Objectives Chronic exertional compartment syndrome is one of the main causes of exertional leg pain. Diagnosis is based on the history and intracompartmental muscle pressure testing during exercise prior to consideration of fasciotomy for treatment. We present the data gathered at Defence Medical Rehabilitation Centre Headley Court during the first year of a revised protocol on dynamic pressure testing from May 2007.
Methods The exercise protocol involved exercising patients using a representative military task: the Combat Fitness Test with a 15 kg Bergen on a treadmill, set at 6.5 km/h with zero incline up to 15 min and if completed, a further 5 min at 7.5 km/h. Subjects informed us when the exertional leg pain was 7/10 on a visual analogue scale and were instructed to carry on till failure (pain 10/10) or till the test finished. Mean pressure during this time period (7/10 to 10/10) was calculated by computer.
Results Over 1 year, we performed 151 intracompartmental pressure studies in 76 patients. 120 were successful in 68 patients, with 31 technical failures. All studies were performed in the anterior or deep posterior muscle compartments as these were the symptomatic compartments; no patients had symptoms in the lateral or superficial posterior compartments and these were not tested. There was only one complication with a posterior tibial artery puncture. In 119 compartment studies, the mean pressure was 97.8 mm Hg (SD 31.7). These data are normally distributed (Shapiro Wilk test, W=0.98 p=0.125).
Conclusions Our data based on this exercise protocol are comparable with the few studies that record dynamic pressure during running-based exercise. There is no accepted diagnostic pressure or exercise protocol. Due to the uncertainty of diagnostic criteria, it is necessary to perform a study measuring dynamic pressures in normal asymptomatic subjects.
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Patients complaining of exercise-induced leg pain may have several possible diagnoses which commonly include stress fracture, traction periostitis/medial tibial stress syndrome or chronic exertional compartment syndrome (CECS).1 Other less common causes can be more serious and include vascular pathology such as claudication, popliteal artery entrapment syndrome, nerve pathology from diabetes, spinal claudication or nerve entrapments, fascial hernias, McArdle syndrome or tumours. CECS was first described by Mavor2 in 1956 in a professional footballer where he distinguished this chronic variant due to exercise from acute compartment syndrome due to trauma with haemorrhage into the muscle. The association with raised pressure within the muscle compartment due to exercise was made soon after.3
CECS is defined as a reversible rise in tissue pressure to abnormal levels brought on by exertion and relieved by rest. The pressure rise within the closed anatomical space of the muscle compartment compromises circulation and tissue function.4 The aetiology is due to inadequacy of musculofascial compartment size and/or tight inelastic fascia, along with muscles increasing in volume by 20% with exercise. When the rising pressure in the compartment exceeds that of the capillaries and small arterioles, they will close (critical closure theory) and decrease perfusion, resulting in ischaemia.5 The pain is believed to be due to hypoxia as well as metabolic waste products such as lactate, which have increased washout times with poorer perfusion.
In CECS, the typical history reported by patients is recurrent episodes of pain often localised to a muscle compartment that occurs at a well defined and reproducible point in exercise and increases if the training persists, with relief of symptoms only with discontinuation of activity.4 There may be associated sensory disturbances (numbness, paraesthesia) and sometimes motor disturbances in nerves that pass through the affected compartment during exercise, for example, first web space numbness or foot drop from the deep peroneal nerve in anterior compartment CECS, or plantar sole numbness from the tibial nerve in deep posterior compartment CECS. Examination is usually normal, although between 40% and 60% of patients have fascial defects with muscle hernias.4 ,6
CECS has traditionally been treated surgically by fasciotomy, which allows an increase in size of the compartment boundaries, thus reducing intracompartmental pressure on exercise.7 ,8 As examination is largely normal, the diagnosis of CECS is dependent on investigations, a variety of which have been described. The gold standard is invasive intracompartmental pressure monitoring using a variety of techniques.9–14 Non-invasive alternatives include standard radiological tests,15–17 radioisotope techniques,18–21 near-infrared spectroscopy22–24 and measuring muscle hardness,25 but non-invasive methods currently remain experimental.
Commercial devices for measuring intracompartmental muscle pressure exist such as the Kodiag monitor (B. Braun Melsungen AG, Melsungen, Germany) or the Stryker Intracompartmental Pressure Monitor (Stryker, Kalamazoo, Michigan, USA). However, these devices give an instantaneous reading on a digital display and are unable to monitor pressure over time. Hence they are suitable for a measurement of pressure that is not changing rapidly such as acute compartment syndrome measurement or static readings pre-exercise and post-exercise, but not to provide continuous readings during exercise. As exercise is the pain-provoking activity, running on a treadmill while dynamically measuring the pressure has been used to reproduce the symptoms and confirm that there is raised intramuscular pressure during this period.8 ,11 ,26–28 The diagnosis of CECS requires both symptoms and raised pressure to occur at the same time.
