Background

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.
Anatomy
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.
Pathophysiology
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]
Etiology
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.
Epidemiology
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.
Prognosis
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.

History
Chronic exertional compartment syndrome (CECS) is usually observed in competitive or
collegiate athletes. Patients report pain or tightness, cramping, burning, or aching over the
affected compartment during exercise. The affected extremity may feel weak.
The anterior and lateral compartments of the lower leg are commonly affected; the deep and
posterior compartments are less commonly involved. Case studies of CECS in the forearm,
thigh, [21] and gluteal regions have been published, but they are rare. CECS is often bilateral,
although involvement of a single extremity may occur.
Like claudication, the pain may develop predictably at a specific point in an exercise session (ie,
distance, time interval, level of intensity). 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.
A sense of fullness in the compartment typically has a gradual onset, which usually worsens as
activity progresses. Pain may be increased with active contraction and passive stretching during
symptomatic episodes. Commonly, the patient notes the sensation of weakness, which is usually
described as a loss of control of the affected extremity. For example, a runner may develop foot
slap on heel-strike due to weakness of the tibialis anterior muscle. Paresthesia or dysesthesia may
develop in the distribution of the affected nerve.
Symptoms tend to subside with rest. Any persistent symptoms are usually minimal during
normal daily activities.
The patient may note bumps or herniations over the affected compartment. The patient usually
denies any edema, temperature changes, or color changes of the affected extremity.
Physical Examination
Physical examination findings in patients with CECS are usually normal, unless the patient has a
history of recent exercise. The musculature in the affected compartment may feel firm or tense to
palpation.
If the anterior compartment is affected, the patient may exhibit weakness on dorsiflexion and
loss of sensation in the web of the first toe due to involvement of the deep peroneal nerve. [22] In
addition, evidence of muscle hernias is present in 20-60% of patients with anterior CECS.
If the lateral compartment is affected, the patient may exhibit weakness upon inversion, with loss
of sensation on the anterolateral part of the shin and the dorsum of the foot due to involvement of
the superficial peroneal nerve.
If the deep posterior compartment is affected, the patient may exhibit weakness in the foot
muscles and loss of sensation in the foot arch due to involvement of the tibial nerve.
The patient should have normal distal pulses. If the pulses are decreased, an arterial source
should be considered, and evaluation for arterial insufficiency including popliteal artery
entrapment should be undertaken.
The neurologic examination results should be normal. If not, then a primary neurologic process
should be considered.
Patients with CECS usually do not have tenderness over the posterior medial tibial cortex in the
distal leg. This contrasts with medial tibial stress syndrome, in which tenderness is typically
located in this area.
Patients with CECS usually do not present with focal tenderness with overlying edema. This
finding is more indicative of a stress fracture.

Diagnostic Considerations
The clinician must perform a full evaluation and assessment to appropriately diagnose chronic
exertional compartment syndrome (CECS). An error in diagnosis can lead to unnecessary
surgical procedures (eg, fasciotomy, fasciectomy), which may result in further complications.
One should consider the significant overlap between CECS and other lower extremity pain
syndromes and entities. These may include periostitis, tibial or fibular stress fracture, and
anterior tibial pain syndrome (ie, medial tibial stress syndrome, lateral tibial stress syndrome).
Other problems consider include the following:
 Infection
  Periostitis
 Vascular entrapment syndromes
 Vascular claudication
Differential Diagnoses
 Deep Venous Thrombosis
 Diphyllobothriasis
 Hypothyroid Myopathy
 Lumbosacral Radiculopathy
 Myopathies
 Nerve Entrapment Syndromes
 Spinal Stenosis
 Tumor

