According to the almost universally accepted suggestion by the Subcommittee on Reporting Standards for Arterial Aneurysms (from the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery [1]), an aneurysm is a “permanent localized (i.e. focal) dilation of an artery having at least a 50% increase in diameter compared to the expected normal diameter of the artery in question.” The subcommittee accepted as normal value for popliteal artery (PA) a diameter of 0.90 ± 0.20 cm (measurement through B-mode ultrasound by Davis et al. [2]). Another proposed definition, more versatile, is “given the assumption that the arterial diameter proximal to dilation is normal, by common convention, an increase in diameter greater than 50% has been considered evidence of an aneurysm.”

In the practical setting, many authors continue to follow what proposed by Szilagyi et al. [3], considering aneurysmatic a PA with a diameter ≥2 cm. McSweeney et al. [4], from Charing Cross Medical School, stated that “a ratio of ≥1.5 maximum popliteal fossa diameter/supragenicular diameter is likely to represent a true dilation of the artery in the popliteal fossa.” Dawson et al. [5] consider a PA aneurysmatic when its external diameter exceeds 2 cm or 1.5 times the size of the normal artery.

1 A Rare Disease?

Textbooks of Pathology, in the early years of the twentieth century [6, 7], asserted that with the exception of the aortic aneurysms, popliteal artery aneurysms (PAAs) are found more frequently than those of any other artery.

In 1949, Linton [8] stated that the true incidence of atherosclerotic PAAs is probably not given in any available statistic. This assessment was repeatedly confirmed [9,10,11].

The causes of this defective knowledge depend on several factors:

  • A number of PAAs are fully asymptomatic.

  • Postmortem investigations rarely involve the popliteal space unless there are precise indications on the basis of symptomatic lesions or dedicated studies.

  • Palpation of the popliteal fossa is not properly ease, and often, it is not performed as a routine. Theis [12], in 1937, wrote “as a rule, the popliteal space is carefully examined only when serious complications are produced by advanced stage of the aneurysm.” This may be a little surprising because any hospital admission or first visit should include the appreciation of peripheral pulses; however, very frequently, if not constantly, at the lower limb level, only the femoral pulse and eventually the very distal pulses are investigated. This should not apply to angiologists and vascular surgeons, but the fact remains that palpation of the popliteal artery, even if correctly performed (Fig. 8.1), may be difficult and misleading, particularly in the obese patient.

Fig. 8.1
figure 1

Palpation of the popliteal pulse

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An idea about the prevalence of PAAs, at least of those clinically relevant, may derive from the comparison with other more easily detectable aneurysms. In 1959, Crawford et al. [13] reported, during a 5-year period, 650 cases of aortic aneurysms and 54 cases of peripheral aneurysms: of these, 30 (55%) were popliteal. Flamand et al. [14] observed, during 11 years, 131 aortoiliac aneurysms and 41 peripheral aneurysms (in 31 patients), of which 28 (68.2%) were popliteal. MacSweeney et al. [4] registered, during the same period, 232 abdominal aortic aneurysms (AAAs) and 24 PAAs (of which only 11 were detected clinically). Bacciu et al. [15] observed, from 1976 through 1986, 206 AAAs and 24 atherosclerotic PAAs (in 15 patients). In men aged 65–79 years, the prevalence of AAA is reported in 5–10% [16]; in a similar age category, PAA is observed in 1% [17]. These and other observations led to the approximative evaluation [18] that PAAs represent 6–8% with respect to AAAs. Shortell et al. [19] report that, during a 25-year period, PAAs represented almost 7% of all aneurysms submitted to repair. Szilagyi et al. [3] report, in the period 1964–1971, a ratio 15:1 of AAAs vs PAAs; the ratio was 13:1 in the experience of Farina et al. [20] for the period 1972–1988.

The introduction of B-mode ultrasound, shortly after the introduction of duplex scan, would allow a more realistic evaluation of the problem. In 1981, Hirsch et al. [21] reported on 100 consecutive patients, suspected to have aortic or peripheral aneurysm, studied through B-mode ultrasound: they found 53 AAAs and 12 PAAs, of which nine were associated with aortic or femoral aneurysm. Batt et al. [22] found a yearly incidence of five to seven PAAs vs 20–25 AAAs.

