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Exercise-Induced Leg Pain

Sifting Through a Broad Differential

Michael Korkola, MD; Annunziato Amendola, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO.6 - JUNE 2001


In Brief: The causes of exertional leg pain are not always easily determined but are often linked to repetitive stress. Medial tibial stress syndrome or periostitis, tibial stress fractures, deep posterior compartment syndrome, exertional compartment syndrome, fascial hernias, peripheral neuropathy, and blood vessel entrapments have characteristic signs and symptoms. A complete history and exam coupled with wise use of adjunctive investigations will lead to the correct diagnosis and treatment.

Exercise-induced leg pain is a common condition in competitive and recreational athletes. It has been estimated that "shin splints" account for 10% to 15% of all running injuries and may account for up to 60% of leg pain syndromes (1). Many terms have been used in the literature for the diagnosis and description of exercise-induced leg pain, including shin splints, tibial stress syndrome, recurrent exercise-induced ischemia, and chronic exertional compartment syndrome. "Shin splints" has been commonly used as an all-encompassing term for many disorders causing lower-leg pain. To avoid confusion, we prefer "exercise-induced" or "exertional" leg pain to describe symptoms until a clear diagnosis has been made.

Etiology

The causes of exertional leg pain in the athlete are numerous. The etiology and subsequent investigations can be organized in terms of the tissue of origin (table 1) or in terms of local versus distant causes (table 2). The conditions in table 2 provide a practical approach to exertional leg pain and the more common conditions of medial tibial stress syndrome (MTSS) and exertional compartment syndrome (ECS).


TABLE 1. Tissue of Origin and Examples of Pathology of Exercise-Induced Leg Pain

Tissue of Origin Examples of Pathology

Bone Tibial stress fracture, fibular stress fracture
Periosteum Periostitis (medial tibial stress syndrome)
Muscle or fascia Exertional compartment syndrome, fascial herniation
Tendon Achilles, peroneal, or tibialis posterior tendinopathy
Nerve Sural or superficial peroneal nerve entrapment
Blood vessel Popliteal artery entrapment, intermittent claudication, or other insufficiency
Distant (referred) Spinal radiculopathy


TABLE 2. Local vs Distant Pathology of Exercise-Induced Leg Pain

Local Pathology Distant Pathology
Periostitis (medial tibial stress syndrome) Popliteal artery entrapment
Tibial or fibular stress fracture Arterial insufficiency, claudication
Exertional compartment syndrome Venous insufficiency
Fascial herniation Spinal radiculopathy
Peroneal tendinopathy, Achilles posterior tibial tendinopathy Sural or superficial peroneal nerve entrapment, common peroneal nerve entrapment

The age of the patient is also a key factor in formulating a differential diagnosis. For example, distant causes (intermittent claudication, spinal stenosis, and venous stasis) are more common in the mature athlete, whereas a diagnosis of ECS would be much more common in a young, healthy athlete. The importance of a complete history and physical examination cannot be overemphasized. Adjunctive investigations (imaging, electrodiagnostic studies, and compartment pressure measurements) must be instituted with a clear differential diagnosis in mind.

In addition, conditions that alter biomechanics and gait, such as tarsal tunnel syndrome or pes planus with tibialis posterior tendon dysfunction, may cause leg pain, but further discussion of these is beyond the scope of this article.

Medial Tibial Stress Syndrome

The true incidence of MTSS is unknown, but it is the most common cause of exertional leg pain in athletes, especially in those participating in repetitive activities, particularly jumping and running. In their definition of MTSS, Michael and Holder (2) included the clinical characteristics of dull aching to intense pain that is alleviated by rest, and tenderness over the posteromedial border of the tibia with the absence of any neurovascular abnormalities. We reserve the term MTSS for periostitis of the posteromedial tibia or use it as a synonym for periostitis.

Detmer (3) classified the disorder into three distinct entities: periostitis, deep posterior compartment syndrome, and tibial stress fracture. Although these conditions are related and may coexist, they should be considered three distinct diagnoses with different presentations and treatments.

