional CS, exertional CS, recurrent CS, and subacute CS, is a distinct entity from acute CS and was not described until 1956 and 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. ProblemThe literature is somewhat confusing due to the interchangeable use of the terms compartment syndrome; 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 CCS is a recurrent syndrome that occurs with exercise or work and is characterized by pain and disability that subside when the precipitating activity is stopped but 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
FrequencyIn isolated humerus fractures or isolated forearm fractures, the incidence of 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%.10 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.11 Feliciano et al similarly reported that overall, 19% of patients with a vascular injury required fasciotomy.12 (Note: These frequency data are from literature published by US authors studying US populations.) EtiologyElevated intracompartmental pressure within the forearm is most common in the volar compartment or the combined volar and dorsal compartments. Although rare, 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 has been reported in conjunction with fractures of the radial or ulnar diaphysis and 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 due to extravasation. Swaringen et al reported a rare case of multiple compartment involvement in a 10-year-old boy with influenza-induced myositis.13 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:
PathophysiologyCS 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:
Ashton examined the effect of increased compartment pressure on regional blood flow and concluded that at least 2 mechanisms were involved, as follows15:
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. Thus, a relatively small increase in osmotically active particles in a closed compartment can attract sufficient fluid to cause a further rise in intramuscular pressure. Thus, 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.16 Reneman described the pathogenesis of CCS in the leg.17 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. ClinicalThe patient afflicted by 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.18 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). 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. Suspect bilateral CCS 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. INDICATIONSSection 3 of 12
In the setting of the classic 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. In 1975, 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 BP (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 patients19: (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 BP and a compartment pressure of 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 ANATOMYSection 4 of 12
Four interconnected compartments of the forearm are recognized, as follows:
Elevated pressures most commonly affect the volar compartments, but the dorsal and mobile wad 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 when performing a volar release is warranted. Mostly, the dorsal compartments are channels for tendons and rarely are afflicted by CS.
The hand has 10 compartments, as follows:
CONTRAINDICATIONSSection 5 of 12
If CS is diagnosed late, fasciotomy is of no benefit. In fact, fasciotomy is probably 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. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Diagnostic Procedures
TREATMENTSection 7 of 12
Medical therapyIf a developing CS is suspected, place the affected limb or limbs at the level of the heart. Elevation is contraindicated because it decreases arterial flow and narrows the arterial-venous pressure gradient. Releasing one side of a plaster cast can reduce compartment pressure by 30%, bivalving can produce an additional 35% reduction,2 and complete removal of the cast reduces the pressure by another 15%, for a total decrease of 85% from baseline.21 Cutting Webril (Kendall Healthcare Products Co) may decrease compartmental pressure by 10-30%.22 Hence, when CS is identified or suspected, all bandages and casts must be removed. In cases of snake envenomation, administration of antivenin may reverse a developing CS. In the setting of an acute CS, capillary permeability is altered after 3 hours, resulting in postischemia tissue swelling of 30-60%. The role of mannitol in decreasing tissue edema is still under investigation; it may reduce compartment pressures and lessen reperfusion injury.23, 24 Ischemia that lasts 4 hours leads to significant myoglobinuria, which reaches a maximum about 3 hours after the circulation is restored but persists for as long as 12 hours. In the face of rhabdomyolysis, IV fluid administration and, potentially, bicarbonate may be used to keep urine output at 1-2 mL/kg/h. Contractures are produced after 12 hours of total ischemia. Relative hypertension and correction of acute anemia may help prevent the development of an impending acute CS. Ongoing research continues to examine the role of nitric oxide. The combination of hypovolemia, acidemia, and myoglobinemia may cause acute renal failure. Alkalization of the urine and diuresis appear to be renal-protective, presumably because hemoglobin and myoglobin are more soluble in an alkaline solution. Patients who survive the crush syndrome and acute renal failure almost always recover renal function, even those patients who require prolonged hemodialysis. Current recommendations are as follows:
