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 exact mechanism that causes exertional compartment syndrome is unknown. The increased intra-compartmental pressures are thought to impede tissue perfusion, create a relative oxygen debt, and result in symptom onset. The exact mechanism by which this occurs remains unclear.
There are several proposed contributing factors, which vary from noncompliant anatomical tissues to deviations of anatomical features and build-up of metabolic byproducts.1 It has been recently suggested that venous outflow occlusion may play a significant role in increased compartment pressures and symptom development.2 Functional muscular compression and associated occlusion of vasculature has been proposed to create elevated hydrostatic pressures and fluid accumulation within the compartments, thereby explaining the elevated IMPs and common findings on imaging modalities.
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.3,4 A vast majority (87%) of patients with LLECS participate in sports, with running accounting for 69%.3
LLECS has a median age of onset of 20 years old, and the prevalence decreases with age, though it has been suggested that there is an underdiagnosed population within older adults, plateauing around age 50.5 Bilateral lower extremity involvement occurs in 85-95% of cases with a predilection for the anterior and deep compartments.5,6 The presence of unilateral symptoms is associated with prior trauma and vasculopathy.5 Risk factors include jumping, cutting, and skating 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.7,8 Amongst this group, women and Caucasian ancestry were found to be independent risk factors. The Army had the highest prevalence of LLCES.7
While there are conflicting reports, there is no clear sex bias. Most recently, a large study has found equal prevalence of CECS in males and females, however, males were more likely to receive a diagnosis of CECS; they also noted that findings of a higher prevalence of CECS in males in other studies may have limitations for interpretation due to selection bias of those enrolled.5 New research has also questioned if sex may influence the diagnostic testing criteria for CECS.
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.9 Most common associated activities were running then soccer.
Chronic exertional compartment syndrome predominantly affects the lower leg, although CECS may also present in the upper extremity and rarely in the upper leg. CECS of the foot has been reported and is likely under-recognized.10 This should be considered and assessed via a similar diagnostic pathway, though there are few studies into the diagnostic criteria, testing modalities, and therapeutic interventions.
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, intracompartmental fluid, and fascial thickening, whose effect is enhanced by a 20% muscle volume increase during strenuous physical activity.2,11
At a population level, involvement of the various compartments may follow different patterns. While they can present in isolation, a portion of patients may have multiple compartments contributing to their symptoms. For example, in those with anterolateral leg pain, the anterior and lateral compartments have simultaneous involvement in 58% of individuals, while the anterior and lateral compartments have isolated involvement in 26% and 7%, respectfully.12 These presentations more commonly affect bilateral lower extremities, while deep posterior compartment involvement may be more common in a unilateral presentation.5
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 Compartments 3,4,13
|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|
|Deep Posterior||Flexor hallucis longus muscle|
Flexor digitorum longus muscle
Posterior tibialis 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 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.
Symptoms begin as a sensation of tightness within a muscle compartment and advance to an aching, pressure-like discomfort.
Symptoms are reproduced at a clearly defined volume of exercise. Pain may progress to a sharp, burning quality, especially if one continues to engage in the provoking activity. Transient weakness and paresthesias may develop with correlation to the affected compartment(s).
