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CASE REPORT
Year : 2020  |  Volume : 68  |  Issue : 4  |  Page : 897--899

Blindness Following Carotid Artery Stenting Due to Ocular Hyperperfusion - Report and Review of Literature

Hilal A Ganaie1, Vipul Gupta1, Rajsrinivas Parthasarathy1, Shrikant Londhe1, Saurabh Anand2,  
1 Department of Stroke, Neurointerventional Surgery, Artemis Agrim Institue of Neuroscience, Artemis Hospital, Gurugram, Haryana, India
2 Department of Neuroanaesthesia, Artemis Agrim Institue of Neuroscience, Artemis Hospital, Gurugram, Haryana, India

Correspondence Address:
Dr. Rajsrinivas Parthasarathy
Consultant Stroke Neurology and Neurointerventional Surgery, Artemis Agrim Institute of Neuroscience, Gurgaon, Haryana
India

Abstract

Cerebral hyperperfusion syndrome is a well-recognised phenomenon following carotid revascularisation. It is defined as cerebral blood flow increase of more than 100% of the baseline. A similar phenomenon can occur in the eye and maybe termed as ocular hyperperfusion syndrome. We present a 65-year-old male who developed an ipsilateral red eye with visual loss following carotid artery stenting. There was a past history of recurrent right middle cereberal artery (MCA) territory embolic infarcts and recurrent trasient episodes of vision loss in the right eye. Flow reversal was noted in the ophthalmic artery on Transcranial doppler (TCD). Digital subtraction angiography (DSA) showed more than 95% stenosis in right internal carotid artery (ICA) ostium and completely occluded left ICA. Following carotid artery, stenting patient developed severe headache and right eye pain along with vision loss despite intensive blood pressure monitoring and control. NCCT head showed mild right cortical SAH and the intra-ocular pressure (IOP) in the right eye was high. It was hypopthesised that aqueous over production due to neovascularity secondary to chronic ocular ischemia, lack of outflow and sudden change in ocular hemodynamics post stenting was the pathogenic mechanism. The patient was commenced on measures to reduce aqueous production along with strict blood pressure control. Prestenting evalvation for chronic ocular ischemia with tanscranial dopplar and angiographic flow reversal in ophthalmic artery, fluorescein angiography to look for watershed zones and slit lamp for neovascularity and angle closure can help in identifing high-risk patients, particularly in patients with bilateral carotid artery disease.



How to cite this article:
Ganaie HA, Gupta V, Parthasarathy R, Londhe S, Anand S. Blindness Following Carotid Artery Stenting Due to Ocular Hyperperfusion - Report and Review of Literature.Neurol India 2020;68:897-899


How to cite this URL:
Ganaie HA, Gupta V, Parthasarathy R, Londhe S, Anand S. Blindness Following Carotid Artery Stenting Due to Ocular Hyperperfusion - Report and Review of Literature. Neurol India [serial online] 2020 [cited 2020 Oct 23 ];68:897-899
Available from: https://www.neurologyindia.com/text.asp?2020/68/4/897/293455


Full Text



Carotid artery stenting (CAS) for symptomatic stenosis is a standard endovascular procedure that encompasses multiple risks, one of the important factors being cerebral hyperperfusion. Cerebral hyperperfusion occurs as a result of transient increase in cerebral blood flow after revascularization as well as alteration of the cerebral vascular autoregulatory mechanisms.[1] Similary, ocular hyperperfusion following carotid revascularization can present with acute red eye secondary to neovascular glaucoma in chronic ocular ischemia patients. In patients with ocular ischemic syndrome (OIS), a stenosis of 90% or more of the common or internal carotid arteries on the same side is usually found. The patients of OIS also have decreased blood flow in the retrobulbar vessels and reversal of blood flow in the ophthalmic artery. The blood flow is shunted away from the eye to the low-resistance intracranial circuit, with further reduction of retrobulbar blood flow.[2] Ocular hyperperfusion post revascularization is an extremely rare condition.

