Table of Contents  
Year : 2021  |  Volume : 8  |  Issue : 3  |  Page : 293-296

The persistent sciatic artery aneurysm a cause of recurrent limb ischemia – A rare case report

1 Department of Vascular and Endovascular Surgery, Ruby Hall Clinic, Pune, Maharashtra, India
2 Departement of Vascular and Endovascular Surgery, Jehangir Hospital, Pune, Maharashtra, India

Date of Submission22-Jul-2020
Date of Decision03-Aug-2020
Date of Acceptance06-Aug-2020
Date of Web Publication6-Jul-2021

Correspondence Address:
Bhushan Shinde
Departement of Vascular and Endovascular Surgery, Jehangir Hospital, Pune, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijves.ijves_104_20

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A persistent sciatic artery (PSA) is a rare vascular anomaly. It can cause complications, including acute and chronic limb ischemia, aneurysm formation, and compression of adjacent tissues during early embryonic development, the sciatic artery usually disappears when the superficial femoral artery has developed properly. PSA is usually an incidental finding and is exceedingly rare to find bilaterally. We are presenting a rare case of unilateral PSA aneurysm presented as an episode of recurrent acutely ischemic limb.

Keywords: Cause of acute limb ischemia, congenital vascular anomaly, persistent sciatic artery

How to cite this article:
Kamerkar DR, Pathak N, Purandare N, Sarkar N, Shinde B, Jaiswal S. The persistent sciatic artery aneurysm a cause of recurrent limb ischemia – A rare case report. Indian J Vasc Endovasc Surg 2021;8:293-6

How to cite this URL:
Kamerkar DR, Pathak N, Purandare N, Sarkar N, Shinde B, Jaiswal S. The persistent sciatic artery aneurysm a cause of recurrent limb ischemia – A rare case report. Indian J Vasc Endovasc Surg [serial online] 2021 [cited 2022 Nov 26];8:293-6. Available from:

  Introduction Top

A persistent sciatic artery (PSA) is a rare vascular anomaly with an estimated incidence of 0.025%-0.04%.[1] The first description of such an anomaly was published as early as 1832 in the lancet.[2] The first description of fatal ruptured aneurysm was reported in 1864.[3] The embryological basis and aberrant anatomy of this artery were elucidated in 1919 by reviewing a number of published case reports highlighting this condition.[3],[4]

The incidence of PSA is estimated to be 0.025%–0.04%. Bilateral PSAs are exceedingly rare and account for only 12%–32% of known cases. It is right-sided in 50% of known cases, left-sided in 20%, and bilateral in <30% of known cases.[1] Both sexes are equally affected.[5] Most patients with PSA are asymptomatic in their youth and present between the ages of 40–50-year-old (mean age of 44 years) with claudication, aneurysm, and rarely, sciatica.[5],[6] Asymptomatic cases are found rarely and incidentally. PSA has been associated with an assortment of coexisting anomalies, including Müllerian agenesis, arteriovenous fistulae, hypertrophy of the lower limb, varicose veins of an atypical pattern, and right retroesophageal subclavian artery. A genetic mutation or environmentally triggered vascular event in utero has been suggested to be the cause of this combined malformations.[7]

  Case Report Top

A 65-year-old male presented with left lower limb pain acute in onset for a week with discoloration of the left forefoot. The patient had no comorbidities. No history of tobacco in any form.

The patient gave a history of left popliteal thrombectomy with fasciotomy performed 9 months back. Doppler findings at that time were showed mixed plaque in proximal and mid portion of persistent trigeminal artery (PTA) causing 30%–40% narrowing with monophasic flow in PTA distally.

Three days before, the patient was again operated in another hospital (other vascular center in same city) for left popliteal thrombectomy. The patient presented to us postpopliteal thrombectomy (first 1 year ago, second 3 days back).

Routine blood investigations were normal.

Preoperatively, the patient had left forefoot cyanosis with foot drop. Forefoot was cold; there was mild tenderness along the anterior aspect of the leg. In index limb, only femoral pulse was palpable. Poor Doppler flows in anterior tibial artery (ATA) and PTA. Rightly lower limb had normal pulses.