Approach Considerations
The diagnosis of chronic exertional compartment syndrome (CECS) may be one of exclusion,
based on the clinical history, the physical examination findings, and the exclusion of various
differential diagnoses. Compartment pressure readings with and without exercise are the gold
standard for the diagnosis of CECS. [7, 8, 9]
Laboratory studies are generally not helpful, but specific tests may be ordered to help rule out
other causes of lower leg pain on an individual case-by-case basis. Similarly, imaging studies are
not helpful in the diagnosis of CECS but may help rule out related disorders.
Blood and Urine Studies
The following studies may be useful for excluding other diagnoses in patients with suspected
CECS:
 Serum creatine kinase (CK) and myoglobin level (identifies myopathy or rhabdomyolysis)
 Urinalysis (UA) and urine myoglobin (rhabdomyolysis)
 D-dimer level (deep venous thrombosis)
 Complete blood cell count with differential (infection, osteomyelitis)
 Complete metabolic panel (metabolic derangements, acidosis, hypercalcemia,
hyperkalemia)
 Thyroid-stimulating hormone (thyroid myopathy)
  Erythrocyte sedimentation rate (ESR) (infection, rheumatologic conditions)
Lower-Extremity Imaging Studies
Imaging studies may help exclude related disorders in patients with suspected CECS.
Anteroposterior, lateral, and oblique views may help rule out stress fractures. In addition,
radiographs of the spine may help identify spinal stenosis or disc degeneration that may be the
source of lower extremity pain.
Bone scanning helps exclude stress fracture, periostitis, and malignancy of the lower extremity.
Ultrasonography can be performed to visualize blood flow (ie, to rule out hematoma, deep
venous thrombosis, or vascular entrapment).
Computed tomography (CT) scanning and magnetic resonance imaging (MRI) can help rule
other significant causes of chronic lower leg pain. MRI may be helpful in the diagnosis of CECS,
although its exact role is unclear. [18]
A study of thallous chloride scintigraphy with single-photon emission CT (SPECT) scanning
showed that thallous chloride scintigraphy with SPECT scanning was a sensitive method of
diagnosis. [23] The study was able to show (1) reversible areas of ischemia in the affected
compartment during exercise testing and (2) multiple compartments with elevated
pressures. [23] However, larger studies need to be conducted to prove the efficacy of this imaging
modality in CECS.
Compartment Pressure Testing
Compartment pressure readings with and without exercise are the gold standard for the diagnosis
of CECS. Pain reproduced during exercise in combination with elevated compartment pressures
can confirm the diagnosis. If symptoms are not reproduced with exertion, the diagnosis is less
certain. [7, 8, 9]
Most, but not all, sports medicine centers have the facilities to perform compartment pressure
testing. Occasionally, the clinician may have to rely on history and physical examination
findings. History and examination findings alone are not usually sufficient to confirm the
diagnosis of CECS; however, some authors do not advocate measurement of compartment
pressures when the findings of the history and clinical examination are clear and the patient is
selected for surgery.
For this procedure, a large-bore needle or a wick catheter is inserted into the affected muscular
compartment and is then connected to a solid-state pressure monitor. See the image below.
 An illustration that depicts
measurement of compartment pressures in the forearm.
Compartment pressure testing must be performed under sterile conditions. The needle tip
location, the depth of penetration, and the knee and ankle position are controlled to obtain
reliable measurements. The anterior, lateral, and superficial posterior compartments are
relatively easy to test; testing the deep posterior compartment is more difficult.
The generally accepted method of testing is to measure the resting compartment pressure,
exercise the patient until a symptomatic level is reached, and then measure again, noting pressure
readings at 1 minute and 5 minutes postexercise.
Pedowitz et al defined the criteria for the diagnosis of CECS in the leg. [24] One or more of the
following is required:
 A preexercise/rest pressure of 15 mm Hg or higher
 A 1-minute postexercise pressure of 30 mm Hg or higher
 A 5-minute postexercise pressure of 20 mm Hg or higher
Although the diagnosis of CECS) can be made if just 1 of the above criteria is met, the greater
the number of criteria that are satisfied, the greater the confidence level of the diagnosis.
Electromyography
Nerve conduction studies may be helpful for detecting neurologic involvement of affected
compartments. However, their role in the diagnosis of CECS is questionable. Such studies may
be helpful for excluding other related disorders such as peripheral nerve entrapment. One study
of pre- and postexercise electromyography demonstrated only a loss of the postexercise
amplitude potentiation in patients with CECS compared with controls.
Approach Considerations
A trial of conservative treatment may be undertaken for chronic exertional compartment
syndrome (CECS). However, symptoms generally recur when the patient returns to exercise. If
conservative therapy is unsuccessful, the patient should be referred to an orthopedic surgeon for
consideration of fasciotomy. [25, 26,27, 28]
Fasciotomy of the anterior compartment has a better outcome than fasciotomy of the posterior
compartment. [29, 30, 31, 32, 33] Furthermore, the rehabilitation phase is longer for patients who
undergo deep posterior compartment fasciotomy than it is for those who undergo anterior
compartment fasciotomy. The reasons for this difference in outcome remain unclear.
Multiple techniques have been described for fasciotomy of the lower leg. Newer techniques have
been developed to minimize the skin incision and maximize the fascial release. [34] For example,
Wittstein et al have suggested that "endoscopic assistance may minimize the intraoperative and
postoperative complications associated with compartment release and offer improved
cosmesis." [10] These investigators used a balloon dissector that was designed to address the
shortcomings of open and semi-blind techniques.
In cases of fasciotomy for anterior CECS, lateral compartment fasciotomy may not be necessary.
A study by Schepsis et al demonstrated similar outcomes in athletes with CECS who were
treated either by single-compartment or dual-compartment release. [35]
Recurrence after fasciotomy is unusual. If fasciotomy fails, the diagnosis of CECS should be
fully reevaluated. Repeat pressure measurements are usually required. For a true recurrence, a
second decompression is performed via fasciectomy and is usually successful.
Physical Therapy
Conservative therapy has been attempted for CECS, but it is generally unsuccessful; symptoms
typically recur once the patient returns to exercise. [10]Discontinuing participation in sports is an
option, but it is a choice that most athletes refuse.
Conservative therapy

