Chronic anterior exertional compartment syndrome: A conservative clinical pathway for CAECS

Author: By Steve “The Footman” Manning Founder of intraini  

This Article was the winner of the 2002 QUT

Texas Peak: Brooks Award for Sports Medicine


Chronic anterior exertional compartment syndrome (CAECS) is one differential diagnosis of shin pain. Neither the pathophysiology, nor the etiology is clearly understood.  Current theories are discussed and a number of pathomechanical etiologies are proposed.  Surgery appears to be the most definitive treatment with few conservative modalities discussed in the literature.  For this reason, a conservative clinical pathway has been developed to guide the podiatrist in treatment of this common cause of shin pain in athletes.


Since the early 1970’s ‘running boom’ began the number of individuals participating in regular endurance exercise has increased dramatically. Along with this increase in participation rates has been an equal increase in injury incidence and prevalence rates. This has generated new industries and activities to service this large group of active people - including sports medicine practitioners and researchers. There has been an evolution of sports medicine knowledge and an increasing sophistication in the sporting public. ‘Shin splints’ are a generic term that in most patient’s eyes can cover any cause of pain in the lower leg. Sports medicine practitioners have needed to develop more specific terms to differentiate conditions that exist in the leg. The new terms try to reflect the tissues affected and the different pathological processes. Chronic anterior exertional compartment syndrome is one common cause of leg pain. Table 1 gives a list of various differential diagnoses for Exercise Induced Leg Pain.

(Subotnik, 1999:287; Bouche, 2001:40; Bruckner and Khan 2002:511)

Overuse injuries:

  • Medial tibial stress syndrome, (tibial faciitis/periostitis)
  • Stress fractures and fractures
  • Muscle or tendon ruptures and strains
  • Bursitis (pes anserinus)
  • Delayed onset muscle soreness.

Claudication syndromes:

  • Compartment syndromes (acute/chronic)
  • Nerve entrapments and claudication (common peroneal for anterior CECS)
  • Popliteal and anterior tibial artery claudication
  • Venous claudication


  • Exertional rhabdomyolysis
  • Muscle cramps
  • Muscle herniation
  • Referred pain
  • Tumours
  • Hyperparathyroidism
  • Rickets
  • Pagets’s disease
  • Myositis ossificans
  • Neural irritation

Compartment syndrome has more recently been separated into ‘acute’ or ‘chronic exertional’ compartment syndrome (Hester, 2001:295).  This is to differentiate the two similar pathological conditions that have very different prognoses.  Both are thought to be the result of increased pressures within a fascial compartment.  The acute version has significantly higher pressures that do not resolve on rest.  Immediate surgical decompression is necessary to avoid necrosis of the neural and muscular structures (Bruckner and Khan, 2002:724).

The success of surgery may have influenced the treatment of the lower risk chronic form of compartment syndrome.  Little research has been conducted on conservative measures for CECS in comparison to surgical treatments.

The purpose of this paper is to give a thorough review of chronic exercise induced compartment syndrome with a focus on the possible pathomechanical etiologies of CECS of the anterior compartment.  A conservative clinical pathway will be suggested that is relevant for treatment by podiatrists.

Functional anatomy

The lower leg is anatomically divided into four compartments – anterior, lateral, deep posterior and superficial posterior with the posterior tibialis sometimes found to be a fifth compartment (Rorabeck, 1986).

These compartments are enclosed within fascial and osseous walls that resist expansion.  Compartments contain neurovascular structures as well as muscles, tendons and fascia.

The anterior compartment contains: (Subotnik, 1999:287)

The muscles:

  • Anterior tibialis
  • Extensor hallicus longus
  • Extensor digitorum longus
  • Peroneous tertius
  • The neurovascular structures
  • Deep peroneal nerve
  • The anterior tibial artery, its branches, and venae comittantes

And deep fascia.

