Materials and Methods
Literature Review
A search of PubMed, Scopus and the Cochrane Collaboration was performed using a combination
of keywords including truncated and wildcard variations and relevant subject headings,
focusing on PAES and functional PAES, as well as terms relevant to the succeeding
subheadings. Non-English abstracts were not included. Reference lists of reviewed
articles were trawled to identify relevant articles not identified in the literature
search.
Anatomy of the Popliteal Artery and Classification of PAES
The popliteal artery passes from the adductor hiatus into the popliteal fossa, where
it typically passes lateral to the medial head of the gastrocnemius, and runs down
posterior to the knee joint, superficial to the popliteus muscle. At the lower border
of the popliteus, it divides into the anterior tibial artery and tibioperoneal trunk
[8]. The popliteal artery is fixed at both ends, to the adductor hiatus and to the soleal
fascia [8]
[9]. It is worth noting that over 75 variations of this “normal” anatomy have been described
[10], which may impact on the presentation and pathogenesis of PAES.
A classification system for PAES was proposed by Love and Whelan and further modified
by Rich [11], who described six subtypes of PAES, defined by the relationship of the popliteal
artery to the medial head of gastrocnemius (MHOG) ([Figure 1a–f]). Type 1 PAES describes a variation whereby the popliteal artery runs medial to
the MHOG. This occurs because the popliteal artery matures prior to the medial migration
of the MHOG and is swept medially by the migrating muscle. In type 2, the popliteal
artery is again medial to the MHOG, but it partially arrests the medial migration
of the MHOG, such that the muscle attaches more laterally on the femur. In type 3,
an accessory band of gastrocnemius entraps the popliteal artery. Part of the axial
popliteal artery does not involute in type 4, so the mature distal popliteal artery
runs deep to the popliteus muscle. If the popliteal vein accompanies the popliteal
artery in any of these anatomical variations, it is termed type 5. In type 6, none
of the above anatomical variations are present [2]
[11]. Type 6 is also known as functional popliteal entrapment syndrome (Functional PAES).
Fig. 1 Subtypes of Popliteal Artery Entrapment Syndrome (PAES). In Type 1, the popliteal
artery runs medial to the medial head of gastrocnemius (MHOG) [a]. In Type 2, the popliteal artery again runs medial to the MHOG; however, the MHOG
has a more lateral attachment on the femur [b]. In Type 3, an accessory band of gastrocnemius entraps the popliteal artery [c]. In Type 4, the popliteal artery runs deep to the popliteus muscle [d]. If the popliteal vein accompanies the artery in any subtype it is classified as
Type 5 [e]. In Type 6, functional PAES, there is no anatomical abnormality present [f].
Functional PAES defines a group of patients who experience reproducible symptoms of
PAES without an identifiable developmental anatomical abnormality [10]. Rignault described this in 1985, having studied in digital subtraction angiography
(DSA) of French military recruits’ lateral displacement of the popliteal artery at
rest, and occlusion of the artery with plantarflexion. At operation, no anatomical
cause was found in these patients, aside from hypertrophy of the medial gastrocnemius
muscle belly [2]
[12].
The exact mechanism of functional PAES is incompletely understood. As aforementioned,
the pathology was initially believed to occur secondary to hypertrophy of the medial
gastrocnemius muscle in athletes, with compression of the posteromedial aspect of
the popliteal artery during stress maneuvers [12]
[13]. Others have postulated that the neurovascular bundle – the popliteal artery, popliteal
vein, and tibial nerve – is compressed where it passes below the soleal arch (the
so-called “popliteal outlet”), the tendinous band that spans between the muscle’s
proximal attachment at the tibia and the head of the fibula, and that symptoms may
arise from compression of the tibial nerve at this point. Hypertrophy of the soleus,
gastrocnemius, plantaris and popliteus muscles may contribute to this compression
[12]
[13]
[14]. One study using Magnetic Resonance Imaging (MRI) found that the insertion of the
medial head of gastrocnemius may extend further towards the midline of the femur,
further crowding the region [15].