Periostitis

The exact cause of periostitis is unclear, and it is controversial whether there is any active inflammation at the site of maximal tenderness (4). It may represent a continuum from the normal stress response of bone to pathologic stress fracture. Detmer (3) suggests that traction from the soleus muscle may actually be responsible for overloading the tibial periosteum. The soleus muscle has been implicated as a cause of "shin splints syndrome," although magnetic resonance imaging (MRI) has shown periosteal edema at the origin of the tibialis posterior and flexor digitorum longus, as well as the soleus (5) (figure 1).

[Figure 1]

In addition, posterior tibial dysfunction with pes planus deformity may cause similar findings along the posterior and distal third of the medial tibia because of pain and inflammation caused by overuse of the posterior tibial tendon. Patients typically have pain over the distal posteromedial tibia. In contrast to a stress fracture, the pain tends to be more diffuse from the soleus bridge to the distal supramalleolar region. The soleus inserts on the posteromedial aspect of the calcaneus, which predisposes the pronated foot to stress changes at both the origin and insertion. The pain is activity related, and neurologic symptoms are generally absent.

The clinical diagnosis of periostitis is made by history and examination. Diffuse pain and tenderness along the posteromedial border of the tibia, normal x-rays, and the absence of neurologic findings generally are enough to make this diagnosis. If the diagnosis is not clear, further investigation with bone scan or possibly MRI (figure 2) should be diagnostic. Periostitis has a distinct scintigraphic appearance with increased uptake along the posteromedial border of the tibia on delayed-phase images. The uptake is longitudinally oriented, and one third or more of the tibia is involved; stress fractures show a more localized uptake. Radionucleotide angiograms and blood-pool images are typically normal.

[Figure 2]

MTSS, unlike ECS, appears to be an inflammatory condition; therefore, clinical examinations and investigations are positive in MTSS. Leg pain is cumulative with activity and is present longer (ie, for days) before it improves with rest. In contrast, pain from ECS subsides within minutes after cessation of exercise, and the clinical investigation for ECS is often negative.

Treatment for periostitis is initially conservative. Modification of activities is often most successful. Modalities to decrease inflammation, including nonsteroidal anti-inflammatory drugs (NSAIDs), local phonophoresis with corticosteroids, ointments, and leg wraps, may be useful. If foot alignment needs correction, orthoses may help. A dedicated program of strengthening of the invertors and evertors of the calf is very important in preventing recurrence; nevertheless, recurrence is common after patients resume heavy activity.

The results of surgery are variable given the absence of rigid diagnostic clinical criteria and variability in the surgery performed. If nonoperative treatment fails and the patient remains symptomatic, we recommend a fasciotomy of the deep posterior compartment with release of the painful portion of periosteum (6). The procedure is not without complications because the saphenous nerve and vein are present posteromedially in the area of surgery and must be protected to avoid injury. A strengthening and stretching program is begun shortly after surgery, progressing to functional exercises as tolerated. Expected return to activity depends on postoperative recovery but is generally 8 to 12 weeks.

Deep Posterior Compartment Syndrome

This differs from periostitis or stress fractures in that it usually subsides quickly with rest and is not an inflammatory condition in the classic sense. Chronic deep posterior compartment syndrome is more a biomechanical phenomenon of the muscle compartment and may coexist with MTSS. Compartment pressures may be used to distinguish the two. Methods of measuring compartment pressures are discussed in the "Exertional Compartment Syndrome" section.

Tibial Stress Fractures

Bone is constantly remodeling. When bone is subjected to stresses over and above those normally seen, bone turnover increases in an attempt to strengthen. There is a fine balance between the amount and duration of stress and the bone's reparative capabilities. With repetitive stresses, the bone weakens to the point of failure if the resorptive process tips the scale (7). A stress fracture occurs when the repetitive loads exceed the bone's reparative abilities. Tibial stress fractures represent 10% to 20% of injuries in athletes (8,9).

