eMedicine Specialties > Orthopedic Surgery > Trauma

Compartment Syndrome, Lower Extremity

Author: Stephen Wallace, MD, Staff, Department of Emergency Medicine, Eastern Idaho Regional Medical Center
Coauthor(s): Stuart Goodman, MD, PhD, FRCSC, FACS, Associate Chairman, Professor, Department of Functional Restoration, Division of Orthopedic Surgery, Stanford University; Head, Division of Orthopedic Surgery, Stanford University Medical Center; Douglas G Smith, MD, Associate Professor, Department of Orthopedic Surgery, University of Washington, Harborview Medical Center
Contributor Information and Disclosures

Updated: Feb 9, 2009

Introduction

Compartment syndrome (CS) is a condition in which the perfusion pressure falls below the tissue pressure in a closed anatomic space, with subsequent compromise of tissue circulation and function. Each muscle or muscle group is enclosed in a compartment bound by relatively rigid walls of bone and fascia. The compartments of the lower leg and the volar forearm are particularly prone to developing elevated compartment pressures.

(Click Image to enlarge.) Single-incision fasciot...

(Click Image to enlarge.) Single-incision fasciotomy. Photographs courtesy of DG Smith, MD, Harborview Hospital, Seattle, WA.

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(Click Image to enlarge.) Single-incision fasciot...

(Click Image to enlarge.) Single-incision fasciotomy. Photographs courtesy of DG Smith, MD, Harborview Hospital, Seattle, WA.


(Click Image to enlarge.) Two-incision posteromed...

(Click Image to enlarge.) Two-incision posteromedial fasciotomy. Photographs courtesy of DG Smith, MD, Department of Orthopedics, Harborview Hospital, Seattle, WA.

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(Click Image to enlarge.) Two-incision posteromed...

(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.) Two-incision anterolate...

(Click Image to enlarge.) Two-incision anterolateral fasciotomy. Photographs courtesy of DG Smith, MD, Harborview Hospital, Seattle, WA.

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(Click Image to enlarge.) Two-incision anterolate...

(Click Image to enlarge.) Two-incision anterolateral fasciotomy. Photographs courtesy of DG Smith, MD, Harborview Hospital, Seattle, WA.


As many as 45% of all cases of CS are caused by tibial fractures. Other causes include any long-bone fracture, vascular injury, compression in the setting of a crush injury, drug overdose, and a tight cast or dressing. Late manifestations of CS include the absence of a distal pulse, extremity paresis, and hypoesthesia. If CS is strongly suspected in the clinical examination, operative decompression is the mainstay of therapy. Compartment-pressure measurements are usually reserved for diagnosing chronic CS, for evaluating comatose patients, or for other conditions in which the clinical examination findings are equivocal.

Although rhabdomyolysis and subsequent renal failure are among the most severe life-threatening complications, Volkmann contractures are the more commonly observed limb deformities. This article discusses the current understanding of CS of the lower extremity.

History of the Procedure

The original description of compartment syndrome (CS) was by Richard von Volkmann in 1872.1 Volkmann described contractures of the forearm muscles following tight bandaging for a closed reduction of an elbow fracture. The contractures resulted from ischemic muscle necrosis, which was later termed CS. In 1926, Paul Jepson published his classic paper in which he described prompt surgical decompression for the prevention of paralysis and contracture.2 In 1941, Bywaters and Beall published research on the occurrence of CS following significant crush injuries during World War II.3

In the early 1900s, capsule and balloon measuring devices were implanted surgically and used to make the diagnosis of CS. In 1968, the wick-catheter technique was introduced; its application for compartment-pressure measurements was popularized by Mubarak et al in 1976.4 Almost concurrently in 1976, Matsen et al documented the high incidence of CS and recommended an infusion technique for continuous compartment-pressure measurements.5 More recently, portable surgical-tissue-pressure monitoring devices that are convenient and easy to use have become available from commercial sources.