Clinical Features of Functional PAES
Functional PAES predominantly affects young, fit individuals and presents with symptoms
of exertional calf pain, weakness, cramping and a sensation of tenseness. There may
be associated paraesthesia of either the dorsal or plantar aspect of the foot [1]
[16]. It is unclear whether the genesis of these symptoms is from ischemic pain secondary
to popliteal artery occlusion or compression of the neurovascular bundle (including
the tibial nerve) as it passes under the soleal arch [14]. Compression of the tibial nerve (and its innervation of the dorsum of the foot
via its calcaneal and plantar branches) may explain the frequent complaint of paraesthesia
of the plantar surface of the foot. Compared to anatomical (type 1 to 5) PAES, patients
with functional PAES tend to be younger, more active, and more commonly female [3]
[17]. There is often a significant delay between the onset of symptoms and diagnosis,
owing to their non-specific nature [18]
[19].
There are no specific examination signs indicative of functional PAES. Patients may
present with hypertrophy of the lower limbs [4]. There may be a loss of the dorsalis pedis or posterior tibial pulse on resisted
plantar or dorsiflexion with the knees extended [20]
[21]. A drop in the Ankle-Brachial Index (ABI) or significant flattening of a plethysmography
waveform with these same maneuvers is considered a positive “entrapment test” [16]. A positive entrapment test and symptoms of atypical claudication are not of themselves
sufficient to make the diagnosis of functional PAES, as somewhere between 20–85% of
normal legs may demonstrate occlusion of the popliteal artery on duplex ultrasound
or MRI in plantarflexion [10]
[22]. Provocative maneuvers, such as hopping on one leg, can induce symptoms including
weakness and paraesthesia of the toes; and the foot can appear cold and pale, followed
by reactive hyperemia following cessation of exercise [23].
Potential long-term sequelae of anatomical PAES stem from the effects of repetitive
arterial micro-trauma on the popliteal artery and include distal embolization, dissection,
acute limb ischemia secondary to acute thrombosis, post-stenotic dilatation and aneurysm
formation [4]
[7]
[21]. This repetitive micro-trauma can be divided into three phases: in the first phase
there is damage to the arterial adventitia; in the second, damage to the media; and
in the third, the intima. Damage to the media may cause post-stenotic dilatation or
aneurysmal degeneration of the artery, while damage to the intima can lead to thrombosis
[24]. Sinha’s 2012 meta-analysis reported a median prevalence of 24% of popliteal artery
occlusion and 13.5% of post-stenotic dilatation or aneurysm formation amongst patients
with PAES [7]. There are reports of patients presenting with complications from functional PAES;
however, the incidence of these complications appears to be much rarer than in their
anatomical counterparts [24].
Differential Diagnosis
Functional PAES represents one of a number of diagnoses that exist on the spectrum
of exercise induced leg pain. These differential diagnoses are important to consider,
as many may masquerade as functional PAES.
Vascular causes of exertional leg pain
Arterial endofibrosis is a non-atherosclerotic cause of exertional leg pain in young
athletes, particularly cyclists [25]. It primarily afflicts the external iliac artery [26]. The exact pathophysiology of the disease is unknown but there is suspected to be
an association between duration of time spent cycling and the development of the disease
[25]
[26]. Typical symptoms include leg weakness and thigh pain on exertion, which resolve
with cessation of exercise. Patients will have a drop in exercise ankle-brachial index
pressures, of at least 20–40% [25]. Duplex ultrasonography may demonstrate increased intimal-medial thickness, and
exercise duplex ultrasonography may show elevated peak systolic velocities (>350 cm/s)
with dampened waveforms [20]. DSA may show iliac artery stenosis or occlusion, with kinking of the vessels either
at rest or when provoked with hip flexion. Most commonly, this is managed with open
endarterectomy and patch angioplasty [20], while surgical release of the iliac artery from its sheath to prevent kinking has
also been described [27]. Endovascular interventions may offer temporary relief; however, they have not been
shown to confer long-term results [20].
Adductor canal compression syndrome is a rare entrapment condition where the superficial
femoral artery (SFA) is compressed in the adductor canal. Etiology can be either anatomical,
with compression of the SFA by fibrous or musculotendinous bands arising from the
adductor magnus, or functional, where the SFA is compressed between the hypertrophied
vastus medialis and adductor magnus muscles [28]. Patients either present with intermittent claudication or medial knee pain secondary
to compression of the saphenous nerve [29]. Relevant investigations include exercise ABIs, duplex ultrasonography, Computed
Tomography (CT) angiography, and MRI [28]. Management of symptomatic individuals is with open surgery, namely patch angioplasty
or bypass of the affected region, accompanied by removal of any accessory musculotendinous
or fibrous bands [28].