As a consequence, the suggestion by Buxton et al. [23] that PAA would occur more frequently than generally thought was confirmed.

A further and deeper insight could derive, always approximatively, by some studies relying on series of patients investigated by duplex scan. Diwan et al. [24] studied 313 consecutive patients affected with AAA: of these, 24 (7.6%) presented also a PAA (for a total of 39 lesions); the authors specified that most of these aneurysms were not detectable clinically. Trickett et al. [17] screened 1076 male subjects aged 75–80 years, finding 11 patients (about 1%) with PAA. Morris-Stiff et al. [25], screening 449 subjects for AAA, extended duplex-scan evaluation to lower limb arteries: they did not find any PAA, but 39/898 (4.3%) popliteal arteries were dilated, with a diameter >1 cm. This finding could be significant: Magee et al. [26], following up for 3.1 years 67 patients with mono- or bilateral ectasia of the PA, observed that within 2 years, seven of them progressed to aneurysm (diameter >2 cm); these cases presented a statistically significant association with extra-popliteal aneurysms.

In spite of a growing mass of information, the true prevalence of PAA remains speculative.

More than 50 years ago, Hunter et al. [10] concluded that apparently PAAs are less common than aneurysms of aortic bifurcation and more common than aneurysms within the chest and of the major arteries of limbs or neck.

The latter assessment was confirmed by several experiences. Abelleyra et al. [27] reported 31 peripheral aneurysms, of which 18 (58%) were popliteal. Hands and Collin [28] observed 25 femoral and 34 popliteal (57.6% of the total) aneurysms. Agrifoglio et al. [29] stated that, on the basis of the available literature, PAAs represent 62% of peripheral aneurysms. In contrast with this general consensus, Whitehouse et al. [30] reported, during a 40-year period, 88 PAAs and 172 femoral artery aneurysms, considering however that many PAAs are small and asymptomatic and that palpation of the groin is much easier and more reliable than that of the popliteal fossa.

Trying to define, if not the prevalence, at least the eventual increase in diagnosis (and consequently the improvement in treatment), we tried to tabulate the data from several series, applying a dividing watershed represented by the year 1985, when duplex-scan apparatuses became widely available. This was a milestone event, as awareness of the importance of the disease, due to the ominous sequelae observed in undiagnosed/misdiagnosed cases, was already established following the reports of Gifford et al. [31], Wychulis et al. [32], and Bouhoutsos and Martin [33].

In the first review (Table 8.1), with the fair exception of the Mayo Clinic (reporting a mean of more than 25 cases/year), the single experiences relied on 1.5–9.8 cases/year, with only two series approaching ten cases/year. In the second review (Table 8.2), the Mayo Clinic remains the leading center, with more than 30 cases/year; however, eight centers reported an annual mean approaching or trespassing ten cases/year (one approaching 30 cases/year).

Table 8.1 Series of atherosclerotic popliteal aneurysms collected (or largely collected) before 1985
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Table 8.2 Series of atherosclerotic popliteal aneurysms collected (or largely collected) after 1985
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Given the characteristics of the various experiences, essentially clinical, the impression is that PAAs are diagnosed with increasing frequency, but this is the consequence of an increased attention in the search of contralateral asymptomatic PAA or of PAA in patients with AAA. Large screenings are still lacking, and therefore, the true prevalence of PAA remains unknown. Perhaps PAA is not really a rare disease, and, in any case, it has been a companion of surgeons during the centuries, so as to justify and share the statement by Laskar et al. [49]: “Il n’est pas étonnant que les premiers balbutiements de la chirurgie vasculaire se soient concentrés autour du diagnostic et du traitement des anévrismes poplités en raison de la fréquence de ces lésions.”

