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Popliteal entrapment syndromes

Popliteal entrapment syndromes
Literature review current through: Jan 2024.
This topic last updated: Oct 30, 2023.

INTRODUCTION — Popliteal entrapment syndrome (PES) is a condition in which the anatomic relationship between the neurovascular structures of the popliteal fossa and nearby musculotendinous structures is abnormal. Popliteal artery entrapment is the most common form, and popliteal artery compression can reduce blood flow to the leg causing ischemic symptoms. Symptoms are usually chronic, but acute ischemia can also occur. Much less commonly, the popliteal vein is compressed manifesting with chronic venous symptoms [1,2].

The pathogenesis, clinical features, diagnosis, and treatment of PES are reviewed. Other nonatheromatous vascular diseases are reviewed separately. (See "Nonatheromatous popliteal artery diseases causing claudication or limb-threatening ischemia".)

INCIDENCE, ETIOLOGY, AND RISK FACTORS — PES is an overall rare condition, but its prevalence has increased in recent years likely because of increased awareness in the medical community. The overall prevalence of PES is estimated to range from 0.17 to 3.5 percent of the general population [3]. PES is most commonly seen in young, otherwise healthy individuals with a male predominance [4]. Typical atherosclerotic risk factors such as smoking, hypertension, hypercholesterolemia, and diabetes are absent [5]. Based on a systemic review published in 2021, the mean age at PES diagnosis was 32 years, and 83 percent of affected patients were male [4]. Popliteal entrapment is most common in athletes participating in long-distance running, basketball, football, rugby, soccer, and martial arts [6].

CLASSIFICATIONS

Congenital versus acquired (functional) PES — PES can occur as either a congenital or acquired condition.

Congenital PES – Congenital popliteal entrapment (types I to VI (see 'Anatomic types' below)) is a result of abnormal fetal development and migration of the popliteal artery and/or vein in relation to the muscles in the leg, resulting in displacement or compression of the popliteal artery.

Acquired PES – In the acquired form of PES (type F (see 'Anatomic types' below)), one of the calf muscles becomes enlarged, resulting in compression of the popliteal artery. The acquired form is commonly referred to as functional PES.

Arterial versus venous PES — PES can cause compression of the popliteal artery, popliteal vein(s), or both. The clinical syndromes differ, with arterial PES leading to variable clinical presentations of limb ischemia (eg, claudication, limb-threatening ischemia) while venous PES leads to symptoms or signs of acute or chronic venous insufficiency. (See 'Clinical presentations' below.)

Anatomic types — Several classification schemes have been used to describe PES based on the course of the popliteal vessels in relation to the medial head of the gastrocnemius muscle (MGH), popliteus muscle, or other fibrous bands/muscle slips [4,7-10]. The Popliteal Vascular Entrapment Forum described a classification system consisting of six congenital forms of PES as well as the acquired form:

Type I – An aberrant medial course of the popliteal artery around a normally positioned MGH.

Type II – The popliteal artery courses more inferolaterally than normal due to an abnormal lateral attachment of the MGH to the femur.

Type III – The popliteal artery is in its normal position but is encircled by an aberrant accessory muscle slip from the MGH.

Type IV – The popliteal artery is in its normal position but is encircled by the popliteus muscle or a fibrous band.

Type V – Primarily venous entrapment. The popliteal vein is most often compressed by the MGH but may also be compressed by a fibrous band.

Type VI – Other variants.

Type F – The popliteal artery is in its normal position but is entrapped by a hypertrophied gastrocnemius muscle, resulting in a functional entrapment syndrome.

CLINICAL PRESENTATIONS — Individuals with PES can be asymptomatic or symptomatic. The estimated prevalence of asymptomatic arterial PES ranges from 25 to 80 percent [4,11]. Although compression of the popliteal vein may be seen during provocative maneuvers in 27 to 47 percent of healthy adults, it is generally asymptomatic [1,12]. For patients with symptoms a constellation of symptoms related to compression of the popliteal neurovascular structures can occur.