Cystic adventitial disease is a rare condition of mucinous cyst formation within the
adventitia of the artery [30]. This disease affects males between 5 to 15 times more than females, and occurs
approximately 85% of the time in the popliteal artery [31]. Patients typically experience short distance claudication, with a prolonged recovery
of symptoms after cessation of exercise [32]. Ishikawa’s sign (loss of pedal pulses with knee flexion) may be present [31]. Duplex ultrasonography is the most sensitive test for the disorder, although CT
angiography and MRI may also prove useful [31]. DSA demonstrates a smooth curvi-linear stenosis, referred to as the “scimitar sign”
[30]
[31]. In the symptomatic patient, treatment options include resectional (resection of
diseased vessel with patch or interposition graft repair) and non-resectional techniques
(such as ultrasound guided cyst aspiration) [30]
[31]. Non-resectional techniques have a higher rate of recurrence and often a need for
repeat intervention [31]. Endovascular approaches have not been shown to be successful in this setting [30].
Non-vascular causes of exertional leg pain
Chronic Exertional Compartment Syndrome (CECS) is the most common cause of atypical
claudication in the young athlete, occurring in approximately 30% of athletes with
exertional leg pain [16]
[33]. It may present alongside PAES, with one cohort of patients with PAES reported to
have an 86% incidence of concomitant CECS [20], and is a mandatory consideration in the work-up of exertional leg pain. Many functional
PAES patients may have already undergone surgery for CECS [23]
[34]. It is predominantly reported in young athletes who run, but may also affect non-athletes
[35]. Symptoms include pain over one of the four leg compartments, which increases during
exercise, and resolves within minutes to hours of ceasing activity [35]. Generally, there are no examination findings, although there may be point tenderness
or muscle atrophy in the affected compartment [35]. The investigation of choice is intra-compartmental pressures, measured at rest,
and both 1 and 5 minutes after exercise [35]
[36]. More recently, the reproducibility of results between different intra-compartmental
pressure measuring systems, and the accuracy of proposed diagnostic criteria have
been brought into question [35]. Accordingly, the diagnosis remains largely a clinical one.
Non-operative strategies including massage, gait changes and chemo-denervation appear
to be successful in approximately 50 percent of cases [36]
[37]. Operative management includes fasciotomy, which can be undertaken either via a
single (lateral) or double (anterolateral and medial) incisions [36]. It is important to ensure that all compartments, including the deep posterior compartment,
are decompressed. Alternative techniques include endoscopically assisted fasciotomy
and minimally invasive fasciotomy, which appear to confer similar results [35]
[36]. Given the similarities in presentation between functional PAES and CECS, patients
may often present with overlapping symptoms. Where there is uncertainty as to which
is the predominant cause of the patient’s symptoms, it has been advocated to perform
fasciotomies first [16]
[19].
Compression of the tibial nerve as it passes under the soleal sling (“Soleal Sling
Syndrome”) is gaining recognition as a separate entity to functional PAES and CECS.
In this syndrome, patients develop plantar numbness or pain, with associated pain
or tightness in the calf [38]. As there is no popliteal artery compression, patients do not experience the claudication
symptoms typical of functional PAES [38]. As previously mentioned, there is likely a degree of overlap between patients with
functional PAES and soleal sling syndrome, as patients with functional PAES often
experience symptoms of plantar pain or numbness. Patients often have their plantar
numbness mistaken for tarsal tunnel syndrome, and may have already undergone unsuccessful
surgical decompression of this [38]
[39]. A key examination finding is tenderness on palpation of the tibial nerve as it
passes under the soleal sling (approximately 9 cm below the posterior knee crease)
[38]
[39]. Patients may have sensory changes in the distribution of the tibial nerve, and
there may be weakness, particularly in extensor hallucis longus [39]. MRI may demonstrate a thickened soleus sling with T2 hyperintensity of the compressed
tibial nerve [40]
[41]. Conservative management involves modifying activities to avoid those that induce
pain and wearing non-constrictive clothing and shoes [39]. Surgical decompression involves detaching the soleal arch, via a medial calf incision,
with promising results from the small case numbers reported thus far [38]
[39].
Medial tibial stress syndrome (MTSS) and stress fractures are two other important
differential diagnoses to consider in the young patient with exertional leg pain.
MTSS is a common affliction in runners with symptoms of pain at the posteromedial
border of the tibia after exercise. Symptoms typically persist for hours to days (compared
with minutes to hours of CECS) [36]
[42]. Patients with stress fractures, however, experience pain at a focal site, which
worsens over time as training loads increase. They may also experience significant
pain at night [35]. Patients with MTSS will experience diffuse pain across the medial aspect of the
tibia, while patients with stress fractures will have tenderness concentrated over
an area of less than 5 cm [35]. Plain X-ray imaging is a primary method of investigation, and MRI is the preferred
choice [35]. Both conditions should be managed conservatively [35].
