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Overview

Practice Essentials

Acute compartment syndrome occurs when the tissue pressure within a closed muscle compartment exceeds the perfusion pressure and results in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event, most commonly a fracture.^[1]

The cycle of events leading to acute compartment syndrome begins when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products result in pain and decreased peripheral sensation secondary to nerve irritation.

Late manifestations of compartment syndrome 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 or if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis, and a limb contracture, called a Volkmann contracture, results. Severe cases may lead to renal failure and death.

The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Crush syndrome is distinct from compartment syndrome; it is defined as a severe systemic manifestation (eg, rhabdomyolysis) of trauma and ischemia involving soft tissues, principally skeletal muscle, as a result of prolonged severe crushing. Crush syndrome trauma or rhabdomyolysis may also lead to an acute compartment syndrome.

Chronic compartment syndrome (CCS) is a recurrent syndrome during exercise or work. CCS is characterized by pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed. Although CCS is more common in the anterior compartment of the lower leg, it has been described in the forearm of motocross racers and other athletes.^{[2, 3, 4]}For more information, see the Medscape Reference article Chronic Exertional Compartment Syndrome.

The incidence of compartment syndrome depends on the patient population studied and the etiology of the syndrome. In a study by Qvarfordt and colleagues, 14% of patients with leg pain were noted to have anterior compartment syndrome^[5]; compartment syndrome was seen in 1-9% of leg fractures.

Compartment syndrome may affect any compartment, including the hand, forearm, upper arm, abdomen, buttock,^[6]and entire lower extremity. Almost any injury can cause this syndrome, including injury resulting from vigorous exercise. Clinicians need to maintain a high level of suspicion when dealing with complaints of extremity pain.^[7]

The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. (See Treatment.)

Historical aspects

The original description of the consequences of unchecked rising intracompartmental pressures is widely attributed to Richard von Volkmann. His 1872 publication documented nerve injury and subsequent contracture from compartment syndrome following supracondylar fracture.^[8]That injury remains known as Volkmann contracture.

Although long bone fractures are a common cause of compartment syndrome, other injuries are also a common antecedent to compartment syndrome. Approximately 50 years after von Volkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction.^[9]

Wilson first described the initial case of exertional compartment syndrome in 1912. Mavor, in 1956, first reported a case of chronic compartment syndrome. Since then, various cases of compartment syndrome have been reported in the literature, and pathophysiology and treatment options have been discussed.

In 1941, Bywaters and Beall reported on the significance of crush injury while working with victims of the London Blitz. These pioneers revealed mechanisms and consequences of compartment syndrome. In the 1970s, the importance of measuring intracompartmental pressures became apparent.

Owen et al published a series of articles describing the use of the wick catheter for pressure measurement and then documented high compartmental pressures in various circumstances.^[10]Almost simultaneously, Matsen published his findings, which are the most commonly annotated group of articles in present literature.^[11]

Symptoms of acute compartment syndrome

Common symptoms observed in compartment syndrome include a feeling of tightness and swelling. Pain with certain movements, particularly passive stretching of the muscles, is the earliest clinical indicator of compartment syndrome. A patient may report pain with active flexion. The pain in compartment syndrome is often described as burning; it is also deep and aching in nature and is worsened by passive stretching of the involved muscles.

Workup in acute compartment syndrome

In a patient with the classic compartment syndrome presentation and physical examination findings, no laboratory workup is needed. Laboratory results are often normal, are not necessary to diagnose compartment syndrome, and are not helpful to rule out compartment syndrome. However, in acute compartment syndrome, especially with trauma, consider performing a workup for rhabdomyolysis, with measurement of the following:

Creatine phosphokinase (CPK)
Renal function studies
Urinalysis
Urine myoglobin

Muscle tears can be observed using magnetic resonance imaging (MRI) or ultrasonography.^[12]MRI may show increased signal intensity in an entire compartment on T2-weighted, spin-echo sequences.