Chronic CS was not described until 1956 and was thought to be a form of shin splints (anterior tibial enthesitis).6 However, with the advent of the fitness boom and the increased popularity of endurance sports, additional research on exercise-induced leg pain has demonstrated that chronic CS is a well-defined clinical entity.

Problem

Compartment syndrome (CS) occurs whenever increased tissue pressure in a myofascial compartment compromises blood flow to the muscles and nerves within that compartment, resulting in tissue and nerve damage. Two types of CS have been identified, acute and chronic.

Acute CS typically occurs subsequent to a traumatic event, most commonly fractures. Symptoms worsen acutely, and irreversible nerve injury and muscle necrosis occur within hours.

Chronic CS (also known as chronic exertional CS, exertional CS, recurrent CS, or subacute CS) is a recurrent syndrome that occurs with exercise or work. Originally described in 1956, chronic exertional CS was previously thought to be an atypical form of shin splints.6 This syndrome is usually observed in competitive or collegiate athletes. Often, it occurs bilaterally, and similar to claudication, the pain it causes may be reproducible at a specific exercise distance or time interval. For example, most long-distance runners reproducibly experience the onset of pain within 15 minutes of initiating their run. Athletes may not be able to play through the severe pain. However, runners may be able to continue running with a modified flatfoot strike. Symptoms tend to subside within 1 hour of terminating the activity and are minimal during normal daily activities but return when activity is resumed.

Pedowitz et al proposed criteria for the diagnosis of chronic CS.7 One or more of the following is required:

  • A resting compartment pressure of greater than or equal to 15 millimeters of mercury (mm Hg)
  • A 1-minute postexercise compartment pressure of greater than or equal to 30 mm Hg
  • A 5-minute postexercise compartment pressure of greater than or equal to 20 mm Hg (95% confidence level)

Frequency

The incidence of acute compartment syndrome (CS) varies depending on the inciting event. DeLee and Stiehl found that 6% of patients with open tibia fractures developed CS, compared with only 1.2% of patients with closed tibia fractures.8

The reported incidence of CS may underestimate the true incidence because the syndrome may go undetected in severely traumatized patients. The prevalence of CS is much higher in patients who have an associated vascular injury. Feliciano et al reported that 19% of patients with vascular injury required fasciotomy, but other patients have an estimated 30% incidence.9 The true incidence of CS that is 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.

The incidence of chronic CS in athletes has not been determined.

Related eMedicine topics:
Tibia Fractures, Open

Diaphyseal Tibial Fractures

Tibial Plateau Fractures

Tibial Shaft Fractures

The Polytraumatized Patient

Etiology

Compartment syndrome (CS) may be the result of either externally applied compressive forces or internally expanding forces. Fractures, vascular injuries, deep venous thrombosis (DVT), overexertion, fluid sequestration, or prolonged compression (as from a cast or other cause) may lead to CS. As many as 45% of all CS cases are caused by tibial fractures. DVT rarely leads to CS, except in the most severe form of DVT, phlegmasia cerulea dolens.10,11 Acute CS has also been reported to follow minor trauma, such as twisting the calf while running, skiing on moguls, and weightlifting.12 Verdolin et al reported a case of bilateral lower extremity CS following prolonged surgery in the lithotomy position with the use of compression-stocking devices.13

Chronic CS is usually observed in long-distance runners, basketball players, skiers, and soccer players. This condition is usually the result of minor trauma or repetitive microtrauma (overexertion).

