Recurrent thrombus formation in a carotid web: highlighting the importance of timely surgical intervention. Illustrative case

Abstract

BACKGROUND

Carotid webs are rare nonatherosclerotic disorders in the carotid artery and are increasingly recognized as factors of ischemic stroke in the young population. Asymptomatic webs can be treated with antithrombotic therapy, whereas symptomatic cases frequently require surgical interventions, including carotid endarterectomy (CEA). However, guidelines for the optimal timing of these treatments remain unestablished, especially compared to atherosclerotic stenotic lesions, due to the rarity of carotid webs.

OBSERVATIONS

A 50-year-old female patient had a carotid web–induced left hemispheric ischemic stroke. Mechanical thrombectomy successfully restored blood flow, but a thrombus reformed in the carotid web within 1 month following the procedure. This caused early CEA, during which the carotid web and thrombus were removed. This case highlights rapid thrombus reformation, indicating that some carotid webs can be more unstable than previously thought.

LESSONS

This case emphasizes the importance of timely surgical intervention in symptomatic carotid webs to prevent recurrent strokes. Additionally, antithrombotic therapy can manage asymptomatic webs, but surgical treatment may be required in unstable cases. Thus, further studies are warranted to establish standardized treatment guidelines for carotid webs.

https://thejns.org/doi/10.3171/CASE24682

Carotid webs, which are rare nonatherosclerotic formations in the carotid bulb, have a reported incidence of 0.62%.^{1, 2} These webs disrupt blood flow, causing thrombus formation and ischemic stroke.³ Asymptomatic carotid webs can be treated with antithrombotic therapy, such as aspirin, but this may be insufficient for symptomatic carotid webs, which frequently require surgical intervention, including carotid endarterectomy (CEA) or carotid artery stenting (CAS).^{4, 5} Surgical intervention for symptomatic carotid webs is predominantly performed early after onset. However, unlike the case of atherosclerotic carotid artery stenosis, guidelines on optimal treatment timing for carotid webs remain unestablished, as these cases are less common than atherosclerotic lesions.⁶ We have observed a case in which a thrombus was reformed in the carotid web approximately 1 month following mechanical thrombectomy for carotid web–induced ischemic stroke, requiring early CEA. This report emphasizes the potential for rapid thrombus reformation and highlights the importance of timely surgical intervention.

Illustrative Case

A 50-year-old female with an unremarkable medical history presented to the emergency department after the abrupt onset of unconsciousness, right hemiparesis, and aphasia. Head magnetic resonance imaging demonstrated evidence of a left hemispheric ischemic stroke. Subsequent head and neck magnetic resonance angiography demonstrated proximal occlusion of the left middle cerebral artery (Fig. 1A–C). Mechanical thrombectomy was performed after administering intravenous recombinant tissue–type plasminogen activator, considering the patient’s diffusion-weighted imaging (DWI)–Alberta Stroke Programme Early CT Score of 6 and the presence of a DWI-clinical mismatch.

FIG. 1.

Admission diffusion-weighted images (A and B) demonstrating high-intensity signals in the left middle cerebral artery region. Magnetic resonance angiogram (C) showing a faintly visualized left internal carotid artery but not beyond the proximal M1 segment. Left common carotid artery angiograms, anteroposterior view, obtained before (D) and after (E) thrombectomy, revealing no visualization beyond the proximal left M1 segment and a clearly demonstrated left middle cerebral artery, respectively.

Left common carotid artery angiography during thrombectomy revealed a 6.5-mm carotid web in the posterior wall of the origin of the left internal carotid artery, where contrast medium stagnation and thrombus formation were observed (Fig. 2A and B). An occlusion was observed in the left M1 segment, and the thrombus was retrieved with a direct aspiration first-pass technique, resulting in thrombolysis in cerebral infarction grade 3 reperfusion (Fig. 1D and E) and detecting no further thrombus (Fig. 2C). CAS for the carotid web was considered just after thrombectomy, but it was deferred because the patient demonstrated a relatively large ischemic lesion and the antithrombotic therapy required following CAS would be unfavorable if hemorrhagic changes occurred.

FIG. 2.

Left common carotid artery angiography, lateral view, before (A and B) and after (C) thrombectomy. A shadow defect on the posterior wall of the left internal carotid artery origin, indicating the presence of an embolic source (A). As contrast flows, the area shows a double contour (arrow, B), with the slightly lighter area at the bottom indicating the thrombus and the darker area at the top denoting contrast retention. Thrombus in the carotid web was not seen after thrombectomy (double arrows, C).

