Incidence and Clinical Features of Neovascularization of the Iris following Acute Central Retinal Artery Occlusion

Abstract

PurposeTo investigate the incidence of neovascularization of the iris (NVI) and clinical features of patients with NVI following acute central retinal artery occlusion (CRAO).MethodsA retrospective review of 214 consecutive CRAO patients who visited one tertiary hospital between January 2009 and January 2015 was conducted. In total, 110 patients were eligible for this study after excluding patients with arteritic CRAO, a lack of follow-up, iatrogenic CRAO secondary to cosmetic filler injection, or NVI detected before CRAO attack. Fluorescein angiography (FA) was applied until retinal arterial reperfusion was achieved, typically within 1 to 3 months.ResultsThe incidence of NVI was 10.9% (12 out of 110 patients). Neovascular glaucoma was found in seven patients (6.4%). The mean time to NVI diagnosis after CRAO events was 3.0 months (range, 1 week to 15 months). The cumulative incidence was 5.5% at 3 months, 7.3% at 6 months, and 10.9% at 15 months. Severely narrowed ipsilateral carotid arteries were observed in only three patients (27.3%). The other nine patients (75.0%) showed no predisposing conditions for NVI, such as proliferative diabetic retinopathy or central retinal vein occlusion. Reperfusion rate and prevalence of diabetes were significantly different between patients with NVI and patients without NVI (reperfusion: 0% [NVI] vs. 94.7% [no NVI], p < 0.001; diabetes: 50.0% [NVI] vs. 17.3% [no NVI], p = 0.017).ConclusionsCRAO may lead to NVI and neovascular glaucoma caused by chronic retinal ischemia from reperfusion failure. Our results indicate that follow-up fluorescein angiography is important to evaluate retinal artery reperfusion after acute CRAO events, and that prophylactic treatment such as panretinal photocoagulation should be considered if retinal arterial perfusion is not recovered.

Early Development of Two Neovascular Glaucoma Cases Following Central Retinal Artery Occlusion

“…8 Despite all these treatments, permanent chronic ischemia occurring after occlusion is the main factor in the development of neovascularization. 9 Despite not being treated earlier, we applied medical treatment and ocular massage, initiated carbogen treatment immediately in order to reduce intraocular pressure. We referred the patients who did not have regression in their findings, to hyperbaric oxygen treatment urgently after examining etiological reasons.…”

The Penumbra Obscura Stimulates Iris Neovascularisation after Isolated Central Retinal Artery Occlusion

“…Theoretically, the volume of the penumbra obscura (and the risk of rubeosis iridis) will also be reduced if there is associated posterior ciliary arterial occlusion (e.g., due to cranial arteritis) since penumbral (hypo-)oxygenation by the choroid will be compromised. This may help to explain Jung et al's [1] observation of eyes with failed CRA recanalization but no NVI.…”

“…Jung et al [1] are to be congratulated on definitively demonstrating what could only be surmised in the past—that intraocular angiogenesis after central retinal artery occlusion (CRAO) occurs in that small proportion of cases wherein retinal reperfusion fails to materialize [23]. However, your contributors appear to be unsure as to the mechanism whereby neovascularisation of the iris (NVI) arises after “CRAO alone.” While they reject Hayreh's [4] assertion that “chronically hypoxic retina ... is totally missing” after what is otherwise called “isolated CRAO” (and implicating ocular ischemia in NVI development due, for example, to carotid arterial stenosis), the crucial link between isolated CRAO and NVI was not elucidated.…”

“…However, the majority of eyes with CRAO will undergo spontaneous or therapeutic CRA recanalization and inner retinal reperfusion, resulting in hypoxia-to-normoxia conversion within the penumbra obscura and cessation of VEGF secretion. As Jung et al [1] point out, therefore, documentation of retinal reperfusion by fluorescein angiography (or other means) dictates that close follow-up of the patient for signs of NVI is no longer necessary. Theoretically, the volume of the penumbra obscura (and the risk of rubeosis iridis) will also be reduced if there is associated posterior ciliary arterial occlusion (e.g., due to cranial arteritis) since penumbral (hypo-)oxygenation by the choroid will be compromised.…”

Neovascular glaucoma: Handling in the future

“…Around 40%~45% of ischemic retinal venous occlusion eyes would develop NVG, and 80% of them would happen within 6–8 months, especially in the first quarter. [ 1 2 ] For PDR patients, there are 22% suffered NVG, majorly bilaterally; intraocular surgeries such as cataract surgery or vitrectomy would promote NVG progressing in DR cases. [ 3 ] As to OIS, NVG can occur in about 68% eyes and the risk increases with the length of time between symptom onset and diagnosis, as well as with the severity of ipsilateral carotid artery stenosis.…”