It is bounded by:

  • The tibia medially
  • The fibula and the anterior intermuscular septum laterally
  • The interosseous membrane posteriorly

Fascial compartments of the leg

The muscles of the anterior compartment are all extensors of the foot causing primarily dorsiflexion with motion in the other planes dependent on the position of the foot and the insertion site of each muscle.

During the contact phase of gait they contract eccentrically to lower the foot to the ground while they contract concentrically during swing phase to gain ground clearance. (Michaud, 1997:54)


Since the early 1970’s ‘running boom’ began the number of individuals participating in regular endurance exercise has increased dramatically.  Along with this increase in participation rates has been an equal increase in injury incidence and prevalence rates.

This has generated new industries and activities to service this large group of active people - including sports medicine practitioners and researchers.  There has been an evolution of sports medicine knowledge and an increasing sophistication in the sporting public.

‘Shin splints’ are a generic term that in most patient’s eyes can cover any cause of pain in the lower leg.   Sports medicine practitioners have needed to develop more specific terms to differentiate conditions that exist in the leg.  The new terms try to reflect the tissues affected and the different pathological processes.

Chronic anterior exertional compartment syndrome is one common cause of leg pain.  Table 1 gives a list of various differential diagnoses for Exercise Induced Leg Pain.


A compartment syndrome can be defined as the increase in pressure within the limited anatomical space of a fascial compartment “which compromises the circulation and function of the tissues within that space resulting in temporary or permanent damage to muscles and nerves” (Bouche, 2001:44).  The pressure can be from increased volume of tissues within the compartment or external pressure.  (Guten, 1997:126)  If compartment volume is limited or decreased due to tight or thickened fascia (Subotnik, 1999:286) then compartment pressures can increase upon normal muscle swelling during exercise.


 Exercise increases the oxygen demands on muscular tissue.  Increased compartment pressures somehow cause local ischemia reducing oxygen supply to muscle tissue. Pain and muscle dysfunction is probably the result of the oxygen demands of the exercising muscles exceeding the supply through blood flow.  There are a number of possible theories of why muscular ischemia may occur.

Arterio-venous gradient theory

The most current theory is that when increased fluid pressure causes internal compression on vascular structures above the critical threshold level of capillary perfusion pressure, local flow is restricted leading to ischemia and compromised tissue function and viability (Bouche, 2001:44, Guten, 1997:126).

Muscle hypertrophy theory

Blackman (2000:S5) says muscle volume increases of 20% are normal during exercise but that chronic exercise may cause lasting hypertrophy.  Contrary to some studies Chalk, McPoil and Cornwall (1995:470) found no variation in foot volume before and after exercise.

Fascial sclerosis theory

Bruckner (2000:S1) says that muscle compartments may become swollen and painful especially if there is excessive scarring of the fascia. Blackman (2000:S5) says there is some suggestion that fascial hypertrophy can cause the deep fascia to become tight and unyielding.



Guten states that runners average one injury for every 250 hours of running or one to two injuries per year, with shin splints making up about 20% of those injuries (1997:61).   CECS has been estimated to occur in 5-15% of Runners. (Guten, 1997:126). CECS has also been linked to soccer players (Martens and Moeyersoons, 1992:23) and inline skaters (Garcia-Mata, 2001).

The anterior compartment is more frequently affected then the other compartments (Hester 2001:292), and more commonly occurs in running then other sports (Martens and Moeyersoons, 1992:23).

Considering that the patient profile of CECS is sports participants, the possibility that overuse is a factor is very high. Guten says CECS can follow episodes of intensive running or endurance activities (1997:126).

Acute Compartment syndrome is more likely the result of trauma or tight casts and dressings and is not specifically sports related (Guten, 1997:126), however Esmail Flynn, Ganley, Pill and Harnly (2001) discuss a case of exercise induced acute anterior compartment syndrome.