Various methods and equipment can be used for compartment pressure measurement. A transducer connected to a catheter usually is introduced into the compartment to be measured. This is the most accurate method of measuring compartment pressure and diagnosing compartment syndrome. Measurement of the compartment pressure then can be performed at rest, as well as during and after exercise.

Management of acute compartment syndrome

The treatment of choice for acute compartment syndrome is early decompression. If the tissue pressure remains elevated in a patient with any other signs or symptoms of a compartment syndrome, adequate decompressive fasciotomy must be performed as an emergency procedure. Following fasciotomy, fracture reduction or stabilization and vascular repair can be performed, if needed.

If a developing compartment syndrome 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.^{[13, 14]}

In patients with tibial fracture and suspected compartment syndrome, immobilize the lower leg with the ankle in slight plantar flexion, which decreases the deep posterior compartment pressure and does not increase the anterior compartment pressure. (Postoperatively, the ankle is held at 90° to prevent equinus deformity.)

The definitive surgical therapy for compartment syndrome is emergent fasciotomy to release the involved compartment, with subsequent fracture reduction or stabilization and vascular repair, if needed.

The patient who undergoes fasciotomy requires a physical therapy program to regain function. Postoperative care and rehabilitation are just as important as the procedure itself.

Anatomy

Compartment syndrome may develop wherever a compartment is present. Possible sites include the lower leg, forearm, wrist, and hand.

Lower leg

The lower leg is divided into 4 compartments. A fifth compartment has been documented, but the clinical significance of this compartment has yet to be established. The 5 compartments are as follows:

Anterior
Lateral
Superficial posterior
Deep posterior
Tibialis posterior

Anterior compartment

Muscles in the anterior compartment are as follows:

Tibialis anterior
Extensor digitorum longus
Extensor hallucis longus
Peroneus tertius

The borders of the anterior compartment are as follows:

Tibia
Fibula
Interosseous membrane
Anterior intermuscular septum

Lateral compartment

The lateral compartment includes the peroneus longus and brevis. Within the compartment lies the common peroneal nerve superficial branch. The borders of this compartment are as follows:

Anterior intermuscular septum
Fibula
Posterior intermuscular septum
Deep fascia

Superficial posterior compartment

The superficial posterior compartment contains the gastrocnemius, soleus, and plantaris. It is surrounded by the deep fascia of the leg.

Deep posterior compartment

The muscles within the deep posterior compartment are as follows:

Flexor digitorum longus
Flexor hallucis longus
Popliteus
Tibialis posterior

Also within this compartment lie the posterior tibial artery and vein and the tibial nerve.

The borders of the deep posterior compartment are as follows:

Tibia
Fibula
Deep transverse fascia
Interosseous membrane

Tibialis posteriorcompartment

The tibialis posterior compartment is a more recently described subdivision of the deep posterior compartment. It consists of the tibialis posterior, which has been shown to have its own fascial layer.

Forearm

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

Superficial volar (flexor)
Deep volar
Dorsal (extensor) compartment
Compartment containing the mobile wad of Henry

The deep volar compartment contains the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus muscles and tendons. The mobile wad of Henry comprises the 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.

Wrist

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. The dorsal compartments are primarily channels for tendons and are rarely afflicted by compartment syndrome.

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

Hand

The hand has 10 compartments, as follows:

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

Pathophysiology

Compartment syndrome results primarily from increased intracompartmental pressure. The mechanism involved in the development of increased pressure depends on the precipitating event.

Two distinct types of compartment syndrome have been recognized. The first type is associated with trauma to the affected compartment, as seen in fractures or muscle injuries. The second form, called exertional compartment syndrome, is associated with repetitive loading or microtrauma related to physical activity.^{[15, 16, 17, 18, 19, 20, 21, 22, 23]}Thus, compartment syndrome may be acute or chronic in nature.

Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure, which is stated by the following formula:

LBF = (PA - PV)/R

In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance.

Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.^[24]

When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

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.

One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure. When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate.

Some reduction in the local AV gradient can be compensated for by changes in local vascular resistance (autoregulation). However, compartment tamponade occurs as arterial blood flow is occluded. Shrier and Magder questioned this traditional hypothesis for the pathophysiology of compartment syndrome and postulated that within muscle compartments, a critical closing pressure exists (similar to West zone II in lung physiology).^[25]These authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow.

