EXERTIONAL COMPARTMENT SYNDROMES OF THE LEG
July 5th, 1995
Peter Edwards, MD and Mark S. Myerson, MD
Abstract
Exertional compartment syndromes of the leg are typically characterized by exercise-induced pain and swelling that are reduced by rest. The symptoms are caused by raised intracompartmental pressure measurements before and after exercise. Although activity modification may alleviate the symptoms, treatment by fasciotomy is recommended.
Introduction
Exertional compartment syndrome (ECS) of the leg is a condition characterized by exercise-induced pain and swelling of the leg that is relieved by rest. Weakness and paresthesia may accompany the pain and are related to ischemic changes within the compartment. In 1975, Reneman1 defined the clinical manifestations of this condition and identified increased intracompartmental pressure as the etiology. Although ECS has been described in the forearm, thigh, and gluteal regions, the leg remains the most common site of involvement.
Anatomy and Pathophysiology
The leg consists of four osseofascial compartments. Each compartment is surrounded by a relatively inelastic fascial covering, and each contains a major nerve: the deep peroneal nerve in the anterior compartment, the superficial peroneal nerve in the lateral compartment, the saphenous nerve in the superficial posterior compartment, and the tibial nerve in the deep posterior compartment (Fig. 1). For a detailed description of the compartments of the leg, we suggest referring to previous reports.2,3
The common peroneal nerve winds around the fibular neck deep to the peroneus longus and divides into two branches, the deep and superficial peroneal nerves. These nerve branches are of special importance in cases of ECS because they can be affected by swelling in the lateral compartment that compresses the common peroneal nerve against the neck of the fibula. The superficial branch continues in the lateral compartment between the peroneus longus and fibula, whereas the deep branch transverses the lateral compartment to continue in the anterior compartment where it lies anterior to the interosseous membrane. Although the literature describes variations in the superficial peroneal nerve's anterior compartment course, as well as atypical crossover, it usually lies in the interval between the two peroneal muscles for a short distance and then emerges anterior to the peroneus brevis.2 At the junction of the mid and distal one-third of the leg, the nerve pierces the lateral compartment fascia and continues distally in a superficial position. The superficial peroneal nerve is prone to injury at this junction, since fascial hernias occur commonly at the point of exit of the nerve and can cause a compression neuropathy.
The anatomy of the two posterior compartments may vary, but both, particularly the deep compartment, are frequently involved in ECS.4-8 The posterior compartment has two distinct fascial coverings. A thin investing fascia covers the entire compartment as it runs beneath the soleus muscle belly. Distal to the edge of the soleus muscle, a thickened band of fascia is present where the anterior and posterior fascial layers of the soleus combine. This "soleus bridge" then crosses over the distal deep posterior compartment to insert on the posterior medial distal tibia. The importance of the soleus bridge is three-fold. Irritation at its tibial insertion has been implicated in medial tibial stress syndrome, which is commonly confused with ECS. Secondly, failure to release the soleus bridge during deep posterior compartment fasciotomy may result in recurrent symptoms. Finally, the soleus bridge is substantially tightened by pronation of the foot. Patients with ECS related to soleus bridge compression will therefore benefit from orthotic support, which controls rapid pronation of the midfoot in the stance phase of gait.
The pathophysiology of ECS clearly depends on increased intracompartmental tissue pressure (Pven) and its resultant effect on the arteriovenous gradient (Part) and local blood flow (LBF), as shown by the equation
Part - Pven
LBF = -----------
Resistance
Skeletal muscle is perfused only during muscular relaxation, and when relaxation pressure exceeds 35 to 45 mmHg, muscle blood flow is decreased. The muscle relaxation pressure is that intracompartmental tissue pressure between muscular contractions. In ECS, relaxation pressures are increased, resulting in decreased perfusion pressure (mean arterial blood pressure - muscle relaxation pressure), resulting in decreased blood flow and myoneural ischemia.
The etiology of the increased relaxation pressures in ECS is unknown, although two theories have been proposed to explain these changes. Normal compartmental volume may increase 20% with exercise due to fiber swelling and increased intracompartmental blood volume. In the conditioned athlete, muscles may hypertrophy, and these anatomic changes alone may be sufficient to raise the local pressure enough to cause decreased perfusion pressure and resultant myoneural ischemia. This is clearly not a sufficient explanation since not all athletes with hypertrophy develop increased compartmental pressure. Alternately, the mechanical damage theory proposes that eccentric exercise results in myofiber damage and release of protein-bound ions. Repetitive eccentric contraction, such as occurs in the anterior compartment of runners, results in increased ion release and increased osmotic pressure within the compartment. The resultant osmotic pressure gradient increases capillary filtration, leading to increased interstitial fluid retention. This raises the relaxation pressure and consequently decreases blood flow.