Conservative treatment of CECS mainly involves a decrease in activity or load to the affected
compartment. The activity level gradually is increased, depending on the patient’s symptoms.
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. [36]

Presurgical therapy

Presurgical therapy in CECS includes reduction of activity, with encouragement of cross-training

exercises (eg, swimming, bicycling, other low-impact activities) and muscle stretching before
initiating exercise. This approach may also be helpful for primary prevention of CECS, although
only limited information is available on this topic. Other preoperative measures are rest, shoe
modification, and the use of nonsteroidal anti-inflammatory medications (NSAIDs) to reduce
inflammation. It is recommended to avoid casting, splinting, or compression of the affected limb.

Postsurgical therapy

Postsurgical therapy for CECS includes assisted weight bearing with some variation, depending
on surgical technique. Some physicians recommend immediate postsurgical range-of-motion
activity that may include walking (unaided by 3-5 d). Early mobilization as soon as is feasible is
recommended by many surgeons to minimize scarring, which can lead to adhesions and a
recurrence of the syndrome.
Activity can be upgraded to stationary cycling and swimming after healing of the surgical
wounds. Isokinetic muscle strengthening exercises can begin at 3-4 weeks. Running is integrated
into the activity program at 3-6 weeks. Full activity is introduced at approximately 6-12 weeks,
with a focus on speed and agility.

Medication Summary
Analgesics may be warranted in patients with chronic exertional compartment syndrome
(CECS), but they play a minimal role in the treatment of this condition. Acetaminophen and/or
nonsteroidal anti-inflammatory drugs (NSAIDs) can be used for pain management. [37]
Adverse effects and patient profiles should be considered when choosing medications.
Acetaminophen can result in liver damage. NSAIDs can result in gastrointestinal upset,
gastrointestinal bleeding, renal damage, and impaired coagulation.
Analgesic Agents
Class Summary
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)

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Acetaminophen is the drug of choice for pain in patients with documented hypersensitivity to
aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
Nonsteroidal Anti-Inflammatory Drugs
Class Summary
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action
may include inhibition of 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)

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Naproxen is indicated for relief of mild to moderate pain. This agent inhibits inflammatory
reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of
prostaglandin synthesis.
Ketorolac

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Ketorolac is an intravenously administered NSAID and a very powerful analgesic. It inhibits
prostaglandin synthesis by decreasing activity of the enzyme cyclooxygenase, which results in
decreased formation of prostaglandin precursors. In turn, this results in reduced inflammation.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

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Aspirin treats mild to moderate pain. It inhibits prostaglandin synthesis, which prevents
formation of platelet-aggregating thromboxane A2.

Ibuprofen (Advil, Motrin)

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Ibuprofen is usually the drug of choice for treatment of mild to moderate pain, if no
contraindications exist. It inhibits inflammatory reactions and pain by decreasing the activity of
the enzyme cyclo-oxygenase, resulting in inhibition of prostaglandin synthesis.

Celecoxib (Celebrex)

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Unlike nonselective NSAIDs, which inhibit both cyclooxygenase-1 (COX-1) and COX-2,
celecoxib primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme that is induced
during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI
toxicity. At therapeutic concentrations celecoxib does not inhibit COX-1; thus GI toxicity may
be decreased.
Although the higher cost of celecoxib can be a drawback, the incidence of costly and potentially
fatal GI bleeds is clearly less with this agent 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. Seek the lowest dose of celecoxib for each patient.