Chronic Exertional Compartment Syndrome

  • Author: Gregory A Rowdon, MD; Chief Editor: Craig C Young, MD  more...
Updated: Oct 08, 2015


Chronic exertional compartment syndrome (CECS) is a condition in athletes that can occur from repetitive loading or exertional activities. CECS is usually observed in competitive or collegiate athletes; long-distance runners, basketball players, skiers, and soccer players. Although it is most common in the lower legs, CECS can occur in any compartment of the extremities; for example, it has been described in the forearms of motocross racers and other athletes.[1, 2, 3]

CECS is characterized by exercise-induced pain that is relieved by rest. In some cases, weakness and paresthesia may accompany the pain. Onset of symptoms typically occurs at a specific exercise distance or time interval or intensity level (eg, within 15 min of initiating a run). Symptoms tend to subside with rest and are minimal during normal daily activities but return when activity is resumed.

Unlike acute compartment syndrome, which usually results from trauma, the pathophysiology of CECS is not well understood. CECS may result from ischemic changes within the compartment; however, multiple theories and mechanisms have been suggested (see Pathophysiology and Etiology).

Although physicians have been aware of CECS symptoms since the early part of the 20th century, it was not until the late 1950s that the first reports on CECS were documented. Mavor was the first to describe the entity in 1956 in a patient who experienced recurrent anterior leg pain with exertion that was associated with herniation of the muscle and numbness of the affected extremity.[4] In 1975, Reneman defined the clinical manifestations of CECS and identified increased intracompartmental pressure as the cause.

CECS was initially thought to be a form of shin splints (anterior tibial enthesitis).[5, 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 CECS is a well-defined clinical entity.

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. Compartment syndrome is a condition in which increased tissue pressure within a closed osteofascial compartment compromises blood flow to the muscles and nerves within that compartment, resulting in the potential for tissue and nerve damage (acute compartment syndrome), as well as in symptoms/disability (CECS).

Crush syndrome is distinct from compartment syndrome and occurs when primary muscle necrosis initiates the cycle of events that may lead to an acute compartment syndrome. Volkmann ischemic contracture is a sequela of untreated or inadequately treated compartment syndrome, in which necrotic muscle and nerve tissue have been replaced with fibrous tissue.

Compartment pressure readings with and without exercise are the gold standard for the diagnosis of CECS (see Workup).[7, 8, 9] A trial of conservative treatment may be undertaken for CECS, but symptoms generally recur when the patient returns to exercise.[10] If conservative treatment is unsuccessful, the patient should be referred to an orthopedic surgeon for consideration of fasciotomy (see Treatment).

For patient education information, see the Sports Injury Center.



A firm grasp of lower extremity anatomy is central to understanding the pathophysiology, diagnosis, and treatment of CECS. The lower leg is divided into 4 compartments: anterior, lateral, superficial posterior, and deep posterior. A fifth compartment, the tibialis posterior, has been documented, but its clinical significance has yet to be established.

The anterior compartment consists of the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius. The borders of this compartment are the tibia, fibula, interosseous membrane, and anterior intermuscular septum. Typically, the anterior compartment of the leg is the most frequently affected compartment in cases of CECS.

The lateral compartment includes the peroneus longus and brevis. Within the compartment lie the common peroneal nerve and its superficial and deep branches. This compartment is bordered by the anterior intermuscular septum, the fibula, the posterior intermuscular septum, and the deep fascia.

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

The deep posterior compartment lies between the tibia, fibula, deep transverse fascia, and interosseous membrane. The muscles within the deep posterior compartment are the flexor digitorum longus, flexor hallucis longus, popliteus, and tibialis posterior. Also within this compartment lie the posterior tibial artery and vein and the tibial nerve.

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



The pathology of CECS is not well established and is still debated; a general discussion follows.

CECS is associated with increased pressure in muscles at rest. Transient increases in compartmental pressure have been demonstrated experimentally as a normal response to exercise. Repetitive muscle contraction alone can increase intramuscular pressure to levels that may cause transient ischemia.

Elevated pressures usually normalize within 5 minutes after cessation of exercise. In CECS, however, 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.[11] Pressures may remain elevated for 30 minutes or longer in persons with CECS.