The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures higher than 30 mm Hg require surgical intervention. If such high compartmental pressures are left untreated, within 6-10 hours, muscle infarction, tissue necrosis, and nerve injury occur. For unclear reasons, compartment syndrome that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.^[26]

Pressure-induced functional deficits are likely caused by decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion. In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis, and conversely, rhabdomyolysis may result in compartment syndrome.^[27]Mortality is usually due to renal failure or sepsis from difficult wound management.

The mechanism of compartment syndrome following vascular trauma may differ slightly from the above scenario because most cases occur with reperfusion. This reperfusion syndrome is likely related to the ischemic depletion of high-energy phosphate forms and ischemic muscle injury.

Muscle has considerable ability to regenerate by forming new muscle cells. Therefore, it is extremely important to decompress ischemic muscle as early as possible. Compartment pressures return to normal after a fasciotomy.^[28]

Etiology

Any internal or external event that increases pressure within a compartment can cause compartment syndrome. Thus, increased fluid content or decreased compartment size can lead to the condition.^[29]

Increased fluid content can be caused by the following:

Intensive muscle use (eg, tetany, vigorous exercise, seizures)^[30]
Everyday exercise activities (eg, stationary bicycle use, horseback riding^[31])
Burns^[32]
Envenomation
Decreased serum osmolarity (eg, nephrotic syndrome)
Hemorrhage (particularly from a large vessel injury)^{[33, 34]}
Postischemic swelling
Drug/alcohol abuse and coma
Rhabdomyolysis^[35]
Gastrocnemius or peroneus muscle tear (lower extremity)
Ruptured Baker cyst
Influenza myositis^[36]
Autoimmune vasculitis^[37]
Androgen abuse/muscle hypertrophy
Deep venous thrombosis^[38]

Fractures or gunshot wounds may be the source of hemorrhage underlying compartment syndrome.^[4]Upper extremity fractures most frequently associated with compartment syndrome are supracondylar fractures of the humerus, but cases have also been reported in conjunction with fractures of the radial or ulnar diaphysis, fractures of the surgical neck of the humerus, and Colles fractures.

Although trauma is the most common etiology, compartment syndrome has been shown to occur in neonates from intrauterine malposition or strangulation of the extremity by the umbilical cord.

Lying on a limb can cause compartment syndrome. In 1979, Owen et al published a landmark study in which researchers measured intracompartmental pressures in various positions common in drug overdoses.^[10]Average pressures were 48 mm Hg with the head resting on the forearm; 178 mm Hg when the forearm was under the ribcage; and 72 mm Hg when one leg was folded under the other.

A study by Shadgan et al indicated that in adult patients with tibial diaphyseal fractures, younger age is a risk factor for acute compartment syndrome. The study, of 1125 patients, found that the mean age of those who developed the syndrome was significantly below that of the rest of the cohort (33.08 years vs 42.01 years). Patient sex, whether the fracture was open or closed, and the use of intramedullary nailing were not found to be risk factors.^[39]

In contrast, in a retrospective study by Robertson et al of pediatric patients with supracondylar humerus fractures, regression analysis indicated that compartment syndrome is more likely to occur in patients who are older or male, as well as in those who exhibit a floating elbow fracture pattern or have neurovascular injury.^[40]

Another pediatric study, a literature review by Mortensen et al, indicated that in children, risk factors for the development of acute compartment syndrome include open radius/ulna fractures (odds ratio [OR]: 3.56), high-energy trauma (OR: 3.51), humerus fractures sustained concurrently with forearm fractures (OR: 3.49), open tibia fractures (OR: 2.29), and male gender (OR: 2.06).^[41]

