Deep state: getting to the heart of CECS

Chris Mallac explores chronic exertional compartment syndrome (CECS), focussing on the deep posterior compartment. What are the signs and symptoms of CECS, and how can clinicians most effectively manage this condition in athletes?



Acute chronic exertional compartment syndrome was first described by Dr Edward Wilson when he suffered what sounds like this condition in his own lower limb during a race to the South Pole in 1912⁽¹⁾. Since those early days, a more chronic version, called CECS was described in 1956 by Marvar when he illustrated a case study of a soccer player who underwent bilateral leg surgery after suffering leg pain from chronic exertion⁽²⁾.

This condition was further elucidated in 1962 by French and Price, who first measured intra-compartmental pressure and then compared this with the patient’s history and symptoms to develop the idea that CECS was a distinct clinical entity⁽³⁾. Finally, deep posterior CECS – the topic of this piece - was originally identified by Puranen in 1974⁽⁴⁾, and confirmed by pressure measurements in 1981.

CECS is regarded as an overuse injury of the lower limb and is reasonably common in running-based athletes⁽⁵⁾. It is considered to be more common in the early 20’s athlete; the anterior, lateral and deep posterior compartments are the most affected, while the superficial compartment is rarely affected^(6,7). The deep posterior variant is considered the more difficult type of CECS to diagnose and to manage. This is due to the variety of differential diagnosis that exists for posteromedial exertional leg pain in the shin and the difficulty in accessing the deep compartment in both testing and surgical treatment.

Anatomy

The four compartments of the lower limb (see figure 1) are as follows^(8,9):

1. Anterior - Consisting of the tibialis anterior, extensor digitorum longus, extensor hallucis longus, peroneus tertius. This compartment is bordered by the tibia, interosseous membrane, fibula, anterior intermuscular septum, and anteriorly the deep fascia. The neurovascular bundle includes the anterior tibial artery and vein, and the deep branch of the common peroneal nerve.
2. Lateral - Made up of the peroneus longus and brevis muscles, the common peroneal nerve, and with the deep branch continuing into the anterior compartment. This compartment is bordered by the anterior intermuscular spetum, the fibula, posterior intermuscular septum and the lateral deep fascia.
3. Deep posterior - Comprised of the flexor hallucis longus, the flexor digitorum longus and the tibialis posterior, along with the posterior tibial artery and vein, and the tibial nerve. The deep transverse fascia separates this from the superficial compartment posteriorly. The anterior boundaries are the tibia, interosseous membrane and fibula.
4. Superficial posterior – Comprising of gastrocnemius, soleus, plantaris, the sural nerve, and a branch of the tibial artery/vein. The crural fascia surrounds this posteriorly.

Occasionally a separate sheath surrounds the tibialis posterior muscle forming an extra compartment⁽¹⁰⁾. This has sometimes been referred to as the fifth compartment⁽¹⁾.

Figure 1: Four compartments of the lower leg

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Pathogenesis

Chronic exertional compartment syndrome primarily affects the lower limb (estimated at 95% of CECS cases), and usually the anterior and deep posterior compartment ^(11,12).  A small percentage (8%) of cases may actually involve both compartments simultaneously ⁽¹³⁾. Overall, it is a very common cause of exercise induced leg pain (26-33% of cases)^(5,14).

It has always been thought that the pain associated with CECS was due to purely an ischaemic phenomenon caused by an increase in muscle compartment volume. Muscle volume can increase up to 20% of its resting size during exercise. Increased muscle volume causes a rise in the internal pressure within the fascial compartment⁽⁶⁾. Most think this increase in pressure ‘chokes’ blood flow to the compartment and reduces tissue perfusion. The tissue ischemia causes pain, increases cell permeability, fosters a fluid shift into the interstitial space, and results in swelling.

The proposed mechanisms involved in this ischemia argument include arterial spasm⁽¹⁵⁾, obstruction of microcirculation⁽¹⁶⁾and arteriolar/venous collapse⁽¹⁷⁾. This theory is further supported by muscle biopsies, which show characteristic blood vessel factors that may contribute to the development of CECS or be associated with CECS^(18,19). Findings such as the lower number of capillaries surrounding muscle fibres and lower capillary density per muscle fibre area may be associated factors in CECS.

However, the idea that tissue ischemia is the source of pain has been questioned^(20,21). In a straightforward study that looked at the ischemia/tissue perfusion concept, Trease et al (2001) showed (using SPECT scanning) that there was in fact no significant difference in the relative perfusion in patients diagnosed with CECS and those in a control group⁽²²⁾.

