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Lower limb exertional compartment syndrome (LLECS), also known as chronic exertional compartment syndrome (CECS), is an overuse syndrome characterized by exercise-induced elevation of intramuscular pressures (IMP) that results in reproducible transient pain, paresthesias, and neuromuscular dysfunction. Symptoms are absent at rest, occur at a well-defined distance, duration or intensity of exercise, and only subside by discontinuation of provoking activity once elicited.


The increased intra-compartmental pressures impede tissue perfusion, causing a relative oxygen debt resulting in symptom onset. The exact mechanism by which this occurs remains unclear. However, there are several proposed contributing factors, which vary from noncompliant anatomical tissues to deviations of anatomical features and build-up of metabolic byproducts such as lactate.1

Epidemiology including risk factors and primary prevention

The incidence of LLECS in the general population is unknown; although some estimate that it accounts for 14-27% of previously undiagnosed exercise-induced leg pain. In fact, this may be under-appreciated secondary to poor awareness among medical providers and the public, as illustrated by an average of 22 months from symptom onset to treatment.2,3 A vast majority (87%) of patients with LLECS participate in sports, with running accounting for 69%.2 While there are conflicting reports, there is no clear gender bias. LLECS has a median age of onset of 20 years old, and the prevalence decreases with age.4 Bilateral lower extremity involvement occurs in 85-95% of cases with a predilection for the anterior and deep compartments.4,5 The presence of unilateral symptoms is associated with prior trauma and vasculopathy.4 Risk factors include jumping and cutting sports.  Location of LLECS can be sport or activity-dependent. The deep posterior compartment is more often affected in soccer players, while the anterior compartment is associated with speed skating and non-sports activities.

The United States military is considered a high-risk cohort with an adjusted annual incidence of up to 0.33-0.5 cases per 1000 person-years.6,7 Amongst this group, women and Caucasian ancestry were found to be independent risk factors.  The Army had the highest prevalence of LLCES.6

In the pediatric population, one study has suggested that females are at highest risk of LLECS with a peak age incidence of 16 years-old.8 Most common associated activities were running then soccer.


The lower leg is divided into 4 main compartments: anterior, lateral, superficial posterior and deep posterior. Each consists of specific muscles and nerves contained within non-compliant fascial and osseous boundaries. The anterior and deep posterior compartments contain the anterior tibial and posterior tibial artery and vein, respectively. The fascia surrounding the posterior tibialis muscle is theorized to form a 5th compartment.

Elevation of IMP is believed to occur in response to physiologic and pathologic changes, including muscle hypertrophy and fascial thickening, whose effect is enhanced by a 20% muscle volume increase during strenuous physical activity.9

Table 1 lists the components of the lower limb compartments.  Please note that fibularis musculature and fibular neurovascular structures are also known as peroneus or peroneal. 

Table 1 – Components of the Lower Limb Compartments2,3,10

Compartment Muscles Nerves Vasculature
Anterior Anterior tibialis muscle
Extensor hallucis longus muscle
Extensor digitorum longus muscle
Fibularis (peroneus) tertius muscle
Deep fibular (peroneal) nerve Anterior tibial artery and vein
Lateral Fibularis (peroneus) longus muscle
Fibularis (peroneus) brevis muscle
Superficial fibular (peroneal) nerve
Superficial Posterior Gastrocnemius muscle
Soleus muscle
Plantaris muscle
Sural nerve
Deep Posterior Flexor hallucis longus muscle
Flexor digitorum longus muscle
Posterior tibialis muscle
Popliteus muscle
Posterior tibial nerve Posterior tibial artery and vein
Fibular (peroneal) artery and vein
5th Posterior tibialis muscle