Plantar fasciitis is a degenerative condition, with overuse or excessive loading causing
repeated micro-trauma to the plantar fascia. It typically presents with localized
heel pain, though in severe cases, the pain can radiate proximally into the lower
limb [43]
[44]. The pain is typically worst early in the morning or after prolonged activity. Risk
factors include anatomical deformity (pes planus and pes cavus) and obesity, and it
is more prevalent in athletes and the elderly. On examination, focal tenderness at
the origin of the plantar fascia is expected. Pain may also be elicited with passive
dorsiflexion. Some patients with plantar fasciitis have limited ankle dorsiflexion,
attributable to gastrocnemius tightness [43]
[44]. In plantar fasciitis, there is not any reduction in sensitivity in the innervation
of the plantar nerves, in contrast to tarsal tunnel syndrome where this is commonplace.
Recently, surgical resection of the medial head of gastrocnemius (a typical surgical
treatment for functional PAES) and gastrocnemius tendon lengthening have been investigated
as alternatives to traditional open plantar fasciotomy (albeit in small numbers) [43]
[44].
Lower back pain may be accompanied by leg pain. This may either be referred pain,
where pathology in the muscles, joints or ligaments in the lumbar spine or pelvis
(including the sacroiliac joint) may produce both pain at the site of nociception
and also in the leg, or radicular pain, where there is shooting pain down the leg
as a result of lumbar intervertebral disc herniation [44]
[45]
[46]
[47]. Both of these syndromes can have a gradual or sudden onset. Referred pain is provoked
by mechanical pressure on the afflicted structures and tends to be more dull or aching,
while radicular pain is elicited by stretching the neural elements through standing
or bending and is described as shocking and electric in character. Both can be severe
and debilitating for patients. History and examination, including straight leg raise
and femoral stretch tests, may help delineate the cause. Patients with radicular pain
may have motor, sensory or reflexive deficits in their limbs. Imaging, including plain
X-ray and MRI scans, nerve conduction studies and electromyography, may be indicated
[44]
[45]
[46]
[47]. Treatment of referred pain is directed towards increasing mobility and return to
pre-morbid function levels, whereas radicular pain treatment ranges on a spectrum
from conservative management with analgesia and physiotherapy to surgery [47].
Investigations
There is no consensus as to the best series of investigations for functional PAES.
Investigations most commonly performed include exercise ankle-brachial pressures (exercise
ABIs) and duplex ultrasound (typically performed with the ankle in dorsiflexion and
plantarflexion), CT angiography, MRI (encompassing plain MRI, stress positional MRI
and MR angiography), and DSA [7]
[48].
Most patients with anatomical and functional PAES will have normal resting ABIs [49]. Turnipseed and others have suggested that exercise ABIs should be the first investigation
of choice when diagnosing functional PAES [3]. Exercise ABIs have been shown to successfully distinguish symptomatic from asymptomatic
patients in a cohort of young patients with exertional leg pain, with the greatest
difference demonstrated after strenuous exercise, specifically running [50]. ABIs should be measured after exercise vigorous enough to produce symptoms (such
as running outside or at high speed on a treadmill) to maximize sensitivity. Furthermore,
the test should also be performed as quickly as possible after cessation of exercise
as pressures may return to baseline rapidly in these patients [23].
Duplex ultrasound with dynamic maneuvers (ankle dorsi and plantar-flexion) is often
the first test ordered when specifically investigating for functional PAES. There
are no defined ultrasound criteria for the diagnosis of popliteal entrapment [24], and between 20–85% of normal legs may demonstrate transient occlusion of the popliteal
artery on duplex ultrasound with dynamic maneuvers, leading to a high rate of false
positives [10]. Typically, the popliteal artery is examined in the region where it is thought to
be compressed by the medial head of gastrocnemius; however, this does not investigate
for compression of the neurovascular bundle at the “popliteal outlet,” a prominent
etiological theory in functional PAES. One study examining compression of the popliteal
artery at this “popliteal outlet” found that only 10% of a cohort of young patients
with exertional leg pain had popliteal artery occlusion when examined with dynamic
ultrasound with ankle plantarflexion [50], with mean compression of the artery that was less than 2.5 mm [50]. This technique has not, however, been validated in a specific cohort of patients
with suspected functional PAES.
