Exercise-induced leg pain can be related to a number of etiologies, some more elusive than others. Differential diagnoses in the workup of exercise-induced leg pain should include musculotendinous injury, exertional compartment syndrome, popliteal artery entrapment syndrome, medial tibial stress syndrome (MTSS) and stress fracture.
Other less common causes of exercise-induced leg pain include lumbosacral radiculopathy, lumbosacral spinal stenosis, focal nerve entrapment, vascular claudication from atherosclerosis, venous insufficiency, neoplasm and various myopathies.
With these considerations in mind, let us take a closer look at the diagnosis and treatment of exertional compartment syndrome, popliteal artery entrapment syndrome, MTSS and stress fracture.
An exertional compartment syndrome is due to a decrease in the compartment volume, which is related to increased muscle edema and capillary ingress. Compartmental pressure increases and this creates a pressure gradient, which is not favorable to arterial inflow. In turn, muscle hypoxia and eventual myonecrosis can result. Upon rest, a decrease in intracompartmental pressure occurs and arterial inflow returns, relieving myofascial ischemia and pain.
The diagnosis of an exertional compartment syndrome requires a high index of suspicion and further clinical investigation using a device such as a wick or slit catheter, a side ported needle (Stryker® manometer) or a simple needle to measure compartment pressures. In the clinic setting, physicians can test pre-exercise compartment pressures and then have the patient engage in exercise until the onset of symptoms. One can then remeasure compartment pressures immediately upon the cessation of activity. This often takes appropriate planning by the clinician and patient.
Intracompartmental pressures > 10 mmHg at rest and/or > 25 mmHg five minutes after exercise have been defined as abnormally elevated.1
Leg pressures that may indicate exercise-induced compartment syndrome are pressures > 30 mmHg one minute after exercise and/or > 20 mmHg five minutes after exercise. Leg pressures > 40 mmHg are diagnostic for exercise-induced compartment syndrome.1-3
The treatment for exertional compartment syndrome can include conservative care, which essentially is limitation of activity. Surgical intervention with decompression fasciotomy has a fairly high success rate of resolving symptoms.1 Traditionally, surgeons have performed open fasciotomy but endoscopic fasciotomy is also an option. Using an endoscope and fasciotomy blade, one can use minimal incisions that may facilitate recovery.
Popliteal artery entrapment syndrome is less common than exertional compartment syndrome. The reported prevalence is 0.16 to 3.5 percent and occurs typically in young men 20 to 40 years of age who have well developed leg musculature.4 The condition can be due to abnormal positioning of the popliteal artery in relation to its surrounding structures. In turn, extrinsic compression leads to an irreversible lesion of the popliteal artery, such as aneurysmal dilatation, thrombosis or intimal thickening.
Typically, patients present with claudication symptoms that are often positional and exercise-induced, leg edema, aching pain, pain at rest, tiredness or calf cramping. Knee extension and/or hyperextension and a plantarflexed foot will elicit non-palpable distal pulses, and when the knee is neutral or slightly flexed, pulses are palpable.5-8
Diagnostic imaging can include duplex ultrasonography, computed tomography (CT) with contrast, digital subtraction angiography and conventional arteriography, all of which one performs with dynamization of the limb. For a patient with popliteal artery entrapment syndrome, this allows visualization of popliteal artery occlusion when the knee is hyperextended and the foot is plantarflexed.
Treatment typically requires consultation with a vascular surgeon and surgical intervention. In the early stages, surgical decompression of the popliteal artery can often alleviate symptoms. However, in the late stages, use of a saphenous vein bypass graft is appropriate.
Medial tibial stress syndrome and tibial stress fracture can both be correlated with biomechanical and structural conditions such as hindfoot varus, excessive forefoot pronation, genu valgum, excessive femoral anteversion and external tibial torsion. The pathomechanics for MTSS typically involve two proposed theories: tibial bending and fascial traction.
In regard to MTSS, Bouche and Johnson concluded in a cadaver study that fascial tension increased with increased strain on the posterior tibial, flexor digitorum longus and soleus tendons, possibly giving some merit to the fascial traction theory.9
Both MTSS and stress fracture occur often in athletes partaking in high impact activities such as running or jumping sports. Both conditions are rare in adolescents under 15 years of age.