It is important to distinguish stress fractures—or more appropriately named, fatigue fractures—from pathologic fractures that occur as a result of normal stresses to abnormal bone (10). A number of mechanisms, all of which ultimately lead to a fatigue fracture, are commonly seen in athletes who have increased their training intensity, altered their footwear, started training on harder surfaces, or failed to modify their activities at the onset of symptoms (11). Abnormal lower- limb alignment may be a predisposing factor. Risk factors associated with a higher incidence of fatigue fractures are lower body weight (<75% of ideal), eating disorders such as anorexia and bulimia, previous levels of inactivity, white race, and female sex (10).

The athlete usually experiences exertional pain localized to the posteromedial aspect of the tibia. The pain and tenderness may not be completely alleviated by rest, as would be more typical of ECS or periostitis. If athletes do not modify their regimens, the pain will occur earlier in the activity (12). A history of trauma preceded by an aching discomfort in the leg may exist in as many as 10% of patients. On physical examination, the most important sign to note is localized tenderness at the affected site rather than the diffuse longitudinal tenderness found in periostitis. Helpful signs include pain reproduced with a sustained one-leg hop, and percussion at a distant site that localizes pain to the site of the lesion.

A complete history and physical exam will lead to the diagnosis of stress fracture in the vast majority of cases. If the history includes stress fractures, patient education is an important factor. Identifiable risk factors should be avoided or modified. Management of stress fractures, although difficult, should first be aimed at prevention.

Plain film radiographs have not been particularly helpful (8) but occasionally may be diagnostic. Important indirect clues to look for are periosteal new bone formation or cortical breaks. These findings, however, may not appear on x-rays for up to 12 weeks (13). A delay in diagnosis may in turn increase the length of the recovery in some cases.

Three-phase bone scan is a useful diagnostic tool when the history and physical examination are not clear-cut (figure 3). It is a sensitive test but not particularly specific and therefore must be correlated with the clinical presentation. More recently, MRI has been described as a sensitive and specific adjunctive diagnostic tool. Fredericson (5) advocates its use in diagnosing and treating tibial stress fractures. He has devised a classification system to aid in correlating the clinical findings with MRI findings. The main drawbacks are cost and availability.

[Figure 3]

Matheson et al (9) outlined a stepwise approach to the management of an established stress fracture. The first step consists of rest and restricted weight bearing. Crutches may be required. A cast is rarely required for proximal and distal tibial stress fractures in the compliant patient. If the patient has a limp with normal weight bearing, initial cast immobilization for 3 weeks may be useful. Casting may be required in diaphyseal fractures, especially on the anterior tension side of the bone. Alternatively, a removable leg brace or walker may be used. Acetaminophen, NSAIDs, ice, and massage may also aid in pain relief. Symptoms usually resolve in 2 to 4 weeks but may last several months in the noncompliant patient or if the diagnosis is delayed. Continuation of nonimpact aerobic activities such as cycling, swimming, and water running is encouraged during this phase.

After symptoms resolve, the second phase of treatment begins. The patient gradually increases activities on soft surfaces and continues nonimpact aerobic activities on alternate days for about 6 weeks. The importance of activity modification, proper footwear, and sensible diet is stressed. Orthoses may be an important adjunctive treatment if any biomechanical predisposition or overload is detected. The vast majority of fractures will heal if the patient adheres to the recommendations.

Delayed union, nonunion, and progression. Stress fractures in the anterior tibial shaft are less common but warrant further discussion given the increased incidence of delayed union, nonunion, and progression to complete fracture. Currently, anecdotal reports detail the use of extra-corporeal shock-wave therapy to treat recalcitrant tibial stress fractures and nonunions. The evidence for the widespread use of this modality is quite limited, but it may be something to consider, short of surgery, to stimulate healing.