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

  • Acute
    • Acute compartment syndrome (ACS) is a separate and distinct etiology from LLECS. Although there is an extremely low risk of LLECS converting to ACS, quick recognition of its clinical features including pain, paresthesias, pulselessness, pallor, paralysis and poikilothermia is imperative as it is a surgical emergency that requires prompt evaluation by an orthopaedic surgeon.
  • Subacute
    • Symptoms begin as a sensation of tightness within a muscle compartment and advance to an aching, pressure-like discomfort.
  • Chronic/stable
    • Symptoms are reproduced at a clearly defined volume of exercise. Pain may progress to a sharp, burning quality, especially if patient continues to engage in the provoking activity. Transient weakness and paresthesias may develop with correlation to the affected compartment(s).
  • Pre-terminal
    • A lower threshold of activity is required for symptom provocation. They become more intense and last for a longer duration after cessation of causative action. Also, neuromuscular dysfunction may become more pronounced. Despite worsening of symptoms, no evidence of permanent cellular damage has been found in histologic studies.11,12

Specific secondary or associated conditions and complications

LLECS can occur in sedentary individuals, especially those with diabetes mellitus. Other predisposing conditions include supplementation with creatine monophosphate and anabolic steroids, secondary to fluid retention and rapid muscle hypertrophy. Aberrant gait mechanics, including rear foot landing and over pronation, contribute to exaggerated weight loading and strain on isolated muscle groups.13



A thorough history is paramount as LLECS is a clinically diagnosed pathology. Patients are asymptomatic at rest and develop tightness and aching pain within the affected compartment(s) at a specific, reproducible duration or intensity of exercise. Symptoms intensify with activity and cause discontinuation of provoking exercise stimulus. Upon rest, symptoms resolve.

Physical examination

Findings are normal when performed at rest; therefore, patient needs to undergo an exercise challenge to elicit symptoms. Once pain is produced, affected compartment(s) may have a bulging or full appearance and be tender to palpation. Muscle herniations via fascial defects are found in 40% of cases.12 Distal pulses are intact with warm extremities. Depending on the involved compartment(s), patients may demonstrate relative weakness and sensory impairment within a peripheral nerve distribution. For example, weak foot inversion with plantar paresthesias may represent posterior compartment involvement.  While ankle eversion weakness with development of an equinus deformity and anterolateral leg paresthesias may be attributed to lateral compartment involvement.

Functional assessment

Gait analysis should be performed as this can provide insight on the compartment involved and its severity. LLECS of the anterior compartment, which is the most commonly affected (45%), can cause dorsiflexion weakness, resulting in a transient or persistent foot drop.9

Table 2 – Clinical Findings Consistent with Compartments Effected by LLECS3,14-16

Compartment Motor Dysfunction Sensory Impairment
Anterior weak dorsiflexion
weak toe extension
foot drop (transient or persistent)
paresthesias of dorsal foot
1st web space numbness
Lateral weak foot eversion
weak dorsiflexion
equinus deformity
inversion deformity
1st web space numbness
paresthesias of dorsal foot
paresthesias of anterolateral distal shin
Superficial Posterior weak plantar flexion dorsolateral foot paresthesias
Deep Posterior weak foot inversion
weak toe flexion
cramping of foot intrinsics
paresthesias of medial arch of foot
5th weak inversion


Non-invasive diagnostic techniques are under investigation; however, their clinical utility warrants further investigation as there is a paucity of information regarding physiologic ranges, specifically fascial and compartment thickness, which eliminates the predictive value of ultrasound. Nevertheless, several studies show promise, especially near infrared spectroscopy (NIRS).17 NIRS measures hemoglobin saturation of tissues and thus detects variations of tissue oxygenation. Unfortunately, quantitative values cannot be extrapolated at the current time which eliminates the ability to develop diagnostic criteria. This method of evaluation may also have limited applicability as thicker layers of adipose tissue negatively influence findings. T2-weighted MRI images can detect increased intra-compartment signal intensity indicating edema, which correlates well with elevated IMP.18 All imaging studies need to be performed pre- and post-elicitation of symptoms.

