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Endovascular Treatment of Chronic Total Occlusion of a Persistent Sciatic Artery and Acute Thrombosis of High Take-Off Anterior Tibial Artery

Case Report

Endovascular Treatment of Chronic Total Occlusion of a Persistent Sciatic Artery and Acute Thrombosis of High Take-Off Anterior Tibial Artery

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Author Information:

Zoran Stankov, MD; Iveta Tasheva, MD; Lyubinka Yanevska, MD; Georgi Dobrev, MD;  Ivo Petrov, MD, PhD

Department of Cardiology and Angiology, Acibadem City Clinic, Cardiovascular Center, Sofia, Bulgaria


Persistent sciatic artery (PSA) is a rare, lower extremity vascular anomaly with an estimated incidence of 0.025% to 0.04% in the general population and bilateral involvement in 12 to 32% of cases. Around 200 cases worldwide have been described thus far. We present a case of a 50-year-old man with bilateral PSA, chronic occlusion of the left PSA, acute thrombosis of a high take-off left anterior tibial artery (ATA), and a recanalized thrombosis of the left popliteal artery (PA). Successful endovascular treatment with recanalization balloon angioplasty and stent placement was performed for the PSA and balloon angioplasty for the ATA. Although there is no well-defined treatment method for PSA -related lesions, in this case, endovascular management proved to be a feasible, relatively easy, and durable option.

Key words: persistent sciatic artery, balloon angioplasty  

Persistent sciatic artery (PSA) is a rare congenital vascular anomaly. The sciatic artery usually disappears early in the embryonic life with the development of the superficial femoral artery as the main blood supply for the lower extremities.1 The estimated incidence in the general population is 0.025% to 0.04% with bilateral involvement in 12% to 32% of the cases.2,3 Around 200 cases of PSA have been described, with variable treatment methods used, depending on the clinical presentation.4

PSA is predisposed to early atheromatous degeneration, aneurysm formation, and arterial occlusion.5,6 Clinical presentation is remarkable with palpable buttock formation, and neurologic (mostly due to compression of the sciatic nerve), or ischemic leg pain (distal embolization from a preexisting aneurysm or atherosclerotic occlusion).3 Pillet and colleagues described 4 different types of PSA, with Gauffre and colleagues adding a fifth type based on the anatomy of the artery.7,8 Three years earlier, Bower and colleagues proposed a more clinically oriented classification by dividing the PSA into  a complete (the vessel being the main source of blood supply for the lower extremities) and incomplete types – with the PSA usually being hypoplastic and terminating in the thigh.6

Case Report

A 50-year-old man with known hypertension, dyslipidemia, and a history of smoking presented with claudication in the left leg after 200-300 meters of walking. He had experienced the leg pain over the past 6 months, but it had worsened significantly in the 10 days prior to admission, with the patient being unable to walk for more than 10 meters without pain. On clinical examination, the left leg was colder than the right, and there was a palpable but weakened pulse of the common femoral artery with markedly weakened pulsations of the arteries of the foot (possibly positive Cowie sign.4) The ankle-brachial index (ABI) of the left leg was 0.3 and the right leg was 1.01. A Doppler ultrasonography (USG) examination suggested occlusion of the left superficial femoral artery (SFA), a probable thrombosis of the left anterior tibial artery (ATA), and stenosis of the left popliteal artery (PA).

Figure 1Without further imaging diagnostics, conventional angiography was performed, revealing bilateral persistent sciatic artery type 2a7,8, with ostial occlusion of the left PSA and distal filling from a collateral arising from an otherwise rudimentary SFA. Additionally, acute thrombosis of a high take-off anterior tibial artery (ATA) and a recanalized thrombosis of the proximal segment of the popliteal artery (PA) with distal collateral filling were observed (Figure 1). Through right femoral access, a 45 cm, 6 French crossover guiding sheath (Flexor Ansel Guiding Sheath, Cook Medical) was placed in the left PSA over a .035-inch Storq Soft guidewire (Cordis, A Cardinal Health Company). Additionally, a TrailBlazer .035-inch support catheter (Medtronic) and a hydrophilic Half Stiff Angled J .035-inch guidewire (Terumo) were used to get through the occlusion of the PSA – first retrograde, using the collateral from the SFA, and then antegrade. Balloon angioplasty was performed using a 5.0 mm × 300 mm over .035-inch Admiral Xtreme (Medtronic) balloon catheter, followed by implantation of 3 overlapping stents: EverFlex 6.0 mm × 150 mm, EverFlex 7.0 mm × 150 mm (Medtronic), and a Complete SE 7.0 mm × 20 mm (Complete) due to remaining significant stenoses. To cross the thrombosis of the ATA and the recanalized thrombosis of the PA, a .014-inch Asahi Sion ( Asahi Intecc) guidewire was used and balloon angioplasty was performed with a 2.5 mm × 100 mm over .014-inch Pacific Xtreme (Medtronic Medical) balloon catheter (Figure 2). An excellent result was noted for the treated lesions. The patient's postprocedure period was unremarkable, and he was discharged the following day with an ABI of 0.81 in the left leg. Double antiplatelet therapy in standard doses with acetylsalicylic acid and clopidogrel was initiated. On day 15 of the first and third month of the follow-up period, marked clinical improvement was noted, with the patient being able to walk for more than a kilometer with no claudication, a Doppler ultrasonography examination revealed patent stents. Figure 2