A literature review by Mortensen et al involving adult patients indicated that risk factors for acute compartment syndrome include age 18-64 years (pooled OR: 1.34), male gender (pooled OR: 2.18), gunshot wound with fracture and vascular injury (pooled OR: 12.5), combined forefoot and midfoot injury (pooled OR: 3.3), an Injury Severity Score (ISS) of 0-9 compared with an ISS of greater than 9 (pooled OR: 1.58), Orthopaedic Trauma Association (OTA)/AO Foundation (AO) type C fracture (pooled OR: 2.75), vascular injury (pooled OR: 9.05), and high-energy trauma (pooled OR: 3.10).^[42]

A study by Bouklouch et al of over 200,000 patients with tibial fractures indicated that, regarding fracture location, proximal and midshaft tibial fractures increase the risk of acute compartment syndrome by the greatest amount. Moreover, open fractures were found to carry twice the risk of acute compartment syndrome, the OR being 2.20-2.42. Other reported risk factors included complex fractures, substance abuse disorders, cirrhosis, and smoking. The likelihood of discovering significant muscle necrosis was determined to be greater with fasciotomies for open tibial fractures than for closed fractures.^[43]

A study by Allmon et al of radiographic predictors of compartment syndrome in patients with tibial fractures found that each 10% increase in the ratio of fracture length to tibial length increased the odds of compartment syndrome by 1.67. The report also found that the likelihood of compartment syndrome after plateau fracture was 12%, compared with 3% and 2% for shaft and pilon fractures, respectively. In addition, patients with Schatzker VI fractures were at greater risk for compartment syndrome than were those with other types of Schatzker fractures, while in patients with plateau fractures, accompanying fibular fractures also raised the likelihood of compartment syndrome.^[44]

A retrospective cohort study by Wuarin et al indicated that risk factors for the development of acute compartment syndrome during the treatment of tibial shaft fractures include a distance of 15 cm or more from the center of the tibial fracture to the talar dome, associated tibial plateau or pilon fracture, closed fracture, and polytrauma.^[45]

In a study of nonfracture acute compartment syndrome in pediatric patients (37 children, 39 cases total), Livingston et al found that vascular causes were the most prevalent (28% of cases), followed by trauma (26%), postoperative causes (21%), exertion (15%), and infection (10%). The study also reported that pediatric nonfracture acute compartment syndrome was associated with a high rate of myonecrosis at surgery and with diagnostic delay (average of 48 h from symptom onset to diagnosis).^[46]

Iatrogenic causes

Iatrogenic causes of compartment syndrome include the following:

Military antishock trousers^[47]
Tight splints, casts, dressings^[48]
Lithotomy position (lower extremity cases)^[49]
Malfunctioning sequential compression devices
Intramuscular, intra-arterial, or intracompartmental injection^[50]
Intraosseous infusion
Massive hypertonic IV fluid infusion
Pressurized intravenous (IV) infusion of parenteral hypertonic contrast agent
Attempts at cannulating veins and arteries of the arm in patients on systemic anticoagulants or patients treated with thrombolytic drugs
Intraoperative use of a pressurized pulsatile irrigation system
Use of a pump for infusion of fluids into the joint during an arthroscopic procedure

Chemotherapy drugs can produce true compartment syndrome. Alternatively, extravasation of these drugs can cause pain and swelling that mimics compartment syndrome.

Compartment syndrome may follow operations for orthopedic fixation (eg, open reduction and internal fixation). These cases may result from 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.

In rare cases, acute compartment syndrome can develop in the lower leg after coronary artery bypass grafting (CABG), with systemic and local factors increasing the risk, according to a report by Te Kolste et al. The study, which involved five patients who developed acute compartment syndrome as a result of CABG, as well as a literature review, noted such risk factors as cardiopulmonary bypass, which can increase microvascular permeability; cardiac-assist devices, which can produce arterial occlusion and reperfusion injury; harvesting of the greater saphenous vein, which can result in hematoma; and, in patients with peripheral vascular disease, use of the lithotomy position and the employment of elastic bandages, which can reduce arterial blood flow.^[51]

Abdominal surgery can lead to well-leg compartment syndrome (WLCS), with a study by Christoffersen et al finding that of 40 prospectively collected cases of WLCS and 124 retrospectively collected cases, 68% of legs had under-knee support during the abdominal operation. The investigators also found that in 56% of cases, WLCS symptoms presented within 2 hours postsurgery.^[52]