2 Etiopathogenesis

In the past, several factors were the object of speculation as responsible for PAA formation. Broca [104] took into consideration the abuse of alcohol and the prolonged use of mercurial drugs, but he thought that trauma and syphilis were the more frequent causes of the disease. Trauma could be acute, under the form of a contusion, but more often iterative and, in some way, inherent to daily activities. Home [105] observed a high incidence of PAA in coachmen, postilions, and horse-riding men (as cavalry soldiers), attributing the cause of chronic trauma not only to repeated strenuous movements but also to the superior border of rigid leather boots. Delbet [106] favored the traumatic etiology, observing that PAAs are more frequent in the laboring class, and also the predominant involvement of men was explained with the harder physical activity proper of male individuals. Syphilis was recognized as a frequent cause of aneurysms, but as for PAA, several doubts arose about its true role. Broca [104] observed that in colonized countries, syphilis was a diffuse disease but aneurysms were rare. Delbet [106] reported a similar and important incidence of syphilis in soldiers and sailors, but PAAs were more frequent in soldiers; contrarily, Erichsen [107] observed a particularly high incidence of PAA in sailors.

Shortly before World War II, Wells et al. [108] stated that atherosclerosis is frequently the only demonstrable disease of the aneurysm wall and that trauma or strain may precipitate the dilatation and, in particular, give rise to symptoms. Linton [8] reported on 42 patients with PAA observed at the Massachusetts General Hospital in Boston during the period 1908–1947: in 35 of them, atherosclerosis was identified as the etiological factor (even if four patients were luetic); moreover, he stressed the fact that syphilis was never recognized as the etiological factor in the 25 aneurysms collected from 1938. The facts are that atherosclerotic lesions are observed also in post-stenotic aneurysms [20] and that atherosclerotic involvement per se cannot explain the predilection of aneurysmal disease for the popliteal artery.

The particular anatomic situation of the popliteal artery is considered relevant to the formation of aneurysm in this site. In 1957, Lord [35] textually wrote: “the popliteal artery is adaptable, in that it may change from a straight line course to one forming an angle of 45 degrees when the leg is fully flexed on the thigh. This change is no trick for the young, healthy, flexible vessel, but it is less readily tolerated by an artery that is more rigid and less elastic due to the presence of atheromatous plaques and deposits of Calcium in the wall...Unquestionably, frequent bending is a factor favoring the development of aneurysms in this particular vessel….”

The importance of repeated trauma from flexion/extension of the knee had been already stressed by Boyd et al. [109] and by Lindbom [110].

An attractive etiopathogenetic theory is that PAA may represent a post-stenotic arterial dilatation. A clinical support to this hypothesis relies on the not rarely observed post-stenotic aneurysms in subjects affected with popliteal artery entrapment. The phenomenon is largely recognized both clinically and experimentally. Subclavian artery aneurysms due to anatomical variants in the thoracic outlet were known in the nineteenth century [111]; in 1916, Halsted and Reid [112] produced a circumscribed dilation of an artery downstream a partially occluding band. In 1954, Holman [113] thoroughly studied in the laboratory the phenomenon of post-stenotic dilatation (Fig. 8.2) and concluded:

“a mass of fluid ejected through a narrow and limited constriction under high velocity strikes against a more slowly moving mass of fluid distal to the stenosis, resulting, first, in the conversion of high kinetic energy into high potential energy or lateral pressure and, second, in the lateral deflection of the rapid stream and even in a complete reversal in the direction of flow, thus producing eddies of alternating high and low pressure whose repeated impacts over prolonged periods against an elastic wall are capable of inducing structural fatigue and distention of the wall, resulting eventually and inevitably in the phenomenon of poststenotic dilatation.”

Fig. 8.2
figure 2

The post-stenotic dilation. Orthograde flow is not represented within the dilated segment, to enhance the effect of the lateral and retrograde deflection of stream lines. (From Holman [113], with permission)

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Parietal vibrations of post-stenotic aneurysms were later studied by Simkins and Stehbens [114].

Several zones of possible narrowing of the arterial line, able to produce a post-stenotic dilation of the popliteal artery at different levels, have been described (outside the anatomical variants giving rise to popliteal artery entrapment). The adductor hiatus is probably the more largely known. At this site, which is rather rigid, continuing microtraumas due to the systolic expansion of the vessel wall could be responsible for atherosclerotic lesions [115], giving rise to anatomical and functional narrowing of the vessel. Already in 1946, Lilly [116] had stressed the concept of arterial narrowing by atheromata at the distal end of Hunter’s canal; Friesen et al. [36] suggested that PAAs soon distal to the adductor hiatus may well be post-stenotic in origin. But the entire adductor canal, where the superficial femoral artery is pressed against the femur by the repeated action of the adductor muscles, may represent a zone of functional stenosis.