CT angiography (CTA) using iodinated contrast media is a less invasive imaging modality
that provides both high spatial resolution and good soft tissue contrast resolution
[51]. It may prove a useful investigation in the work-up of patients for atypical causes
of claudication. Separately phased scans can be performed with ankle dorsiflexion
or plantarflexion to investigate specifically for evidence of popliteal entrapment
[51]. Plethysmography using an oximeter on the hallux of the afflicted side can ensure
the ankle has been sufficiently positioned or flexed [16]
[52]. CTA may demonstrate mild to severe popliteal artery stenosis, popliteal artery
occlusion, and even popliteal venous compression [51]. Multiplanar reconstructions and maximal intensity projections allow good visualization
of the complete course of the artery and may identify muscular or tendinous abnormalities
in the case of anatomical PAES [53]. Alternative diagnoses such as cystic adventitial disease may also be readily identified
[53]. Its less invasive nature has led many to prefer it over DSA in the investigation
of functional PAES [53]. Some patients with symptoms of PAES and signs of popliteal artery compression on
CTA demonstrate minimal drop in pressure on exercise ABIs [52] – it is unclear whether this subset of patients did not exercise vigorously enough
to incur a drop in ABI, or if there is a subset of patients with functional PAES who
have symptoms and imaging consistent with the diagnosis, but normal exercise ABIs.
MRI is a valuable imaging modality to assess the lower limb arterial tree and soft
tissue structures. It is the most commonly used investigation in the work-up for functional
PAES [48]. MRI has greater specificity and sensitivity in the detection of lower limb peripheral
arterial disease, when compared to duplex ultrasound [54] and does not expose the patient to ionizing radiation, an important consideration
in this typically younger cohort of patients. T1-weighted MRI sequences display the
muscular anatomy and its relation to the popliteal artery, and as such can be used
to diagnose or exclude anatomical PAES as the cause of the patient’s symptoms [55]
[56]. Time-of-flight MR angiography (MRA) can demonstrate arterial compression in either
ankle dorsiflexion or plantarflexion without the need for administration of intravenous
contrast media. However, MRI is acutely sensitive to motion artefacts, and the scan
duration is typically longer than CTA [55]. Contrast-enhanced MRA may act as a less invasive substitute for DSA, with correlation
between MRI and DSA findings of approximately 95% in patients with lower limb atherosclerotic
disease, although MRI may tend to underestimate the degree of stenosis [57]. Use of blood pool MRI contrast agents, which stay in the intravascular space for
a longer period of time, may allow for the acquisition of higher spatial resolution
sequences, which may overcome the tendency to underestimate the degree of stenosis,
as well as permitting arterial imaging with dynamic maneuvers [58]. There are a number of absolute and relative contraindications to MRI, including
some implantable cardiac devices, endovascular stent grafts and orthopedic implants
to name a few. These may prohibit the use of MRI, and hamper image quality if they
are within the region of interest. Similarly, gadolinium-based contrast is contraindicated
in patients with severe kidney impairment due to the risk of nephrogenic systemic
fibrosis. These contraindications are less commonly encountered in the typically young,
fit cohort of functional PAES patients.
DSA is still considered by many to be the “gold standard” imaging modality in the
identification of patients with functional PAES [51]. DSA with stress maneuvers may identify a stenosis or occlusion of the popliteal
artery if present, either at rest or with ankle dorsi- and plantarflexion [51]
[59]; however, it is an invasive procedure and it exposes the patient to ionizing radiation.
DSA can be particularly useful when MRA is inconclusive, or the diagnosis is still
suspected despite normal MRA findings. In patients with complicated presentations,
DSA could allow for simultaneous therapeutic endovascular intervention in the rare
situation of a patient presenting with acute limb ischemia [60].
Management
In patients with anatomical PAES, surgery is indicated to release the entrapment and
prevent complications such as arterial stenosis, occlusion and aneurysm formation.
It appears that functional PAES is much less likely to result in these complications.
Thus, intervention is generally reserved for patients with functional PAES who have
typical symptoms that are severe and repetitive [12]
[17]. Non-operative intervention is in the form of massage and stretching with the intent
to reduce gastrocnemius contraction and retraction, although this is unlikely to be
effective as it does not affect muscle morphotype or volume [61].