Brahms et al (8) discuss an anterolateral tibia fracture in a professional football player that progressed to a complete fracture 3 years after incomplete healing. Green et al (14) discuss six cases of anterior tibial stress fractures, all of which were resistant to the usual nonoperative treatment measures. They note that an incomplete fracture on the tension side of the bone, with large posterior muscle forces, is more likely to progress to completion. They suggest that if no healing has occurred within 4 to 6 months of nonoperative treatment, an iliac crest graft should be considered. The athlete should not return to sport until healing is complete.

In contrast, Rettig et al (15) presented 8 patients with similar fractures who were treated with rest and/or pulsing electromagnetic therapy. Seven of the 8 healed without grafting; however, the average time from the onset of symptoms until return to competition was 12.5 months. More recently, intramedulary fixation has been used for recalcitrant diaphyseal stress fractures rather than open grafting.

Exertional Compartment Syndrome

The muscles of the lower limb are divided into compartments enclosed by relatively noncompliant fascia. Many terms have been used for the elevated compartment pressure of ECS, including chronic compartment syndrome, recurrent compartmental ischemia, and anterolateral compartmental syndrome. We believe ECS is the most descriptive and accurate term because this condition is present during exertion but goes away between activities.

The pathophysiology of ECS is not as well defined in the acute form. Experimental evidence has been unable to demonstrate a decrease in blood flow despite documented elevated compartment pressure and a consistent clinical presentation. MRI, MRI spectroscopy, and nuclear medicine blood-flow studies have all been used with limited success (16). Muscle biopsies have provided conflicting results regarding the role of muscle ischemia in the generation of pain.

Embree (17) demonstrated a decrease in phosphofructase after performing fasciotomies in patients with documented elevated compartment pressures. Phosphofructase is a marker of glycolytic metabolism that indicates a shift from preoperative anaerobic metabolism to a lower anaerobic level postfasciotomy. In general, the pain in this syndrome is likely caused by ischemia secondary to insufficient oxygen and nutrient transfer to muscle capillary beds. Further studies are required to better define the pathophysiology.

The diagnosis of ECS has long been considered to be one of exclusion; however, with a better understanding of the presentation, the diagnosis is usually readily apparent. The patient's history is paramount. The syndrome has been previously described as local pain associated with swelling and paresthesias (18). Pedowitz et al (19) describe a variable presentation in which patients may have pain described as achy, sharp, or dull. Cramping, swelling, associated muscle tightness, or paresthesias may occur if exercise continues.

Rampersaud and Amendola (6) indicated that the diagnosis of ECS need not be one of exclusion. The patient characteristically has reproducible exercise-induced leg pain that is completely relieved by cessation of the offending activity, no pain at rest, and a normal physical examination. These patients warrant intracompartmental pressure measurements to confirm the diagnosis (see "Measuring Intracompartmental Pressure," below), rather than the extensive imaging studies or other investigations that are usually conducted. Predictors that may also add weight to the clinical diagnosis include bilateral symptoms, young age (<30 years old), and running or repetitive-stress sports.

Electromyography and nerve-conduction velocities have a limited role in the diagnostic workup. The test results are generally normal preoperatively and remain normal following fasciotomy (17). ECS is a biomechanical problem and is therefore usually not amenable to nonoperative management. Intracompartmental pressure normally rises and falls with activity; therefore, nonsurgical modalities do not effect pressure. Physical therapy, anti-inflammatory medications, and orthoses have generally been ineffective.

Operative treatment is indicated for patients who have appropriate clinical presentations with confirmatory pressure measurements and are unwilling to modify or give up their sport of choice. Although various techniques have been described, we use a two-incision fasciotomy of both the lateral and anterior compartments (figure 4) (6). Drains are used postoperatively and are removed before the patient is discharged home the same day. Multiple authors (20-22) have reported excellent results if the appropriate surgical indications and technique are followed.

[Figure 4]

Rehabilitation progresses according to what the patient can tolerate. The first 2 weeks are directed at decreasing swelling, improving range of motion of the ankle and knee, and weight bearing as tolerated. The next 2- to 6-week period is directed at regaining strength and functional exercise. Expectations are to return to activities 6 to 8 weeks postoperatively.