In 1949, Boyd et al. [109] described a fibrous tunnel derived from the fascia of the deep surface of the gastrocnemius; the popliteal artery enters this tunnel after coursing freely mobile through the loose fatty tissue of the popliteal space. The fascial covering of the deep surface of the gastrocnemius would form a definite band, broad 0.25–0.50 in., attached to the capsule of the knee joint and crossing posteriorly the popliteal artery.

In 1961, Gedge et al. [117] highlighted the importance of the arcuate popliteal ligament (Fig. 8.3) in the genesis of aneurysms of the distal popliteal artery: the ligament arches upward from the head of the fibula and the lateral side of the popliteus muscle, crossing this and blending into the posterior ligaments of the knee joint. This fibrous structure, which crosses anteriorly the popliteal artery, becomes particularly sharp and prominent when the leg is fully extended.

Fig. 8.3
figure 3

Schematic representation of two potential sites of PA stenosis. (A) The adductor hiatus (dilation of the proximal PA). (B) The arcuate popliteal ligament (dilation of the distal PA). (From Gedge et al. [117], modified, with permission)

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Stenosis may play a particular role when localized at a bifurcation of the arterial tree. Guvendik et al. [18] observed that both abdominal aortic and popliteal aneurysms occur upstream a bifurcation; if atherosclerosis causes narrowing of one or both limbs, this will greatly enhance the reflection of pressure waves from the bifurcation, and considerable fluctuations will occur from the meeting between orthograde and reflected waves.

One of the characteristics of PAAs is the frequent association with aneurysms in other sites, leading to the observation that “popliteal aneurysms caused by atherosclerosis are only single manifestations of a generalized progressive disease.” This formal assessment, made by Friesen et al. [36] in 1962, was stressed as a basic concept by Bouhoutsos and Martin [33] in 1974. Towne et al. [44] observed that patients with PAA have an inherent tendency for aneurysmal degeneration. Dawson et al. [61] followed up for 15 years a group of 50 patients with PAA: 16 (32%) developed 23 new aneurysms (six thoracoabdominal, 11 femoral, six popliteal contralateral). Cole et al. [59] asserted that the presence of a popliteal aneurysm indicates high probability of another aneurysm either in the contralateral limb or elsewhere.

The exceptional progress in the basic sciences during the last decades has generated a series of cooperative studies between clinicians and scientists aiming to define the origin of arterial aneurysms and particularly of those which are more frequent and more frequently associated, i.e., abdominal aortic and popliteal aneurysms. The research is still ongoing, but probably at the end (if any), the role of atherosclerosis will be redefined. Lindeman et al. [118], in 2008, could assert that abdominal aortic aneurysm (AAA) is a general inflammatory condition characterized by enhanced expression and activation of pro-inflammatory transcription factors accompanied by IL-6 and IL-8 hyperexpression and exaggerated downstream cellular responses (differently from atherosclerosis).

Pioneer papers appeared in the literature between 1980 and 1990: Busuttil et al. [119] and Menashi et al. [120] observed the increase of elastase and collagenase activities in the wall of AAA; other authors [121,122,123] stressed the importance of genetic factors, given the preponderance of involvement of the male sex, particularly striking for PAA. The hypothesis of Ward [124] was that of a systemic abnormality.

MacSweeney et al. [4] studied a series of 232 patients with AAA, 24 of them being also affected with PAA. Genotyping for apolipoprotein β and type III collagen did not yield any characterization for patients having also PAA. Fibrillin-1 genotyping yielded a significant difference between 128 patients with AAA and 24 patients with AAA and PAA.