Mechanic with ideal performance

Heelstrike to FF loading (Contact):

While running, maximum activity of the anterior leg muscles occurs just after heel strike to decelerate ankle plantarflexion (Michaud 1997:54). Eccentric contraction smoothly lowers the forefoot to the ground (Cavanagh, 1990:176).  Tibialis anterior maintains the forefoot in an inverted position along the MTj axis.  It should be noted that the ideal mechanics of heelstrikers cannot be directly transferred to midfoot or forefoot strikers.

FF loading to Heel lift (Midstance):

During midstance the anterior compartment muscles relax although some authors say that the group contracts concentrically to pull the leg over the foot (Cavanagh, 1990:176).

Heel lift to toeoff (Propulsion):

The group then stabilizes the foot as antagonists during propulsion.  EDL and Peroneus Tertius act to dorsiflex the ankle while maintaining a pronated oblique Mtj axis. Tib Ant assists ankle dorsiflexion while dorsiflexing and inverting the first ray.  EHL maintains tension on the hallux (Michaud 1997:54).

Swing phase:

The anterior group contracts concentrically during early swing to gain ground clearance. They then have a period of relaxation before contracting again to prepare for ground contact. The oblique Mtj axis is pronated while the forefoot is inverted around the longitudinal Mtj axis. (Michaud 1997:54). At terminal swing phase the foot is in varus in relation to the ground.  The amount of varus increases in relation to velocity.  This is important to shock attenuation if the anterior compartment is dysfunctional.

Studies on changes in shock attenuation after arthrodesis have indicated that ankle dorsiflexion rather than subtalar joint pronation is the main neuromuscular dampener on excessive shock in the foot. (Thomas et al, 2000)

Common pathomechanics

A large range of pathomechanical etiologies can contribute to CECS.  Most of these are related to overloading the tissues due to excessive movement or velocity of movement.  Table 4 explores some of the possible pathomechanics.

If the anterior muscles are dysfunctional then the most common result will be footdrop and slapping upon forefoot loading.  Slapping occurs when the anterior muscles cannot adequately control the motion of the foot as it rolls through to forefoot loading.  When this happens, excessive force passes up through those muscles further traumatising them.  During swing phase, footdrop will cause excessive flexion of the hip and knee and possible hitching of the hip.  These are compensations to get greater ground clearance for a foot that is inadequately dorsiflexed as it passes over the ground.  In effect it will act as a LLD generated in the swing phase rather than stance phase.

The shoe or orthoses can be a major cause of the slapping when they are too stiff or stable.  A certain amount of flexibility is required to coordinate the transition from heel to toe.  Otherwise, the shoe will act like a stiff plank that pivots over the ground. (Manning, 2002)

Premature strike can cause early ankle plantarflexion forcing the extensors to contract out of coordination - against already initiated motion.  This could cause excessive muscle damage.

Finally, because CECS needs the specific sports activity to raise the intracompartmental pressure (Padhiar and King, 1996:360), it is possible that the biomechanics of that specific activity could be changed to resolve the symptoms.

TABLE 3:  Proposed Pathomechanical Etiologies:

Structure and function:

  • Pes Cavus – rigid foot causing poor shock attenuation and possible forefoot strike
  • Pes Planus – hypermobile foot causing overpronation and Extensor stabilisation
  • Genu recurvatum – causing possible overstriding and delayed toe-off
  • Ankle eqiuinus (Bruckner and Khan, 2002:521) – anterior group overworking to DF ankle
  • Tight or spasming Antagonists (posterior muscles) overloading anterior group.
  • Weak hip flexors – overloads ankle extensors to gain ground clearance
  • 2º to peroneal spasm overloading AT
  • Hallux Limitus causing EHL hyperactivity prior to heel lift
  • LLD – long leg pronation and abduction of foot, short leg FF strike and varus position of foot.
  • Muscle Imbalance - Muscle tightness - Muscle Weakness