Anterior compartment involvement is more common and accounts for approximately 70% to 80% of the cases. Posterior compartment involvement is less common and has been associated with less predictable surgical outcomes. If the symptoms are posterior, and elevated posterior compartment pressures are documented, a single incision is used to release the tibialis posterior and remainder of the deep compartment. The tourniquet is released prior to closure to ensure adequate hemostasis.

A number of reasons may explain the inferior results noted after release of the posterior compartment. Deep posterior calf pain is often associated with coexisting MTSS. Rorabeck et al (20) indicate that the most likely explanation is that the tibialis posterior muscle is not completely decompressed. They recommend exposing the tibialis posterior muscle and tendon before incising its fascia.

A potential postsurgical cause of pain is scarring of the fasciotomy incision. Patients undergoing posterior releases are often more uncomfortable than those who have undergone anterior releases. Aggressive range of motion of the ankle and knee is essential postoperatively to prevent plantar flexion contracture of the ankle.

Other Compartment-Related Causes of Pain

Acute compartment syndrome. When compartmental pressure acutely exceeds the microvascular perfusion pressure, ischemia and subsequent neuromuscular necrosis develop if the pressure is not relieved. In acute compartment syndrome, the chronic sequelae of contracture, nerve dysfunction, and muscle function become constant rather than arising from exertion. Fractures of the tibia are the most common cause of acute compartment syndrome.

When the diagnosis is made, the compartments must be decompressed as soon as possible. Chronic ECS must be distinguished from acute compartment syndrome because the urgency to perform a fasciotomy is quite different.

Fascial hernia. Patients who have fascial hernias will report a variety of symptoms in addition to exercise-induced leg pain. Physical examination will usually reveal a mass over the anterior compartment with a palpable fascial defect that may vary in size with exercise. There is no indication to repair the fascial defect, even if cosmetic appearance is an issue in an otherwise asymptomatic leg, because closure of the defect will likely increase intracompartmental pressure and can precipitate an acute compartment syndrome.

Mubarak (23) states that there is frequently a hernia at the exit of the superficial peroneal nerve, or of one of its branches, in "chronic compartment syndrome." According to Touliopolous and Hershman (12) a hernia becomes symptomatic because of chronic ECS, a compressive neuropathy, or ischemia of the herniated muscle tissue.

Miniaci and Rorabeck (24) have outlined a management approach. Patients with asymptomatic hernias require no treatment. Symptomatic hernias should be initially managed with education, activity modification, and, possibly, use of support hose. Failure of these modalities may be an indication for surgery. Good results have been obtained from decompressing the entire compartment.

Peripheral Neuropathy

Compression or nerve entrapment can lead to a functional disturbance or pathologic change in the peripheral nerve that may be documented by further investigation.

The common peroneal nerve may be compressed where it passes around the fibular neck. History and physical examination in the setting of exercise-induced leg pain should lead to the correct diagnosis. Electrodiagnostic studies before and after exercise are helpful in determining the exact location of the lesion. If a mass effect is suspected (eg, ganglion from the proximal tibiofibular articulation), further imaging with x-rays, MRI, or computed tomography may be warranted. Compartment pressure measurements may be used to differentiate peroneal nerve lesions from chronic anterior compartment syndrome, which may have a similar presentation.

Leach et al (25) described peroneal nerve entrapment in a group of 7 runners and 1 soccer player who all had exercise-induced leg pain, paresthesia, postexercise weakness, and positive percussion signs at the fibular neck. Diagnosis was confirmed in all subjects by nerve conduction studies made before and after running. Pre-exercise values were normal; a decrease in the conduction velocity of the common peroneal nerve at the fibular neck was noted postexercise. Three of the 7 runners underwent compartment pressure monitoring; the results were normal. All 8 patients had surgical decompression just proximal to the fibular neck. The soccer player noted dramatic relief and returned to full activities; 6 of the 7 runners had similar results. The other runner noted relief of symptoms but was unable to return to his previous level of activity.