Supplemental assessment tools

The gold standard for diagnosis is intra-compartmental manometry, which must be performed at rest, then 1 and 5 minutes post symptom-provoking exercise. This can be performed with fluid-filled catheters (needle, wick, or slit), transducer-tipped catheters, or solid-state transducer intra-compartment catheters (STIC). All instruments are reported to have comparable accuracy if used properly. Potential confounding variables include catheter depth, insertion distance and angle, underlying structures, muscle contraction and position of lower extremity. Though highly debated, the most widely accepted diagnostic values are 15mm Hg at rest, 30mm Hg at 1-minute post-exercise, and 20mm Hg at 5-minutes post-exercise.19


Use of running shoes with a minimal heel and sole can reduce IMP by greater than 20mm Hg secondary to biofeedback, which naturally encourages a forefoot running technique resulting in a decreased plantarflexion angle at heel strike and reduced eccentric contraction of anterior tibialis muscle due to reduced duration of plantarflexion.11


Available or current treatment guidelines

The mainstay of treatment is medical and rehabilitation management with activity modification, avoidance of provocation, rest, ice, stretching, and anti-inflammatory medications until resolution of symptoms. Other measures include deep tissue massage, osteopathic manipulative treatment, therapeutic ultrasound, orthotics and change of footwear. Unfortunately, symptoms tend to recur with reintroduction of the aggravating activity; however, studies examining the effect of forefoot running (FFR) biomechanics on LLECS renew hope of non-surgical treatment for running-induced LLECS in the 89% of shod runners with a rearfoot strike pattern.20 In one study, patients who completed 6 weeks of FFR training returned to play, reduced their pain, and improved their performance.13 In cases that fail conservative efforts, elective surgical intervention should be considered.

At different disease stages

  • Acute
    • If LLECS converts to an ACS, patient requires emergent fasciotomy by an orthopaedic surgeon.
  • Subacute
    • Encourage conservative management. If inflaming activity is running, undergo gait analysis and subsequent training to develop forefoot running pattern. Barefoot running or minimalistic shoes may help achieve this goal; however, they should not act as a substitute for professional guidance as one study demonstrated a low-conversion rate to FFR following an 8-week graduated running program without formal gait coaching.21,22
  • Chronic/stable
    • Continue conservative measurements. Elective fasciotomy may provide an alternative course for patients such as professional athletes who wish or need to continue engaging in their sporting activity.
  • Pre-terminal
    • If patient has failed 6-12 weeks of conservative treatment, symptoms are produced at lower thresholds, and symptom intensity has increased, fasciotomy of affected compartment should be considered. There are multiple methods to perform this procedure, including open, subcutaneous, endoscopic-assisted subcutaneous, and ultrasound-guided percutaneous.9,23 Note all techniques require inclusion of any hernias within the fascial incision. Patients who do not obtain relief with surgery may need to repeat the procedure with a more extensive release. Fasciectomy is reserved for recalcitrant cases.

Coordination of care

Treatment of LLECS requires an interdisciplinary approach that should be led by a physiatrist or sports medicine physician and include physical therapy and orthopaedic surgery as needed.

