Paradoxical development of neovascular glaucoma following carotid angioplasty and stenting

Abstract

This report describes a very rare ocular complication of carotid intervention. A 74-year-old patient presented with left-sided weakness and was diagnosed with right cerebral border-zone infarctions caused by severe stenosis of the right proximal internal carotid artery. Staged carotid intervention (balloon angioplasty followed by stenting) was successfully performed. However, neovascular glaucoma developed following carotid angioplasty and stenting. We concluded that although carotid angioplasty and stenting improves vision in patients with ischemic oculopathy, it can rarely induce paradoxical visual deterioration such as development or aggravation of neovascular glaucoma.

Introduction

Ischemic oculopathy and neovascular glaucoma may be related to carotid atherosclerotic disease. Visual dysfunction is often improved after carotid reperfusion therapy such as carotid endarterectomy (CEA) and carotid artery stenting (CAS).^1,2 However, a few reports have shown that CEA occasionally aggravates neovascular glaucoma.^3–6 There has been no report of such an occurrence after CAS. We report a case of acute deterioration of neovascular glaucoma after carotid angioplasty and stenting. The patient gave informed consent for this review.

Case report

A 74-year-old man presented with sudden-onset left hemiparesis and was admitted to our hospital for further evaluation. He was a chronic alcoholic and had a one-year history of hypertension. He also had a medical history of senile cataract, and had undergone intracapsular cataract extraction and phacoemulsification in the right eye one month before admission. Brain magnetic resonance imaging (MRI) showed acute border-zone infarctions in the right cerebral white matter, and MR angiography revealed severe stenosis (more than 70%) of the ipsilateral proximal internal carotid artery (Figure 1(a), (b)). Preoperative Diamox single-photon emission computed tomography (SPECT) showed markedly decreased vascular reserve in the right cerebral hemisphere. Therefore, we planned a staged CAS (two-step endovascular therapy including stent insertion a few days after balloon angioplasty) because he was considered to be at high risk of developing postoperative cerebral hyperperfusion syndrome (CHS).

Figure 1.

(a) Diffusion-weighted magnetic resonance (MR) images obtained at the onset of symptoms showing acute border-zone infarctions in the right cerebral white matter. (b) MR angiography showing severe stenosis of the right proximal internal carotid artery.

Initially, he underwent percutaneous angioplasty using an undersized balloon and had no immediate complications (Figure 2(a)–(c)). However, five days later, he complained of severe ocular pain with visual disturbance in the right eye. Intraocular pressure (IOP) of the right eye was markedly elevated to 43 mmHg and new iris vessels (rubeosis iridis) were detected, consistent with neovascular glaucoma (Figure 3). A preoperative ophthalmological exam showed normal visual acuity, and right eye IOP was normal (16 mmHg) one month previously. After active management including intravitreal lucentis injection, IOP was decreased and ocular pain subsided three days later. After his ocular symptom had stabilized, he subsequently underwent a planned CAS at 14 days after balloon angioplasty (Figure 2(d)). However, on the second postoperative day, he complained of worsening ocular pain and IOP was significantly elevated (about 30 mmHg). He received topical agents such as dorzolamide (carbonic anhydrase inhibitor), timolol (beta antagonist), latanoprost (prostaglandin analog), and brimonidine (α2 adrenergic agonist) with serial measurements of IOP and intermittent administration of 20% mannitol. Blood pressure was also maintained at a systemic target of less than 140 mmHg with medical therapy. IOP in the right eye was maintained within 25∼35 mmHg for a few days. He recovered well with no neurological progression or ocular symptoms and was discharged on the 15th day post-stenting.

Figure 2.

Right carotid angiogram revealing severe stenosis (80%) of the proximal internal carotid artery prior to angioplasty (a) and slight reduction of this stenosis following balloon angioplasty ((b),(c)). (d) Two weeks after angioplasty, carotid artery stenting was performed. After staged carotid stenting, the patency was well restored.

Figure 3.

The anterior segment photograph of the right eye shows rubeosis iridis (white arrows) and corneal edema caused by increased intraocular pressure (IOP). At this time, the right eye IOP was elevated up to 43 mmHg.

Discussion

Carotid angioplasty provides an alternative to CEA in patients with carotid stenosis and angioplasty-related complications are being increasingly observed: cerebral embolism, vessel dissection, hemodynamic compromise and CHS, all of which are well documented in the literature. Among these, CHS is a rare but potentially devastating complication. According to the preoperative diamox SPECT, this patient was at risk for postoperative complications such as CHS. Yoshimura et al.⁷ demonstrated that two-stage angioplasty is a relatively effective method to avoid CHS in a high-risk patient population and this was the reason for performing the staged CAS.

The development of neovascular glaucoma after carotid reperfusion therapy is extremely rare. Several reports of glaucoma deterioration after CEA have been published.^3–6 However, most cases have been reported in the field of ophthalmology or neurosurgery rather than the interventional field. Although the incidence of ocular complication caused by carotid reperfusion therapy is relatively low, the prognosis of this complication is variable. To the best of our knowledge, this is the first reported case of neovascular glaucoma development after CAS.

There are some theories for the development of neovascular glaucoma after carotid reperfusion therapy. Ocular ischemia causes not only neovascularization of the iris, which leads to insufficient resorption of the aqueous humor, but also insufficient production of the aqueous humor. Neovascularization of the iris subsequently causes adhesion between the iris and the cornea, causing closure of the anterior chamber angle leading to insufficient aqueous humor resorption, and this results in increased IOP.^4,5 After CAS or CEA, production of the humor is immediately activated by improved ocular circulation as well as the cerebral circulation, but the resorption capacity does not change, which results in an extraordinary increase in IOP.⁵ Another prevailing theory describes a model of increased angiogenic growth factor production as a result of stimuli from increased perfusion, leading to ophthalmic changes that result in neovascular glaucoma.⁵

According to previous reports, deterioration is likely to occur several days to weeks after CEA.^3,5,6 Also, elevated IOP was maintained for two weeks, which is similar to that in our case. This may be caused by extensive peripheral anterior synechiae disturbing the flow of aqueous humor to the angle. Furthermore, in cases of carotid intervention, carotid baroreceptors are stimulated by balloon angioplasty or carotid stent and this induces prolonged bradycardia and hypotension; and subsequent rebound arterial hypertension may induce a delayed ocular complication such as neovascular glaucoma.⁸

Although neovascular glaucoma is not a common postoperative complication, Aiello et al. reported a 7.8% incidence of development of neovascular glaucoma after intracapsular cataract extraction.⁹ Furthermore, Lon et al. reported that the incidence of neovascular glaucoma was higher in patients who underwent intracapsular cataract extraction than in those undergoing extracapsular extraction with preservation of an intact posterior capsule (8.9% vs. 0%, p < 0.01).¹⁰ After intracapsular cataract extraction, alterations in intraocular fluid dynamics may permit such an angiogenetic growth factor to reach the anterior segment and stimulate iris neovascularization with progression to neovascular glaucoma. We proposed that CAS is a major cause of developing neovascular glaucoma, but also suggest that intracapsular cataract extraction can have an adverse effect on developing or aggravation of neovascular glaucoma.

We should be aware that although CAS improves vision in patients with ischemic oculopathy, it can rarely induce paradoxical visual deterioration such as aggravation of neovascular glaucoma. This emphasizes the potential need for a preoperative assessment of visual function in patients undergoing elective carotid reperfusion procedure at least in those who have risk factors for ocular sequelae due to the nonspecific ocular pain in imminent neovascular glaucoma.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.