The superficial peroneal nerve is a branch of the common peroneal nerve. The nerve is most commonly compressed as it exits the deep fascia to become subcutaneous, a point where localized tenderness may be encountered. In addition to muscle herniation, the nerve can also be compressed by the fascial edge or be subjected to repeated traction by recurrent inversion ankle sprains; 25% of patients note a history of trauma, particularly recurrent ankle sprains (26).

Patients may have activity-related pain and neurologic symptoms in the distal third of the leg or the dorsum of the foot and ankle. Weakness is not expected because the innervation of the peroneals is proximal to the site of compression.

Physical examination should include a detailed neurovascular examination from the spine to the foot. Additional tests include palpation at the site where the nerve exits the deep fascia (11 cm above the tip of the lateral malleolus) while the patient actively dorsiflexes and averts against resistance. Alternatively, the foot is passively plantar flexed while the nerve is percussed along its length (26). Tinel's percussion sign is often present. Treatment includes activity modification with surgical release for resistant cases.

The sural nerve originates in the popliteal fossa as a branch of the tibial nerve and subsequently anastomoses with the peroneal communicating nerve. It runs adjacent to the Achilles tendon with the short saphenous vein and terminates in the lateral aspect of the foot. It can be compressed anywhere along its course, usually from trauma but occasionally from a tumor.

Sural nerve entrapment is a less common neuropathy in patients who have exercise-induced leg pain. Patients may present with pain or paresthesias within the posterolateral aspect of the calf and foot. There may or may not be a history of trauma. Electrodiagnostic studies are useful to pinpoint the exact site of compression. Other imaging modalities, such as MRI, are useful when planning surgery. Treatment of resistant cases includes surgical release at the site of compression followed by specific rehabilitation.

Lumbar Radiculopathy and Spinal Stenosis

Patients suffering from spinal stenosis are often middle-aged or older. They may have a long-standing history of low-back pain with a more recent onset of lower-extremity symptoms. Again, the history and physical examination are paramount. The physical exam may or may not reveal significant neurologic signs. Often the symptoms and physical signs can be elicited by having the patient exercise for a short period. Investigations include plain film radiograph flexion and extension views to check for dynamic instability. MRI is the imaging modality of choice to confirm the diagnosis and rule out other more worrisome causes such as malignancy.

Treatment consists of education, activity modification, a structured physical therapy program, and a short course of NSAIDs. Epidural corticosteroid injections may be useful for radicular symptoms. Indications for surgery include an objective neurologic deficit and disabling pain resistant to nonoperative treatment. A number of good reviews discuss management of spinal stenosis (27-29).

Peripheral Vascular Disease

Lesions or entrapments of the anterior tibial artery and vein, great or small saphenous vein, popliteal vein, peroneal vein, or other blood vessels can be a source of exertional leg pain.

Intermittent claudication is caused by insufficient blood supply to exercising muscle. Patients are usually in the active older age-group and may have comorbid illnesses. They typically report an aching sensation or cramp that occurs with walking; usually a consistent distance will bring on the symptoms. Symptoms quickly resolve with rest. Progression to symptoms at rest usually indicates progression of the disease. Symptoms depend on the site of the lesion, the extent of the obstruction, and the development of collateral flow.

Physical examination readily identifies an abnormality, but angiography is helpful to determine the exact location of the lesion as well as its size and extent. The severity of the lesion will govern further treatment that may include regular moderate exercise to promote the development of collateral flow and smoking cessation, if needed. Percutaneous transluminal angioplasty plays a role in localized lesions and yields good results in the iliac arteries (95%) and acceptable results in the thigh and calf arteries (50% to 60%) (30). Pharmacotherapy is beyond the scope of this discussion.

Popliteal artery entrapment syndrome is uncommon. It should be included in the differential diagnosis of young adults presenting with ischemic lower-extremity symptoms. Compression may occur at the origin of the medial head of the gastrocnemius or plantaris (30), or as a result of an aberrant course of the vessel. Compression of the popliteal vein occurs in 10% to 15% of patients (31) and may be responsible for the initial presentation of leg pain, edema, and even deep vein thrombosis.

