Neovascular glaucoma masked by cerebral hyperperfusion syndrome following carotid artery stent placement: illustrative case

Abstract

BACKGROUND

Carotid artery stent (CAS) placement and carotid endarterectomy can improve ocular ischemic syndrome (OIS). However, paradoxical visual deterioration due to neovascular glaucoma (NVG) may rarely occur after revascularization. The authors report a case of NVG developing after CAS placement, resulting in severe and irreversible vision loss.

OBSERVATIONS

A 74-year-old man with severe right internal carotid artery stenosis and preoperative retinal ischemia underwent CAS placement. The stenosis was successfully resolved. On the day after the procedure, he developed a headache and was diagnosed with cerebral hyperperfusion syndrome, which stabilized with strict blood pressure control. Despite this, his headache persisted, accompanied by progressive visual deterioration. On postoperative day 10, ophthalmological evaluation confirmed NVG, and topical treatment was initiated. Nevertheless, the visual impairment remained irreversible.

LESSONS

NVG following carotid revascularization has no established preventive strategies and often leads to profound vision loss. Neurosurgeons and neurointerventionalists should recognize this potential complication. The authors recommend conducting preoperative and postoperative ophthalmological assessments for high-risk patients, including those with OIS or a history of cataract surgery.

https://thejns.org/doi/10.3171/CASE25746

Ocular ischemic syndrome (OIS) results from ocular hypoperfusion secondary to stenosis or occlusion of the common or internal carotid arteries. It typically presents as vision loss, orbital pain, and visual field defects. Characteristic ocular findings may include rubeosis iridis and retinal edema.¹ Ocular hypoperfusion leads to anterior segment ischemia. Anterior segment ischemia can promote neovascularization of the iris and angle, ultimately resulting in neovascular glaucoma (NVG).²

Carotid revascularization, including carotid artery stent (CAS) placement and carotid endarterectomy (CEA), is an established intervention for carotid stenosis and can improve ischemic complications such as OIS.³ However, revascularization carries potential risks. Cerebral hyperperfusion syndrome (CHS) is a rare but serious complication, particularly in patients with impaired cerebrovascular reserve.⁴

Paradoxical worsening of NVG after carotid revascularization has been reported in rare cases. To date, no definitive risk factors or preventive strategies have been identified for NVG in this context.

Here, we report a case in which CAS placement was followed by CHS and progressive NVG, resulting in severe and irreversible vision loss.

Illustrative Case

A 74-year-old man was referred with blurred vision. His medical history included cataract surgery in the right eye. On examination, his Glasgow Coma Scale score was 15, and he had no motor or sensory deficits. He reported blurred vision in the right eye. Laboratory tests, including hemoglobin A1c and lipid profile, were within normal limits. Ophthalmological evaluation showed corrected visual acuity of 20/20 (1.0) in both eyes, with no evidence of rubeosis iridis or NVG. Intraocular pressure measured 14 mm Hg in the right eye and 17 mm Hg in the left. Optical coherence tomography demonstrated regional retinal thickening consistent with ischemic retinal changes (Fig. 1A).

FIG. 1.

A: Optical coherence tomogram showing regional retinal thickening attributable to ischemic changes in the retina (circle). B: MR image revealing scattered high-intensity lesions in the right hemisphere on diffusion-weighted imaging (arrow). C: T1-weighted black-blood MR image demonstrating the plaque as approximately isointense relative to surrounding muscle (arrow). D and E: MR angiogram revealing severe stenosis of the right ICA (D; arrow) with diminished distal flow signal (E). F: CT angiogram confirming marked stenosis (95%) of the right ICA according to the NASCET criteria (arrow). G: Ultrasonogram showing a heterogeneous plaque containing hypoechoic regions (circle).

MRI revealed multiple scattered infarctions in the right cerebral hemisphere and reduced flow in the right internal carotid artery (ICA) (Fig. 1B–E). CT angiography confirmed severe stenosis of the right ICA, with a stenosis of 95% according to North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria (Fig. 1F). Ultrasonography revealed a heterogeneous plaque with hypoechoic regions (Fig. 1G), suggesting that severe stenosis with an unstable plaque underlay both the thromboembolic events and ocular ischemic syndrome (OIS). CAS placement was recommended to address symptomatic carotid stenosis.

Prior to the procedure, dual antiplatelet therapy was initiated. Transfemoral CAS placement was performed under flow reversal. A low-profile balloon was used to predilate the stenosis before stent deployment. A CASPER Rx stent (MicroVention) was successfully placed in the right ICA (Fig. 2A and B), followed by postdilation. Vital signs remained stable throughout, and atropine was not administered. Postprocedural angiography confirmed improved antegrade flow in the right ICA with no thromboembolic complications (Fig. 2C).

FIG. 2.