  • Overuse hill running (particularly racing downhill without practice) increasing eccentric load
  • Overtraining with excessive intensity increasing forefoot strike ratio while fatigued
  • Speedwork while fatigued (eg after race or long run)
  • Inadequate warm-up
  • Increase in training intensity or volume too quickly
  • Technique and biomechanics

  • Extensor substitution
  • Overstriding creating functional equinus and premature strike
  • Changing gait from Heelstrike to Forefoot strike
  • Slapping
  • Premature strike
  • Overpronation – overworking tib ant with extensor stabilisation
  • Compensatory gait patterns
  • Environment:

  • Running on slippery surfaces causes clawing and sudden over-contraction
  • Treadmill running.  Surface keeps moving after strike to throw off coordination
  • Changing surfaces between racing and training
  • Running on surfaces that are either too hard or too soft
  • Footwear and orthoses

  • Footwear: inappropriate support, heavy shoes, too much flexibility
  • Running with orthoses made for walking
  • Shoes that do not flex at FF overload extensors to move body over shank
  • Poorly fitting shoes cause change in foot shape and mechanics.
  • Assessment of pathology and etiology

    Diagnosis is mainly based on the history of symptoms related to exercise (Bruckner, 2000:S2).  There is a unique presentation of onset after a specific exercise interval followed by resolution soon after exercise is stopped. Diagnosis is then by exclusion (Guten, 1997:127; Blackman, 2000:S7). Radiographs, bone scan or Ct are used to rule out osseous conditions.  Blackman (2001:S6) says symptoms are “cramping, burning or aching pain and tightness in the lower leg with exercise.  Pain is “usually constant and unrelated to ground impact”, with “onset at a relatively fixed point in the patient’s activity”. Blackman further states that the hallmark of CECS is the lack of physical signs at rest.  There may be herniations and associated dysfunction of muscles and nerves, and “anterior CECS may cause weakness of dorsiflexion and paresthesiae in the first web space” (Blackman 2000:S7).  Clinical presentation of CECS and arterial entrapment are identical except pain in CECS is

    usually related to volume and in claudication it is related to intensity (Bradshaw 2000:S34).  A definitive diagnosis is most commonly achieved through compartment pressure testing.

    Stryker handheld pressure monitor

    A Stryker handheld digital monitor measures intracompartment pressure. Pedowitz (1990) established objective criteria for normal and abnormal pressures.  Slight increases in compartment pressures were found during exercise in asymptomatic subjects but a return to near the pre-exercise pressures was achieved within five minutes.  Symptomatic subjects had higher pre exercise values with significantly increased exercise values and 5 min post-exercise values. Normal at rest is under 10mmHg. A positive diagnosis can be made with 15mmHg at rest, 35mmHg during exercise and 25mmHg after exercise. (Bruckner and Khan, 2002:520)  Dynamic pressure tests have not been as reliable as pre- and post-exercise tests (Blackman, 2000:S8).  More recently Mollica and Duyshart (2002) established that these values might be consistent for other muscle compartments in the body.

    An accurate diagnosis may require an exercise test for symptoms to arise. Mollica and Duyshart suggested that “resting pressures considered in isolation are insufficient for diagnosis of chronic exertional compartment syndrome” (2002:271) CECS can not be excluded without the specific sports activity being used to raise the intracompartmental pressure” (Padhiar and King, 1996,360).  What is universally accepted is that the test should continue until symptoms are reproduced.

    Functional assessments

    Timing of onset with exercise can be used to determine the extent of injury while gait analysis and gait related tests can help to identify the cause or causes of injury.

    1.          Muscle testing immediately post-exercise induced onset (ankle dorsiflexion)

    2.          Palpation post exercise for pain and firmness with active DF/PF

    3.          Neurovascular tests post exercise - first interspace paresthesia, pulses.

    4.          Gait Analysis – with skipping, jumps and hurdles to identify foot drop.

    5.          Increased slapping noise at onset of pain during running caused by dysfunction of anterior compartment muscles at heel strike.

