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Competitive Sports and Pain Management

Exertional Leg Pain

Teasing Out Arterial Entrapments

Pham, Thomas T. DO; Kapur, Rahul MD; Harwood, Marc I. MD

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Current Sports Medicine Reports: December 2007 - Volume 6 - Issue 6 - p 371-375
doi: 10.1097/01.CSMR.0000305615.98295.2b
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The vascular etiologies of exercise-induced leg pain include popliteal artery entrapment syndrome (PAES), endofibrosis (intimal hyperplasia), kinking or stenosis of the iliac artery, and arterial aneurysm or dissection. Vascular pathology as the cause of exercise-induced leg pain can be difficult to differentiate from the more common causes such as chronic exertional compartment syndrome (CECS), medial tibial stress syndrome (MTSS), and stress fractures. Understanding the common causes of exercise-induced lower leg pain and the various arterial etiologies will improve care for the athletic population, particularly the highly competitive athletes.

Chronic Exertional Compartment Syndrome (CECS)

CECS is a condition in which increased pressure in the fascial compartments of the lower extremities leads to recurrent episodes of leg discomfort [1••]. In an athletic population, this increased pressure is the result of increased oxygen demand of exercising muscle and the subsequent inflow of blood to supply the exercising muscle. There are four major compartments in the lower leg, each containing specific muscles and neurovascular structures bound by fascia and bone [1••,2]. The anterior compartment is most commonly involved (45%), followed by deep posterior (40%), lateral (10%), and superficial posterior (5%) compartments [1••].

The classic clinical presentation is recurrent, exercise-induced leg discomfort that occurs at a predictable distance or activity intensity, which increases with continued exertion and subsides with rest. The pain is usually described as cramping, burning, or a squeezing ache usually over a specific involved compartment, and the pain is often worse on the second day of hard workouts. Physical examination at rest is usually benign but may reveal a fascial defect and/or muscle hernia. Examination postexertion usually reveals a tense, firm compartment that is tender to deep palpation and passive stretch [2]. Neurological examination may exhibit findings specific to the compartment affected, such as foot drop and paresthesia over the dorsum of the foot with anterior compartment involvement [1••,2].

Diagnosis relies on confirmation of elevated compartment pressures coinciding with reproduction of the patient's symptoms [3]. Treatment of CECS is largely considered to be surgical, although aggressive fascial massage can alleviate symptoms in some athletes. Operative treatment involves fasciotomy of the involved compartments, and the anterior compartment releases generally achieve more successful outcomes. Verleisdonk et al. [4] reported an 87% improvement in symptoms at 2-year follow-up from anterior compartment fasciotomy.

Medial Tibial Stress Syndrome (MTSS)

MTSS is characterized by pain and tenderness over the posteromedial aspect of the distal tibia [5]. It is an overuse injury accounting for 6% to 16% of injuries in runners and 4% to 10% of military recruits [6]. The etiology is believed to be a stress reaction at the tibial attachment of the soleus and deep crural fascia resulting in a periostitis or traction fasciitis [5]. Intrinsic risk factors include excessive foot pronation and increased hindfoot varus. Training errors contribute to the majority of cases [5,6].

Patients typically present with diffuse tenderness over the distal posteromedial tibia that occurs with exercise, but may persist at rest in severe cases. Plain radiographs are usually normal, although rare cases show evidence of periosteal reaction [5]. Triple phase bone scan will show a classic diffuse longitudinal uptake along the tibial periosteum on the delayed images only [1••]. MRI has also shown utility in diagnosing and distinguishing MTSS from stress fractures [7]. The mainstay of treatment is relative rest and correction of intrinsic and extrinsic risk factors [1••]. Posterior fasciotomy to relieve traction from the deep crural fascia is indicated for refractory cases, with reported success rates of 69% to 90% [8].

Stress Fractures

Stress fractures result when bone fails to adapt adequately to the repetitive stress of exercise. Risk factors include previous stress fracture, low bone mineral density, menstrual irregularity, poor nutritional status, and biomechanical factors such as pes cavus [1••]. Presentation differs from MTSS in that individuals will often complain of insidious onset of pain and tenderness in a focal region. Radiographs are initially negative in the majority of patients and only half of patients with stress fractures eventually demonstrate radiographic abnormalities. Triple phase bone scan will show focal uptake in all three phases and MRI is highly sensitive and specific for stress fractures [1••]. Treatment for medial tibia stress fractures may require a short period of immobilization in a walking boot with gradual return to play, generally in 6 to 8 weeks. Anterior cortex tibial stress fractures are prone to nonunion and often require prolonged rest and immobilization for up to 6 months, use of a bone stimulator, and surgical intervention for refractory cases [1••].