Botulinum Toxin A (BTA) has emerged in the past five years as a non-operative treatment
for functional PAES. BTA is injected under electromyographic guidance into the medial
head of gastrocnemius and/or the plantaris muscles [48]. Typically, between one and three treatments are performed, with the further “top
up” treatments provided at patient request [48]
[62]. In total, less than 50 patients cumulatively have been reported in the literature
as having undergone this technique [48]
[61]
[62]. Post-procedural success rates appear to be greater than 50 percent, and advantages
of this therapy are that it is minimally invasive and potentially diagnostic in identifying
patients who are likely to benefit from surgery. It may function as a bridge to surgery,
and in particular cases, alleviate the need for surgery altogether [48]. The long-term outcomes of BTA therapy for functional PAES remain unclear. It is
less likely to be effective, if there is already arterial pathology, such as popliteal
artery stenosis or occlusion [48].
Surgery remains the most widely accepted treatment for functional PAES. Three predominant
surgical approaches have been described: posterior, medial and the Turnipseed approach.
A posterior approach may be undertaken by a lazy S incision over the popliteal fossa.
The popliteal fascia is incised, protecting the sural nerve and short saphenous vein,
to expose the medial head of gastrocnemius. This is divided using either a right angle
and diathermy, or a LigaSure [23]
[52]. The plantaris may also be divided at this point [63]. Proponents of this approach state that it allows better access and visualization
of the neurovascular bundle, and easy access to the medial head of gastrocnemius [13]
[16]
[23]
[52]. Potential drawbacks are the difficulty of proximal arterial access, should an arterial
bypass be necessary, and that the patient must be positioned in a prone position.
The medial approach is via an incision in the medial lower thigh, facilitating access
to the above-knee popliteal artery. This allows division of the medial head of gastrocnemius,
but does not permit division of the plantaris or popliteus [34]. Advantages of this approach are that patients are supine for the procedure, and
that more proximal access to the artery may be gained if a bypass is required [24]; additionally, it provides easy access to the greater saphenous vein. However, visualization
of the distal popliteal artery, particularly at the level of the “popliteal outlet,”
is more difficult. The final approach is that described by Turnipseed. A superomedial
calf incision is made, similar to that for exposure of the below-knee popliteal artery.
The fascial attachments of the gastrocnemius and soleus are excised off the medial
tibia. The tendon and proximal third of the plantaris muscle are excised. The soleus
is taken down at its medial attachment to the tibia. The anterior soleal fascia is
taken down at the level of the popliteal outlet [16]. Possible advantages of this procedure are that it spares resection of the musculature
of the medial head of gastrocnemius (which may be less debilitating in an athletic
cohort of patients), and that it releases the medial tibial origin of the musculature
and the anterior soleal fascia which may cause compression of the neurovascular bundle
at the popliteal outlet. Concerns, however, have been raised that insufficient debulking
of the medial head of gastrocnemius may result in post-operative compression of the
popliteal vein, even if the artery has been successfully freed [23]
[52]. It is unclear whether this is a possibility in patients undergoing this technique.
Another possible drawback of the approach is the limited access to the above-knee
popliteal artery. Currently, there is no comparative data regarding the relative efficacy
of these approaches.
Vascular reconstruction has not been reported in patients with functional PAES [48]. Experience extrapolated from patients with anatomical PAES suggests that treatment
would involve thromboendarterectomy with or without patching or interposition or exclusion
bypass, as vessel damage generally necessitates resection of the intima and/or media
[24]
[48]. Data from patient cohorts who have undergone vascular reconstruction for anatomical
PAES suggests that the 5- and 10-year patency rates of these reconstructions are excellent
(>90%); however, patients who require extensive or distal bypass have a significantly
lower patency rate, approaching 20% in Lejay’s cohort [5]
[64]
[65].
There is no validated method of assessing post-operative outcomes in functional PAES.
Some authors have measured the percentage of patients who have successfully returned
to their pre-morbid level of sport post-operatively [52], while others have recorded post-procedural exercise ABIs and compared them to pre-procedural
figures [23]. There is also no evidence regarding whether patients should be surveilled long-term
after surgery. Qualitative observations suggest that long-term recurrence in patients
with functional PAES may be secondary to fibrosis around the neurovascular bundle
[23].
Endovascular treatment of functional PAES has not been described. Endovascular treatment
is not recommended for the management of anatomical PAES. An endovascular approach
is not preferred in functional PAES, as it does not correct the compression of the
popliteal artery. Furthermore, there are concerns regarding the durability of endovascular
angioplasty and stenting in young patients.