Therefore, alternative theories abound. One theory is that as blood volume increases during exercise and the muscle starts to swell, the fascia cannot distend to accommodate the increase in intra-compartment volume. The pressure in the compartment builds and this may then stimulate sensory receptors in the fascia or periosteum, or possibly biochemical factors are released due to the minimal blood flow⁽²⁰⁾.

Another possible - and more recent - train of thought is that CECS may be caused by inflammation-induced fibrosis of the surrounding fascia around a muscle, and subsequent reduction in the elasticity of this fascia caused by repetitive overuse.

The basis of this proposal is from a study from Barbour et al (2004), which looked at the histology of the fascial-periosteal interface in subjects with deep posterior compartment syndrome, and who underwent surgery for this condition⁽²³⁾. The tissue pathogenesis is loosely confirmed by biopsies that show that the fascia has abnormally thickened. Interestingly, the fascia in these subjects appears more organised than normal subjects, possibly hinting at a remodelling process in the fascia due to the histological changes encountered. Biopsies of the fascial-periosteal interface also show⁽²³⁾:

• Fibrocytic activity
• Chronic inflammatory cells
• Vascular proliferation
• Decreased collagen irregularity (suggestive of an attempted healing and remodelling process)

The flow chart from Barbour et al (see figure 2) shows the sequence of events that may lead to CECS⁽²³⁾.

Figure 2: Possible sequence of events leading to CECS⁽²³⁾

From Barbour et al (2004)

Biomechanical overload syndrome

In another view on the pathogenesis of CECS, Franklyn-Miller et al propose a model known as the ‘biomechanical overload syndrome’⁽²⁴⁾. This theory postulates that intra-compartmental pressure theories and tissue ischaemia models are all irrelevant as the pain may actually stem from muscle overload. They argue that this is the reason why in their series of surgical subjects, poor results are often seen after surgical fasciotomy.

Instead of focusing the treatment direction towards fascial compliance (via massage or surgery), they managed conditions of CECS with running re-education to reduce the loads on the tibialis anterior (anterior CECS) and tibialis posterior (deep posterior CECS). The focus was on mid-foot running styles and higher cadence running (decreased stride length) and other individual running biomechanical variations.

Furthermore, patients underwent a program of dynamic core and gluteal strengthening, podiatric input and hip, knee ankle triple flexion alignment improvement and education. The in-patient course was followed by a 3-month individualised gait rehabilitation programme based around return to running and improved lower-limb conditioning. They found at three months follow ups, the subjects had retained the gait changes they had been taught and 70% experienced a resolution of their CECS symptoms⁽²⁴⁾.

In summary, it is most likely that the cause of CECS is multifactorial. The factors that may be relevant are as follows⁽²⁵⁾:

1. Constraints of an inelastic, fixed, osseofascial muscular compartment.
2. Normal and abnormal swelling of the muscle with exercise.
3. Abnormally thickened fascia.
4. Normal muscle hypertrophy in response to weight training.
5. Supplement use (creatine and steroids).
6. Dynamic or prolonged contractions due to abnormal gait patterns.

A number of risk factors may be associated with CECS. These include:

• Anabolic steroid and creatine use. Both increase muscle volume⁽²⁵⁾.
• Eccentric exercise - increases the risk due to decreased fascial compliance and this may be more relevant in younger growing athletes⁽²⁵⁾.
• Pathomechanics in a runner such as overpronation can increase the risk of compartment syndrome secondary to pressure on individual muscle groups in the lower leg⁽²⁴⁾.

Signs and symptoms

The usual signs and symptoms of deep posterior CECS include the following:

1. No pain at rest but builds with exertion.
2. Exertional pain, ache, burning, cramping or tightness in and around the medial tibia. Possible tingling and numbness in the plantar aspect of the foot. These recover quickly with rest.
3. The pain usually comes on at a fixed point during exercise eg at the 3-mile mark of a run.
4. The compartment may feel hard and tense upon palpation and may be tender. Deep posterior syndromes do not feel as tense or painful as anterior and lateral compartment syndromes.
5. Weakness with toe off, plantar flexion and flexion of the big toe.
6. Possible to have the ‘second day’ phenomenon⁽²⁶⁾– ie pain and ache beginning much earlier during the exercise session on the day after the initial episode of CECS.
7. Fascial herniations (bulges) may appear along the medial shin or anterior shin.
8. X-rays and bone scans are normal.

NB: A few other conditions may mimic a CECS. These include popliteal artery syndrome. medial tibial stress syndrome, vascular claudication and tibial stress fractures⁽²⁷⁾.

