Persistent Sciatic Artery in Right Lower Extremity Complicated by Thrombosis: A Case Report

Introduction

Persistent sciatic artery (PSA) is a rare congenital vascular malformation with an incidence of approximately 0.025% to 0.04%. ¹ Previous studies have shown that the mean age of onset is 57 years, with almost no sex differences. ² Embryologically, the sciatic artery originates from the umbilical artery and supplies blood to the lower extremities. When the femoral artery is incompletely developed or the sciatic artery has not degenerated in the third trimester, the sciatic artery persists as a continuation of the internal iliac artery and is referred to as a persistent sciatic artery. ³ In this article, we report a case of severe ischemia caused by thrombosis in the right lower extremity PSA. After endovascular staging treatment, blood flow to the right lower extremity was restored and the ischemic symptoms disappeared.

Case Report

A 65-year-old man visited the outpatient clinic with pain and chills in the right lower extremity for 2 months, with progressively worsening symptoms and numbness in the right foot for 10 days. Computed tomography angiography (CTA) of both lower extremities showed that the right inferior gluteal artery and right popliteal artery of the right internal iliac artery were connected, which is considered a congenital developmental variant. This was complicated by multiple thromboses of the right internal and external iliac arteries and the right femoral artery (Figure 1). The patient had a history of hypertension and diabetes mellitus for >2 years, was not compliant with his medications and had poor blood pressure and glucose control. Physical examination showed pale skin on the right foot, low temperature on the skin below the knee, hypofunction of motor senses, weak pulsation of the right femoral artery, and undetectable popliteal, posterior tibial, and dorsalis pedis arterial pulses.

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Figure 1.

(A) Computed tomography angiography (CTA) three-dimensional reconstruction showed thickened right persistent sciatic artery (PSA) without descending and slender right superficial femoral artery (SFA). (B) Rugged travel of the right PSA, with many thrombi. (C) The right PSA traveled posterior to the pelvis and was not visible.

The patient was admitted to the emergency department and immediately treated with clopidogrel (75 mg) and nadroparin (4100 IU), which was to be continued once daily. After the preoperative preparation, the left femoral artery was punctured for right lower limb arteriography, during which a PSA was confirmed with luminal thrombosis. Catheter-retaining urokinase (13 000 U/h) was then used. Right lower extremity arteriography was performed again 2 days later, showing a reduced thrombus load. We continued to pump 5000 U/h of urokinase through a 40 cm thrombolytic catheter for thrombolytic therapy. Lower extremity angiography was performed 2 days later. During the operation, the PSA lumen thrombus was almost completely removed. A 90 cm Mach1 Guide catheter (Boston Scientific, Maple Grove, MN, USA) was used to aspirate parts of the old thrombus, and lower thigh vessels were stenosed (more than 90%). Balloon dilation and stenting were then performed step by step: two 6 × 150 mm self-expanding bare stents (LifeStent; Bard Peripheral Vascular, Tempe, AZ, USA) were implanted at the proximal end of the PSA, a 5 × 150 mm self-expanding bare stent (LifeStent; Bard Peripheral Vascular, Tempe, AZ, USA) was implanted distally, and a 4.5×120 mm self-expanding bare stent (Supera; Abbott Vascular, Santa Clara, CA, USA) was implanted in the popliteal artery segment (Figure 2). The angiogram showed good blood flow in the PSA. After the surgery, the patient continued to receive treatment with clopidogrel (75 mg) and nadroparin (4100 IU) once daily, which relieved the lower extremity chills and pain. Computed tomography angiography of the lower extremity 3 days later revealed smooth blood flow in the stent, no thrombus, and smoothly flowing blood in the PSA and superficial femoral artery (SFA) (Figure 3). Anticoagulation therapy with rivaroxaban (10 mg) once daily was continued after discharge.

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Figure 2.

Intraoperative digital subtraction angiography (DSA) confirmed multiple stenoses of the persistent sciatic artery (PSA). (B and C) Post-stent implantation angiogram showed patent blood flow in the stent and visualized vessels in the distal extremity.

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Figure 3.

(A) Computed tomography angiography (CTA) showed that the right persistent sciatic artery (PSA) stent was unobstructed and the popliteal artery was well developed. (B) CTA suggested that the right PSA was located in the gluteus and posterior thigh muscle groups, with patent blood flow in the stent and good vessel morphology.

At the 5-month postoperative follow-up, the patient reported walking freely, no lower extremity pain or discomfort, and normal right lower extremity skin temperature. Computed tomography angiography of both lower extremities showed smooth blood flow in the right PSA stent with a slight mural thrombus below the stent (Figure 4). The patient was advised to continue rivaroxaban (20 mg) orally once daily and to come for reexamination regularly.