He underwent computed tomography (CT) angiogram which showed a saccular pseudo-aneurysm with wide neck, arising from the anterior aspect of dominant internal illiac artery which is posterior to hip joint, internal iliac artery traversed the gluteal region and posterior thigh to form popliteal artery which was normal in caliber [Figure 1]. ATA shows multiple luminal narrowing with collaterals around it. Posterior tibial artery was well opacified in the proximal 15 cm, but the mid and distal parts were not opacified. Rich collaterals reformed of PTA at ankle, with good foot vascularity.
Figure 1: Preoperative computed tomography angio showing persistent sciatic artery aneurysm

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Left external iliac artery and left superficial femoral arteries up to distal thigh were smaller in calibre compared to right, but well opacified. Left superficial femoral artery distally does not continue as popliteal artery. Left profunda femoris and branches well opacified. No other abnormal finding in the aorta or right leg.

Findings were diagnostic of complete PSA with embolization from saccular aneurysm.

MRI was performed to see relation of PSA to other soft tissues and sciatic nerve of the left gluteal region showed persistent left sciatic artery and aneurysm of it seen in the left gluteal region, predominantly anterior to gluteal maximus, it is partially thrombosed, 37 cm × 57 cm × 48 cm in size.

Two-dimensional echocardiogram (2D echo) showed 60% ejection fraction no abnormal findings.

Patient operated for left PSA aneurysm repair with interposition inter-ringed graft (8 × 40) along with aneurysmorrhaphy.

Intraoperative description

After induction of anesthesia, the patient was operated in prone position after taking care of all pressure points. PSA was approached from the lateral side of gluteal fold. Flap was raised along with muscle to identify and secure sciatic nerve. PSA aneurysm appreciated. Controls taken over the healthy part of the artery. After 3 min, heparinization clamps applied proximally and distally, aneurysm sac opened and interposition graft-interringed poly-tetra fluoro ethylene (PTFE) (8 × 40) sutured. Anerysmorrhaphy was done.

Ten days later, CT angio showed near complete thrombosis of aneurysm, graft patent. Good run off below knee with foot vascularity satisfactory [Figure 2].
Figure 2: Postoperative computed tomography angio showing graft patency and thrombosed aneurysm

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The patient discharged on dual antiplatelet (anticoagulation was not used as there was no course of embolization left after putting interposition graft) and advised to avoid persistent pressure on graft by changing sitting position or with water bed for sitting and sleeping.

On serial follow-up, the patient is doing well. Doppler showed patent graft. Recent telephonic follow-up, the patient was symptom free, was able to do day to day activities.

  Discussion Top

Embryologically, the sciatic artery is a branch of the umbilical artery that forms a confluence of the capillary plexus in the limb bud;[8] this confluence consolidates to form the sciatic artery that serves as the primary arterial supply to the lower limbs during the 6–9-mm stage of the embryo. During the 10-mm stage, the femoral artery begins to develop as a continuation of the external iliac artery. By 12 mm, the femoral and deep femoral arteries are present.[7] The femoral artery enlarges and branches, eventually dominating arterial delivery to the lower limb. The 14-mm stage of the embryo is the only time during development that the lower limb receives dual blood supply from both the sciatic and the femoral arteries. Normally, by the 22-mm embryologic stage, the sciatic artery has atrophied at its midpoint in the distal thigh.[8] Its proximal portion becomes the inferior and superior gluteal arteries, and the distal sciatic artery develops into the peroneal and popliteal arteries. The femoral artery continues to develop and establishes continuity with the popliteal artery, becoming the primary arterial supply of the distal lower limb.[9] Simultaneously, the umbilical artery develops into the internal iliac artery.[7] Several authors have suggested that the sciatic artery persists when the femoral arterial system is hypoplastic to deliver adequate blood flow to the developing limb.[7]

