eMedicine Specialties > Physical Medicine and Rehabilitation > Lower Limb Musculoskeletal Conditions

Compartment Syndrome

Abraham T Rasul Jr, MD, Medical Director for Rehabilitation, Specialty Hospital of Washington; Medical Director for Rehabilitation, St Thomas More Medical Complex; Founder, Arizona Golf Medicine Institute

Updated: Mar 11, 2009

Introduction

Background

In 1881, Richard von Volkmann reported the effects of ischemia on the soft-tissue components of a limb compartment. The contractures that developed were named after him. 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. The incidence of compartment syndrome varies depending on the patient population studied and the etiology of the syndrome. In a group of patients with leg pain, according to Qvarfordt and colleagues, 14% of them were noted to have anterior compartment syndrome.¹ Compartment syndrome was seen in 1-9% of leg fractures.

Related eMedicine articles:
Compartment Syndromes
Compartment Syndrome, Extremity
Compartment Syndrome, Lower Extremity
Compartment Syndrome, Upper Extremity
Volkmann Contracture

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 contained in a compartment of the limb. The second form, called exertional compartment syndrome, is associated with repetitive loading or microtrauma related to physical activity.^{2,3,4,5,6,7,8,9} Thus, compartment syndrome may be acute or chronic in nature.

Various theories have been proposed to explain the increase in compartment pressure.¹⁰ One commonly accepted theory is that the inflammatory response associated with trauma results in vascular permeability and vasodilatation that drives fluid out of the intravascular channels into the interstitial compartment. The presence of plasma proteins attracts more fluid into the compartment. Lactic acid has been shown to be in high concentration in the leg muscles of patients with exercise-induced pain.

The increase in compartment pressure has deleterious effects on the soft-tissue contents of the compartment. The increased tissue pressure results in decreased blood flow that, in turn, causes ischemia. Compartment pressures of 50 mm Hg have been associated with blood flow that has been decreased to 70%. At 80 mm Hg, the pressure has been reduced to 5%. Other studies have shown that compartment pressures return to normal after a fasciotomy.¹¹

How long can soft tissues tolerate the increased compartmental pressure? Whitesides and colleagues noted that muscle necrosis was seen when compartment pressures of 50 mm Hg were left for 4-8 hours. Compartment pressures of 40 mm Hg left for 6 hours were associated with early neuromuscular deficits, according to Sheridan and coauthors. According to Gelberman and colleagues, tissue pressures of more than 50 mm Hg applied to the median nerve for 4 hours resulted in sensorimotor abnormalities.

Clinical

History

The clinical presentation of patients with compartment syndrome is typically pain that appears out of proportion to the injury. In severe trauma, such as an open fracture, it is difficult to differentiate pain from the fracture from pain resulting from increased compartment pressure. In exertional compartment syndrome, pain is associated with prolonged or repetitive exercise and is relieved by rest.

Physical

• Common symptoms observed in compartment syndrome include a feeling of tightness and swelling. The 5 Ps (ie, pain, pallor, paresthesias, paralysis, pulselessness) are pathognomonic of compartment syndrome; however, these usually are late signs. Extensive and irreversible injuries to the soft tissues may have taken place by then.
• Peripheral pulses and capillary refill remain normal in most cases of acute compartment syndrome. The pain may be associated with paresthesia involving the superficial sensory nerve in that compartment.
• The acute syndrome most commonly involves the forearm and leg. With the chronic syndrome, the anterior pretibial compartment in the leg is most often involved. Gluteal and thigh involvement is uncommon.¹²
• Measurement of compartment pressures still remains the standard for diagnosis of compartment syndrome. Various methods, as well as equipment, can be used for this purpose. 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.
  • With the acute syndrome, the exact pressure threshold is controversial, but typical ranges are from 30-45 mm Hg at rest. Some sources state that it is better to associate this pressure to diastolic pressure (that is, within 10-30 mm Hg of diastolic pressure).
  • With chronic compartment syndrome, resting intracompartmental pressure above 15 mm Hg or exertional pressure greater than 30 mm Hg generally is considered to be elevated. A prolonged elevated pressure of more than 20 mm Hg for 5 minutes or more after completion of exercise also is considered to be abnormal.
  • In a 2009 study, Arato et al measured intracompartmental pressure and tissular oxygenation to determine the progression of compartment syndrome in patients who had undergone revascularization surgery for lower limb ischemia.¹³ The investigators used near-infrared spectroscopy to evaluate whether postsurgery oxygenation was low, an indication of insufficient secondary microcirculation. According to the study, the derived pressure and oxygenation measurements aided in determining whether patients required conservative or surgical treatment for compartment syndrome. 
• The first deficits may be subclinical, with a decrease in vibratory sensation to a 256 cycle per second tuning fork.
• A soft-tissue mass may be noticed as a result of herniation of fat and/or muscle tissue from the fascial defect that is often found in the lower third of the leg.