Blood tests, hypercoagulability analysis, electrocardiography, continuous electrocardiographic monitoring, and transthoracic echocardiography were performed to investigate other possible etiologies of the ischemic stroke, but all exhibited unremarkable results. Hence, a carotid web was considered the only etiology of the current stroke.

The patient developed cerebral infarction in the left frontal and temporal lobes 2 days after thrombectomy, causing uncal herniation due to cerebral edema. Decompressive craniectomy was performed. Aspirin was administered to prevent a carotid web–induced stroke recurrence despite prolonged postoperative unconsciousness, and the patient’s condition gradually stabilized.

Carotid ultrasonography revealed blood flow within the carotid web without any apparent thrombus formation 2 weeks after the initial event (Fig. 3A and B). However, subsequent neck contrast-enhanced computed tomography (CT), conducted on day 29 postonset, revealed a carotid web with a 10-mm filling defect, strongly indicating a thrombus (Fig. 3C and D). Early CEA was performed to remove the carotid web and associated thrombus, considering the significant risk of recurrent stroke posed by this newly formed thrombus.

FIG. 3.

Carotid ultrasounds on day 14 of onset (A and B) and neck contrast-enhanced CT on day 29 of onset, axial (C) and sagittal (D) views. Shelf echo along the posterior wall of the left internal carotid artery origin (arrow, A). Color Doppler showing blood flow within the shelf echo (B). Membrane-like septal shadow visible on the posterior wall of the left internal carotid artery origin (double arrows, C). Posterior wall of the left internal carotid artery showing a contrast defect measuring 10 mm in length, suspected to be a thrombus (arrowhead, D).

A shelf-like structure and a thrombus inside were observed when the common and internal carotid arteries were incised during CEA (Fig. 4A and B). The carotid web surface was smooth, and a relatively uniform and firm thrombus formed inside the carotid web was observed. Part of the thrombus appeared to protrude from the pocket. The carotid web and the thrombus were removed (Fig. 4C). Intraoperative common carotid arteriography confirmed the carotid web disappearance (Fig. 4D).

FIG. 4.

Intraoperative images (A–C) and intraoperative left common carotid artery angiogram (D). Intimal flap and thrombus (arrow, A) on the posterior wall of the left internal carotid artery. Pocketed carotid web after thrombus removal (B). Intimal flap being excised (double arrows, C). Absence of intimal flap or contrast medium accumulation in the posterior wall of the internal carotid artery after the procedure (arrowhead, D).

The pathological assessment revealed vitreous or mucous-like tissue within the intravascular space of the endomembrane section of the internal carotid artery. No atheromatous components were found. However, a fresh thrombus composed of red blood cells and fibrin adhered to part of the intimal surface, resulting in a carotid web–induced thrombosis diagnosis (Fig. 5).

FIG. 5.

Pathological specimen of the removed shelf-like structure showing that the intima-media section of the internal carotid artery reveals vitreous or mucous-like intravascular tissue. No atheromatous components are observed, and a fresh thrombus, composed of red blood cells and fibrin, is seen adhering to a portion of the intimal surface (single arrow). Double arrows represent the inner elastic plate. Phosphotungstic acid hematoxylin, original magnification ×20.

No postoperative complications were reported, and the carotid web had disappeared on carotid ultrasound that was performed 9 days after CEA. No recurrence of stroke was reported for approximately 6 months after CEA, and the patient is continuing with rehabilitation.

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Carotid webs are increasingly recognized as a crucial cause of cryptogenic stroke, particularly in younger patients without other stroke risk factors.⁷ Medical treatment plays a role in managing symptomatic carotid webs, but it is generally not considered sufficient as a stand-alone treatment.⁸ Evidence is currently lacking, but several case studies indicate that early surgical intervention can effectively prevent recurrent ischemic attacks.⁹ However, evidence to support this approach remains limited, perhaps because of the small number of cases. Our case indicates a rare documentation of thrombus reformation within a carotid web. The rapid timeline of this recurrence offers evidence in favor of early surgical intervention for symptomatic carotid webs. Additionally, it is the second reported case in which a thrombus in the carotid web was directly observed.¹⁰ Such rare observations are crucial in advancing our understanding of the condition’s natural history and guiding optimal treatment strategies to mitigate the risk of recurrent cerebrovascular events.