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.14,15
It is important to note that it is not uncommon for symptoms to develop in multiple compartments over time. This may represent a natural progression of the condition or reemergence of symptoms in a new compartment after treatment, such as a fasciotomy.5
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.16 Recently, there has been some speculation if LLECS is associated with other forms of vascular pathology, including popliteal artery entrapment syndrome, or PAES, which also causes exertional leg pain.2,17
Essentials of Assessment
A thorough history and physical exam is paramount as LLECS is a clinically diagnosed pathology. The differential for exertional leg pain is broad and contains entities both rare and common. Targeted history should help distinguish if patients are asymptomatic at rest and develop tightness and aching pain within the affected muscular region at a specific, reproducible duration or intensity of exercise. In CECS, symptoms intensify with activity and cause discontinuation of provoking exercise stimulus. Upon rest, symptoms resolve, though they may last for several minutes after cessation, differing from PAD, where symptoms will likely resolve immediately.18
Table 2: Differential Diagnoses of Exercise-Associated Leg Pain19, 20
|Diagnosis||Distinguishing History||Physical exam||Key Diagnostic Testing|
|Popliteal Artery Entrapment Syndrome (PAES)||Insidious severe leg and foot claudicationLower extremity numbness, paresthesias, discoloration to pallor, and thermal changes||Calf hypertrophyPedal pulse aberrations with dorsiflexion / plantar flexion||Vascular studies: ABI, duplex ultrasonography, MR angiography|
|Peripheral Arterial Disease (PAD)||Exercise inducedResolution quickly following (<5 mins)||Decreased pulsationsTrophic changesDecreased cap refill||Vascular studies|
|Medial Tibial Stress Syndrome (MTSS)||Pain located over inner, distal 2/3s of tibiaabsence of other findings (feelings of fullness, paresthesias, etc)||Tenderness to palpation along posteromedial tibiaLocalized edema||MRI, bone scan|
|Stress Fracture||Focal painPersistent during rest||Localized tibial pain with palpationWorsened with hopping||XR, MRI, Bone scan|
|Fascial Hernia||Palpable muscle herniations Absence of other symptoms||Visible defects, +/- tenderness||MRI, ultrasound|
|MSK disorder (strain, tendon injury, etc)||Localized painAggravates with stretching||Often reproducible with targeted physical exam maneuvers||MRI, ultrasound|
|Nerve entrapment/ mononeuropathy/ polyneuropathy||Paresthesias or sensory deficitsLack of control||Objective sensory changesWeakness||EMG/NCS|
Findings are normal when performed at rest; therefore, patients need to undergo an exercise challenge to elicit symptoms. Once pain is produced, affected compartment(s) may have a bulging or full appearance and be firm and tender to palpation. Muscle herniations via fascial defects are found in 40% of cases.15 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.
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.11
Table 3 – Clinical Findings Consistent with Compartments Affected by LLECS 4,21,22,23
|Compartment||Motor Dysfunction||Sensory Impairment|
weak toe extension
foot drop (transient or persistent)
|paresthesias of dorsal foot|
1st web space numbness
|Lateral||weak foot eversion|
|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|
Several imaging modalities show promise in assisting with diagnosis of LLCECS when imaging is completed both at rest and during exercise, often either immediately post-exercise or during isometric contraction.
T2-weighted MRI images can detect increased intra-compartment signal intensity indicating edema, which correlates well with elevated IMP and has been found to have a high sensitivity (96%) and specificity (88%).25,26 All imaging studies need to be performed pre- and post-elicitation of symptoms. Near infrared spectroscopy (NIRS) measures hemoglobin saturation of tissues and thus detects variations of tissue oxygenation.24 This method of evaluation may also have limited applicability as thicker layers of adipose tissue negatively influence findings. While it has demonstrated high sensitivity (94%), specificity is significantly limited (20%).25 Single proton emission computed tomography (SPECT) has also been found to have a sensitivity of 80% and specificity of 97%.25 There may be some role for ultrasound shear wave elastography, though studies remain limited.27
These non-invasive diagnostic techniques are under investigation and 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. Currently, more publications are using imaging modalities in place of ICP monitoring due to some of the questionable diagnostic criteria cutoffs and increasing thoughts that vascular pathology may be playing a role in the etiology of CECS.2,17
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 the lower extremity. Though highly debated, the most widely accepted diagnostic values are 15 mm Hg at rest, 30 mm Hg at 1-minute post-exercise, and 20 mm Hg at 5-minutes post-exercise.28
Recently, there has been further debate on if this diagnostic criterion requires adjustment based on which compartment is being tested and the biologic sex of the patient. When examined separately in those with the diagnosis of CECS, the anterior and lateral compartments have been found to have significantly lower ICP, raising concern that the current diagnostic criteria may be too high to adequately capture some affected individuals. The patient’s height and biologic sex as also been noted to significantly increase the ICP of the lateral and anterior compartments, respectfully.29 Differences in intracompartmental pressure values across male and female cohorts, which is a key diagnostic tool, often used in combination with the Pedowitz reference values, for diagnosing CECS. Females were found to have lower intracompartmental pressure values in the anterior compartment.30 These findings are relevant for clinical interventions and diagnostic interpretations, as those with results just below the Pedowitz diagnostic threshold may require further follow-up to optimize care.30
Use of running shoes with a minimal heel and sole can reduce IMP by greater than 20 mm 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.14
Rehabilitation Management and Treatments
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.31 In one study, patients who completed 6 weeks of FFR training returned to play, reduced their pain, and improved their performance.16 In addition to implementing a FFR pattern to reduce loading of anterior and lateral compartments, formal gait retraining recommendations also include increasing cadence >180 steps/min to reduce stride length and adopting a more upright running posture to minimize ground reaction forces.32 In cases that fail conservative efforts, elective surgical intervention should be considered.