Diagnostic testing

It is beyond the scope of this paper to discuss all the possible lower limb investigations. However, the clinician should keep in mind that CECS does mimic other lower limb overuse conditions and investigations may be required to rule these out as a possible source of exertional lower limb pain. For example, technetium-99 bone scans may be required to observe increased uptake on the medial tibia that would be suggestive of medial tibial stress syndrome or a tibial stress fracture as being the source of exertional lower leg pain⁽²¹⁾. Also, degree of overlap can exist between many of these conditions. The confirmation of one does not necessarily rule out the existence of the others.

The gold standard in diagnosis has for a long time been the Strkyer catheter pressure measurements for intra-compartmental pressure. During normal exertion, the compartment pressure typically increases 3-4 times from resting levels and then returns to normal a few minutes after cessation of activity. In patients with CECS however, the levels remain elevated for much longer.

The Stryker catheter is a hand-held needle device that includes a pressure scale. The needle is placed into one of the four compartments (see figure 3). Normal saline is injected into the compartment and the pressure of the compartment is taken. After entering the compartment the proper placement of the needle can be verified by externally compressing the compartment being measured and observing a pressure increase on the device⁽⁷⁾.

Figure 3: Stryker catheter

Testing the lateral and anterior compartments is reasonably simple as these compartments are easy to access. The deep posterior compartment is harder to access anatomically. To test for intra-compartmental pressure in the deep posterior compartment, the needle is inserted posterior to the tibia on the medial side at the junction of the lower and middle thirds of the tibia, and through the two layers of the fascia. The patient is then taken through some exercises that will increase the intra-compartmental pressure such as calf raises and running. It is important however that the actual activity that causes the pain is used to increase compartment pressure.

Pressure measurements are taken before exercise, immediately after exercise and then five minutes after. The most commonly used criteria for diagnosis has been as follows⁽²⁸⁾:

1. Basal intra-compartmental pressure >15 mmHg
2. One minute post exercise >30mmHg
3. Five minutes post exercise >20mmHg

However, a recent systematic review of standard pressure measurements has suggested that symptomatic patients overlap normal subjects in compartment pressure studies, which therefore may lead clinicians to over emphasise the importance of measuring compartmental pressure to definitively diagnose compartment syndrome^(24,29).

As compartment testing is invasive and painful, other testing methods have been sought. Near-infrared spectroscopy is a test that shows some promise. This test measures oxygenated and deoxygenated blood in the muscles pre and post-exercise. Results that indicate that with CECS, there is a delayed return to the level of oxygen at baseline when the muscle is measured post exercise, and an increased ratio of deoxygenated to oxygenated muscle post-exercise⁽²⁵⁾. Infrared spectroscopy is very sensitive and has been shown to be more sensitive than MRI or intra-compartmental measurements⁽²⁵⁾.

Other new methods are that are non-invasive include diffusion tensor magnetic resonance imaging (DTI) and ultrasound. However, the studies on ultrasound have been performed on the anterior compartment and not deep posterior compartment^(30,31). Post-exertional MRI has also been used to test for CECS. The basis for this is the evaluation of changes in soft tissue composition that MRI may detect. With CECS, abnormal fluid shifts and compartmental oedema has been implicated, and post-exertional MRI may see this fluid change⁽³²⁾.

Treatment

*Conservative

Initially, conservative management may be attempted prior to surgical intervention, and this may prove effective⁽³³⁾. Conservative strategies involve the following:

• Reducing exercise volume
• Deep tissue massage
• Active release techniques
• Dry needling techniques
• Assessment and correction of causative factors such as biomechanical faults, training faults and orthotic/shoe selection

The use of extensive soft tissue myofascial massage (sometimes twice per day) with reduced running/training loads for a 4 to 6-week period does fit with some of the theories as to why CECS develops. If CECS is due to a tight fascial envelope then myofascial soft tissue massage may give the compartment fascia some extra compliance. If it is due to sensitisation of nerve endings in the fascia, then deep tissue massage may desensitise the fascial nerve endings over time.

*Surgical

Surgery via fasciotomy (slits in the fascia) or fasciectomy (removal of fascia) is based on the idea that pressure needs to be released from the compartment. There are a few different forms of fasciotomy⁽⁷⁾. These include open fasciotomy, subcutaneous fasciotomy and endoscopic fasciotomy. These procedures inherently all aim to do the same thing - to divide the restricting envelope of the fascia and thus effectively increase the size of the compartment. The logic for surgery is that if it’s true that a tight, non-compliant fascial envelope is the root cause of CECS, then long term rest and conservative measures are likely to be ineffective. If the tight fascial envelope is irreversible, then surgery must be the only effective treatment.