A: Preoperative angiogram via the right common carotid artery (CCA) demonstrating severe proximal ICA stenosis. B:Deployment of a CASPER Rx stent resolved the stenosis. C: Postprocedural angiogram via the CCA showing improved antegrade flow in the right ICA. D and E: On postoperative day 1, MR image revealing a cerebral hemorrhage in the right temporal lobe (D), and SPECT scan showing increased perfusion in the right hemisphere (E). F:SPECT scan on postoperative day 9 demonstrating resolution of hyperperfusion.

On the day after CAS placement, the patient developed a headache. MRI revealed a cerebral hemorrhage in the right temporal lobe (Fig. 2D), and single-photon emission CT (SPECT) demonstrated increased perfusion in the right hemisphere (Fig. 2E). A diagnosis of CHS was made, and strict blood pressure control was implemented (systolic < 120 mm Hg). By postoperative day 9, SPECT showed resolution of hyperperfusion (Fig. 2F). Despite this, the headache persisted, accompanied by visual deterioration. In contrast to preoperative findings, ophthalmological evaluation revealed corrected visual acuity of 1/10 (0.1) in the right eye, elevated intraocular pressure (29 mm Hg), and rubeosis iridis (Fig. 3), confirming NVG. The left eye remained unchanged. Topical therapy was initiated with prostaglandin F2α analogs, α2-adrenergic agonists, and carbonic anhydrase inhibitors; however, intraocular pressure remained inadequately controlled, and vision in the right eye declined to light perception.

FIG. 3.

Anterior segment photograph obtained on postoperative day 10 showing small, fine blood vessels developing on the anterior surface of the iris, indicating rubeosis iridis (arrows).

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Observations

We report a rare case of NVG accompanied by CHS following CAS placement and review the literature on NVG after carotid revascularization. This case suggests that CHS may contribute to delayed recognition of NVG after revascularization.

In NVG, neovascularization occurs in the eye, including the anterior chamber. Fibrovascular tissue in the anterior chamber obstructs aqueous humor outflow, leading to elevated intraocular pressure. In patients with severe carotid stenosis, chronic ocular hypoperfusion often reduces aqueous humor production, so intraocular pressure may remain normal or even low.⁵ After revascularization, neovascularization can increase aqueous humor production via the ciliary body, while resorption capacity remains unchanged, creating an imbalance that triggers a rapid rise in intraocular pressure and NVG.⁶ In this case, prior cataract extraction likely facilitated anterior segment neovascularization, as vascular endothelial growth factor can more easily diffuse into the anterior chamber.⁵

To clarify the characteristics of NVG following carotid revascularization, we reviewed 20 reported cases (Table 1).^6–21 Of these, 7 patients underwent CAS placement and 13 underwent CEA. All patients had underlying conditions predisposing them to intraocular neovascularization, including diabetes mellitus, hypertension, or prior cataract surgery. Severe carotid stenosis was present in all cases, and 90% of patients exhibited OIS. Preoperative ophthalmological findings revealed rubeosis iridis or NVG in approximately 80% of patients. Postoperatively, patients with any symptoms, such as ocular pain or visual disturbance, often experienced severe visual deterioration, with more than half declining to counting fingers or worse. Thus, the visual prognosis of NVG after carotid revascularization is generally poor. Although preventive strategies are not established, early therapeutic intervention is critical. Measures to control intraocular pressure, including topical medications and panretinal photocoagulation, should be initiated promptly in collaboration with ophthalmologists. If a preoperative ophthalmological evaluation reveals ocular neovascularization, appropriate interventions may help prevent a sudden postoperative rise in intraocular pressure. In high-risk patients, such as those with OIS or prior cataract surgery, preoperative and early postoperative ophthalmological evaluation are essential for timely detection of NVG. Staged CAS placement (balloon angioplasty followed by stent placement) is commonly used to prevent CHS and may also reduce NVG risk. However, NVG has been reported despite staged CAS placement, suggesting limited preventive efficacy.¹⁶ In the present case, a single-stage procedure was performed due to the presence of an unstable plaque.

TABLE 1.