Epidemiology

The anterior distal lower extremity is the most common studied site of compartment syndrome. Tibial fracture is the most common precipitating event, accounting for 2-12% of all compartment syndrome cases, according to the literature. In a retrospective study by McQueen and Court-Brown in 164 patients with diagnosed compartment syndrome, 69% of cases were associated with a fracture, and half of those involved the tibia. In the study, compartment syndrome was diagnosed more often in men than in women. This finding likely represents selection bias, however, because most patients with traumatic injuries are male.^[53]In a 10-year study, McQueen et al studied 850 patients and concluded that continuous intracompartmental pressure monitoring should be considered following tibial diaphyseal fracture because these patients are at risk for acute compartment syndrome.^[54]

The incidence of acute compartment syndrome varies depending on the inciting event. DeLee and Stiehl found that 6% of patients with open tibial fractures developed compartment syndrome, compared with only 1.2% of patients with closed tibial fractures.^[55]The reported incidence of compartment syndrome may underestimate the true incidence because the syndrome may go undetected in severely traumatized patients.

In the aforementioned study by Robertson et al of pediatric patients with supracondylar humerus fractures, acute traumatic compartment syndrome developed in approximately 2-3 fractures per 1000.^[40]

The frequency of compartment syndrome is much higher in patients who have an associated vascular injury. Feliciano et al reported that 19% of patients with vascular injury required fasciotomy^[56]; an incidence of 30% has also been suggested, but this figure is not well documented and is most likely an estimate. The true incidence of cases associated with vascular trauma may not be known because many vascular surgeons perform a prophylactic fasciotomy at the time of the vascular repair in high-risk patients.

Prognosis

Compartment syndrome outcome depends on both the diagnosis and the time from injury to intervention. Rorabeck and Macnab reported almost complete recovery of limb function if fasciotomy was performed within 6 hours.^[57]Matsen found necrosis after 6 hours of ischemia, which currently is the accepted upper limit of viability.^[58]

When fasciotomy was performed within 12 hours after the onset of acute compartment syndrome, Sheridan and Matsen reported that normal limb function was regained in 68% of patients.^[59]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 are delayed. Tendon transfers and stabilization may be indicated as late treatment for CS.

Long-term follow-up of patients who have undergone fasciotomies has shown good results, with a return to premorbid activity level. Pain also has been found to significantly improve.

In the lower leg, the results of fasciotomies for posterior compartment syndrome are not as good as those for the anterior compartment. A possible explanation is that it is difficult to do a complete decompression of the deeper posterior compartment, because of the morbidity associated with this procedure. In general, however, early diagnosis, with institution of the appropriate treatment, results in a good outcome.

With late diagnosis, irreversible tissue ischemia can develop in the acute setting. Thus, permanent muscle and nerve damage, along with chronic pain, may occur. In the lower leg, peroneal nerve palsy, in particular, may develop.

Volkmann contracture is the residual limb deformity that results over weeks to months following untreated acute compartment syndrome or ischemia from an uncorrected arterial injury. Approximately 1-10% of patients develop a Volkmann contracture.^[60]Calcific myonecrosis of lower extremity muscles has been identified as an uncommon late complication of posttraumatic compartment syndrome.

Recurrent compartment syndrome has been reported in athletes. It is thought to be related to severe scarring and the subsequent closing of the initial compartment release.

Infection is a serious complication of compartment syndrome. In a retrospective review by Matsen et al, 11 of 24 extremities that had late surgical decompression developed infections, and 5 of these infections led to an amputation.^[61]Infection after fasciotomy may become chronic. Patients, especially those with multiple traumatic injuries, may die because of infections or metabolic complications. Renal failure or multiple organ failure may occur preoperatively or postoperatively. Most fatalities are due to prolonged intensive care admissions with sepsis and multisystem organ failure.