The etiology of CS is as follows:

  • External restriction of the lower extremity compartment
    • Military antishock trousers (MAST)14
    • Splints, casts, dressings15
    • Burns
    • Lithotomy position
    • Malfunctioning sequential compression devices (SCDs)
    • Tight ski boots
  • Internal increase in compartment volume
    • Hemorrhage (trauma, warfarin [Coumadin], tissue plasminogen activator [TPA])
    • Hemophilia
    • Fractures
    • Gunshot wound to thigh
    • Massive intravenous (IV) fluid infusion
    • Drug/alcohol abuse and coma
    • Compartment fluid injection
    • Crush injuries
    • Rhabdomyolysis
    • Gastrocnemius or peroneus muscle tear
    • Weightlifting or overuse of weights
    • Androgen abuse/muscle hypertrophy
    • Knee arthroscopy
    • Ruptured Baker cyst
    • Snake envenomation

Pathophysiology

Compartment syndrome (CS) develops after elevated compartment pressure causes muscle and nerve ischemia. Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure. This is also 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.16

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. With myocyte necrosis, 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 CS and postulated that within muscle compartments, a critical closing pressure exists (similar to West zone II in lung physiology).17 The 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. Untreated, within 6-10 hours, the final result of such high compartmental pressures is muscle infarction, tissue necrosis, and nerve injury. For unclear reasons, CS that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.18

Pressure-induced functional deficits are likely due to 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 CS may result in rhabdomyolysis, and conversely, rhabdomyolysis may result in CS.19 Patient mortality is usually due to renal failure or sepsis from difficult wound management.

The mechanism of CS 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.

The pathogenesis of chronic CS was described by Reneman.20 Muscle bulk increases 20% during exercise and contributes to the transient increase in intracompartmental pressure. Repetitive muscle contraction alone can increase intramuscular pressure to levels that may cause transient ischemia. Chronic CS occurs when the pressure between successive contractions remains high and impedes blood flow. As the pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping. The anterior and lateral compartments of the lower leg are commonly affected; the deep and posterior compartments are less commonly involved.

Presentation

The traditional 5 P's of acute ischemia in a limb (ie, pain, paresthesia, pallor, pulselessness, poikilothermia) are not clinically reliable and manifest only in the late stages of compartment syndrome (CS). Symptomatically, the patient with CS may experience crescendo pain that is out of proportion to the original injury. The pain is also deep and aching in nature and is worsened by passive stretching of the involved muscles. The patient may describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of CS. Paresthesia, or numbness, is an unreliable early symptom.

On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of a developing CS. Comparison of the affected limb to the unaffected limb is useful. Excessively vigorous examination of a tibial fracture should be avoided because this may exacerbate irritation of the deep posterior compartment.

In the clinical scenario in which there is evidence of trauma and gross deformity, a claw-toe deformity might occur; therefore, the patient should be evaluated for such a condition. Sensory nerves tend to be affected before the motor nerves, and selected nerves may be more susceptible than others in the same compartment. For example, in acute anterior lower leg CS, the first sign to present may be numbness between the first 2 toes (superficial peroneal nerve). Decreased 2-point discrimination is the most consistent early finding, and correlation has also been reported between diminished vibration sense (256 cycles/s) and increasing compartment pressure. On deep palpation, a firm wooden feeling is a specific sign when present. Bullae may also be observed. If objective evidence of a major sensory deficit or loss of peripheral pulse is found, the syndrome is far advanced.

Laboratory testing that reveals a creatine kinase (CK) measurement that is greater than or equal to 1000-5000 U/mL or demonstrates the presence of myoglobinuria may alert the physician to the occurrence of CS.

Patients with chronic CS typically have pain, a tight sensation, and weakness of the muscles of the involved compartment. In anterior CS, a runner may develop foot slap on heel-strike due to weakness of the tibialis anterior.

Indications

In the setting of classic compartment syndrome (CS) presentation and physical examination findings, no further diagnostic workup is needed. No consensus exists regarding the pressure for which fasciotomy should be performed. Whitesides et al noted that fasciotomy should be performed when compartment pressure rises to within 10-30 mm Hg of the patient's diastolic blood pressure (this value has been coined the delta-P).6 McQueen and Court-Brown, studying CS in dogs, affirmed the difference of 30 mm Hg between the compartment pressure and the diastolic blood pressure as a more reliable measure than absolute pressure measurements.21 Many surgeons now use a measured compartment pressure of 30 mm Hg as a cutoff for fasciotomy. Multiple pressure readings are often obtained, and the clinician must decide how to incorporate these readings with the clinical picture in the decision-making process.