The various techniques have various exercise protocols and pressures have been measured either by taking static measurements pre-exercise and post-exercise or dynamic measurements during exercise. Two extensive review articles4 ,29 discuss 16 and 21 studies respectively and provide excellent summaries of the literature and both essentially conclude that there is no consensus for diagnostic pressure or exercise regimes used. The 2006 survey by Tzortziou et al30 of UK orthopaedic surgeons reported that 42% used a dynamic compartment pressure (ie, during exercise) >35 mm Hg as the criterion for anterior CECS diagnosis and 35% used Pedowitz's modified criteria. These are based on static measurements (with one or more fulfilled criteria being diagnostic) of a pre-exercise pressure ≥15 mm Hg, a 1 min post-exercise pressure ≥30 mm Hg or a 5 min post-exercise pressure ≥20 mm Hg.31
Previous work at the Defence Medical Rehabilitation Centre (DMRC) Headley Court prior to 2007 had settled on a protocol based around the work of Allen and Barnes,8 ,32 using an exercise regime of dorsi-/plantarflexing the ankle while the patient was supine on a couch. A positive diagnosis was made if the mean pressure during this exercise test was ≥50 mm Hg with reproduction of symptoms. However, our experience of several years of using this exercise protocol was that it was hard to reproduce symptoms and did not correlate with the required functional activities of Service personnel such as running or the loaded march which drove the decision to change the protocol. When changing the exercise protocol to the loaded march, we continued to use 50 mm Hg as the diagnostic pressure.
We also revised our technique of dynamically measuring intracompartmental muscle pressure using off-the-shelf equipment that had been validated. We used a saline-filled indwelling catheter connected to a pressure transducer.10 ,13 ,14 The alternative implantable miniaturised transducer (Millar Mikro-Tip Pressure Transducer Catheter, Millar Instruments, Inc., Houston, Texas, USA)11 was at that time prohibitively expensive. The signal from the transducer was recorded by a computer that could analyse these data.
Approval for this study was obtained from the Ministry of Defence Research Ethics Committee. New patient referrals from Primary Care, Regional Rehabilitation Units or Secondary Care were reviewed in a Legs Multi-Disciplinary Injury Assessment Clinic where a thorough history and examination were undertaken to ascertain if the patient might have CECS. Any biomechanical problems were identified at this time, which might lead to another cause of exertional leg pain rather than CECS. Patients with a suitable history and negative examination were referred to the Lower Leg Pain Clinic for invasive compartment monitoring to measure the dynamic pressures within the affected muscle compartments during exercise.
The skin was prepared with alcoholic chlorhexidine and shaved over the affected compartment of the leg. The skin and subcutaneous tissue but not the muscle compartment, were anaesthetised with 5 ml of 1% lidocaine. For the anterior compartment, the insertion point was 2 cm lateral to the anterior tibial crest and 5 cm distal to the tibial tuberosity. The break-away needle was angled at 30° to the skin and inserted in the line of the tibia to its full length of 75 mm. For the deep posterior compartment, the insertion point required a medial approach at the point where gastrocnemius ends and soleus overlies tibialis posterior which is palpable in most individuals. The 75 mm break-away needle was inserted perpendicular to the skin and it was necessary to feel for a ‘double pop’ as the needle pierced the superficial posterior fascia and deep posterior fascia. This position could be confirmed with ultrasound and corresponded to half the length of the needle in most patients.
The slit catheter (Stryker Corp, Kalamazoo, Michigan, USA) was primed with heparinised saline, which was used to prevent thrombus occlusion of the catheter, and connected to a pressure transducer BHT-2000 (pvb-cc GmBH, Germany) which outputted to a computerised manometer SmartGraph 7900 Pressure Monitoring System (Albyn Medical, Dingwall, UK). The catheter tip and the transducer were placed on the leg and the manometer was zeroed. The catheter was inserted via the break-away needle into the muscle compartment, the needle withdrawn and peeled apart, leaving the catheter alone emerging from the muscle and skin. The catheter was secured to the skin with benzoin compound tincture B.P. and Mefix dressing (Mölnlycke Health Care, Dunstable, UK). The transducer was then also attached to the leg with short strips of Micropore tape (3M PLC, Bracknell, UK) at the same level to minimise the saline column height between muscle and transducer, without circumferentially wrapping the leg to avoid a tourniquet effect (Figures 1 and 2). A total of 0.2 ml of saline was injected into the muscle compartment to form a pressure transmitting pocket at the tip of the slit catheter (according to the manufacturer instructions). The computerised manometer recorded the muscle pressure at 50 Hz and provided graphical displays of these data as well as minimum, maximum and mean calculations.