Patient & family education

  • Following symptom resolution with conservative management, patients should gradually resume the inciting exercise at a 10% increase in intensity or duration per week.
  • Surgical release of anterior and lateral compartments is associated with an 80-100% success rate.10
  • Fasciotomy of the deep posterior compartment has a success rate of 30-65%, attributed to more complex anatomy, inadequate visualization, and presence of 5th compartment.10,24
  • Recurrence rates of LLECS range from 6-11% and are often secondary to incomplete release, suboptimal rehabilitation, and non-adherence to post-operative instructions.15
  • There is a 15% surgical complication rate in athletes and military members.7
  • Although a majority of patients’ symptoms improve after surgery, 58% of individuals may not be able to return to their pre-condition activity levels.25 Due to persistent symptoms, 17% of US military service personnel who underwent surgery for LLECS are medically discharged.7
  • In order to maximize benefits from surgery and accelerate recovery, patients must control edema within the first 48 hours post-operation with compression wraps and elevation and immediately begin range of motion exercises to reduce adhesion formation.
  • Post-operative instructions and progression of activity can be surgeon and case-specific. However, the following strategy represents a generalized course of recovery.
    • A compression dressing typically stays intact for 48 hours.
    • For alleviation of pain and swelling, patients employ standard strategies including rest, ice, compression and elevation.
    • Active ankle range of motion exercises may be performed immediately and walking may begin on post-operative day 1 with crutches. The crutches may be weaned over a week per tolerance.
    • Non-impact activities to light jogging may be resumed within 2-4 weeks and run training within 6 weeks.
    • Sport specific drills may begin around 8 weeks with full recovery occurring around 8-12 weeks.9,16,24

Emerging/unique Interventions

Preliminary studies of the use of intramuscular botulinum toxin A injections show potential for reduction of IMP and pain without causing functional impairment; however, this novel treatment warrants further investigation to establish proper dosing regimens, as well as elucidating its therapeutic mechanism.26,27 Ultrasound-guided percutaneous fenestration and/or fasciotomy have also been reported to alleviate symptoms.23,28 Such ultra-minimally invasive techniques may offer symptom relief while optimizing cosmesis.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

LLECS is a relatively common cause of exertional leg pain that not only causes functional impairment but can impact patients’ quality of life. It predominantly affects younger runners. The most commonly involved compartment is the anterior, closely followed by the deep posterior. Non-invasive imaging studies are best suited to evaluate the superficial compartments, especially the anterior. Although intra-compartmental manometry is the gold standard for objective testing, the diagnosis of LLECS remains clinical. Conservative treatment with activity modification and rest is the mainstay of treatment; however, surgical intervention is a viable option for those unwilling or unable to discontinue the inciting activity.


Cutting edge concepts and practice

Simultaneous use of surface electromyography with intra-compartmental manometry looks to be a promising adjunct to the diagnosis of LLECS, as it can eliminate false positives caused by muscle contractions, which can create confounding elevation of IMP.29  Despite a case report of isolated absence of F-waves in a patient with LLECS, electrodiagnostic studies have no clinical value for diagnostic purposes, as transiently elevated IMP are not sustained long enough to produce electrical abnormalities.30,31 Histopathology studies of biopsied specimens from LLECS patients compared to controls have revealed lower capillary density and relatively thicker fascia but no consistent inflammatory markers. 1  Diagnostic ultrasound measuring compartment thickness is a non-invasive diagnostic test that requires further investigation and development of normative data.32


Gaps in the evidence-based knowledge

Prior studies designed to establish diagnostic IMP criteria for LLECS are fraught with methodological flaws. Additional studies are needed to identify normal values for IMP,fascial thickness and an optimal exercise protocol to aid the validation of a standardized diagnostic criteria.  Image-guided catheter placement may provide a higher diagnostic value as 58% of palpation-guided catheters meant for the deep posterior compartment have suboptimal to inaccurate placement.33


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Aweid O, Buono A, Malliaras P, et al. Systematic review and recommendations for intracompartmental pressure monitoring in diagnosing chronic exertional compartment syndrome of the leg. Clin J Sport Med. 2012;22(4):356-370.

Birtles DB, Rayson MP, Jones DA, Padhiar N, Casey A, Newham DJ. Effect of eccentric exercise on patients with chronic exertional compartment syndrome. Eur J Appl Physiol. 2003;88(6):565-571.

Original version of the topic

Brionn K. Tonkin, MD and Alexander M. Senk, MD. Lower limb exertional compartment syndrome. Original Publication Date: 1/30/2014

Author Disclosure

Brionn K. Tonkin, MD
Nothing to Disclose

Alexander M. Senk, MD
Nothing to Disclose

Deborah Hudleston, MD
Nothing to Disclose