In asymptomatic patients, intracompartmental pressure studies have shown that transient increases in compartment pressure during exercise are tolerated without becoming symptomatic. These pressures normalize quickly after completion of exercise, usually within 5 minutes. In ECS, abnormally high intracompartmental exercise pressures are found and maintained after exercise completion. Pressures may remain elevated for 20 minutes or longer before returning to normal. As ECS worsens, the periods of pressure elevation after exercise lengthen. If elevated pressures are maintained long enough, then an irreversible cycle of swelling and ischemia can occur, leading to an acute ECS. In this situation, tissue metabolic demands are not met, leading to more swelling, which further restricts local blood flow. The clinical presentation of chronic and acute ECS differs only in severity, although the pathogenesis of the elevated pressures in both is similar.
Clinical Presentation
Acute ECS is generally present in relatively sedentary patients who are involved in an exercise event that is markedly strenuous. In this situation, severe muscular swelling and intracompartmental volume increase, resulting in perfusion deficits severe enough to cause irreversible ischemia of nerves and muscles within the compartment. Athletes with ECS who markedly increase their training are also at risk for the development of acute ECS. These patients present with symptoms and signs of an acute compartment syndrome, including agonizing pain, tense swelling, and pain on passive stretch of the involved muscles. Sensory deficits, such as paraesthesia or anesthesia to light touch, in the distribution of the involved nerves and motor loss (including foot drop) may be present.
ECS usually occurs in well-conditioned athletes less than 40 years old. They complain of the gradual onset of aching leg pain and fullness over the involved compartments of the leg, most commonly, the anterior and deep posterior compartments (Fig. 2). Activity-related pain begins at a set time after commencing exercise or after reaching a certain exercise intensity level. Fifty to seventy percent of patients will have bilateral involvement, with one side being somewhat worse than the other. The pain is always fully relieved by rest, usually within 20 minutes of exercise completion, only to recur on resuming exercise. Patients occasionally complain of paresthesia in the leg and dorsum of the foot during exercise. It is important to remember that superficial peroneal nerve paresthesias may be secondary to ischemic change in the lateral compartment as well as local compression from fascial hernias in either the lateral or anterior compartments. Physical examination in ECS is usually normal unless the patient has recently exercised. Many patients who experience symptoms of anterior compartment pain will have demonstrable fascial defects or hernias, usually in the distal third of the leg over the intramuscular septum.
Patients with ECS do not have tenderness over the posterior medial tibial cortex in the distal leg, which contrasts with posterior medial stress syndrome where tenderness is quite specific and located in this area. In posterior medial stress syndrome, local inflammation of the periosteum results in activity-related pain early in the exercise period and tends to improve with subsequent exercise or improved conditioning. However, pain may persist for hours or even days after exercise and may progress to involve nonexercise activity. In ECS, tenderness (if present) is located more proximally, although typically patients with ECS have no focal pain. Furthermore, they have no pain with vibratory testing of the tibia or circumferential bony tenderness, as seen with stress fractures. No accessory muscle or identifiable bony abnormalities are present (Fig. 3), and Tinel's sign over the common or superficial peroneal nerve is negative, as are other provocative tests for neural irritability. Finally, these patients have no evidence of vascular abnormality with resisted ankle plantarflexion, as seen with anomalous gastrocnemius compression of the popliteal artery.
Physical examination after exercise strenuous enough to reproduce the patient's symptoms is somewhat more helpful. Involved compartments are swollen and tense, and leg girth is increased. The leg is tender over the involved muscles and, with severe ECS, muscle weakness and paresthesia to light touch are present.
Diagnostic Evaluation
Anteroposterior, lateral, and oblique radiographs of the leg are obtained but are usually normal. As part of the diagnostic workup, a bone scan should be obtained to rule out stress fracture or periostitis, although this is rarely positive in ECS. A transverse linear pattern is noted with stress fracture and a longitudinal linear uptake in the cortex is noted in posterior medial stress syndrome. The presence of atypical neurologic symptoms or signs may occasionally necessitate electromyography and nerve conduction studies, although these are not routinely necessary. In the presence of foot drop, electrophysiologic testing is quite helpful to document the extent of motor loss. Compression neuropathy of the superficial peroneal nerve is the most common finding, although the saphenous nerve may also be involved. Finally, magnetic resonance imaging may be used to evaluate intracompartmental contents for muscular abnormalities (Fig. 3). Preliminary reports suggest that magnetic resonance imaging may be used to diagnose ECS, although its routine use is not recommended at this time.