Diagnosis begins with a complete history, physical examination (specifically, the distal pulses), and a high index of suspicion. MRI combined with MR angiography has recently been advocated as the most effective way to view these lesions (32). Treatment is usually surgical and depends on the patient's underlying condition. Removal of the offending compressive structure with reconstruction of the artery has been advocated in the medical literature (33).

Venous stasis is another uncommon cause of exertional leg pain in the mature athlete. Patients most commonly experience skin and vascular changes in the supramalleolar region. The plexus of veins in this area of the leg contribute to the saphenous vein and are usually inflamed and tender to palpation by the examiner. Often, patients experience pain that is worse at the end of the day and aggravated by repetitive daily activities. Treatment modalities center around modification of offending activity and the use of pressure support hose.

Meeting the Challenge

Exercise-induced leg pain is common in today's active population. The importance of a detailed history and physical examination cannot be overemphasized. It is a challenging problem to treat, but satisfactory results will be obtained with an accurate, timely diagnosis and a multidisciplinary approach to treatment.

References

  1. Bates P: Shin splints: a literature review. Br J Sports Med 1985;19(3):132-137
  2. Michael RH, Holder LE: The soleus syndrome: a cause of medial tibial stress (shin splints). Am J Sports Med 1985;13(2):87-94
  3. Detmer DE: Chronic shin splints: classification and management of medial tibial stress syndrome. Sports Med 1986;3(6):436-446
  4. Chambers HG: Medial tibial stress syndrome: evaluation and management, in Drez D Jr, DeLee JC (eds): Operative Techniques in Sport Medicine: Compartment Disorders: Classification, Pathophysiology, Diagnosis, and Treatment. WB Saunders Co, 1995, vol 3, no. 4, pp 247-277
  5. Fredericson M: Diagnosing tibial stress injuries in athletes. West J Med 1995;162(2):150
  6. Rampersaud YR, Amendola A: The evaluation and treatment of exertional compartment syndrome, in Drez D Jr, DeLee JC (eds): Operative Techniques in Sport Medicine: Compartment Disorders: Classification, Pathophysiology, Diagnosis, and Treatment. WB Saunders Co, 1995, vol 3, no. 4, pp 267-273
  7. Clanton TO, Solcher BW: Chronic leg pain in the athlete. Clin Sports Med 1994;13(4):743-759
  8. Brahms MA, Fumich RM, Ippolito VD: Atypical stress fracture of the tibia in a professional athlete. Am J Sports Med 1980;8(2):131-132
  9. Matheson GO, Clement DB, McKenzie DC, et al: Stress fractures in athletes: a study of 320 cases. Am J Sports Med 1987;15(1):46-58
  10. Amendola A, Bell D: Stress fractures and exertional compartment syndrome, in Bull CR (ed): Handbook of Sports Injuries. New York City, McGraw-Hill, 1999, pp 245-263
  11. McBryde AM: Stress fractures in runners. Clin Sports Med 1985;4(4):737-752
  12. Touliopolous S, Hershman EB: Lower leg pain: diagnosis and treatment of compartment syndromes and other pain syndromes of the leg. Sports Med 1999;27(3):193-204
  13. Sullivan D, Warren RF, Pavlov H, et al: Stress fractures in 51 runners. Clin Orthop 1984;187(Jul-Aug):188-192
  14. Green NE, Rogers RA, Lipscomb AB: Nonunions of stress fractures of the tibia. Am J Sports Med 1985;13(3):171-176
  15. Rettig AC, Shelboume KD, McCarroll JR, et al: The natural history and treatment of delayed union stress fractures of the anterior cortex of the tibia. Am J Sports Med 1988;16(3):250-255
  16. Amendola A, Rorabeck CH, Vellett D, et al: The use of magnetic resonance imaging in exertional compartment syndromes. Am J Sports Med 1990;18(1):29-34
