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Ann Indian Acad Neurol
Ann Indian Acad Neurol
AIAN
Ann Indian Acad Neurol
Annals of Indian Academy of Neurology
0972-2327
1998-3549
Wolters Kluwer - Medknow India

39172080
AIAN-27-426
10.4103/aian.aian_267_24
Case Report
Carotid Stump Syndrome: Rare Cause of Recurrent Stroke Post-Ipsilateral Carotid Occlusion – A Case Report
Chinchure Swati D.
Kataria Varun 1
Department of Neurointerventions, Institute of Neurosciences, Medanta Super Speciality Hospital, Indore, Madhya Pradesh, India
1 Department of Neurology, Institute of Neurosciences, Medanta Super Speciality Hospital, Indore, Madhya Pradesh, India
Address for correspondence: Dr. Swati D. Chinchure, Medanta Superspeciality Hospital, Vijay Nagar, Indore - 452 010, Madhya Pradesh, India. E-mail: swatichinchure@yahoo.com
Jul-Aug 2024
22 8 2024
27 4 426429
06 4 2024
16 6 2024
21 6 2024
Copyright: © 2024 Annals of Indian Academy of Neurology
2024
https://creativecommons.org/licenses/by-nc-sa/4.0/ This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
Carotid stump is blind remnant of occluded proximal segment of the internal carotid artery (ICA) that can become the potential source of embolism. Carotid stump syndrome is a potentially treatable cause of recurrent ischemic events in the carotid territory in the setting of occlusion of the ipsilateral ICA. It is thought to be caused by turbulent blood flow in the patent stump of the occluded ICA causing microemboli migrating in the brain through external carotid–ophthalmic anastomotic channels and retrograde flow. Here, we report a patient with known ipsilateral chronic ICA occlusion, who was on best medical management, presented on two separate occasions with recurrent embolic infarctions in ipsilateral carotid territory. She was diagnosed with carotid stump syndrome and treated through endovascular route with clinical and angiographic follow-up.

Carotid stump syndrome
internal carotid occlusion
stroke
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pmcINTRODUCTION

Carotid stump syndrome (CSS) is a rare cause of recurrent cerebrovascular events after ipsilateral internal carotid artery (ICA) occlusion. Carotid stump is blind remnant of occluded proximal segment of ICA. CSS is a treatable cause of recurrent ischemic symptoms.[1] Here, we report a case of CSS that was treated through endovascular route which relieved her recurrent symptoms.

CASE PRESENTATION

A 53-year-old female, who was a known hypertensive, presented with recurrent right-sided weakness with reduced vision in the left eye. Magnetic resonance imaging showed watershed infarcts in the left hemisphere and complete occlusion of ICA with a small stump at the origin [Figure 1]. Computed tomography angiography confirmed complete occlusion. She was started on double antiplatelets (Aspirin 150, Clopidogrel 75 once a day). She came with recurrent symptoms after a month. Cardiac workup to rule out cardioembolic etiology was negative. She was started on Ticagrelor along with Aspirin. She presented again after 20 days with another infarct in the left frontal cortex [Figure 2a, b]. Catheter angiography showed normal contralateral carotid bifurcation [Figure 2c] with good cross circulation across anterior communicating artery (ACOM) [Figure 2d, e]. Left carotid injection showed patent carotid stump with vortex flow and distal complete occlusion. There was reformation of left ICA via external carotid artery (ECA)–ophthalmic artery collaterals [Figure 2f, g]. Diagnosis of CSS was made in view of her presentation on two separate occasions with recurrent symptoms and evidence of ongoing embolic strokes. A CGuard embolic protection stent was placed from the common carotid artery to ECA to block the flow in patent stump [Figure 2h]. Follow-up angiography after 2 months documented complete exclusion of the stump [Figure 2i]. On clinical follow-up at 9 months, she is free from recurrent episodes.