Observations

Anticipating when a symptomatic carotid web will cause recurrent ischemic attacks is a crucial consideration in timing a therapeutic intervention. The recurrence rate of cerebral ischemia in patients with medically managed symptomatic carotid webs has been up to 20% over 2 years and 26.8% over a follow-up period of 2–55 months.^{6, 8, 11} The median time until recurrence is approximately 12 months (range 0–97 months).¹² CEA performed within 2 weeks of symptom onset in atherosclerotic carotid stenosis has maximized stroke-free survival. It is predominantly performed early in the carotid web, but the timing is more variable, probably because the carotid web is considered more stable and intervention is less urgent. Previous reports have revealed that CEA of carotid webs is performed between 18 days and several months following the initial stroke, which is less hasty than for atherosclerotic lesions.^{13, 14} However, imaging confirmed the reformation of the disappeared thrombus in this case approximately 4 weeks later. Similarly, 2 reports of imaging confirmed the reformation of a disappeared thrombus, with reformation occurring 72 hours and 8 days after the disappearance.^{15, 16} These cases indicate that some carotid webs may be less stable than previously thought and may warrant urgent therapeutic intervention.

Current evidence indicates that multiple factors, including the size and location of the web, as well as individual hemodynamics, such as flow disturbances, low shear rates, flow stasis, local blood flow stagnation, platelet adhesion and coagulation, and recirculation, affect thrombus formation.¹⁷ Perry da Camara et al. demonstrated that symptomatic carotid webs appear longer (mean 3.2 mm), have a larger cross-sectional area and volume, and are thinner than asymptomatic ones.¹⁸ In our case, the length of the carotid web was 6.5 mm, which was longer than the average for symptomatic carotid webs, thereby contributing to thrombus reformation in a short period.

Moreover, in this case, the reason for the previously asymptomatic carotid web to suddenly become repeatedly thrombus-forming in a short period remains unclear. Vercelli et al. reported de novo carotid webs, indicating that they can enlarge over time.¹⁹ Hassani et al. investigated 47 children with ischemic stroke and found no cases of carotid webs, indicating that carotid webs are acquired and can enlarge over time.²⁰ These reports indicate that carotid webs can initially form as small structures and then enlarge, making them susceptible to thrombus formation. Furthermore, we reported similarities between intimal dissections and carotid webs. Localized intimal dissections could have evolved into shelf-like structures and undergone reactive changes, causing “trapped” areas of fibrous tissue within the media, thereby forming the carotid web.²¹ Therefore, some carotid webs might be acquired later in life, possibly caused by hemodynamic stress or endothelial injury.

More research is required to establish definitive guidelines, but our case and others indicate that timely surgical procedures, such as CEA, should be considered the primary therapeutic intervention for symptomatic carotid webs. Antithrombotic therapy could be considered for asymptomatic or medically managed cases, but its limitations in preventing recurrence highlight the potential need for timely surgical intervention in symptomatic patients. Ultimately, the selection between surgical intervention and medical management should be individualized, with early surgical intervention preferred in cases with recurrent thrombus formation or large and symptomatic webs. Additionally, postoperative management, including antithrombotic therapy and regular imaging follow-up, is crucial to monitor for recurrence and ensure long-term stroke prevention. Continuously increasing the number of cases and thoroughly investigating the effectiveness of surgical intervention, drug therapy, and follow-up are necessary. Future large-scale studies are important for developing standardized guidelines and ensuring optimal outcomes for patients with carotid webs. Case-by-case evaluations remain crucial until more data are available.

Lessons

We reported a case of thrombus reformation within the carotid web just 1 month after mechanical thrombectomy for ischemic stroke, which requires early CEA. Aspirin alone was insufficient to prevent thrombus reformation, suggesting that dual antiplatelet therapy or anticoagulation may have been necessary. This case indicated that some carotid webs could be more unstable than previously thought, and timely surgical intervention is crucial to prevent recurrence.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: T Takahashi, Yanaka, Matsumaru. Acquisition of data: T Takahashi, N Takahashi. Analysis and interpretation of data: T Takahashi, Yanaka, N Takahashi. Drafting the article: Ishikawa, T Takahashi. Critically revising the article: T Takahashi, Yanaka, Marushima. Reviewed submitted version of manuscript: Ishikawa, Yanaka, Saura, Aiyama, Marushima. Approved the final version of the manuscript on behalf of all authors: Ishikawa. Study supervision: Ishikawa, Yanaka, Matsumaru.

Correspondence

Eiichi Ishikawa: Institute of Medicine, University of Tsukuba, Ibaraki, Japan. e-ishikawa@md.tsukuba.ac.jp.