Clinical Presentation

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Media Gallery

(Click Image to enlarge.) Volar release in the forearm. The upper illustration shows the incision that is used. The lower left picture depicts the relevant incisional anatomy. The lower right picture depicts the cross-sectional anatomy.
Surgical anatomy of the volar forearm. Photo courtesy of Dr. Smith, Harborview/UW Medical Center, Department of Orthopaedics, Seattle, Wash.
(Click Image to enlarge.) Two-incision anterolateral fasciotomy. Photographs courtesy of DG Smith, MD, Harborview Hospital, Seattle, WA.
(Click Image to enlarge.) Two-incision posteromedial fasciotomy. Photographs courtesy of DG Smith, MD, Department of Orthopedics, Harborview Hospital, Seattle, WA.
(Click Image to enlarge.) Single-incision fasciotomy. Photographs courtesy of DG Smith, MD, Harborview Hospital, Seattle, WA.
Picture of compartment pressure measuring device for use when commercial devices are unavailable.
Stryker STIC Monitor. Image courtesy of Stryker Corporation, used with permission.

of 7

Author

Abraham T Rasul, Jr, MD, FAAPMR, FCCP NeuroSciences, SLO

Abraham T Rasul, Jr, MD, FAAPMR, FCCP is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, American Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD Medical Director, Senior Products, Central North Region, Humana, Inc

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Acknowledgements

Samuel Agnew, MD, FACS Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma, University of Florida at Jacksonville College of Medicine; Consulting Surgeon, Department of Orthopedic Surgery, McLeod Regional Medical Center

Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic Association

Disclosure: Nothing to disclose.

Jason H Calhoun, MD, FACS Frank J Kloenne Chair in Orthopedic Surgery, Professor and Chair, Department of Orthopedics, The Ohio State University Medical Center

Jason H Calhoun, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Diabetes Association, American Medical Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Missouri State Medical Association, Musculoskeletal Infection Society, Southern Medical Association, Southern Orthopaedic Association, Texas Medical Association, and Texas Orthopaedic Association

Disclosure: Nothing to disclose.

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Stuart B Goodman, MD, PhD, FRCS(C), FACS, FBSE Robert L and Mary Ellenburg Professor of Surgery, Professor, Department of Orthopedic Surgery, Fellowship Director, Orthopedic Adult Reconstruction, Affiliated Faculty, Department of Bioengineering, Affiliated Faculty, Stanford Center on Longevity, Stanford University School of Medicine, Stanford University Medical Center

Stuart B Goodman, MD, PhD, FRCS(C), FACS, FBSE is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, California Medical Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Orthopaedic Trauma Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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

Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association

Disclosure: Nothing to disclose.

Rick Kulkarni, MD

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Eric L Legome, MD Chief, Department of Emergency Medicine, Kings County Hospital Center; Associate Professor, Department of Emergency Medicine, New York Medical College

Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Richard Paula, MD Assistant Professor of Emergency Medicine, Director of Research, University of South Florida College of Medicine

Richard Paula, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Steven I Rabin, MD Clinical Associate Professor, Loyola University Medical Center; Chair, Department of Orthopedic Surgery, Dreyer Medical Clinic

Steven I Rabin, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Fracture Association, AO Foundation, and Orthopaedic Trauma Association

Disclosure: Nothing to disclose.

Douglas G Smith, MD Associate Professor, Department of Orthopedic Surgery, Harborview Medical Center, University of Washington School of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Drug Reference Salary Employment

Jeffrey L Visotsky, MD Assistant Professor, Department of Clinical Orthopedic Surgery, Northwestern University, The Feinberg School of Medicine

Jeffrey L Visotsky, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association for Hand Surgery, American College of Physician Executives, American College of Surgeons, American Medical Association, American Society for Surgery of the Hand, Arthroscopy Association of North America, Chicago Medical Society, and Illinois State Medical Society

Disclosure: Depuy Consulting fee Speaking and teaching; Pegasus Honoraria Board membership

Stephen Wallace, MD Staff Physician, Department of Emergency Medicine, Memorial Hospital of Sweetwater County

Stephen Wallace, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Rajesh R Yadav, MD Associate Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas Medical School at Houston

Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.