One would make the diagnosis of MTSS via a clinical exam with patients experiencing diffuse tenderness to palpation along the posteromedial border of the mid- to distal one-third of the tibia. Trace to mild edema may be present as well.
Stress fractures tend to have more focal pain on exam. When it comes to imaging, one should begin with radiographs, which are usually normal for MTSS but may show periosteal reaction for a stress fracture. Physicians can obtain a three-phase Tc-99 bone scan as well. This scan may demonstrate linear streaking for MTSS versus a “hot spot” and focal uptake that occur in a stress fracture. Magnetic resonance imaging (MRI), although more expensive, can be more specific and is also an option for differentiating MTSS from a stress fracture.
Treatment for both conditions includes cessation of high impact activities until symptoms resolve and this can take up to 12 weeks. Patients should substitute non-impact activities such as biking, swimming and aqua jogging for running during the recovery period. Ice massage for 20 minutes twice daily and nonsteroidal anti-inflammatory (NSAID) use can decrease symptoms as well. Use of a compression leg sleeve or taping for MTSS can allow relief of symptoms during impact activity if it were necessary for one to compete or continue an activity.
Upon the return to activity, it is important to evaluate the biomechanics of the patient and his or her shoe gear, and consider custom orthotics. Encourage cross training with low to no impact activities such as swimming and biking as well as a gradual return to a walk/jog program.
In determining a patient’s etiology of exercise-induced leg pain, it is important for the clinician to take a thorough history and physical to uncover all potential etiologies. It is important to remember that certain medications such as statin drugs or drugs such as diuretics that cause electrolyte imbalance can lead to myofascial pain and cramping.
Additionally, being aware of the patient’s diet as well as his or her family and social history can lend insight to diagnosis. Lower extremity specialists should be aware of the multiple pathologies that can cause exercise-induced leg pain. They should also be well versed in the diagnosis and treatment of these conditions, or ensure a proper referral when appropriate.
Dr. Jennings is affiliated with the Department of Orthopedics and Podiatry at the Palo Alto Medical Foundation in Mountain View, Calif.
Dr. Richie is an Adjunct Associate Professor in the Department of Applied Biomechanics at the California School of Podiatric Medicine at Samuel Merritt University. He is a Fellow and Past President of the American Academy of Podiatric Sports Medicine.
1. Fronek J, Mubarak SJ, Hargens AR, Lee YF, Gershuni DH, Garfin SR, Akeson WH. Management of chronic exertional anterior compartment syndrome. Clin Ortho. 1987; 220:217-27.
2. Pedowitz RA, et al. Chronic exercise-induced compartment pressure elevation measured with a miniaturized fluid pressure monitor. A laboratory and clinical study. Am J Sports Med. 1990; 18(1):35-40.
3. Awbrey BJ, et al. Chronic exercise-induced compartment pressure elevation measured with a miniaturized fluid pressure monitor. A laboratory and clinical study. Am J Sports Med. 1988; 16(6):610-5
4. Baltopoulos P, Filippou DK, Sigala F. Popliteal artery entrapment syndrome: anatomic or functional syndrome? Clin J Sport Med. 2004; 14(1):8-12.
5. Ring DH, et al, Popliteal artery entrapment syndrome: arteriographic findings and thrombolytic therapy. J Vasc Interv Radiol. 1999; 10(6):713-21.
6. Sipponen J, et al. Popliteal artery entrapment. Ann Chir Gyn. 1989; 78(2):103-9.
7. Iwai T, et al. Diagnostic and pathological considerations in the popliteal artery entrapment syndrome. Cardiovasc Surg (Torino). 1983; 24(3):243-9.
8. Radonić V, KoplićS, Giunio L, et al. Popliteal artery entrapment syndrome: diagnosis and management, with report of three cases. Tex Heart Inst J. 2000; 27(1):3-13.
9. Bouche RT, Johnson CH. Medial tibial stress syndrome (tibial fasciitis): a proposed pathomechanical model involving fascial traction. JAPMA 2007; 97(1):31-6.
Editor’s note: For further reading, see “Current Concepts In Treating Medial Tibial Stress Syndrome” in the April 2010 issue of Podiatry Today.