Deep posterior fasciotomies have a success rate of 50% compared with the success rate of fasciotomies of the superficial fascia and lateral fascia⁽²⁵⁾. Ambramowitz and Schepsis found that all 16 patients who underwent anterior compartment fasciotomy had good results⁽³⁴⁾. However, only 13 out of 20 had satisfactory results for the same procedure to the deep posterior compartment. Decreased success in the release of the deep posterior compartment has been attributed to its more complex anatomy, poor visualisation of this compartment during surgery, inaccessible small muscular subdivisions and initial misdiagnosis such as tibial stress fractures, vascular insufficiency and popliteal entrapment.

Early mobilisation after surgery is required to maximise the effect of the fasciotomy. If the patient remains inactive in bed for several days after surgery, then the fascia may well heal back to its original size and make the surgery ineffective. The typical post-surgical factors to consider are⁽¹⁾:

1. Post-operative antibiotics to reduce infection and cellulitis.
2. Full ankle plantarflexion and dorsiflexion post-operative to encourage early and optimal loading.
3. Non-weightbearing or limited weightbearing in the first five days then full weightbearing.
4. Strengthening work once scars have healed.
5. Gradual return to running 4-6 weeks post-surgery.
6. Full return to sport at 6-8 weeks (1 compartment) and 8-12 weeks (multiple compartments).

It is beyond the scope of this paper to explain a thorough rehabilitation guideline for CECS both conservative management and post-surgical rehabilitation. For a comprehensive guide, refer to Amy Schubert’s piece in the International Journal of Sports Physical Therapy⁽²⁷⁾.

Summary

CECS of the deep posterior compartment is a reasonably common lower overuse injury affecting primarily those in running sports. It usually presents as a deep ache and stiffness in the postero-medial shin that typically comes on a specified time/distance during exercise. It usually resolves soon after cessation of activity. The exact pathogenesis of this condition in open to debate. The gold standard investigation for CECS has for a long time been catheter compartment pressure testing. However, new methods of investigation show some promise as non-invasive tests for CECS. Treatment can be either conservative through stretching, myofascial release and biomechanical modifications. If these fail then surgical release has been advocated. The return to competition time is reasonably fast following surgical interventions.

References

1. Med Sci Sports Exerc 2000;32 (3 Suppl):S4–10
2. J Bone Joint Surg Br 1956;38:513–17
3. BMJ 1962;ii: 1290-96
4. J BoneJoint Surg Am 1981;63A: 1304309
5. Clin Sports Med; 1994. 13:743-759
6. Am Journal of Orthop, 2004: 33. 335-41
7. Curr Rev Musculoskeletal Med, 2010; 3. 32-37
8. Amendola, A and C.H Rorabeck (1985). Chronic exertional compartment syndrome. In: Current Therapy in Sports Medicine. Welsh and Shepard (Eds). Toronto. B.C.Decker
9. Am J Sports Medicine, 1989. 17: 747-750
10. Am J Sports Med 2003;31(5):770–6
11. Br J Sports Med 1997;31:21–7
12. Sports Med 1990; 9:62–8
13. Foot Ankle Int. 2005;26: 1007–1011
14. Am J Sports Med 1988;16:165–9
15. Clin Orthop and Related Research. 1975, 113. 8-14
16. Clin Orthop and Related Research. 1975, 113. 52-57
17. Clin Orthop and Related Research. 1975, 113. 69-80
18. Scand J Med Sci Sports 2010;20(6): 805–13
19. Br J Sports Med 1999;33:49–53
20. Clin Sports Med 1993;12(1):151–65
21. Amendola 1990 Am J Sports Med. 1990; 18. 29-34
22. Eur J Nucl Med. 2001;28(6):688–95
23. Br J Sports Med 2004;38(6):709–17
24. Franklyn-Miller (2014) Br J Sports Med 2014;48:415–416
25. Curr Sport Med Rep. 2003;2:247–50
26. Physician and Sportsmedicine. 1987; 15. 111-120
27. The Int J of Sp Phys Th. 2011 6(2); 126-141
28. Am J Sports Med 1990;18(1):35–40
29. Scand J Med Sci Sports.2012 Oct;22(5):585-95
30. Clin J Sport Med 2013;23(4):305–11
31. Med Sci Sports Exerc 2002;34(12):1900–6
32. Magn Reson Imaging Clin N Am. 2001;9(3):544–7
33. Sports Med 1994; 17. 200-208
34. Orthopaedic Review 1994; 23:219-26