 Case Report



A 65-year-old male hypertensive for 25 years and chronic smoker presented with history of two episodes of left hemiparesis and left facial weakness and four episodes of transient right eye vision loss over last six months before admission. Computed topographic angiography (CTA) showed right ICA origin stenosis of >90 percent stenosis and left ICA total occlusion from the origin. Digital subtraction angiography (DSA) confirmed the above findings [Figure 1].{Figure 1}

The patient subsequently underwent right carotid artery stenting [Figure 2]. Post procedure within 24 hours patient developed severe right hemi cranial headache, vomiting, red eye and visual loss despite invasive blood pressure monitoring and control [Figure 3]. An urgent ophthalmology review revealed a non-reactive right pupil, an elevated IOP of 60 mmHg in the right eye as compared to 20 mm Hg in the left eye. The right eye changes were consistent with severe acute neovascular glaucoma (2C). Slit lamp examination revealed right iris neovascularisation. Patient was managed with Mannitol 200 ml IV twice daily, Tab acetazolamide (Diamox) 250 mg twice daily, timolol (beta antagonist), daily ocular pressure monitoring and strict blood pressure management. Intravenous Mannitol was continued till IOP in right eye was <30 mm Hg. The patient gradually started improving and the vision of the right eye also improved. Patient was discharged on 12th day of admission without any neurological or visual deficit.{Figure 2}{Figure 3}

 Discussion



Proximal ICA stenosis at its origin has a significant influence on the flow dynamics of the ocular circulation. The flow in the ophthalmic artery (OA) can be 'anterograde' in the presence of a good circle of Willis collaterals or 'retrograde' when OA acts as a conduit (collateral) from the external to the ICA. The outer layers of the retina and the choroid are supplied by the medial and lateral posterior ciliary arteries, both branches of the OA.[3] According to Giuffre et al., posterior ciliary arteries supply the choroid in a segmental manner. The zones between segmentally vascularized areas are amenable to ischemia and are termed 'watershed zone'.[4] Poor collateral circulation in patients with proximal stenosis can result in OIS secondary to expansion in the watershed zones.[5] Patients with a healthy collateral circulation may not develop OIS even with total occlusion of the ICA, whereas in those with poor collaterals an ICA stenosis <50% may be sufficient to develop OIS.[5]

The disturbed ocular circulation correlates with chronic ocular ischemic syndrome (OIS) symptoms that included frequent amaurosis fugax, a decline of visual acuity and chronic ischemic ocular pain.[6] Carotid revascularization may restore the cerebral perfusion pressure and improve the intracranial vascular hemodynamics and improve ocular circulation. However, severe carotid artery disease with poor collateral circulation can predispose to flow reversal in ophthalmic artery and ophthalmic artery steal syndrome. The secondary chronic ophthalmic artery insufficiency and resultant retinal ischemia and choroidal hypoperfusion with expansion in watershed zones leads to neovascularization in iris (NVI). NVI subsequently causes adhesion between the iris and the cornea, causing closure of the anterior chamber angle leading to insufficient aqueous humor resorption. To start with, the production and resorption are matched and therefore ocular pressures remain stable. Following revascularization, there is a sudden increase in aqueous humor production by the ciliary body while the resorptive capacity remains low. This imbalance in aqueous humor production and resorption results in a drastic increase in intraocular pressure and subsequent neovascular glaucoma.

In a series of 25 patients, reversed ophthalmic artery flow was significantly seen in 15 patients (60%) showing chronic ocular ischemic syndrome.[7] Further, Kawaguchi et al. found that Type 2b and type 3 ocular flow on TCD is associated rubeosis iridis formation in approximately 50% and 30% of patients respectively.[8] In our patient reversal of blood flow in right ophthalmic artery on the TCD was noted prior to intervention. Right external carotid artery angiogram revealed retrograde OphA flow reversal confirming the TCD findings [Figure 1]e and [Figure 1]f. Many studies have shown that ophthalmic artery flow direction on colour flow duplex imaging is highly specific for severe carotid stenosis.

The manifestation of acute red eye due neovascular glaucoma post CAS is extremely rare. Only two cases of acute neovascular glaucoma after carotid artery stenting have been published till date[9],[10] however flow reversal has not been demonstrated. Flow reversal in ophthalmic artery is likely to be a surrogate marker for poor collateral circulation and a predictor of ocular ischemia and neovascularization. In this patient, the contra lateral carotid artery was also occluded. The finding of flow reversal may bear more relevance for the subset of patients with contralateral carotid disease and should prompt careful preoperative exam for rubeosis iridis and angle closure, fluorescein angiography for assessing watershed zones alongside vasomotor reserve testing and stringent invasive blood pressure monitoring and control.

 Conclusion



Ocular hyperperfusion syndrome is a rare but serious complication of carotid artery stenting. OA flow reversal on TCD appears to be a surrogate marker for poor collateral circulation and ocular ischemia. Preoperative ocular exam for rubeosis iridis and angle closure could allow for stringent blood pressure monitoring and effective blood pressure control and careful watch for cerebral and ocular hyperperfusion.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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