At different disease stages
If LLECS converts to an ACS, patients require emergent fasciotomy by an orthopaedic surgeon.
Encourage conservative management. If the inflaming activity is running, undergo gait analysis and subsequent training to develop forefoot running pattern and other retraining strategies.32 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.33,34
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.
If patients fail 6-12 weeks of conservative treatment, symptoms are produced at lower thresholds, and symptom intensity has increased, fasciotomy of the affected compartment(s) should be considered. There are multiple methods to perform this procedure, including open, subcutaneous, endoscopic-assisted subcutaneous, and ultrasound-guided percutaneous.11,35 Not 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 may be clinically indicated following a completed fasciotomy and subsequent recurrence of CECS symptoms.19,36
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.13
- 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.13,37
- Recurrence rates of LLECS range from 6-11% and are often secondary to incomplete release, suboptimal rehabilitation, and non-adherence to post-operative instructions.22
- There is a 15% surgical complication rate in athletes and military members.8
- Although a majority of patients’ symptoms improve after surgery, 58% of individuals may not be able to return to their pre-condition activity levels.38 Due to persistent symptoms, 17% of US military service personnel who underwent surgery for LLECS are medically discharged.8
- 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.11,23,37
Preliminary studies of the use of intramuscular botulinum toxin A injections show potential for reduction of IMP and pain without causing functional impairment. Despite the significant benefit from these case reports, this novel treatment warrants further investigation to establish proper dosing regimens, as well as elucidating its therapeutic mechanism and protocol for which muscles to target.2,27,39, 40,41,42,43 Ultrasound-guided percutaneous fenestration and/or fasciotomy have also been reported to alleviate symptoms.35,44 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/ Emerging and Unique 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.45 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.46,47 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.48
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. Further investigations are needed to highlight differences that may exist between the different compartments and between different patient populations: civilian vs military, male vs female, etc.5,29,30 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.49
Recent studies have been suggesting some overlap between CECS and vascular pathology.2,17 It will be imperative to continue investigations into this relationship if these entities exist on a spectrum or if they appear commonly present concomitantly.
CECS of the foot requires further development of diagnostic criteria and treatments to help drive awareness about the clinical entity.10
- Barbour TDA, Briggs CA, Bell SN, Bradshaw CJ, Venter DJ, Brukner PD. Histology of the zantfascial-periosteal interface in lower limb chronic deep posterior compartment syndrome. Br J Sports Med. 2004;38(6):709-717. doi:10.1136/bjsm.2003.007039.
- McGinley JC, Thompson TA, Ficken S, White J. Chronic exertional compartment syndrome caused by functional venous outflow obstruction. Clin J Sport Med. 2022;32:355–360
- Rajasekaran S, Kvinlaug K, Finnoff JT. Exertional leg pain in the athlete. PM R. 2012;4(12):985-1000. doi:10.1016/j.pmrj.2012.10.002.
- Detmer D, Sharpe K, Sufit RL, Girdley FM. Chronic compartment syndrome: Diagnosis, management, and outcomes. Am J Sports Med. 1985;13(3):162-170.
- de Bruijn JA, Zantvoort APM Van, Klaveren D Van, et al. Factors Predicting Lower Leg Chronic Exertional Compartment Syndrome in a Large Population. Int J Sports Med. 2018;39(1):58-66. https://doi.org/10.1055/s-0043-119225.