Summary of reported cases of patients with NVG after carotid revascularization

Case No.	Authors & Year	Age (yrs)	Sex	Medical Hx			Degree of Stenosis	Preop Ophthal Findings		Op Procedure	Days to Sx Onset Postop	Ocular Sx	IOP, Preop/Postop (mm Hg)	Vis Det
				DM	HT	CS		IOS	Rubeosis Iridis/NVG
1	Coppeto et al., 19857	67	F	+	+	−	95%	+	+	CEA	−	None	18/46	−
2		49	M	+	+	−	95%	+	+	CEA	−	None	21/43	NA
3	Melamed et al., 19878	60	M	+	+	−	Severe	+	+	CEA	−	None	24/38	−
4		46	M	−	+	−	100%	+	+	CEA	−	None	18/42	NA
5	Wagner et al., 19889	54	F	−	+	−	95%	+	+	CEA	3	Pain	17/50	+
6	Daels et al., 199210	60	M	NA	NA	NA	100%	+	+	CEA	−	None	16/50	−
7	Nguyen et al., 199611	72	F	−	+	+	70%	+	−	CEA	−	None	12/38	NA
8	Masuoka et al., 199712	58	M	+	−	−	95%	−	+	CEA	4	Pain, exophthalmos	20/49	NA
9	Cuevas-Lestienne et al., 200013	NA	NA	−	−	+	NA	NA	+	CEA	1	Pain, visual disturbance	NA/66	+
10	Takagi et al., 200514	59	M	+	−	−	99%	+	+	CEA	1	Pain	30/45	−
11	Katsuta et al., 201315	64	M	+	−	−	83%	+	+	CEA	1	Pain, visual disturbance	10/51	+
12	Ng et al., 20156	58	M	+	−	−	Subtotal occlusion	+	−	CEA	2	Pain, visual disturbance	NA?/47	−
13	Lee et al., 201616	74	M	−	+	+	>70%	−	NA	CAS (staged)	5 (PTA), 2 (CAS)	Pain, visual disturbance	16/43	−
14	Radojcic et al., 201817	69	M	+	+	+	80% (contralat)	+	−	CEA	3	Pain, visual disturbance	NA/35	+
15	Kawano et al., 201818	67	M	+	+	−	90%	+	+	CAS	9	Pain	15/36	+
16		70	M	+	+	−	99%	+	+	CAS	1	Pain	15/54	+
17	Loving et al., 201919	70	M	+	−	−	90%	+	+	CAS	1	Pain	29/40	NA
18	Mannava et al., 202020	66	M	+	+	+	High grade	+	+	CAS	1	Visual disturbance	Rt: 19/29, lt: 19/26	+
19	Witton-Davies et al., 202421	71	F	+	+	−	90%	+	+	CAS	1	Pain, visual disturbance	19/44	+
20	Present case	74	M	−	−	+	95%	+	−	CAS	1	Pain	14/29	+

CAS = carotid artery stent placement; CS = cataract surgery; DM = diabetes mellitus; HT = hypertension; Hx = history; IOP = intraocular pressure; IOS = ischemic ocular syndrome; NA = not available; Ophthal = ophthalmological; PTA = percutaneous transluminal angioplasty; Sx = symptom(s); Vis Det = visual deterioration; + = yes; − = no.

In this case, the patient developed headaches on the day after CAS placement, and SPECT revealed increased cerebral blood flow in the right hemisphere, leading to a diagnosis of CHS. Ten days later, ophthalmological evaluation confirmed NVG, although its onset may have occurred earlier. Preoperative ophthalmological evaluation revealed partial retinal thickening secondary to chronic ischemia without evidence of neovascularization. However, NVG may still develop even in the absence of preoperative neovascularization.^6,17 Patients with severe carotid stenosis and impaired cerebrovascular reserve are at risk for CHS after revascularization,⁴ which typically presents as a headache within the 1st postoperative day. NVG and CHS share overlapping risk factors, onset timing, and clinical manifestations. While CHS is a well-recognized complication, NVG is rare and may be masked by concurrent CHS.

Although visual deterioration is a hallmark symptom of NVG, recognition relies on patient reporting. In this case, the patient did not report visual changes because he kept his eyes closed due to headache. Providing preoperative counseling regarding the risk of NVG may facilitate earlier detection of visual deterioration and prompt ophthalmological intervention.

Lessons

NVG after carotid revascularization is rare, and its visual prognosis is poor once it occurs, with no established preventive strategies. Because its symptoms can overlap with CHS, diagnosis may be delayed when both conditions coexist. Neurosurgeons and neurointerventionalists should be aware of this potential coexistence. Early recognition of NVG and prompt ophthalmological intervention are essential to mitigate vision loss, as illustrated by the present case. We recommend preoperative and postoperative ophthalmological assessments for high-risk patients, including those with OIS or a history of cataract surgery.

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: Dowaki, Watanabe, Okada. Acquisition of data: Dowaki, Okada, Takeishi, Ogawa. Analysis and interpretation of data: Dowaki, Okada, Ogawa. Drafting the article: Dowaki, Okada. Critically revising the article: Dowaki, Okada, Ogawa. Reviewed submitted version of manuscript: Dowaki, Watanabe, Okada, Takechi. Approved the final version of the manuscript on behalf of all authors: Dowaki. Statistical analysis: Okada. Administrative/technical/material support: Okada, Ogawa. Study supervision: Okada, Horie.

Correspondence

Ryosuke Dowaki: Matsuyama Red Cross Hospital, Matsuyama, Ehime, Japan. dowaki.huns@gmail.com.