An important research was performed by Sandgren et al. [125] aimed to ascertain if there is a dilating diathesis involving the peripheral arteries of patients with AAA, starting from the hypothesis that AAA is not only a localized vascular disease but also is associated with altered mechanical properties and dilatation of distant arteries [126] and with modifications of arteriolar resistance [127]. The study group comprised 183 consecutive patients waiting for AAA repair. The common femoral artery was measured in 175 subjects (151 male) and the PA in 109 subjects (95 male). Aneurysmal disease was found in eight common femoral and four popliteal arteries. Excluding these 12 patients, no dilating diathesis could be demonstrated in the examined arteries.

Starting from PAAs, the condition of generalized dilating diathesis, as hypothesized by several authors, was confirmed by Widmer et al. [128]: 33 patients undergoing repair of a PAA during the period 1996–2000 were submitted to ultrasound measurement of infrarenal abdominal aorta and common iliac, common femoral, and contralateral popliteal arteries, finding respectively the following:

  • Dilation: 45.5%; 51.5%; 81.2%; 21.2%

  • Aneurysm: 34.2%; 34.8%; 10.6%; 45.5%

Moreover, patients with multiple aneurysms showed also significantly larger diameters of the brachial and external iliac arteries.

Jacobs et al. [129,130,131]stressed the importance of apoptosis in the wall of PAAs, emphasizing the role of inflammation; they observed a large number of cells, predominantly T lymphocytes, expressing death-promoting molecules. Loss of vascular smooth muscle cells and disruption of elastic lamellae were the more evident signs of architectural derangement in the wall of PAAs and of other peripheral aneurysms.

Abdul-Hussien et al. [132] demonstrated, both in AAA and PAA: marked activation of nuclear factor kβ and activated protein 1 proinflammatory transcription factors; hyperexpression of IL-6 and IL-8 on the cellular level; profuse infiltration of macrophages, neutrophils, and T-helper cells; and increased matrix metalloproteinases 8 and 9. According to their findings, genetic and epidemiologic association between AAA and PAA suggest a common origin.

That PA may behave as AA has been suggested in 2004 by Debasso et al. [133], who studied the mechanical properties of the walls of PA in healthy subjects; they observed, with increasing age, the following modifications, particularly evident in male subjects: increase in diameter, increase in stiffness, increase of intima-media thickness, and decrease of distensibility. All these findings suggested a behavior typical of a central elastic artery and not of a true muscular artery, implying susceptibility to dilation and aneurysm formation.

Recently, Hurks et al. [134], from Utrecht, published a detailed study of 38 PAAs (in 36 patients) and 198 AAAs. They found similar wall degradation for elastin disruption and smooth muscle cell decrease; however, the focus of inflammation was the intima in PAAs and the adventitia in AAAs. Cholesterol core presence was more pronounced in AAAs, while iron deposits were more frequent in PAAs, suggesting previous intramural hemorrhages possibly attributable to trauma. Similar levels of MMP-9 were observed in the two types of aneurysm, while PAAs were characterized by higher levels of MMP-2, TNF-α, TNF-β, and interferon-γ. The conclusion was that AAAs have a pathophysiologic mechanism more closely related to atherosclerosis than PAAs.

A still ongoing research at the 1st Dept. of Surgery of Rome University “Sapienza” [135] is focusing attention on the levels of metalloproteinases MMP-2 and MMP-9 and of their specific inhibitors (TIMP-1 and TIMP-2) in the wall of resected PAAs, both by reverse transcription-polymerase chain reaction (RT-PCR) method and immunohistochemistry. Up to now, specimens have been divided into three groups:

  • 11 isolated atherosclerotic aneurysms

  • Eight atherosclerotic aneurysms associated with AAA

  • Six post-entrapment aneurysms

In group 2, levels of MMPs were significantly higher, and levels of TIMPs were significantly lower. No difference in MMP and TIMP gene expression was observed between groups 1 and 3. Immunohistochemistry confirmed the results of RT-PCR. These preliminary results would suggest that single PAAs and post-entrapment PAAs may share the same origin, different from the one triggering the formation of multiple aneurysms.

The studies aiming to elucidate the origin of PAAs and of arterial aneurysm in general are currently flourishing, but we are still in the dawn of this fascinating research.

Finally, it must not be forgotten that sites of arterial fusion during embryogenesis could present some kind of structural weakness, which could be prone to aneurysm formation [136], and this could be true in some cases of PAA [137].