- Brewer RB, Gregory AJM. Chronic lower leg pain in athletes: a guide for the differential diagnosis, evaluation, and treatment. Sports Health. 2012;4(2):121-127. doi:10.1177/1941738111426115.
- Waterman BR, Liu J, Newcomb R, Schoenfeld AJ, Orr JD, Belmont PJ. Risk factors for chronic exertional compartment syndrome in a physically active military population. Am J Sports Med. 2013;41(11):2545-2549. doi:10.1177/0363546513497922.
- Wuellner JC, Nathe CD, Kreulen CD, Burnham KJ, Giza E. Chronic Exertional Compartment Syndrome: The Athleteʼs Claudication. Oper Tech Sports Med. 2017;25(2):52-58. doi:10.1053/j.otsm.2017.03.004.
- Beck JJ, Tepolt FA, Miller PE, Micheli LJ, Kocher MS. Surgical Treatment of Chronic Exertional Compartment Syndrome in Pediatric Patients. Am J Sports Med. 2016;44(10):2644-2650. doi:10.1177/0363546516651830.
- Ray R. Chronic exertional compartment syndrome of the foot. Clin Podiatr Med Surg. 2021; 38:143–164
- Murray MC, Heckman MM. Chronic Exertional Compartment Syndrome : Diagnostic Techniques and Management. Tech Orthop. 2012;27:75-78.
- Van Zantvoort APM, Hundscheid HPH, de Bruijn JA, et al. Isolated lateral chronic exertional compartment syndrome of the leg, a new entity?The Orthopaedic J of Sports Med. 2019; 7(12), 2325967119890105
- George CA, Hutchinson MR. Chronic exertional compartment syndrome. Clin Sports Med. 2012;31(2):307-319. doi:10.1016/j.csm.2011.09.013.
- 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;22(5):585-595. doi:10.1111/j.1600-0838.2011.01386.x.
- Bresler M, Mar W, Toman J. Diagnostic imaging in the evaluation of leg pain in athletes. Clin Sports Med. 2012;31(2):217-245. doi:10.1016/j.csm.2011.09.006.
- Diebal AR, Gregory R, Alitz C, Gerber JP. Forefoot running improves pain and disability associated with chronic exertional compartment syndrome. Am J Sports Med. 2012;40(5):1060-1067. doi:10.1177/0363546512439182.
- Johnson SEJ, Finnoff JT, Amrami KK, Jelsing EJ. Radiological prevalence of popliteal artery entrapment in individuals with anterior leg compartment chronic exertional compartment syndrome. Clin J Sport Med 2022; 32:e160–e164
- De Bruijn JA, Wijns KCA, van Kuijk SMJ, et al. Chronic exertional compartment syndrome in the differential diagnosis of peripheral artery disease in older patients with exercise-induced lower limb pain. jour Vascular Surg. 2020; 73 (6) 2114-2121
- De Bruijn JA, Winkes M, van Eerten P, Scheltinga M. Chronic exertional compartment syndrome as a cause of anterolateral leg pain. Unfallchirurg 2019 · 123 (Suppl 1):S8–S14
- Davis DD, Shaw PM. Popliteal Artery Entrapment Syndrome. [Updated 2022 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441965/
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- Gustafsson P, Crenshaw AG, Edmundsson D, Toolanen G, Crnalic S. Muscle oxygenation in Type 1 diabetic and non-diabetic patients with and without chronic compartment syndrome. PLoS One. 2017;12(10):1-12. doi:10.1371/journal.pone.0186790.
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Original version of the topic
Brionn K. Tonkin, MD, Alexander M. Senk, MD. Lower limb exertional compartment syndrome. Original Publication Date: 1/30/2014
Previous Revision(s) of the topic
Brionn K. Tonkin, MD, Alexander M. Senk, MD, Deborah Hudleston, MD. Lower limb exertional compartment syndrome. Original Publication Date: 9/6/2018
Alexander M. Senk, MD
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Kersten L Schwanz, MD
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Katherine Weir, MS
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