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.[12]

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. Changes in local vascular resistance (autoregulation) can compensate for some reduction in the local AV gradient. 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 a critical closing pressure exists within muscle compartments (similar to West zone II in lung physiology).[13] 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 that exceed 30 mm Hg and persist for 6-10 hours result in muscle infarction, tissue necrosis, and nerve injury. 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.[14, 15]

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 compartment syndrome may result in rhabdomyolysis (acute compartment syndrome); conversely, rhabdomyolysis may result in compartment syndrome.[16, 17]



CECS usually results from repetitive microtrauma (overexertion). It is typically observed in long-distance runners, basketball players, skiers, and soccer players.

The pain in CECS has been thought to derive from the same pathologic processes that cause pain in acute compartment syndrome—that is, compromise of the vascular supply, which leads to myoneural ischemia.

Various mechanisms have been suggested as to the cause of this tissue ischemia, including arterial spasm, capillary obstruction, arteriovenous collapse, or venous outflow obstruction. However, a magnetic resonance imaging (MRI) study conducted by Amendola et al showed that significant tissue ischemia does not develop.[18]

Other theories suggest that muscle hypertrophy and/or fascial inflexibility is the origin of pain in patients with this CECS. However, not all athletes with muscle hypertrophy develop compartment syndrome.

Another theory, the mechanical damage theory, posits that exercise results in myofibril damage and release of protein-bound ions. Frequent damage, such as that occurring in the anterior compartment of runners, results in an increased release of ions, increased osmotic pressure, and decreased blood flow within the compartment.

Despite these various explanations for the cause of pain in CECS, no single theory has been overwhelmingly accepted. Further investigation is needed, including that regarding the relationship between pain and compartment metabolites.



The true prevalence of CECS is uncertain. One United States study found a 14% prevalence rate of anterior CECS in individuals who reported lower leg pain.

Males and females are affected equally, although Kaper et al have suggested that women may be more susceptible than men to lower leg CECS.[19]

CECS usually occurs in well-conditioned athletes younger than 40 years. Athletes with CECS who markedly increase their training are at risk of developing exacerbation of this condition, as are inactive individuals who initiate rigorous training.



Surgical intervention generally has good success in patients with CECS, with success defined as the return to athletics without significant symptoms. For unknown reasons, the deep posterior compartment does not respond as quickly or as well to fasciotomy as the anterior compartment. In the anterior compartment of the leg, success rates usually exceed 85%. In the deep posterior compartment, success rates are approximately 70%.

In a study by Awbrey, 44 of 46 patients undergoing compartment release for lower leg CECS had excellent pain relief and unimpaired running at 1- and 9-year follow-up.[20]

The majority of complications can be attributed to surgical intervention or misdiagnosis. Complication rates of surgery have been reported in the 11-13% range; complications include hemorrhage, wound breakdown, complications from anesthesia, and postoperative infection.

In addition, surgical patients may experience persistent or CECS, Volkmann contracture, and permanent disability. Persistent pain with activity may result from incomplete or incorrect decompression of a muscle compartment. Recurrent CECS is thought to be related to severe scarring and subsequent closing of the compartment release. Mortality may result from renal failure or sepsis from difficult wound management.

Contributor Information and Disclosures

Gregory A Rowdon, MD Associate Clinical Professor, Department of Medicine, Division of Family Practice, Indiana University Medical Center; Team Physician, Purdue University

Gregory A Rowdon, MD is a member of the following medical societies: American College of Sports Medicine, American Medical Society for Sports Medicine

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.

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 Association for Physician Leadership, American College of Surgeons, American Medical Association, American Society for Surgery of the Hand, Arthroscopy Association of North America, Chicago Medical Society, Illinois State Medical Society

Disclosure: Received consulting fee from Depuy for speaking and teaching; Received honoraria from Pegasus for board membership.

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, Southern Orthopaedic Association

Disclosure: Nothing to disclose.

Stephen Wallace, MD Chief of Emergency Medicine, Sublette County Rural Health Care District

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

Disclosure: Nothing to disclose.