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Figure 4.

(A) Computed tomography angiography (CTA) showed patent blood flow in the right persistent sciatic artery (PSA) stent and normally arranged blood vessels. (B) CTA showed patent blood flow in the right PSA stent.

Discussion

Persistent sciatic artery is a rare congenital vascular malformation. Atherosclerosis and atherothrombosis are complications caused by PSA abnormalities. Approximately, 32.2% of patients had a unilateral PSA solitary on the right side or a bilateral PSA, and 35.6% had a unilateral PSA on the left side. The major complication of PSA is aneurysm-like changes, which account for approximately 48% of complications. Other complications include stenosis and occlusion of the artery, with lower incidences of 7% and 9%, respectively. ² The aneurysm is usually located in the gluteal region; although the reason it occurs mainly in this site is unknown. It may be related to mechanical (traumatic) injury or intrinsic factors related to the body. Dysplasia of the elastic component of the arterial wall may be an important factor in the degeneration of the arterial wall leading to aneurysmal changes. ⁴

These complications can lead to several serious clinical problems, including thrombosis, distal extremity embolism, and aneurysm rupture. Timely recognition and diagnosis of such vascular variants are critical to avoid life-threatening complications in patients. Primary diagnostic methods include vascular ultrasound and CTA. Persistent sciatic artery is usually detected when the patient presents with complications or incidentally when patients undergo routine physical examinations. If patients with asymptomatic PSA are found incidentally, no intervention is required; however, due to the high incidence of aneurysm formation and the high risk of thromboembolic events, regular follow-up is recommended. ⁵

Some studies have proposed a classification system for PSA diagnosis and the selection of surgical options based on the continuity or absence of the femoral artery system. The Pillet classification was proposed in 1980 and further improved by Gauffre in 1994, who summarized the above-mentioned PSA into 5 types.^6,7 This provides a reliable guide for the subsequent treatment of PSA. Although the previous classification may be helpful in understanding PSA anatomy from an embryological perspective, it is of little use in developing treatment plans. In contrast, Ahn et al ⁸ proposed a new PSA classification in 2016. This new classification not only considered the concomitant incomplete persistent sciatic and SFAs but also noted the presence of aneurysms, which is an important guideline for the treatment of patients. According to the latest classification, this case was classified as class IIa with complete PSA and SFA without a complicated aneurysm.

Treatment is recommended for all symptomatic patients with PSA. Treatment methods depend mainly on the symptoms and staging of PSA.^9,10 Surgery and endoluminal therapy are not required for patients with asymptomatic PSA, but regular follow-up is needed. Surgical or vascular endoluminal treatment may be selected for patients with symptomatic PSA based on clinical symptoms, anatomical staging, the presence of an occluded portion of the vessel, and aneurysm characteristics. Attention should be paid to the identification and management of PSA levels to relieve ischemic symptoms in the lower extremities and reduce the amputation rate. A correct surgical approach is important and CTA images should be carefully evaluated preoperatively to maintain longer patency rates. ¹¹ The characteristic clinical sign of PSA is “Cowie’s sign,” which presents as a diminished or absent femoral pulsation with a significant popliteal pulsation. ¹² However, this case was complicated by massive thrombosis in the PSA without Cowie’s sign. Instead, the patient presented with thrombotic disease secondary to atherosclerosis rather than the more common atheromatous disease complicated by thrombosis. Few data are available on simple PSA thrombosis. We carefully assessed the patient’s medical history. The patient was sedentary, and the original vascular lesions were mainly on the buttocks. Considering the possibility of vascular intimal hyperplasia and lumen stenosis caused by repeated local injury as a result of staying in the sitting position for prolonged periods, it is recommended that the patient change his lifestyle and avoid prolonged sitting after surgery.

The goals of treatment are revascularization and prevention of recurrence. Open surgery carries the risk of potential complications, including sciatic nerve injury, which requires surgery in the narrow and deep buttocks. This surgery can be difficult, and because the patient had more thrombotic components in the PSA, a staged surgical plan was adopted in the treatment, after catheter thrombolysis and thrombus aspiration. If there was residual vascular stenosis, balloon dilation and stent implantation would be performed, and good results are usually obtained.

Conclusion

PSA is a rare vascular malformation that could lead to many complications. Therefore, early recognition, diagnosis, and treatment are important. This vascular malformation should be considered when the SFA is slender and the internal iliac artery is larger than the contralateral diameter on CTA. Treatment strategies can be selected based on the anatomical characteristics of PSA and SFA. Asymptomatic patients with PSA can be closely monitored. Surgery or individualized endovascular treatment plans should be considered for patients with aneurysm formation or vascular occlusion.