In addition to direct pressure measurements, other less invasive compartment blood flow–measurement techniques have been studied. These include laser Doppler, methoxy isobutyl isonitrile–enhanced magnetic resonance imaging (MIBI MRI), phosphate nuclear MRI (P-NMR), thallium-201 (201 Tl) and technetium-99m (99m TC) sestamibi, and xenon (Xe) scanning.

In the setting of a vascular injury, a fasciotomy should be performed on high-risk patients before arterial exploration. High-risk patients include those with prolonged ischemia time, significant preoperative hypotension, associated crush injury, combined arterial and venous injury, or the need for a major venous ligation in the popliteal or femoral area.

Relevant Anatomy

  • Anterior compartment
    • Dorsiflexion muscles of the ankle and foot
      • Tibialis anterior
      • Extensor digitorum longus
      • Extensor hallucis longus
      • Peroneus tertius
    • Anterior tibial artery – Commonly injured in lateral tibial plateau fractures
    • Deep peroneal nerve – Provides sensation to the first dorsal web space
  • Lateral compartment
    • Peroneus brevis and peroneus longus – Plantar flexor and evertor muscles of the foot
    • Superficial peroneal nerve – Provides sensation to the dorsum of the foot
  • Deep posterior compartment
    • Plantar flexor and phalangeal flexor muscles
      • Tibialis posterior
      • Flexor digitorum longus (FDL)
      • Flexor hallucis longus
    • Posterior tibial and peroneal arteries
    • Posterior tibial nerve – Provides sensation to the sole of the foot
  • Superficial posterior compartment
    • Plantar flexor muscles of the foot
      • Gastrocnemius
      • Plantaris
      • Soleus
    • Sural nerve – Provides sensation to the lateral aspect of the foot and distal calf

Contraindications

If compartment syndrome (CS) is diagnosed late, fasciotomy is of little benefit. In fact, fasciotomy is probably contraindicated after the third or fourth day following the onset of CS, and when performed late, severe infection usually develops in the necrotic muscle.

More on Compartment Syndrome, Lower Extremity

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Workup: Compartment Syndrome, Lower Extremity
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Follow-up: Compartment Syndrome, Lower Extremity
Multimedia: Compartment Syndrome, Lower Extremity
References
Further Reading
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  67. Wilson SC, Vrahas MS, Berson L, Paul EM. A simple method to measure compartment pressures using an intravenous catheter. Orthopedics. May 1997;20(5):403-6. [Medline].

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Keywords

compartment syndrome, CS, chronic CS, chronic exertional CS, exertional CS, recurrent CS, subacute CS, Volkmann ischemia, chronic exertional compartment syndrome, exertional rhabdomyolysis, recurrent compartment syndrome, subacute compartment syndrome, fasciotomy, compartment release

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Contributor Information and Disclosures

Author

Stephen Wallace, MD, Staff, Department of Emergency Medicine, Eastern Idaho Regional Medical Center
Stephen Wallace, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Stuart Goodman, MD, PhD, FRCSC, FACS, Associate Chairman, Professor, Department of Functional Restoration, Division of Orthopedic Surgery, Stanford University; Head, Division of Orthopedic Surgery, Stanford University Medical Center
Stuart Goodman, MD, PhD, FRCSC, FACS 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.

Douglas G Smith, MD, Associate Professor, Department of Orthopedic Surgery, University of Washington, Harborview Medical Center
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

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

Managing Editor

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
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.

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Physicians of Indian Origin, American College of International Physicians, and American College of Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri
Jason H Calhoun, MD, FAAOS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, and American Orthopaedic Foot and Ankle Society
Disclosure: Nothing to disclose.

 
 
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