Stuart B Goodman, MD, PhD, FRCSC, 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, 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, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Steven I Rabin, MD Clinical Associate Professor, Department of Orthopedic Surgery and Rehabilitation, Loyola University, Chicago Stritch School of Medicine; Medical Director, Orthopedic Surgery, Podiatry, Rheumatology, Sports Medicine, and Pain Management, Dreyer Medical Clinic; Chairman, Department of Surgery, Provena Mercy Medical Center

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Russell D White, MD Clinical Professor of Medicine, Clinical Professor of Orthopedic Surgery, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center-Lakewood

Russell D White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Family Physicians, American Association of Clinical Endocrinologists, American College of Sports Medicine, American Diabetes Association, American Medical Society for Sports Medicine

Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Medical College of Wisconsin

Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Joseph P Garry, MD, FACSM, FAAFP Associate Professor, Department of Family Medicine and Community Health, University of Minnesota Medical School

Joseph P Garry, MD, FACSM, FAAFP is a member of the following medical societies: American Academy of Family Physicians, American Medical Society for Sports Medicine, Minnesota Medical Association, American College of Sports Medicine

Disclosure: Nothing to disclose.

  1. Claes T, Van der Beek D, Claes S, Verfaillie S, Bataillie F. Chronic exertional compartment syndrome of the forearm in motocross racers. Presented at: The European Sports Medicine Congress; Hasselt, Belgium; May 14-16, 2003.

  2. Goubier JN, Saillant G. Chronic compartment syndrome of the forearm in competitive motor cyclists: a report of two cases. Br J Sports Med. 2003. 37(5):452-3; discussion 453-4. [Medline]. [Full Text].

  3. Piasecki DP, Meyer D, Bach BR Jr. Exertional compartment syndrome of the forearm in an elite flatwater sprint kayaker. Am J Sports Med. 2008 Nov. 36(11):2222-5. [Medline].

  4. Blackman PG. A review of chronic exertional compartment syndrome in the lower leg. Med Sci Sports Exerc. 2000 Mar. 32(3 suppl):S4-10. [Medline].

  5. Whitesides TE, Haney TC, Morimoto K, Harada H. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop Relat Res. 1975 Nov-Dec. 43-51. [Medline].

  6. Whitesides TE Jr, Haney TC, Harada H, Holmes HE, Morimoto K. A simple method for tissue pressure determination. Arch Surg. 1975 Nov. 110(11):1311-3. [Medline].

  7. Roberts A, Franklyn-Miller A. The validity of the diagnostic criteria used in chronic exertional compartment syndrome: a systematic review. Scand J Med Sci Sports. 2012 Oct. 22 (5):585-95. [Medline].

  8. Tiidus PM. Is intramuscular pressure a valid diagnostic criterion for chronic exertional compartment syndrome?. Clin J Sport Med. 2014 Jan. 24 (1):87-8. [Medline].

  9. Roscoe D, Roberts AJ, Hulse D. Intramuscular compartment pressure measurement in chronic exertional compartment syndrome: new and improved diagnostic criteria. Am J Sports Med. 2015 Feb. 43 (2):392-8. [Medline].

  10. Wittstein J, Moorman CT 3rd, Levin LS. Endoscopic compartment release for chronic exertional compartment syndrome. J Surg Orthop Adv. 2008 Summer. 17(2):119-21. [Medline].

  11. Reneman RS. The anterior and the lateral compartmental syndrome of the leg due to intensive use of muscles. Clin Orthop Relat Res. 1975 Nov-Dec. 69-80. [Medline].

  12. Clayton JM, Hayes AC, Barnes RW. Tissue pressure and perfusion in the compartment syndrome. J Surg Res. 1977 Apr. 22(4):333-9. [Medline].

  13. Shrier I, Magder S. Pressure-flow relationships in in vitro model of compartment syndrome. J Appl Physiol. 1995 Jul. 79(1):214-21. [Medline].

  14. Beraldo S, Dodds SR. Lower limb acute compartment syndrome after colorectal surgery in prolonged lithotomy position. Dis Colon Rectum. 2006 Nov. 49(11):1772-80. [Medline].

  15. Wassenaar EB, van den Brand JG, van der Werken C. Compartment syndrome of the lower leg after surgery in the modified lithotomy position: report of seven cases. Dis Colon Rectum. 2006 Sep. 49(9):1449-53. [Medline].

  16. Rafiq I, Anderson DJ. Acute rhabdomyolysis following acute compartment syndrome of upper arm. J Coll Physicians Surg Pak. 2006 Nov. 16(11):734-5. [Medline].

  17. Walker JL, Smith GH, Gaston MS, Robinson CM. Spontaneous compartment syndrome in association with simvastatin-induced myositis. Emerg Med J. 2008 May. 25(5):305-6. [Medline].