    Assessment and investigations

    Some noninvasive tests for CECS are showing promise.  Forced dosiflexion MRI post exercise revealed increased T2 signal intensity in the entire anterior muscle compartment. (Lauder etal, 2002:315)  Verleisdonk, van Gils and van der Werken (2001:321) found a significant change in signal intensity following exercise after fasciotomies.  “Thallium stress testing is non-invasive and may be a more physiologic measurement” (Swain and Ross, 1999:159).  Rowden et al (2001:229) concluded that an “absence of postexercise potentiation of the peroneal motor amplitude” might become a

    diagnostic sign of CAECS after further study is conducted.  Vascular studies are used to rule out anterior tibial artery claudication.  Near infrared Spectroscopy is useful only at high pressures >160mmHg where ischaemia is present. (Gentilello, 2001)

    The main question is, what is really damaged, the muscle or the fascia?  Fascial thickness increases in cases of CECS so maybe that is the cause and muscle pathology is the symptom.  Perhaps the underlying cause was a trigger episode (traumatic event) that led to the extensive damage to fascia causing CECS?

    Some etiological theories

    i.  Traumatic fascial stress theory

    1. Episodic with multiple traumas

    2. Single trigger event of overload eccentric damage

    ii.  Chronic overuse muscle theory

    1. Chronic muscle hypertrophy

    2. Unresolved tissue edema

    3. Vascular insufficiency causing damage to neuromuscular structures.

    iii.  Neural control theory

    The pain is a result of efferent neural command inhibiting exercise activity before irreparable damage to muscles occurs (Gibson, Lambert and Noakes 2001:637)

    Treatment Program

    The treatment of choice for compartment syndromes has been surgical fascial release.  Fasciotomy (release of the fascial sheath around compartment) and Fasciectomy (removal of a window of the fascial sheath) have been extensively discussed in the literature and Bruckner and Khan suggest that both should be done for improved success (2002:520). Anterior CECS surgery is a single incision 5-6cm in length in the midportion of the lower leg halfway between the anterior tibial crest and the fibula (Blackman, 2000:S8). Anterior compartment releases tend to recover faster than other compartments (Blackman 2000:S9). Early mobilization prevents excessive scaring and adhesions and running can be commenced 3 to 6 weeks after surgery (Blackman 2000:S9). Garcia-Mata (2001: 328) report that all patients in their study returned to sport 6 weeks after Sx with no symptoms. A new method of one portal endoscopic faciotomy may help to decrease damage to soft tissue and allow patients to return immediately to normal activities of daily living (Kitajima et al, 2001:33).

    While surgery is used extensively to treat chronic exertional compartment syndrome, as podiatrists we need to create conservative treatment options that are related to our scope of practice.  Subotnik says that ‘Conservative treatment has been unsuccessful in patients who continue vigorous exercise’ (1999:288). The evidence for conservative measures is poor.  As Blackman says, “ Many statements discussing conservative methods appear to be based on anecdotal information alone, and more scientific data are needed to draw firm conclusions” (2000:S8).

    The main goal of rehabilitation is to reduce pain and improve function during activity. While full resolution is the long term goal, partial resolution may be more acceptable then surgery to some patients.  This may mean permanently reduced activity levels or activity modification.

    Because CECS needs the specific sports activity to raise the intracompartmental pressure (Padhiar and King, 1996,360), cross training could be an effective way of maintaining fitness without aggravating the symptoms.  A return to the specific sporting activity may need a change to the individuals pathomechanical etiology as discussed in table 3.  Of particular Note for CAECS are the following treatments:

    Structure and function

  • Stretching and exercises targeting tightness and weakness
  • Technique and biomechanics

  • Reduce slapping
  • Prevent over-striding
  • Aim for smooth transfer of forces and optimum path of motion
  • Work on ideal recruitment patterns
  • Training and environment

