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Popliteal artery aneurysms (PAAs) are uncommon, having an estimated incidence in the general population of 0.1%. They are the third most common aneurysmal pathology encountered in clinical practice, ranking behind both aortic and cerebrovascular aneurysms. Half to three quarters of patients with PAAs come to the hospital with bilateral lesions. Patients with PAAs have a 30% to 50% chance of a concomitant abdominal aortic aneurysm (AAA), the latter being more likely in patients with bilateral aneurysms. The converse statement, that a PAA is present in a patient with aortic aneurysms, is true in 3% to 12% of patients.
Diagnosis of a PAA mandates lifelong surveillance. It is estimated that half to three quarters of those with these aneurysms either come to the hospital with synchronous aneurysms or develop a separate aneurysm at a distant location within 10 years, mandating continued surveillance after the PAA is addressed.
Aneurysm formation is typically defined as a greater than 50% increase in diameter relative to the accepted normal size of the artery. The accepted diameter of a normal popliteal artery is between 0.7 and 1.1 cm. PAAs have growth rates between 0.7 and 1.5 mm yearly, and larger aneurysms expand between 1.5 and 3.5 mm yearly. The timing of intervention for asymptomatic aneurysms is somewhat controversial given the lack of prospective randomized data on which to base management decisions.
PAAs were described as early as the 3rd century AD. The earliest strategies for treatment involved inducing thrombosis of the vessel. Various techniques, including knee flexion for prolonged periods, compression bandaging, and direct manual compression, were undertaken in attempts to induce thrombosis. These maneuvers were maintained, on average, for 2 weeks. In the 18th century, John Hunter carried out a surgical intervention consisting of proximal ligation of the aneurysm and reliance on geniculate collaterals to maintain perfusion to the leg.
Reconstructive endoaneurysmorrhaphy, whereby the aneurysm was treated by suturing the walls of the aneurysm together over a catheter, thus maintaining in-line flow to the foot, was described in 1906. This time period also saw the use of interposition grafting using either popliteal or greater saphenous vein as conduit. Exclusion and vein bypass was introduced by Edwards in 1969. Exclusion and bypass remains the most common form of treatment in current surgical practice.
The most limb-threatening presentation of a patient with a PAA is that of acute limb ischemia. This is typically caused by thrombosis of the popliteal aneurysm, with concomitant loss of the runoff vessels through a combination of chronic distal embolization and acute thrombosis of the remaining vessel. This presentation carries with it the worst prognosis with respect to limb salvage and necessitates urgent surgical intervention. From 40% to greater than 50% of all patients in published series present in this manner, a number that has remained distressingly high with little change since the 1980s.
Despite the severity of the initial presentation, limb-salvage rates have remained good. A recent meta-analysis demonstrated 30-day amputation rates of 14.1% in patients presenting acutely, with approximately 20% of the total number of amputations performed as a primary procedure without thrombectomy, thrombolysis, or bypass. Smaller series from other centers have reported higher amputation rates, exceeding a third of patients treated. Rupture as the initial presentation is a relatively uncommon acute presentation occurring in only 2% of patients. Fortunately, in this setting, life-threatening hemorrhage is rare because of the constraints of the popliteal fossa. Although it is not life threatening, a ruptured PAA is limb threatening, with reported amputation rates of 50% to 75%.
A second group of patients come to the hospital with symptoms of arterial insufficiency, ranging from claudication to tissue loss. This group represents up to 40% of all patients with PAAs. Repair of these aneurysms in this subgroup of patients should be undertaken regardless of their size given that distal embolization has already begun to compromise the popliteal artery runoff vessels. In addition, this approach provides better outcomes with respect to graft patency, limb loss, and mortality.
A much smaller group of patients with PAAs have symptoms caused by physical compression of venous or nerve structures surrounding the aneurysm within the popliteal fossa. This occurs almost exclusively in patients with aneurysms that are greater than 3 cm. Surgery for these patients decompresses the aneurysm to relieve symptoms and excludes the aneurysm.
In most published series, asymptomatic patients account for between 25% and 50% of patients who present with a PAA. These patients develop symptoms at a rate of approximately 14% per year. Up to 40% of this group have absent pedal pulses, suggesting the presence of distal embolization even in the absence of any clinical manifestations. When Dawson and colleagues compared asymptomatic patients with and without pulses they found that 34% of patients with pulses developed symptoms within 3 years compared to 86% of those without pulses at their initial presentation.
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