The pain-provoking exercise protocol was called the Exertional Leg Pain Test (ELPT). This involved performing a loaded march according to the standard Combat Fitness Test33 protocol on a treadmill carrying a 15 kg Bergen at 6.5 km/h and zero incline for a maximum of 15 min (Figure 3). The time at which the patient's exertional leg pain reached 7/10 on a visual analogue scale (VAS) was noted on the computer and when the patient was unable to continue due to pain (10/10 VAS) was recorded, at which point the treadmill was stopped and the patient sat down on a high couch with legs hanging free. If the patient was able to complete 15 min on this protocol, the treadmill speed was increased to 7.5 km/h for up to a further 5 min in order to provoke pain to 10/10 or they completed the test (20 min total), at which point the treadmill was stopped. Mean pressure was calculated by the software averaging pressure recordings between the 7/10 and 10/10 VAS markers.
Statistical analysis was performed using Analyse-it for Microsoft Excel v2.24 (Analyse-it Software, Leeds, UK). Normality testing of the data was performed using Shapiro Wilk test, with p<0.05.
During the first year of the study (May 2007–2008), 151 intracompartmental pressure studies were performed in 76 patients. Overall, 120 were successful in 68 patients, with 31 technical failures due to clot occlusion of the catheter, air bubble within the catheter, kinking of the catheter during exercise, catheter falling out while the patient was exercising and various other factors attributed to the operators learning curve. Patients only reported exertional leg pain in the anterior or deep posterior muscle compartments and these were the only compartments tested (Figure 4). The majority of studies were performed in the anterior leg compartment (110 successful in 64 patients), with nine successful studies in five patients in the deep posterior compartment. One subject had unilateral leg symptoms but had bilateral pressure studies, so the normal leg had a pressure study performed, which was below 50 mm Hg and excluded from analysis. There was only one complication which occurred in a patient who had previously had bilateral four-compartment fasciotomies with ongoing symptoms who was undergoing deep posterior compartment studies. On the first occasion, the venae commitantes of the posterior tibial artery were punctured and on a second attempt 1 month later the posterior tibial artery itself was punctured; further attempts were abandoned due to the aberrant post-operative anatomy. Ultrasound guidance was used to site any catheters in previously operated legs subsequently.
The mean age of patient was 28.9 years (SD 6.7). In the 119 compartment studies (Figure 5), the mean pressure was 97.8 mm Hg (SD 31.7). These data were normally distributed (Shapiro Wilk test, W=0.98 p=0.125).
In all, 31 of the 151 (20.5%) compartment studies failed due to technical issues, a rate comparable with other UK centres (authors own data). We identified an operator learning curve, where we learnt over time to flush out air bubbles in the heparinised saline-filled catheter, noting clot occlusion early in the catheter and flushing it, and securing the catheter so that it did not fall out during exercise or kink by leaving too long or short a portion of the catheter outside the skin. One way to remove the issues of kinking, clot occlusion or air bubble formation was to remove saline-filled catheters completely and to place the transducer directly within the exercising muscle; however, this would not eliminate the risk of the transducer falling out of the leg or disconnecting from the computer during exercise. Although the use of the Millar transducer was not feasible in 2007 due to the cost, this subsequently fell such that they can now be considered a cost effective single-use item. Furthermore, the BHT-2000 reusable transducer was withdrawn from the market by its manufacturer and replaced by a disposable unit that was susceptible to movement artefact, which was unacceptable for a dynamic study. DMRC switched to Millar transducers in October 2011.