In 2003, the Undersea and Hyperbaric Medical Society (UHMS) Hyperbaric Oxygen (HBO) Committee reported 13 major syndromes amenable to HBO, of which fourth on the list is crush injury, CS, and other acute traumatic ischemias.25 HBO promotes hyperoxic vasoconstriction, which reduces swelling and edema and improves local blood flow and oxygenation. It also increases tissue oxygen tensions and improves the survival of marginally viable tissue. At the time of surgical debridement, previous treatment with HBO aids in the demarcation of nonviable tissue. The best results are obtained when therapy is begun early. Twice-daily treatments at 2.0-2.5 atmosphere absolute (ATA) for 90-120 minutes are recommended for 5-7 days, with frequent examinations of the affected area. Surgical therapyThe fasciotomy technique is a matter of surgical choice. The goal is salvage of a functional extremity. In no way should the adequacy of decompression be compromised due to concern over cosmesis. It is essential to decompress all tight compartments, and the skin must be considered a potentially significant limiting structure.26 Decompression fasciotomy of the forearm is performed through a volar approach, a dorsal approach, or both. In the forearm, unlike the fascial compartments of the leg, the volar compartment, dorsal compartment, and mobile wad compartment (containing the brachioradialis and radial wrist extensors) are interconnected. Thus, fasciotomies of all 3 compartments may be unnecessary. Superficial fasciotomy is usually adequate to decompress the entire forearm.27 The flexor digitorum profundus and flexor pollicis longus muscles (deep volar compartment) are among the most severely affected muscles due to their deep location adjacent to the radius and ulna. Prefasciotomy and postfasciotomy pressures are often obtained from all compartments of the volar forearm, and if deep compartment pressures remain high after superficial fasciotomy, an additional release is indicated. Forearm fasciotomy requires decompression from the wrist to mid arm, including the lacertus fibrosus fascia, the fascial compartments over the flexor carpi ulnaris, and the edge of the flexor superficialis muscles. With median nerve involvement, in addition to carpal tunnel release, the surgeon must explore the nerve in the proximal forearm. The median nerve is decompressed throughout its course, including high-risk areas that are deep to the bicipital aponeurosis (lacertus fibrosus); between the humeral and ulnar heads of the pronator teres, the proximal arch, and deep fascial surface of the flexor digitorum superficialis; and the carpal tunnel.18 In the surgical treatment of hand CS, anatomically, 10 separate osteofascial compartments can typically be released with a carpal tunnel release and 1 or 2 dorsal incisions. The transverse carpal ligament also requires release. In the digits, 2 dorsal longitudinal incisions are usually made. Schnall et al, however, reported the use of an alternative approach for fasciotomy in cases of pyogenic flexor tenosynovitis28; this approach involved irrigation of the tendon sheath and leaving the lateral incision open, which allowed early active mobilization of the finger. Preoperative detailsProphylactic antibiotics against Staphylococcus aureus are generally recommended. Intraoperative detailsAfter standard surgical preparation and draping, no tourniquet should be used. Fasciotomy for acute compartment syndrome of the forearm: Volar Henry approach for superficial and deep flexors Volar ulna approach (similar to Henry approach) for extensor mechanism This approach is used to release the flexor carpi ulnaris and flexor digitorum superficialis. Watch the proximal edge of the flexor digitorum superficialis, and decompress the ulnar nerve at the wrist. Dorsal approach
Fasciotomy for acute compartment syndrome of the hand 1. Make 2 longitudinal dorsal hand incisions over the second and fourth metacarpals.
Image 2 shows the incision and relevant anatomy of a volar release. Image 3 shows the surgical anatomy of the volar forearm. Postoperative detailsThe postoperative details depend on the etiology of the CS and on the overall clinical condition of the patient. Elevate the affected extremity for 24-48 hours after surgery. If necrotic muscle develops, excise it. Tendinous attachments are retained if possible. Delayed primary closure of the skin can usually be accomplished at 5 days. If closure is not possible within 5 days, a split-thickness skin graft should be applied instead. The rehabilitation protocol is dependent upon the underlying mechanism of injury and the stability of the fracture reduction. Follow-upStandard suture removal and postoperative wound checks are indicated. Patients may require skin grafting if the skin defect is large. COMPLICATIONSSection 8 of 12
VC is the residual limb deformity that results over weeks to months following untreated acute CS or ischemia from an uncorrected arterial injury. Approximately 1-10% of CS cases develop a VC.2 Treatment of VCs can be found elsewhere. Recurrent exertional CS has occurred in athletes and is thought to be related to severe scarring and subsequent closing of the compartment release. OUTCOME AND PROGNOSISSection 9 of 12
If fasciotomy is performed within 12 hours after the onset of acute CS, the prognosis is good; Sheridan and Matsen reported that normal limb function was regained in 68% of patients in such cases.29 However, when fasciotomy was delayed 12 hours or longer, only 8% of patients had normal function. Thus, little or no return of function can be expected when the diagnosis and treatment for CS are delayed. Tendon transfers and stabilization may be indicated as late treatment for CS. FUTURE AND CONTROVERSIESSection 10 of 12
Controversy still exists regarding the treatment of CS that presents more than 3 days after the injury. Most authors suggest that fasciotomy is contraindicated due to the near universal occurrence of severe infection and the difficulty in managing necrotic muscle. Additionally, many authors remark that no generally accepted pressure threshold exists and that fasciotomy should be performed whenever the clinical impression favors the diagnosis of CS. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Compartment Syndrome, Upper Extremity excerpt Article Last Updated: Jul 27, 2007 | ||||||||||||||||||||||||||