PSA is a rare vascular anomaly, with most cases being of the complete type and with no notable sex prevalence.3,4 Around 200 cases have been described since Green published the first postmortem case in 1832.9

When present, the PSA is usually ectatic and enlarged, predisposed to an early atheromatous degeneration and aneurysm formation. The mechanism of these processes is still unclear. Most authors conclude that they are due to chronic mechanical trauma and the hypoplastic characteristics of the vessel tissues.10, 11

In about 80% of reported cases, specific clinical symptoms were reported, with the remaining 20% being asymptomatic and diagnosed in the context of another medical condition.3,6,11 Up to 46% of patients develop an aneurysm of the PSA, which is the main source of complications.3 The aneurysm may lead to a neurologic, even radicular, leg pain due to its proximity to the sciatic nerve and its compression. It is often associated with thrombosis and distal embolization that leads to ischemic leg pain, with only 10% of cases with such symptoms originating from a native stenosis, occlusion, or thrombosis of the artery.3,12-15

Digital subtraction angiography (DSA) shows detailed anatomy of the vessel and its flow pattern, but may fail to reveal the vessel's full occlusion. In cases where understanding of the relationship between the vessel and surrounding tissues is needed, magnetic resonance imaging (MRI) is the method of choice, especially if an aneurysm with suspected communication with the sciatic nerve is present. Doppler ultrasonography (USG) is usually the first, most cost-effective, and least invasive diagnostic method used for evaluation of the vascular anatomy with good diagnostic effectiveness.16-18

The treatment method for patients with PSA pathology is guided by the patient's specific symptoms, anatomy of the artery, presence of a stenosis and/or an aneurysm, and type of PSA.19 Symptoms resulting from ischemic leg pain are most often due to thrombosis of an aneurysm or its distal embolization. Successful surgical exclusion of an aneurysm has been performed by ligation of the artery and, when the PSA is of the complete type, by performing an additional femoropopliteal bypass.20-22 Stent grafts have also been used for the exclusion of an aneurysm, with good results reported.23-25 Endovascular treatment is usually the first method of choice for treating stenoses or thromboses of the lower extremity arteries with either balloon angioplasty and/or stent placement being performed. There are no guidelines or consensus papers regarding the treatment of a stenotic or occluded PSA. Only a few cases of endovascular-treated stenoses or occlusions of the PSA have been reported, and even fewer treated with placement of a stent.26-28 In the first intervention treatment case series, Gabelmann and colleagues reported a 41-year-old patient with a PSA stenosis that was successfully treated with the placement of an 10 × 40 mm stent. In 18 months of follow-up, Duplex scanning confirmed stent patency.29 Shibutani and colleagues managed a 74-year-old patient presenting with limb ischemia due to a 13 cm chronic total occlusion of the PSA using balloon angioplasty and implantation of a 7 mm × 120 mm stent. Three months later, the patient was diagnosed with a newly developed aneurysm above the previously treated lesion, which was again managed endovascularly with a 10 mm × 40 mm stent graft.30

In our case, the patient presented with an ostial occlusion of the PSA that was promptly treated via balloon angioplasty, followed by additional placement of three stents due to remaining significant stenoses of the vessel. A thrombosis of a high take-off ATA and a recanalized thrombosis of a PA were also successfully treated with balloon angioplasty. This proved to be a feasible, quick, and effective method for dealing with such lesions, with a good final result on angiography. Immediate clinical improvement was observed, and patent stents and good blood flow were noted on the USG examination in the early follow-up period. 


PSA is a rare vascular anomaly with various clinical presentations. Each patient with PSA pathology should be approached individually and the management method should be chosen carefully. In patients with leg ischemia caused by stenosis or occlusion of the PSA, as in our particular case, endovascular treatment with balloon angioplasty and stent placement may prove to be a feasible and reliable method. 

Disclosure: The authors report no financial relationships or conflicts of interest regarding the content herein.

Manuscript submitted February 9, 2019; accepted February 27, 2019.

Address for correspondence: Georgi Dobrev, MD, Acibadem City Clinic, Cardiovascular Center, Sofia, Bulgaria. Email:


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