Figure 1 Diffusion images (a-c) showing watershed infarcts in the left hemisphere. MR (d, e) and CT angiography (f) showing complete occlusion of the left carotid with a small patent stump

CT = computed tomography, MR = magnetic resonance

Figure 2 Diffusion (a, b) showing acute infarct in the left frontal cortex. Digital subtraction angiography (DSA) showing normal contralateral bifurcation (c), good cross circulation (d), and no venous delay (e). Left carotid injection (f, g) shows patent stump (single arrow) with vortex flow (g) and ECA. Ophthalmic collaterals causing retrograde opacification of supraclinoid ICA (double arrow). A C Guard stent was placed to block the flow in patent stump (h). Angiography after 2 months documented complete exclusion of the stump (i)

ECA = external carotid artery, ICA = internal carotid artery

DISCUSSION

Clinical spectrum of carotid occlusion ranges from completely asymptomatic to large stroke and death. Risk of recurrent stroke is 3%–5% per year following ipsilateral carotid occlusion.[2] Symptomatic ICA occlusion diagnosed noninvasively should be confirmed angiographically to differentiate total occlusion from pseudo-occlusion/near-total occlusion.[34] Kniemeyer et al.[5] classified “totally occluded” carotids into three types. Type I is near-total occlusion (pseudo-occlusion) at the origin with delayed orthograde filling of ICA. Type II is total occlusion at the origin with slow orthograde filling of cervical ICA by atypical collateral. Type III is complete occlusion at bifurcation with patent siphon due to retrograde flow. With noninvasive imaging, these types are overlooked and broadly labeled as total occlusion. Patients with near-total occlusion are likely to get benefitted by carotid revascularization.[6] However, revascularization is not an option for patients with total occlusion. Missing the residual lumen in near-total occlusion denies the beneficial procedure of carotid revascularization to the patient.[6]

Having confirmed total occlusion of ipsilateral ICA, what can cause recurrent stroke in the occluded carotid territory [Figure 3]? Recurrent stroke can be hemodynamic or thromboembolic or of combined etiology. In the setting of carotid occlusion, perfusion in the ipsilateral hemisphere is maintained through collateral circulation.[7] Insufficient perfusion can lead to failure of collateralization and hemodynamic infarcts in watershed territory. Thromboembolic infarcts can be secondary to

Figure 3 Flow chart for evaluation of recurrent strokes post-ipsilateral ICA occlusion

CT = computed tomography, ECA = external carotid artery, ICA = internal carotid artery

CSS,

contralateral carotid/aortic disease,[8] or

partial recanalization of ipsilateral carotid allowing trickle of blood flow with emboli.[9]

The first case of CSS was described by Barnett et al.[10] It is thought to be caused by turbulent blood flow in the patent stump of the occluded ICA causing microemboli migrating in the brain through the pathway that involves the reversed blood flow of the ophthalmic artery. CSS has been attributed to both hemodynamic and embolic factors which act synergistically. Microembolization is the more supposable cause because attempts to eliminate hypoperfusion using extracranial–intracranial bypass were unsuccessful.[11]

To date, CSS therapy includes medication, surgical treatment, and intravascular intervention. Besides optimal medical therapy, several studies recommend the surgical option for symptomatic patients. Traditionally, ICA stump surgical excision through ipsilateral ECA endarterectomy is described as the mainstay treatment for CSS.[12] Reported outcomes are good but theoretically clamping of ECA can lead to ischemic stroke when ECA is contributing to intracranial ICA reformation.

Endovascular treatment like covered stents, bare stent with or without coils, and coiling of the carotid stump has been described in the literature.[1314] A systemic review by Baker et al.[15] indicated that endovascular treatment of CSS is associated with low intraprocedural risk and is effective at treating recurrent symptoms. Another study compared the outcomes of open versus endovascular treatment for CSS and concluded that both open and endovascular treatments were safe and effective.[5] Future studies with larger cohorts are needed to make a definitive conclusion on optimal management. Direct comparative studies between surgical and endovascular outcomes are needed, but are difficult due to rarity of CSS.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.
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