In patients who fail treatment for these more common diagnoses, other causes must be pursued. Their pain etiology may stem from either external or internal disruption of the vascular tree.

External Factors (Arterial Entrapment)

Popliteal artery entrapment syndrome (PAES)

In 1965, Love and Whelan coined the term popliteal entrapment syndrome to illustrate the collection of neuromuscular and ischemic symptoms in the lower extremity from vascular impingement in the popliteal fossa of the knee [9]. The pain of PAES is ischemic or claudicant pain in the calf or anterior leg. The pain is brought on by exercise, and the severity of the symptoms correlates with the intensity of exercise rather than volume. Symptoms quickly resolve when exercise is stopped. The intensity, length, or character of the pain is unaffected by exercise on the previous day. It is not uncommon to have compartment syndrome coexist with PAES.

The physical examination tends not to assist with diagnosis. Sometimes there is a popliteal bruit at rest that is accentuated with forceful active ankle plantar-flexion or passive dorsiflexion. The bruit tends to be more pronounced immediately postexercise with associated weak or absent peripheral pulses.

A common etiology of PAES involves anatomic variation between the course of the popliteal artery in relation to the surrounding musculotendinous structures as it exits the popliteal fossa [10,11••]. The most common variant involves an accessory medial head of the gastrocnemius muscle that passes behind the popliteal artery [12]. Other anatomic variants include an aberrant course of the popliteal artery, popliteal compression from hypertrophy of the surrounding muscles, and fibrous bands of the gastrocnemius or the popliteus muscle causing vascular constriction [11••]. Clinical evidence suggests that these anatomic variations are associated with development of local occlusive or aneurysmal changes of the popliteal artery, which presents as lower limb pain and ischemia [9]. Chronic anatomic entrapment can lead to endothelial damage, which leads to accelerated atherosclerotic disease [10]. The prevalence and natural history of PAES is still uncertain, particularly in the absence of anatomic abnormalities [10].

Symptomatic patients with anatomic entrapments usually have focal extrinsic compressive bands of tendon or fascia that are associated with the development of intrinsic arterial disease and subsequent ischemic symptoms. These patients are commonly male with a mean age of 43 years. They are typically more sedentary, have more restrictive claudication symptoms, and often have evidence of peripheral occlusive disease on noninvasive testing [9].

Entrapment may also occur in the absence of an anatomic abnormality [9]. Functional popliteal entrapment refers to neuromuscular claudication with lower extremity paresthesias without anatomic abnormality and is due to repetitive overuse or orthopedic injury. It is thought that these symptoms originate from neuromuscular irritation [9]. Patients with functional entrapment have more diffuse lateral compression of disease-free vessels with symptoms caused by peripheral nerve compression. Compared with the anatomical entrapment patients, these patients are younger, with a mean age of 24 years. They are more often female and have an active lifestyle [9]. These patients tend to have normal resting and postexercise noninvasive tests. It appears that functional entrapment is a form of overuse injury and tends to occur in the same population at risk for chronic compartment syndrome [9]. Symptoms from functional entrapment originate from neuromuscular irritation, while compartment syndrome symptoms are due to isolated abnormalities in muscle perfusion caused by increases in compartmental pressure.

Noninvasive tests such as pulse volume recording, plethysmography, or duplex Doppler imaging, done in both the neutral and provocative positions, are good screening tools; however, they are unable to accurately differentiate between anatomic and functional entrapment and have a high false–positive rate in athletes [11••]. Arteriography is the gold standard for establishing a diagnosis. Contrast arteriography has traditionally been used and can provide subtle clues of anatomic impingement. In cases of anatomic impingement, there can be medial displacement of the popliteal artery, plaque in the midpopliteal artery, or development of mild aneurysmal change. If these angiographic findings are encountered, a stress positional arteriogram is the next step. It is important to image the arterial tree with the ankle in active plantar-flexion. The study should also be performed with active and passive dorsiflexion at the ankle [10,12]. Although contrast arteriography is more common and readily available, magnetic resonance arteriography may actually prove to be the better test to differentiate between functional and anatomical entrapment. T-weighted (T1 and T2) musculoskeletal studies show the relationship between vascular and musculotendinous structures within and around the popliteal fossa and can distinguish intrinsic vascular disease from extrinsic compression [9]. It has been proposed that dynamic MRI can be used to characterize the mechanics of impingement to help differentiate intrinsic vascular disease from extrinsic compression [9].