Symptomatic patients classically present with intermittent claudication related to arterial compression; acute limb ischemia has also been reported. In a study of 88 limbs with PES treated over 10 years, claudication was the main presenting symptom in 79.5 percent of cases [13]. In those with chronic symptoms, the pulse examination at rest in these typically young, healthy individuals is normal; resting ankle-brachial index (ABI) values are also typically normal. Passive dorsiflexion or active plantar flexion, which elicit compression of the popliteal artery, may result in loss of palpable pulses. Many cases of arterial compression are bilateral, although the exact prevalence is unknown (25 to 83 percent in the available literature) [13-15]. Acute limb ischemia occurs in approximately 11 percent of patients [14]. (See "Clinical features and diagnosis of acute lower extremity ischemia".)

When venous compression is symptomatic, patients present with symptoms of chronic venous insufficiency, including leg pain, swelling, stasis dermatitis, or ulceration in the affected extremity [1,2,12,14]. (See "Clinical manifestations of lower extremity chronic venous disease".)

Other symptoms such as paresthesias related to tibial nerve compression can occur.

DIAGNOSIS — PES should be suspected in young, otherwise healthy individuals with clinical symptoms and signs consistent with compression of the neurovascular structures of the popliteal fossa. This is more typically arterial compression (claudication), although symptoms of venous compression, nerve compression, or a combination of symptoms can occur. Venous PES should be considered in young, otherwise healthy individuals presenting with symptoms of chronic venous insufficiency and no alternative pathology. (See 'Clinical presentations' above.)

The diagnosis of relatively uncommon condition is made through a combination of physical exam, physiologic testing with exercise, and vascular imaging with provocative maneuvers to elicit vascular compression. Based on a systemic review of PES, digital subtraction angiography (DSA) was the most commonly used imaging modality in the diagnostic workup (28 percent of cases), followed by ABI measurements (18 percent), computed tomographic (CT) angiography (12 percent) or magnetic resonance (MR) angiography (12 percent), duplex ultrasound (10 percent), exercise ABIs (4 percent), and other modalities (4 percent) [4]. On average, patients undergo three investigations prior to confirming the diagnosis of PES [4].

Diagnostic evaluation

Arterial PES – Patients will arterial PES usually have a normal physical exam and diagnostic studies at rest. Thus, to establish a diagnosis, the popliteal artery must be evaluated during provocative maneuvers. Loss of palpable pulses on physical examination and reduced arterial flow on vascular imaging with passive dorsiflexion or active plantar flexion, which elicit compression of the popliteal artery, is considered pathognomonic for arterial PES.

Venous PES – The diagnosis of venous PES can be made with duplex ultrasonography also with provocative maneuvers. Cross-sectional studies can be used as an adjunct to image surrounding anatomy and muscular anomalies. Venography with provocative maneuvers can help identify the precise segment and extent of compression.

Physiologic studies with exercise — In the younger patient with claudication symptoms suspicious for arterial PES, resting ABIs are usually normal. Thus, ABIs should be evaluated before and after exercise that provokes onset of symptoms. During exercise, ABI values decrease as the popliteal artery is compressed by the aberrant calf musculature. (See "Noninvasive diagnosis of upper and lower extremity arterial disease", section on 'Exercise testing'.)

While exercise ABIs are traditionally measured before and after walking on a treadmill with a slight incline, the diagnosis of arterial PES may be better evaluated before and after the patient performs forceful plantarflexion. An average force of plantarflexion between 0 and 70 percent of maximum has been shown to be maximally sensitive and specific for diagnosing arterial PES [7]. Duplex ultrasonography can be used as an adjunct to ABI testing, as it allows for direct imaging of the artery and vein during provocative maneuvers. When the patient is positioned supine with the legs straight, popliteal artery velocities should be normal. However, after exercise or with provocative maneuvers (ie, forceful plantarflexion), flow velocities in the popliteal artery will increase as the popliteal artery is compressed.