  • Exercise reduction (Bruckner and Khan, 2002:520)
  • Run on firm consistent surfaces and avoid hills
  • Footwear

  • Identify functioning rocker sole
  • Cushioned Forefoot
  • Optimum Heel Height differential
  • Aim for guidance rather than blocking control
  • Orthoses

  • Decide on cushioned or controlling device depending on biomechanics
  • Sports Orthotics -separate running and walking orthoses (Kirby, 1997)
  • Assessment and correction of any biomechanical abnormalities
  • Reduce ankle dorsiflexion requirements.
  • Physical therapies

    Massage – myofascial release (Bruckner and Khan, 2002:520-21)

    1. Longitudinal release with active and passive PF/DF to restore fascial flexibility

    2. Transverse frictions to reduce focal regions of muscle thickening

3. Pressure point massage (sustained myofascial tension grade III with active or passive PF and circumduction

4. It is also helpful to release posterior compartment

Icing -  direct ice method during and following releases

Vacuum cupping (Bruckner and Khan, 2002:521)

Myofascial release technique

Treatment may require us to work within a multidisciplinary group.  While orthoses and footwear are the main podiatric contribution to the team, physiotherapists will be responsible for muscle strength and control in rehab, massage therapists can work on myofascial release, sports physicians can do pressure testing and prescribe anti-inflammatories.  Biomechanists and coaches can work with the podiatrist to help to modify pathomechanics and learn new movement patterns.

The podiatrist can direct the conservative clinical pathway as outlined in table 4.  What is needed is an understanding of the appropriate conservative treatments and knowledge of practitioner’s skills and abilities so that the condition can be resolved.

TABLE 4:  Proposed Conservative Clinical Pathway:

Initial Visit - Day 1

  • Dx by History
  • Physical Exam to identify any coexisting conditions
  • Routine Biomechanical exam
  • Footwear evaluation and prescription
  • Refer for radiographs to differentiate osseous and tumours
  • Advise to not run until day of exercise test

Second Visit - Day 3

  • Gait analysis to identify pathomechanical etiologies
  • Exercise Test. with compartment pressure testing
  • If positive advise activity reduction and conservative and surgical alternatives

Begin rehabilitation phase

  • Refer for myofascial release every 48 hours followed by icing to reduce trauma
  • including longitudinal release, transverse friction and deep tissue massage
  • Refer to physio for ultrasound, phonophoresis, vacuum cupping

Third Visit - Week 2

  • Thorough biomechanical exam
  • Casting for orthoses

Fourth Visit - Week 3

         Orthoses dispense

Begin functional phase

  • Return to modified activity not related to onset activity
  • Begin motor relearning sessions

Fifth Visit - Week 5

  • Orthoses review and modification

Sixth Visit - Week 7

  • Exercise test to identify improvement.
  • If no change then refer on for surgery and post surgical pathway
  • If partially resolved, then continue conservative measures until full resolution

Begin return to activity phase

  • If resolved, then return to desired sporting activity with preventative measures

Seventh Visit - 3 months post resolution

  • Check that biomechanics and movement patterns are still under control.


This paper has attempted to give a thorough overview of chronic anterior exertional compartment syndrome.

Diagnosis can be confounded by combined pathologies but is usually differentiated by the unique exercise induced symptomology.  While it is probable that overuse and pathomechanics are the main etiologies, more research is needed to develop an accurate pathophysiological model. Dysfunction and pain of the anterior compartment muscles leads to a characteristic gait pattern of footdrop and slapping upon forefoot loading.  The gold standard method of assessment is pre and post exercise compartment pressure testing.

Treatment has focused on surgical rather than conservative methods.  A conservative clinical pathway has been suggested for podiatrists to follow when treating the patient with CAECS.  This common running injury of the leg falls into the scope of practice of the podiatrist.  What is needed is more research into conservative podiatric treatment of CAECS and its outcomes.

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