Treatment involves open surgical exploration of the popliteal fossa and division of the offending fascial bands, repair of the popliteal artery, resection of musculotendinous anomalies, and/or vascular repair via grafting or bypassing of the troubled section [9,10].

Intrinsic Arterial Defects

Endofibrotic disease

Endofibrotic disease and kinking of a major artery can cause exercise-related calf or thigh pain. In 90% of cases, the affected vessel is the external iliac artery [11••]. External iliac artery endofibrosis has been reported mostly in professional cyclists but there have also been reports in runners and rugby players [10,13]. Complications involving the proximal vessels are seen in cyclists, whereas the distal vessels are affected in individuals participating in running, skiing, rugby, soccer, and basketball [11••]. A typical patient is a young, highly trained athlete with no atherosclerotic risk factors and competing at an elite level, who started training in his/her early teens [11••].

The majority of the time (85%), symptoms are unilateral [11••]. The classic complaint is a perceived lack of power in the leg with intermittent claudication that occurs during high-intensity effort resulting in a subsequent decrease in performance [11••]. Other symptoms include an exercise-related sensation of a swollen thigh or hardening or cramping of the buttocks, thigh, or calf. Paresthesia of the limb and of the plantar aspect of the foot during incline running or repetitive jumping has also been reported. In cyclists, symptoms occur while racing, climbing a hill, or riding into a strong wind [10], associated with a forward-flexed riding position. Symptoms consistently occur at times of intense exercise and rapidly resolve at rest.

It has been postulated that prolonged exercise with the hip in a flexed position, as with cycling, predisposes the artery to undergo fibrotic thickening of the artery intima [10,13]. The chronic stress on the arterial wall when the hip is flexed causes intimal hyperplasia, which leads to stenosis of the artery. At maximal exercise, vascular stress from high cardiac output results in arterial hypertension and increases turbulence in the external iliac artery. In the hip-flexed cycling position, the external iliac artery is sinuous and the vascular stress leads to intimal thickening. It has been found that the external iliac artery tends to be elongated with abnormal loops in these patients [11••]. There have also been reported cases of arterial stenosis caused by medial and adventitial thickening in response to stress-related repetitive trauma [11••].

Diagnosis can be difficult because, in many cases, the physical examination tends to be normal. In some athletes there can be muscle wasting in the thigh and calf. Absent dorsalis pedis or posterior tibial pulses can be seen in extreme cases of ischemia. On postexercise examination, an arterial bruit may be present over the femoral artery with the hip flexed. There may be associated weak or absent distal pulses.

Pre- and postexercise ankle-to-brachial pressure indices are good screening tests and they can also serve to differentiate exercise-induced leg pain of vascular origin from nonvascular origin. It has been reported that 85% of confirmed patients with endofibrosis have a resting ankle-to-brachial pressure index less than 0.5. A value of 0.66 at 1 minute after intense exercise has been reported as the optimal cut-off point for clinical use, with 90% sensitivity and 87% specificity in the diagnosis of moderate disease [11••].

Arterial ultrasound and color Doppler are also useful but heavily operator dependent. The external iliac artery can be visualized at both rest and when exercising or symptomatic. Ultrasound at rest may be diagnostic in 80% of patients with endofibrosis [11••]. Color Doppler is effective in visualizing kinks and intravascular lesions [11••]. The Doppler readings should quickly return to a pre-exercise state once exercise ceases.

Magnetic resonance angiography is another noninvasive option and is not operator dependent. It provides good visualization but is more expensive than ultrasound with Doppler. Magnetic resonance angiography has the added benefit of detecting excessive kink and compression, particularly of the common iliac and popliteal arteries [11••].

The treatment options include angioplastic balloon catheter dilation and stenting, endarterectomy with vein patch angioplasty, vascular reconstruction in cases of intravascular lesions, or lesion bypass surgery [11••]. Balloon angioplasty alone only provides short-term symptomatic relief [11••]. Some authors believe that percutaneous transluminal angioplasty and intravascular stenting is contraindicated because of the high risk of dissection and reactive intimal hyperplasia following the procedure [11••]. For endofibrotic lesions, angioplasty-endofibrosectomy (endarterectomy with vein patch angioplasty), saphenous vein graft, or shortening of the artery may prove to be successful with quick return to competition [11••]. In cases of kinking, excision of the kink followed by vascular reconstruction has been the traditional treatment. Success rates of the different interventions are unknown due to the lack of long-term follow-up of these cases and lack of head-to-head studies comparing one procedure with another [11••].