To confirm the diagnosis of ECS, intracompartmental pressure measurements must be obtained; they are performed most easily with a wick or slit-catheter technique. The needle tip location and depth of penetration, as well as knee and ankle position, are controlled to obtain valid and reliable measurements. Our patients are tested supine with the knee extended and the ankle in neutral dorsiflexion. An 18-gauge needle is used in conjunction with a hand-held compartment measurement device.
Although testing has been recommended before, during, and after exercise, we do not recommend measuring during exercise as this is technically more difficult and measurements are less reliable. We inject small amounts of local anesthetic in the skin alone and measure the pressures at rest and at 1 and 5 minutes after exercise; however, we consider those obtained after exercise to be far more reliable (and confirm the diagnosis). It is essential to be able to reproduce the patient's symptoms of ECS, and the measurements obtained after exercise are considered valid only if the intensity of the exercise is sufficient to reproduce the patient's symptoms. We rarely obtain bilateral measurements since this is unnecessarily uncomfortable for the patient; however, comparison of these extremity measurements may be important if the results of pressure measurements are equivocal.
Rorabeck and coauthors,7,9,10 Fronek et al.,11 and Pedowitz et al.,12 have proposed that elevated resting and postexercise pressures are diagnostic of ECS (Table 1). Although any of these criteria are useful, we have used the guidelines proposed by Pedowitz et al. 13: resting and exercise pressures above 15 and 20 mmHg, respectively, are diagnostic of ECS. The compartmental pressure measurements are rarely equivocal; if they are, measurements are repeated at a later date. In these patients, increasing pressures in successive postexercise measurements are also considered diagnostic.
Treatment
Acute ECS is treated with fasciotomy immediately upon diagnosis. A two-incision technique is used, with generous medial and lateral incisions to completely release all involved compartments. Skin incisions are left open, and delayed closure is performed at 48 to 72 hours.
When a patient first presents with ECS, we almost always commence with a nonoperative course of treatment and address extrinsic and intrinsic patient parameters. Extrinsic factors include training surface, shoe design, and training intensity, all of which can be modified. Intrinsic factors, such as muscular imbalance, flexibility, and limb alignments (especially hindfoot pronation), are treated with strengthening and stretching exercises and orthoses. These modifications are not always successful, although orthoses do decrease hyperpronation and thereby decrease compression of the deep posterior compartment by the soleus bridge. Once a patient presents with ECS, it is most difficult to modify all these parameters. Athletes routinely remain symptomatic unless they abstain from the sports or specific activities that cause their symptoms. These poor results from nonoperative treatment were highlighted by Fronek et al.11 who reported that five of seven patients were unable to return to sports after a conservative program.
If symptoms persist, fasciotomy is the recommended treatment for chronic ECS and, unlike the fasciotomy for acute ECS, may be limited to the involved compartments. If the anterior or lateral compartment is involved, the skin incision is planned over any fascial defect so that both may be incorporated into the fasciotomy. These defects are never closed as doing so may actually increase intracompartmental pressure and precipitate an acute compartment syndrome. Care is taken to avoid the superficial peroneal nerve in the anterior distal leg and the saphenous nerve posteriorly, and to decompress them if clinically indicated. Each compartment is completely released as needed and in the case of the deep posterior compartment, the tibialis posterior investing fascia should also be released. Fasciotomies are performed through lateral, medial, or combination incisions, depending on compartmental involvement as documented by pressure measurements.
The anterior/lateral decompression is performed through an incision 5 to 7 cm in length placed 1 to 2 cm anterior to the intramuscular septum (Fig. 4). After identifying the superficial fascia, a short transverse incision is used to visualize the septum. The anterior and lateral compartment fascia is then released under direct vision.
A medial incision, just posterior to the middle one-third of the tibia, is used to release the posterior compartments (Fig. 5). The deep fascia is opened carefully to avoid damage to the neurovascular bundle that lies just below it. The neurovascular bundle is protected, and the deep compartment fascia is released. The soleus bridge is identified and released in the distal portion of the incision. This completely releases the deep posterior compartment with the exception of the separate tibialis posterior compartment, which is then released.
Postoperatively, patients are treated with immediate range of motion to prevent fascial scarring. Weight-bearing is begun within the first week. Athletes begin exercise on a stationary bicycle at 2 weeks and gentle isokinetic strengthening exercises at 3 to 4 weeks postoperatively. Running is begun at 5 to 6 weeks, with speed and agility drills at 8 weeks.