Causes

Trauma, fractures, bleeding in an enclosed space, external compression of the limb, vigorous exercise, small thrombotic or embolic events, and intramuscular injection have all been implicated in the pathogenesis of compartment syndrome.

Differential Diagnoses

Stress Fracture

Other Problems to Be Considered

Also consider periostitis (ie, shin splints) when entertaining the possible diagnosis of chronic compartment syndrome.

Workup

Laboratory Studies

• Additional workup is needed to rule out other associated pain-producing pathologies in the leg.
• With acute compartment syndrome, especially with trauma, consider obtaining workup for rhabdomyolysis (ie, creatine phosphokinase [CPK], renal functions, urinalysis, urine myoglobin).

Imaging Studies

• Stress fractures and periostitis can be diagnosed with plain radiographs, bone scans, computed tomography (CT) scans, or magnetic resonance images.¹⁴
• Vascular pathologies can be evaluated with arterial and venous Doppler ultrasonography. In some cases, a venogram or arteriogram may be necessary.
• Muscle tears can be observed using magnetic resonance imaging (MRI) or ultrasonography.¹⁵

Other Tests

• Measurement of compartment pressures, as mentioned earlier
• Nerve conduction studies are needed to evaluate nerve entrapment syndromes.

Procedures

• In unusual cases, muscle biopsies may be necessary in primary muscle disorders.

Treatment

Rehabilitation Program

Physical Therapy

Exertional compartment syndrome initially is treated differently from the trauma-induced form. A trial of conservative treatment may result in resolution of symptoms in exertional compartment syndrome. The conservative treatment mainly involves a decrease in activity or load to the affected compartment. The activity level gradually is increased, depending on the symptomatology. Aquatic exercises, such as running in water, can improve mobility and strength without unnecessarily loading the affected compartment. Massage and stretching exercises also have been shown to be effective, according to Hutchinson and Ireland.¹⁶

The patient who undergoes fasciotomy requires a physical therapy program to regain function. Postoperative care and rehabilitation is just as important as the procedure itself. During the immediate postoperative period, weight bearing is limited, and assistive devices (eg, crutches) are needed. Within a few days, and with adequate pain control, the use of crutches can be discontinued. The rehabilitation program then involves range of motion (ROM) and flexibility exercises involving the muscles of the affected compartment. Adjacent joints need to be exercised to maintain their normal ROM.

Once the patient is able to ambulate with a normalized gait pattern, a program of graduated resistive exercises (depending on the person's regular activities or work) is initiated. In the case of athletes, sports-specific exercises are started with the intention of returning to a regular athletic schedule. Cross training is also beneficial for these athletes. Activities such as swimming, pedal exercises, water jogging, or running help athletes to regain muscle strength and flexibility without loading the affected compartment.

Occupational Therapy

With surgical intervention for decompression, occupational therapy consultation should be considered early in the postoperative period for assessment of appropriate treatment and of the patient's deficits with regard to activities of daily living (ADL), as well as for instruction in the use of any necessary assistive device(s).

Medical Issues/Complications

Nonsteroidal anti-inflammatory drugs (NSAIDs) also have been shown to be helpful in relieving the discomfort of compartment syndrome.

Surgical Intervention

When compartment pressures are elevated, especially in acute settings, prompt surgical evaluation should be performed, since elevated pressures can, over a prolonged period, cause irreversible damage.^17,18 The exact pressure at which a fasciotomy may be performed is somewhat debatable.^4,6,8,9

Consultations

An orthopedic surgeon needs to be consulted early in cases in which acute compartment syndrome is suspected. With the chronic picture, if the initial intervention of decreasing the patient's activity level is not helpful or possible, then surgical decompression is necessary.

Other Treatment

Many authors advocate the use of hyperbaric oxygen therapy (HBO) for treatment of compartment syndrome.