Anatomically, therefore, the PSA is essentially an anatomic extension of the internal iliac artery. The internal pudendal and superior gluteal arteries originate from the PSA within the pelvis. Subsequent to this branch point, the PSA courses posteriorly through the lower part of the sciatic foramen, beneath the piriformis musculature. At this level, the vessel is often accompanied by the posterior cutaneous nerve or sciatic nerve. Several authors of PSA cases have reported that the artery actually runs within the sciatic nerve sheath, although this finding is not universal.[7] At the proximal femur, the artery courses medially to the sciatic nerve. Occasionally, perforators from the profunda join with the PSA at this level. The PSA extends to the popliteal fossa through the dorsum of the adductor magnus, becoming contiguous with the popliteal artery. Subsequently, the PSA courses along the anterior aspect of the sciatic nerve and eventually terminates in the dorsal foot.[10] The PSA is typically subcentimeter in diameter, usually on the order of 5–9 mm. Although the sciatic artery and vein develop simultaneously along a similar course, it is extremely rare for the sciatic vein to persist along with the artery.[7]

A complete PSA is the most common variant and accounts for 70%–80% of recorded cases.[7] A complete PSA connects a large internal iliac artery to the popliteal artery. The femoral artery can be normal, incomplete, or absent. In an incomplete PSA, the vessel is interrupted in its course from internal iliac to popliteal fossa but is connected to the popliteal fossa through collaterals.[11] In the case of an incomplete PSA, the femoral artery supplies a crucial fraction of arterial flow to the extremity and is continuous with the popliteal artery. The deep femoral artery can be absent or reduced. Differentiating complete PSA from incomplete PSA is critical as the differences guide appropriate treatment options.[12]

PSA was first described in 1832 by Green during a postmortem dissection.[2] A classification system has been developed to best describe and catalog various PSA anomalies.[7] The classification scheme is outlined by incomplete or complete persistence of the sciatic artery and femoral development.

The PSA classification scheme describes five types. Type 1 is a complete PSA along with a normal femoral artery. Type 2 is a complete PSA with incomplete femoral development. In type 2a, the femoral artery is present but tapers and does not reach the popliteal artery. In type 2b, the femoral artery is completely absent, as in our case. Type 3 is an incomplete PSA in which only the proximal part of the sciatic artery remains, and the femoral arteries are fully developed. Type 4 is an incomplete PSA in which only the distal part of the artery remains, and the femoral arteries are fully developed. Type 5 PSA originates from the median sacral artery. Type 5a has a developed femoral artery, and type 5b has an underdeveloped femoral artery.[7]

PSA is a rare congenital anomaly associated with various complications,[6],[13],[14],[15] including atherosclerotic changes or aneurysms, that are often mechanically compressed because of their anatomical location. These changes can lead to limb ischemia, thrombosis of the PSA or distal embolization, rupture of the aneurysm and buttock pain or sciatic neuralgia because of compression of adjacent tissue.

In our case, 65-year-old male presented with acute limb ischemia with forefoot cyanosis and foot drop with 1-week history of symptoms which were acute in onset.

This was his second episode to get acute limb ischemia in same leg. Nine months back, he had acute onset of leg pain with restricted mobility at ankle and toe joints, when he was operated with preoperative Doppler examination which was suggestive of popliteal and tibial thrombus, for which he underwent popliteal-tibial thrombo-embolectomy with fasciotomy.

A 65-year-old male was presented without any comorbidities with no cardiac history. There was no history of smoking and structural normality on 2D echo presenting with recurrent episode of popliteal and tibial thrombosis made us think about any proximal source of thrmboemolism.

Later on CT-angio, it was confirmed that it is complete PSA type IIa which is continuation from dominant internal iliac artery with aneurysm which is responsible for recurrent distal thrombosis. For confirmation of anatomical location and relation to other structures, surrounding MRI was performed which gave us the location of aneurysm anterior to gluteus maximus away from other important neurovascular structures.

In our case, it was complete PSA with aneurysm arising from the anterior part of PSA having wide neck and 3 cm × 6 cm × 4 cm (ap × tran × cranio-caudal) in measurement.

We decided for open repair of aneurysm with revascularization by inter-ringed PTFE graft along with anneurysmorrhapy.

Surgery and endovascular treatment are both treatment options for PSA aneurysms. In our case, open surgical repair of aneurysmal part of the artery was performed. However, surgical resection of a PSA aneurysm may be complicated by sciatic nerve injury for sciatic artery approach.