Outcome
Generally, we are able to return most athletes to full sports participation by 8 to 12 weeks, and this may be allowed when symmetric strength has returned as documented by instrumented testing. In the literature, the results of fasciotomy for ECS are predictably good: numerous authors have reported rates of 90% good and excellent results. Generally, athletes are able to return to their sport without pain or certainly with greatly diminished symptoms. Fronek et al.11 and Styf and coworkers14-16 have shown normalization of resting pressures and decreased pressures after exercise in postfasciotomy patients. Thus, fasciotomy appears to decrease the inelasticity (or increase the compliance) of the involved compartments. The results of anterior and lateral compartment releases are superior to those of posterior releases in most studies. If recurrent symptoms occur after fasciotomy, they can usually be traced to the deep posterior compartment, particularly if this compartment was not adequately released. Although recurrent symptoms secondary to inadequate release, a soleus bridge, scarring over of the fasciotomy defect, or entrapment of the saphenous nerve in scar have been suggested, in some patients the cause of these symptoms remains unclear. If fasciotomy fails, the diagnosis of ECS should be fully reevaluated.
References
1. Reneman RS: The anterior and the lateral compartmental syndrome of the leg due to intensive use of muscles. Clin Orthop 1975; 113:69-80
2. Abramowitz AJ, Schepsis AA: Chronic exertional compartment syndrome of the lower leg. Orthop Rev 1994; 23:219-226
3. Adkison DP, Bosse MJ, Gaccione DR, Gabriel KR: Anatomical variations in the course of the superficial peroneal nerve. J Bone Joint Surg 1991; 73A:112-114
4. Davey JR, Rorabeck CH, Fowler PJ: The tibialis posterior muscle compartment. An unrecognized cause of exertional compartmental syndrome. Am J Sports Med 1984; 12:391-397
5. Eisele SA, Sammarco GJ: Chronic exertional compartment syndrome. Instr Course Lect 1993; 42:213-217
6. Michael RH, Holder LE: The soleus syndrome. A cause of medial tibial stress (shin splints). Am J Sports Med 1985; 13:87-94
7. Rorabeck CH: Exertional tibialis posterior compartment syndrome. Clin Orthop 1986; 208:61-64
8. Soffer SR, Martin DF, Stanish WD, Michael RH: Chronic compartment syndrome caused by aberrant fascia in an aerobic walker. Med Sci Sports Exerc 1991; 23:304-306
9. Rorabeck CH, Bourne RB, Fowler PJ, Finlay JB, Nott L: The role of tissue pressure measurement in diagnosing chronic anterior compartment syndrome. Am J Sports Med 1988; 16:143-146
10. Rorabeck CH, Fowler PJ, Nott L: The results of fasciotomy in the management of chronic exertional compartment syndrome. Am J Sports Med 1988; 16:224-227
11. Fronek J, Mubarek SJ, Hargens AR, Lee YF, Gershuni DH, Garfin SR, Akeson WH: Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop 1987; 220:217-227
12. Pedowitz RA, Toutounghi FM: Chronic exertional compartment syndrome of the forearm flexor muscles. J Hand Surg 1988; 13A:694-696
13. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990; 18:35-40
14. Styf JR, Korner LM: Chronic anterior-compartment syndrome of the leg. Results of treatment by fasciotomy. J Bone Joint Surg 1986; 68A:1338-1347
15. Styf J, Korner L, Suurkula M: Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome. J Bone Joint Surg 1987; 69B:301-305
16. Styf JR, Korner LM: Microcapillary infusion technique for measurement of intramuscular pressure during exercise. Clin Orthop 1986; 207:253-262
17. Detmer DE, Sharpe K, Sufit RL, Girdley FM: Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med 1985; 13:162-170
Figure Legends
Fig. 1. Cross-sectional anatomy in the proximal and distal thirds of the leg.
Fig. 2. The relative incidence of exercise-induced compartment syndromes of the leg.
Fig. 3. This runner presented with abnormal pain in the distal third of his leg after exercise. Clinical examination was significant for an abnormal soleus muscle causing exercise-induced pain from a "soleus syndrome." A, standing. B, with the foot in dorsiflexion. The magnetic resonance images (C and D) demonstrate an abnormally large soleus muscle occupying the distal superficial posterior compartment of the leg.
Fig. 4. The skin (A) and fasciotomy (B) incisions used to decompress the anterior and lateral compartments of the leg.
Fig. 5. The skin (A) and fasciotomy (B) incisions used to decompress the posterior compartments of the leg.
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