  17. Embree MJ: Chronic compartment syndrome: an analysis at the cellular level, thesis. London, Ontario, Faculty of Graduate Studies, The University of Western Ontario, 1996
  18. Matsen FA, Rorabeck CH: Compartment syndromes. Instr Course Lect 1989;38:463-472
  19. Pedowitz RA, Hargens AR, Mubarak SJ, et al: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990;18(1):35-40
  20. Rorabeck CH, Fowler PJ, Nott L: The results of fasciotomy in the management of chronic exertional compartment syndrome. Am J Sports Med 1988;16(3):224-227
  21. Fronek J, Mubarak SJ, Hargens AR, et al: Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop 1987;220(Jul):217-227
  22. Detmer DE, Sharpe K, Sufit RL, et al: Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med 1985;13(3):162-170
  23. Mubarak SJ: Surgical management of chronic compartment syndromes of the leg, in Drez D Jr, DeLee JC (eds): Operative Techniques in Sport Medicine: Compartment Disorders: Classification, Pathophysiology, Diagnosis, and Treatment. WB Saunders Co, 1995, vol 3, no. 4, pp 259-266
  24. Miniaci A, Rorabeck CH: Compartment syndrome as a complication of repair of a hernia of the tibialis anterior: a case report. J Bone Joint Surg Am 1986;68(9):1444-1445
  25. Leach RE, Purnell MB, Saito A: Peroneal nerve entrapment in runners. Am J Sports Med 1989;17(2):287-291
  26. Baxter DE: Functional nerve disorders in the athlete's foot, ankle and leg. Instr Course Lect 1993;42:185-194
  27. Velan GJ, Currier BL, Yaszemski MJ: Decision making in the evaluation and management of acquired spinal stenosis: an algorithmic approach. Sem Spine Surg 1999;11(3):195-208
  28. Shakil MS, Vaccaro AR, Albert TJ, et al: Efficacy of conservative treatment of lumbar spinal stenosis. Sem Spine Surg 1999;11(3):229-233
  29. Jenis LG, An HS: Spine update: lumbar foraminal stenosis. Spine 2000;25(3):389-394
  30. Taunton JE, Maxwell TM: Intermittent claudication in an athlete—popliteal artery entrapment: a case report. Can J Appl Sport Sci 1982;7(3):161-163
  31. Gerkin TM, Beebe HG, Williams DM, et al: Popliteal vein entrapment presenting as deep venous thrombosis and chronic venous insufficiency. J Vasc Surg 1993;18(5):760-766
  32. Atilla S, Akpek ET, Yucel C, et al: MR imaging and MR angiography in popliteal artery entrapment syndrome. Eur Radiol 1998;8(6):1025-1029
  33. Stager A, Clement D: Popliteal artery entrapment syndrome. Sports Med 1999;28(1):61-70


Measuring Intracompartmental Pressure

Confirmatory pressure measurements are made by many methods. The most symptomatic leg and compartment are usually investigated. The authors' preference is an indwelling slit catheter before, during, and after exercise. Once the catheter is inserted, the patient is asked to exercise, walk, or jog on a treadmill until symptoms are reproduced or the patient is unable to continue. Resting pressure, immediate postexercise pressure, and continuous pressure measurements for 30 minutes after exercise are most important to confirm the diagnosis. A study is considered positive if the insertional pressure is greater than or equal to 15 mm Hg, the immediate postexercise pressure is greater than or equal to 30 mm Hg, or if the pressure at 15 minutes postexercise fails to return to normal or exceeds 15mm Hg.


Dr Korkola is an orthopedic resident and Dr Amendola is an orthopedic consultant at Fowler/Kennedy Sport Medicine Clinic in London, Ontario, Canada. Address correspondence to Annunziato Amendola, MD, Fowler/Kennedy Sport Medicine Clinic, 3M Center, University of Western Ontario, London, Ontario, Canada N6A 3L8; e-mail to [email protected].


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