Patient was kept in prone position, sciatic artery approached from lateral side of gluteual fold by raising flap and securing sciatic nerve. PSA repair was done with inter-ringed interposition graft of size 8 × 40 followed by anneurysmorrhaphy.

Endovascular treatment may avoid surgical complications because it is a less invasive treatment. Endovascular treatment options available are coiling of aneurysm and covered stent.

We chose surgical repair because of wide neck of aneurysm and requirement distal revascularisation by interposition graft.

Interinged graft by surgical approach over covered stent was chosen because site of graft is on usual pressure area.

Patient followed up for 6 months in out patient department, patient was doing well with patent graft checked on Doppler.

Last telephonic follow up 2 years postoperative, patient is ambulating with foot drop splint no other leg symptoms.

  Conclusion Top

Acute limb ischaemia should always be evaluated for proximal source of thromboembolism. Doppler examination should not be only investigation for decision making in acute limb ischaemia. Early management can result in preventing significant limb loss.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Mazet N, Soulier-Guerin K, Ruivard M, Garcier JM, Boyer L. Bilateral persistent sciatic artery aneurysm discovered by atypical sciatica: A case report. Cardiovasc Intervent Radiol 2006;29:1107-10.  Back to cited text no. 1
Green PH. On a new variety of femoral artery. Lancet 1832;17:730-1.  Back to cited text no. 2
Fagge CH. Case of aneurysm, seated on an abnormal main artery of lower limb. Guy's Hosp Rep 1864;10:151-9.  Back to cited text no. 3
Senior HD. The development of arteries of the human lower extremity. Am J Anatomy 1919;25:55-95.  Back to cited text no. 4
Wang B, Liu Z, Shen L. Bilateral persistent sciatic arteries complicated with chronic lower limb ischemia. Int J Surg Case Rep 2011;28:309-12.  Back to cited text no. 5
Patel MV, Patel NH, Schneider JR, Kim S, Verta MJ. Persistent sciatic artery presenting with limb ischemia. J Vasc Surg 2013;571:225-9.  Back to cited text no. 6
van Hooft IM, Zeebregts CJ, van Sterkenburg SM, de Vries WR, Reijnen MM. The persistent sciatic artery. Eur J Vasc Endovasc Surg 2009;375:585-91.  Back to cited text no. 7
Jung AY, Lee W, Chung JW, Song SY, Kim SJ, Ha J, et al. Role of computed tomographic angiography in the detection and comprehensive evaluation of persistent sciatic artery. J Vasc Surg 2005;424:678-83.  Back to cited text no. 8
Brantley SK, Rigdon EE, Raju S. Persistent sciatic artery: Embryology, pathology, and treatment. J Vasc Surg 1993;182:242-8.  Back to cited text no. 9
Bower EB, Smullens SN, Parke WW. Clinical aspects of persistent sciatic artery: Report of two cases and a review of the literature. Surgery 1977;815:588-95.  Back to cited text no. 10
Knight BC, Tait WF. Massive aneurysm in a persistent sciatic artery. Ann Vasc Surg 2010;248:1135.e13-8.  Back to cited text no. 11
Mascarenhas de Oliveira F, de Souza Mourão G. Endovascular repair of symptomatic sciatic artery aneurysm. Vasc Endovascular Surg 2011;452:165-9.  Back to cited text no. 12
Bito Y, Sakaki M, Iida O, Inoue K, Yoshioka Y, Mizoguchi H. Clinical management of lower limb ischemia secondary to a persistent sciatic artery aneurysm: Report of a case. Surg Today 2011;41:402-5.  Back to cited text no. 13
Santaolalla V, Bernabe MH, HipolaUlecia JM, Agundez Gomez ID, Hoyos YG, Mateos Otero FJ, et al. Persistent sciatic artery. Ann Vasc Surg 2010;24:691.e7-10.  Back to cited text no. 14
Ishida K, Imamaki M, Ishida A, Shimura H, Miyazaki M. A ruptured aneurysm in persistent sciatic artery: A case report. J Vasc Surg 2005;42:556-8.  Back to cited text no. 15


  [Figure 1], [Figure 2]


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