Popliteal Artery Aneurysm (PAA)

PAAs are localized dilations of the popliteal artery greater than 2 cm in diameter or greater than 150% of the normal diameter [14]. Although rare in athletes, they represent the most common peripheral arterial aneurysm [15]. PAAs are more common in elderly men and are often bilateral. An abdominal aortic aneurysm is present in almost 50% of patients with a PAA, while PAAs are present in only 10% of those patients with an abdominal aortic aneurysm [16•]. In elderly patients, atherosclerosis is the most common etiology. PAES, cystic adventitial degeneration, osteochondroma, and trauma are implicated in younger patients [15].

Gallant et al. [14] found that 38% of patients studied were asymptomatic at time of diagnosis. Symptoms of intermittent claudication were found in 25% of patients and 5% to 10% of patients also complain of pressure or fullness in their posterior knee or popliteal fossa. Diagnosis is made by ultrasound, which can delineate the dilated vessel and determine whether or not there is thrombus present. Angiography may fail to show a PAA if the artery is occluded [16•].

The main complications of PAA are rupture, embolization, and acute thrombosis, which can lead to acute limb ischemia that requires urgent surgical intervention [15]. Mortality after thrombosis is 5% and limb loss is 20% or higher, leading many surgeons to recommend elective repair of all PAAs greater than 2 cm [15,16•]. Treatment may involve thrombolytics followed by repair of the aneurysm with ligation and bypass grafting. Endovascular repair of PAAs is still being studied [17].

Cystic Adventitial Disease

Cystic adventitial disease is compression of an artery due to mucoid cysts in the vessel adventitia [16•]. The popliteal artery is most commonly affected (85%) and is usually found in men in their mid-40s who present with symptoms of intermittent claudication. The etiology is believed to be from mucin-producing mesenchymal cells incorporated into the vessel wall during development [16•]. Ankle-to-brachial pressure indices will be diminished and ultrasound will show arterial stenosis with surrounding cysts. Both angiography and MRI can be used to confirm the diagnosis [18]. Surgical evacuation of the cysts is the recommended treatment as both cyst aspiration and balloon angioplasty have been shown to be ineffective [16•].

Peripheral Arterial Dissections

Spontaneous peripheral artery dissections are exceedingly rare, with a few case reports of dissecting aneurysms of the femoral and popliteal artery that are most often associated with hypertension [19]. More recently, a few cases of spontaneous, nonaneurysmal dissection of the external iliac arteries [20] and the popliteal artery [21] associated with competitive cycling and running have been reported. Some authors believe this is associated with repetitive, extreme blood pressure swings of exertion, termed “chronic episodic exertional hypertension,” which leads to intimal damage predisposing arteries to dissection [20].


PAES and other vascular etiologies should be considered in any athlete with exertional leg pain. PAES is caused by an anatomic variant of the popliteal artery in relation to its surrounding musculature, which leads to compression of the artery and resultant claudication symptoms. Other important vascular etiologies include endofibrotic disease, PAA, cystic adventitial disease, and peripheral arterial dissections. Endofibrotic disease refers to intimal hyperplasia and subsequent stenosis, and is especially important in the cycling population. Aneurysms (localized dilations) of the popliteal artery may lead to rupture, embolization, or acute thrombosis causing limb-threatening problems. It is important to differentiate vascular causes from CECS, MTSS, and stress fractures in order to guide treatment plans, avoid vascular complications, and return athletes to play.

References and Recommended Reading

Papers of particular interest, published recently, have been highlighted as: • Of importance: •• Of major importance

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Excellent review of CECS, MTSS, and stress fractures.

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Provides a good overview of vascular complications in the lower limb.

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Excellent review of popliteal artery disease.

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20. Cook PS, Erdoes LS, Selzer PM, et al.: Dissection of the external iliac artery in highly trained athletes.J Vasc Surg 1995, 22:173–177.
21. Rabkin DG, Goldstein DJ, Flores RM, Benvenisty AI: Spontaneous popliteal artery dissection: a case report and review of the literature.J Vasc Surg 1999, 29:737–740.
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