Related eMedicine topics:
Hyperbaric Oxygen Therapy [Clinical Procedures]
Hyperbaric Oxygen Therapy [Plastic Surgery]
Hyperbaric Oxygen

Medication

Opioids, nonopioids, and NSAIDs can be used for pain management in compartment syndrome.¹⁹ Side effects and patient profiles should be considered when choosing medications. Acetaminophen can result in liver damage. Narcotics can produce gastrointestinal distress, constipation, and sedation, and they have addictive potential. NSAIDs can result in gastrointestinal upset, gastrointestinal bleeding, renal damage, and impaired coagulation.

Analgesic agents

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Acetaminophen (Tylenol, FeverAll, Aspirin Free Anacin)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Dosing

Adult

500-1000 mg PO q6h prn

Pediatric

Not established

Interactions

Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen (APAP) is contained in many OTC products, and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose

Opioid analgesics

These medications provide control of moderate to severe pain.

Hydrocodone and acetaminophen (Vicodin, Lorcet, Lortab)

Drug combination indicated for moderate to severe pain.

Dosing

Adult

1-2 tabs PO q6h prn

Pediatric

Not established

Interactions

Coadministration with phenothiazines may decrease analgesic effects; toxicity increases with CNS depressants or tricyclic antidepressants

Contraindications

Documented hypersensitivity; high altitude cerebral edema (HACE) or elevated intracranial pressure (ICP)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Tabs contain metabisulfite, which may cause hypersensitivity; caution in patients who are dependent on opiates, since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction

Nonsteroidal anti-inflammatory drugs

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Naproxen (Naprosyn, Aleve, Naprelan, Anaprox)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

500 mg PO bid prn

Pediatric

Not established

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Cyclooxygenase-2 inhibitors

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with cyclooxygenase-2 (COX-2) inhibitors than it is with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme; induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.

Dosing

Adult

200-400 mg PO qd or divided bid

Pediatric

Not established

Interactions

Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease plasma concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention, severe heart failure, and hyponatremia, because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction, or in abnormal liver lab results

Follow-up

Complications

• With late diagnosis, irreversible tissue ischemia can develop in the acute setting. Thus, permanent muscle and nerve damage, along with chronic pain, may occur. Peroneal nerve palsy, in particular, may develop. With muscle damage, muscle contractures may be observed.
• Infection is a major issue after fasciotomy and in some cases becomes 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.
• Calcific myonecrosis of lower extremity muscles has been identified as an uncommon late complication of posttraumatic compartment syndrome. On radiographs, peripheral calcifications may be observed around a fusiform mass.

Prognosis

• 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. 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, due to the morbidity associated with this procedure. In general, however, early diagnosis, with institution of the appropriate treatment, results in a good outcome.

Miscellaneous

Medicolegal Pitfalls

• Delay in diagnosis (or misdiagnosis) can lead to failure to provide appropriate treatment, increasing the risk of complications, such as nerve entrapment, vascular compromise, tissue necrosis, and/or chronic pain.
• As previously mentioned, the long-term prognosis for patients with posterior compartment syndrome is less favorable than that for patients with the anterior variety.
• If surgical management is undertaken, the usual surgical and postsurgical risks must be considered (eg, anesthesia risk, infection, deep vein thrombosis, pulmonary embolism).

References

1. Qvarfordt P, Christenson JT, Eklof B, et al. Intramuscular pressure, muscle blood flow, and skeletal muscle metabolism in chronic anterior tibial compartment syndrome. Clin Orthop. Oct 1983;(179):284-90. [Medline].

2. Amendala A, Rorabeck CH. Chronic exertional compartment syndrome. In: Welsh RP, Shepard RJ, eds. Current Therapy in Sports Medicine. 1985. Toronto, Canada: BC Decker; 250-2.

3. Blackman P, Bradshaw C, Crossley K. Chronic exertional compartment syndrome in the lower leg. A comparison of treatment options and outcome. International Conference of Science and Medicine in Sports, Brisbane, Australia. 1994;56-7.

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Keywords

compartment syndrome, fasciotomy, anterior compartment syndrome, compartmental syndrome, acute compartment syndrome, exertional compartment syndrome, compartment pressure, intracompartmental pressure

Contributor Information and Disclosures

Author

Abraham T Rasul Jr, MD, Medical Director for Rehabilitation, Specialty Hospital of Washington; Medical Director for Rehabilitation, St Thomas More Medical Complex; Founder, Arizona Golf Medicine Institute
Abraham T Rasul Jr, MD 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, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Rajesh R Yadav, MD, Assistant Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, 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, FAAPMR, FAAEM 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.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

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