Vascular imaging with provocative maneuvers — Cross-sectional imaging with CT and MR imaging shows the anatomic relationship of the neurovascular structures in the popliteal fossa to the gastrocnemius muscle. Dynamic CT and MR angiography (ie, with provocative maneuvers) can be useful to identify the location of compression. These are particularly helpful for diagnosing functional PES in which the anatomy is normal, but gastrocnemius hypertrophy causes compression during exercise. Dynamic angiography involves obtaining images first in the static position and then again following a series of provocative maneuvers. In general, MR angiography provides better resolution of muscle anatomy compared with CT angiography but is more time consuming to obtain. By contrast, CT angiography is convenient and can be obtained quickly, but involves radiation exposure and the use of iodinated contrast.

If the diagnosis of PES is not confirmed using one of the above studies, DSA can be performed and is best accomplished by obtaining angiographic images with the patient in a static supine position, and then again following forceful plantarflexion as described above. When performed with provocative maneuvers, DSA is highly sensitive (97 to 100 percent) for making the diagnosis of PES [4]. Some authors have also advocated using intravascular ultrasound (IVUS) as an adjunct to determine the precise location and extent of compression. IVUS also allows the provider to evaluate the lumen for any intimal damage or intraluminal stenosis requiring repair or interposition grafting [16].

MANAGEMENT APPROACH

Asymptomatic patients — For patients with asymptomatic PES, no intervention is necessary. Arterial compression may be present based on imaging studies, but if it is not associated with symptoms, there is no indication for repair. Similarly, in patients with evidence of venous or nerve compression who are not symptomatic, no specific treatment is needed.

Symptomatic patients

Arterial PES — Surgical treatment for PES is generally recommended for symptomatic patients with arterial PES taking into account the goals of treatment and patient preferences.

Congenital arterial PES – For patients with symptomatic congenital arterial PES (types I to VI), open surgery is the mainstay of treatment. Only a few small studies describe outcomes for conservatively managed patients with symptomatic congenital PES. Of these, symptom resolution was described in a small number of patients with moderate symptoms following discontinuation of an extreme exercise program [13].

Functional arterial PES – For patients with functional arterial PES (type F), intervention is indicated for those with lifestyle-limiting symptoms. Because patients who come to medical attention tend to be young and often involved in extreme exercise or athletics, lifestyle-limiting symptoms often include those that affect athletic activities. Decompressive surgery has been the mainstay of treatment for functional PES, but series describing the use of botulinum toxin A injections as an alternative noninvasive treatment have been favorable [17,18]. The authors of a systematic review have suggested that patients with functional arterial PES and normal-appearing popliteal vasculature on CT or MR angiography can be reasonably treated with a trial of botulinum toxin A [14]. If symptoms improve following injection, the diagnosis of functional arterial PES is confirmed. If the symptoms recur, the patients can either undergo a repeat botulinum toxin A injection or proceed with surgical decompression.

Venous PES — Compared with arterial entrapment, venous entrapment may be treated conservatively with compression hosiery and leg elevation in most cases. In refractory cases presenting with stasis ulceration, surgical release of the popliteal space may be considered. Outcomes of these patients are favorable, with significant relief of pain and swelling and resolution of stasis ulceration/dermatitis in 82 percent of patients [12]. Anticoagulation is indicated if thrombosis of the popliteal vein occurs. There is no evidence that prophylactic anticoagulation is beneficial.

SURGERY FOR POPLITEAL ARTERY ENTRAPMENT — Surgical decompression of the popliteal space with or without vascular reconstruction is the mainstay for treatment with the aim of preventing progressive damage including the development of intraluminal stenosis or aneurysmal degeneration of the popliteal artery from persistent, repetitive trauma. Endovascular treatment is not recommended in this setting, as it does not relieve the source of compression and ongoing trauma can lead to stent migration or fracture. Treatment of PES involves open surgical decompression of the popliteal space with or without arterial reconstruction depending on the condition of the vasculature. Surgical decompression is usually achieved by performing a musculotendinous division to release the entrapment.

While endovascular techniques are often the preferred initial treatment for lower extremity revascularization related to peripheral artery disease (PAD), because of the associated anatomic abnormalities with PES, endovascular therapy is not commonplace except perhaps in the form of catheter-directed thrombolysis for patients presenting with acute limb ischemia [13,19]. (See "Intra-arterial thrombolytic therapy for the management of acute limb ischemia".)

