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Single pathology, 2 clinical and therapeutic perspectives: popliteal aneurysm thrombosis as a rare cause of acute lower limb ischemia

Maryla Kuczyńska1, Monika Zbroja-Putowska2, Katarzyna Drelich2, Agata Zarajczyk3, Michał Sojka4, Anna Drelich-Zbroja1
1 Department of Interventional Radiology and Neuroradiology, Medical University of Lublin, Lublin, Poland
2 Department of Pediatric Radiology, Medical University of Lublin, Lublin, Poland
3 Students’ Scientific Society at the Department of Interventional Radiology and Neuroradiology, Medical University of Lublin, Lublin, Poland
4 Department of Vascular Surgery of the University Clinical Hospital No. 4 in Lublin, Lublin, Poland
DOI: 10.20452/pamw.16961
Published online: March 3, 2025.
CCBYCC BY 4.0

In this article

Popliteal artery aneurysm (PAA) is defined as a segmental dilatation exceeding 50% of its normal diameter.1 Aneurysm thrombosis is a rare cause of acute lower limb ischemia (ALI)2 that can bring about serious health implications, including amputation or, when treated, reperfusion syndrome.3 Approximately 17%–46% of patients with PAA may develop severe ALI.4

Two men were admitted to an emergency department due to acute onset of lower limb pain. The first patient, aged 66, had a history of minor contusion of the popliteal area. The second, aged 58, reported mild‑to‑moderate dehydration due to recent food poisoning.

Patient 1

Clinical examination showed no pulse in the dorsal artery of the left foot with considerably prolonged capillary refill, severely compromised motor function, and paresthesia and rest pain. Doppler ultrasound showed 6 cm × 3 cm (length × diameter) PAA filled with heteroechoic masses that exhibited slight movement concurrent with the arterial pulsation in its proximal portion, consistent with acute thrombosis. No flow was detected in the below‑the‑knee arteries (class IIb in the Rutherford classification). The patient required immediate thrombolytic treatment, and he received a continuous infusion of alteplase delivered via an intra‑arterial catheter positioned within the thrombosed PAA. Additionally, an intra‑arterial infusion of heparin (500 IU/h) was administered distally to prevent below‑the‑knee thrombosis.

The next day, clinical improvement of the distal circulation was observed. Follow‑up angiography confirmed recanalization of the popliteal artery and below‑the‑knee arteries.

Femoropopliteal bypass surgery was performed on the same day to exclude PAA from the circulation (Figure 1A–1D). The patient developed symptoms of fascial compartment syndrome requiring urgent fasciotomy. By the following day, the distal pulse was restored and the skin temperature and function of the treated limb normalized.

Figure 1 AD – Patient 1; popliteal aneurysm visible on both B‑mode (A) and color Doppler (B) ultrasound scans. The aneurysmal sac is nearly filled with heterogenous thrombotic material (A, asterisk), with residual blood inflow visible only in the cephalad portion of the aneurysm (B, long arrow). Real‑time imaging additionally showed a free‑floating proximal aspect of the thrombus, that is, a risk factor for embolism. A compressed popliteal vein is seen modelling over the aneurysm (B, short arrows). No flow signals were detected distally to the aneurysm. On the preoperative digital subtraction angiography, complete occlusion of the vessel was visible at the same level as on ultrasound imaging (C, arrow). A successful surgical bypass led to restoration of the blood inflow to the below‑the‑knee arteries (D, arrow). EH – Patient 2; B‑mode imaging showing another case of a thrombosed popliteal ectasia / aneurysm (E, arrow). No flow signals are visible within the artery on either low‑velocity color Doppler (F, arrow), or microvascular flow imaging (G). A patent popliteal vein is visible modeling against the aneurysm (G, arrows). In this case, a biphasic, low‑resistance, low‑velocity flow was detected in the distal below‑the‑knee arteries (H). Although insufficient, it was enough to prevent the patient from developing prominent sensory or motor dysfunction.

Patient 2

The patient presented with symptoms of intermittent claudication occurring after walking short distances (50–100 m) for several days. The pulse on the dorsal pedal artery was absent, and the left foot was considerably colder. Motor function was slightly impaired, and sensation was limited to the distal part of the foot.

Ultrasound showed ectasia / aneurysm (13 mm in diameter) of the popliteal artery filled with heterogeneous thrombus, with no flow signals on Doppler or microvascular imaging. Low‑resistivity poststenotic flow patterns (peak systolic velocity, 5–15 cm/s) were observed in the distal two‑thirds of the posterior tibial and peroneal arteries. A monophasic (vein‑like) waveform was noted in the very distal anterior tibial artery, however, with no color‑coding (class IIa in the Rutherford classification).

Considering the subacute clinical manifestation, a decision was made to start conservative treatment with low‑molecular‑weight heparin (enoxaparin) and pentoxifylline. Popliteal and below‑the‑knee thrombectomy was performed on the following day, resulting in improved peripheral circulation. The second stage of the intervention (stent‑graft implantation) was scheduled in 3 weeks to exclude popliteal ectasia / aneurysm (Figure 1E–1H).

Popliteal artery aneurysms frequently remain asymptomatic. Trauma or dehydration may trigger the clotting cascade, resulting in aneurysmal thrombosis and ALI. While endovascular treatment has proven effective in restoring the arterial patency, selected cases still require open surgical intervention, such as thrombectomy or bypass to ensure optimal outcomes. In the case of ALI, it is essential to not only rely on diagnostic imaging, but also to take into consideration the Rutherford classification, that is, clinical factors, thorough physical examination, evaluation of motor function, possible dermatologic and trophic changes, nerve function evaluation, as well as flow evaluation to determine severity of the treatment. In our case, the thrombosed popliteal aneurysms were atypical cause of ALI.

Acknowledgments: None.
Funding: None.
Conflict of interest: None declared.
References
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