We devised the ELPT as we found from the history that most subjects in the Legs Multi-Disciplinary Injury Assessment Clinic were Army or Royal Marines and complained of being unable to complete the Combat Fitness Test, and we wanted to introduce a representative military task. However, some of our patients were Royal Navy or Royal Air Force and the fitness tests for these subjects are purely running-based (1.5 mile run or Multi-Stage Fitness Test). However, all patients performed the ELPT, irrespective of Service. Some have reported that the rise in pressure in CECS is exercise-specific34 ,35 and the stride and gait pattern of the loaded march or ‘tabbing’ is not comparable with running or normal walking. It was noted from patients’ histories that hills/inclines were particularly apt to provoke symptoms. In order to use more gait patterns and to provoke symptoms quicker (the original ELPT could last up to 20 min), the exercise protocol was modified to make it more arduous and introduced in 2010. It comprised a loaded march with 15 kg Bergen at 6.5 km/h at zero incline (5 min) followed by 5 min at 5° incline; the Bergen was then removed for 5 min running at 9.5 km/h at 5° incline. If patients could complete 15 min, the diagnosis was unlikely to be CECS.
With a threshold diagnostic pressure of 50 mm Hg, we had eight negative studies in patients with a history of CECS, but noted that the mean pressure during the ELPT when a patient was symptomatic from pain was nearly 100 mm Hg, almost double the diagnostic pressure. Although Allen and Barnes8 do not quote mean exercise pressures, Puranen and Alavaikko26 found mean exercise pressures of 100 mm Hg in the anterior and 72 mm Hg in the deep posterior compartments in subjects with a history of CECS against a diagnostic pressure of 50 mm Hg. Likewise, McDermott et al11 described mean exercise pressures in the anterior compartment of 106 mm Hg in symptomatic patients where the diagnostic pressure was 85 mm Hg; Rorabeck27 found mean exercise pressures of 95 mm Hg in the anterior and deep posterior compartments. However, more recently a systematic review by DMRC36 of 38 pressure studies found methodological flaws in these studies used to determine both dynamic and static pre-exercise/post-exercise pressure thresholds to diagnose CECS. The CIs of pre-exercise, during exercise, 1 and 5 min post-exercise pressures overlapped the criteria of Puranen/Allen and Pedowitz, meaning that if a subject had an intracompartmental pressure above the criteria, one could not be sure if they belonged to the upper end of asymptomatic or the lower end of CECS patients. In addition, most studies used to form the basis of the criteria did not include healthy controls for comparison or had very few. We similarly only investigated patients who gave a history of CECS and did not do a control study in asymptomatic subjects. Further work is needed to carry out our own control study to determine whether the intracompartmental pressures in normal subjects while performing a loaded march overlaps with the 50 mm Hg diagnostic pressure.
Although our technique in use today at DMRC has evolved substantially, this 2007 protocol is very similar to the methods currently used at other centres for dynamic intracompartmental pressure studies with an exercise protocol. Our results should be comparable with other groups using this method and we have also presented our lessons learnt to inform practice elsewhere.
In view of potential diagnostic uncertainty, the current practice at DMRC evolved in 2011 to taking all patients presenting with possible CECS symptoms for a rehabilitative approach rather than intracompartmental pressure testing. Studies found that by enforcing a forefoot-strike instead of rearfoot running pattern, either by shoe37 or gait38 modification, the anterior compartment pressure during exercise was reduced. This is thought to be due to decreased tibialis anterior eccentric contraction duration with a forefoot-strike. We have also noted some patients to use their extensor hallucis longus and extensor digitorum longus muscles to dorsiflex their ankle instead of tibialis anterior. Inappropriate use of these smaller muscles will cause early fatigue and anterior compartment pain. These are collectively placed under the term Biomechanical Overload Syndrome which has been coined at DMRC.39 During the rehabilitation course, patients have running gait re-education to correct these biomechanical abnormalities. Only patients who fail this rehabilitative approach are put forward for pressure testing.
We have presented a large series of patients with a history of CECS who underwent dynamic intracompartmental pressure studies in the anterior and deep posterior compartments of the leg, using an exercise protocol based on the Combat Fitness Test. The techniques, difficulties and subsequent modifications are described in detail. Mean pressure using this test of 97.8 mm Hg was comparable with previous studies using running on a treadmill as the exercise protocol and the pressures measured in subjects were normally distributed.
Due to diagnostic uncertainties, we need to perform a control study of normal subjects without CECS symptoms to see if the diagnostic pressure of 50 mm Hg is still justified. Our unit has now switched to a rehabilitative approach using gait re-education to correct biomechanical abnormalities in patients with these symptoms. Only patients whose symptoms persist undergo intracompartmental pressure testing.
This work has been presented at the British Society for Rheumatology Conference, SECC Glasgow, in April 2009, the Combined Services Orthopaedic Society, Gosport, in May 2009 and the Seddon Society Meeting, Royal National Orthopaedic Hospital, Stanmore, in June 2009.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
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