Patients with arterial PES who are treated for acute limb ischemia will still require surgical decompression following restoration of flow to address their anatomic abnormalities. Whether to perform open thrombectomy or endovascular thrombectomy/thrombolysis is determined by the severity of limb ischemia. There is currently no role for an endovascular-only intervention for the management of PES.

Decompression of the popliteal space can be performed via a posterior [10,20-24] or a medial approach [13,25,26]. The selection of approach is based upon the precise location and extent of compression as well as the need for reconstruction of the artery. There are no objective benefits of one approach over another. However, studies including both approaches tend to describe using the posterior approach for decompression alone and the medial approach for cases when arterial reconstruction is anticipated [4].

For the posterior approach, either a longitudinal or S-shaped incision is made on the posterior knee. A simple transverse incision may be appropriate in selected cases with compression that is limited to a short segment of the vascular structures. The popliteal artery is completely exposed, releasing all musculotendinous attachments along its course. The artery is then replaced in its native (ie, orthotopic) position [24].

For the medial approach, a longitudinal incision is made just below the knee, and the gastrocnemius and/or other musculotendinous attachments are fully divided to release the compression of the popliteal artery. If there is a popliteal artery stenosis due to long-term trauma to the vessel, arterial reconstruction is indicated. Sometimes this will be anticipated preoperatively based on cross-sectional or angiographic imaging. If it is unclear, intraoperative duplex ultrasound can be helpful to assess for stenosis in the affected segment following decompression. As with any lower extremity bypass, autogenous conduit using great saphenous vein is preferred whenever possible.

Outcomes after popliteal release are generally favorable, with studies reporting >75 percent and up to 100 percent of patients with relief of symptoms and/or return to athletic activities [27,28].

Complications following surgery for arterial PES are generally related to arterial reconstruction, which occurs in a median of 27.5 percent of cases [4]. Other complications include deep vein thrombosis (11 percent), wound seroma (4.6 percent), and wound infection or hematoma (3 percent).

SUMMARY AND RECOMMENDATIONS

Popliteal entrapment syndromes – Popliteal entrapment syndrome (PES) is a rare condition in which the anatomic relationship between the neurovascular structures of the popliteal fossa and nearby musculotendinous structures is abnormal. The popliteal artery is more commonly affected, but entrapment of the popliteal vein can also occur. (See 'Introduction' above.)

Classification – PES is classified based on whether the etiology is congenital or acquired, and for congenital PES, the anatomic relationship of the vascular and musculotendinous structures to each other. (See 'Classifications' above.)

Clinical presentations – Depending on the involved structures PES and severity of compression, PES can be asymptomatic or present with ischemia (eg, claudication, acute limb ischemia) or chronic venous insufficiency (eg, swelling, pain, skin changes). (See 'Clinical presentations' above.)

Diagnosis – A diagnosis of PES may be suspected based on symptoms and signs of neurovascular popliteal compression in a younger patient lacking typical risk factors for arterial or venous disease. The diagnosis relies on vascular imaging demonstrating flow abnormalities or vascular occlusion during provocative maneuvers. Cross-sectional imaging (eg, MR, CT) can demonstrate the abnormal relationship of the neurovascular and musculoskeletal structures in the popliteal fossa and localize the point of compression. (See 'Diagnosis' above.)

Treatment – Treatment of symptomatic patients depends on the classification of PES. Long-term outcomes following treatment are good with relief of symptoms with low recurrence. (See 'Symptomatic patients' above.)

Arterial PES – Surgical treatment is generally recommended for symptomatic patients with arterial PES, taking into account the goals of treatment and patient preferences.

-For patients with symptomatic congenital arterial PES (types I to IV), open surgery involves musculotendinous release of the compressive muscular components. Decompression can be performed using a posterior or medial approach to the popliteal fossa. A medial approach is more often used when arterial reconstruction is necessary.

-For patients with functional arterial PES (type F), decompressive surgery is indicated only for those with lifestyle-limiting symptoms. An alternative to surgery is botulinum toxin A injection, which can be repeated if symptoms recur, or the patient can proceed with surgery.

Venous PES – For patients with symptomatic venous PES (type V), conservative management including leg elevation and compression hosiery provides sufficient relief in most patients.

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