  18. Amendola A, Rorabeck CH, Vellett D, et al. The use of magnetic resonance imaging in exertional compartment syndromes. Am J Sports Med. 1990 Jan-Feb. 18(1):29-34. [Medline].

  19. Kaper BP, Carr CF, Shirreffs TG. Compartment syndrome after arthroscopic surgery of knee. A report of two cases managed nonoperatively. Am J Sports Med. 1997 Jan-Feb. 25(1):123-5. [Medline].

  20. Awbrey BJ. Office diagnosis and intraoperative pressure-assisted fasciotomy for exercise-induced compartment syndrome. Paper (no. 395) presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; March 19-22, 1998; New Orleans, La.

  21. King TW, Lerman OZ, Carter JJ, Warren SM. Exertional compartment syndrome of the thigh: a rare diagnosis and literature review. J Emerg Med. 2010 Aug. 39(2):e93-9. [Medline].

  22. Rowdon GA, Richardson JK, Hoffmann P, Zaffer M, Barill E. Chronic anterior compartment syndrome and deep peroneal nerve function. Clin J Sport Med. 2001 Oct. 11(4):229-33. [Medline].

  23. Hayes AA, Bower GD, Pitstock KL. Chronic (exertional) compartment syndrome of the legs diagnosed with thallous chloride scintigraphy. J Nucl Med. 1995 Sep. 36(9):1618-24. [Medline]. [Full Text].

  24. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH. Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med. 1990 Jan-Feb. 18(1):35-40. [Medline].

  25. Edwards PH Jr, Wright ML, Hartman JF. A practical approach for the differential diagnosis of chronic leg pain in the athlete. Am J Sports Med. 2005 Aug. 33(8):1241-9. [Medline].

  26. Black KP, Taylor DE. Current concepts in the treatment of common compartment syndromes in athletes. Sports Med. 1993 Jun. 15(6):408-18. [Medline].

  27. Detmer DE, Sharpe K, Sufit RL, Girdley FM. Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med. 1985 May-Jun. 13(3):162-70. [Medline].

  28. Schepsis AA, Martini D, Corbett M. Surgical management of exertional compartment syndrome of the lower leg. Long-term followup. Am J Sports Med. 1993 Nov-Dec. 21(6):811-7; discussion 817. [Medline].

  29. Mouhsine E, Garofalo R, Moretti B, Gremion G, Akiki A. Two minimal incision fasciotomy for chronic exertional compartment syndrome of the lower leg. Knee Surg Sports Traumatol Arthrosc. 2006 Feb. 14(2):193-7. [Medline].

  30. Raikin SM, Rapuri VR, Vitanzo P. Bilateral simultaneous fasciotomy for chronic exertional compartment syndrome. Foot Ankle Int. 2005 Dec. 26(12):1007-11. [Medline].

  31. Styf JR, Körner LM. Chronic anterior-compartment syndrome of the leg. Results of treatment by fasciotomy. J Bone Joint Surg Am. 1986 Dec. 68(9):1338-47. [Medline]. [Full Text].

  32. Rorabeck CH, Fowler PJ, Nott L. The results of fasciotomy in the management of chronic exertional compartment syndrome. Am J Sports Med. 1988 May-Jun. 16(3):224-7. [Medline].

  33. Fronek J, Mubarak SJ, Hargens AR, ET AL. Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop Relat Res. 1987 Jul. 220:217-27. [Medline].

  34. Sebik A, Dogan A. A technique for arthroscopic fasciotomy for the chronic exertional tibialis anterior compartment syndrome. Knee Surg Sports Traumatol Arthrosc. 2008 May. 16(5):531-4. [Medline].

  35. Schepsis AA, Gill SS, Foster TA. Fasciotomy for exertional anterior compartment syndrome: is lateral compartment release necessary?. Am J Sports Med. 1999 Jul-Aug. 27(4):430-5. [Medline].

  36. Hutchinson MR, Ireland ML. Common compartment syndromes in athletes. Treatment and rehabilitation. Sports Med. 1994 Mar. 17(3):200-8. [Medline].

  37. Mar GJ, Barrington MJ, McGuirk BR. Acute compartment syndrome of the lower limb and the effect of postoperative analgesia on diagnosis. Br J Anaesth. 2009 Jan. 102(1):3-11. [Medline].

An illustration that depicts measurement of compartment pressures in the forearm.
Medscape Consult