Korean J Ophthalmol.  2016 Oct;30(5):352-359. 10.3341/kjo.2016.30.5.352.

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

• Jung YH
• Ahn SJ
• Hong JH
• Park KH
• Han MK
• Jung C
• Woo SJ

• KMID: 2353828
• DOI: http://doi.org/10.3341/kjo.2016.30.5.352

Abstract

PURPOSE
To investigate the incidence of neovascularization of the iris (NVI) and clinical features of patients with NVI following acute central retinal artery occlusion (CRAO).
METHODS
A 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.
RESULTS
The 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).
CONCLUSIONS
CRAO 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.

Keyword

Incidence; Neovascularization; Reperfusion; Retinal artery occlusion

MeSH Terms

Carotid Arteries
Diabetic Retinopathy
Diagnosis
Fluorescein Angiography
Follow-Up Studies
Glaucoma, Neovascular
Humans
Incidence*
Iris*
Ischemia
Light Coagulation
Perfusion
Prevalence
Reperfusion
Retinal Artery Occlusion*
Retinal Artery*
Retinal Vein
Retinaldehyde
Retrospective Studies
Tertiary Care Centers
Retinaldehyde

Figure

• 

  Fig. 1 Flow chart of stuy design and exclusion criteria. CRAO = central retinal artery occlusion; NVI = neovascularization of the iris.

• 

  Fig. 2 Case 11. Fundus photography (left), fundus fluorescein angiography (middle), and optical coherence tomography (right) were obtained when the patient initially visited (A) and after 4 months when neovascularization of the iris was detected (B). Text (lower right corner) in the fundus fluorescein angiography indicates the time (54 seconds and 98 seconds) when images were taken after fluorescein infusion. (A) Examination results showed typical acute central retinal artery occlusion, including a cherry red spot. (B) After 4 months, angiography showed delayed retinal arterial perfusion, with inner retinal atrophy from optical coherence tomography.

• 

  Fig. 3 Kaplan-Meier survival curves following onset of central retinal artery occlusion (CRAO). The cumulative incidences were 5.5% at 3 months, 7.3% at 6 months, and 10.9% at 15 months. NVI = neovascularization of the iris.

• 

  Fig. 4 Case 11. Neovascularization of the iris was observed 4 months after the initial event of central retinal artery occlusion.

Reference

1. Park SJ, Choi NK, Seo KH, et al. Nationwide incidence of clinically diagnosed central retinal artery occlusion in Korea, 2008 to 2011. Ophthalmology. 2014; 121:1933–1938.

2. Sagong M, Kim J, Chang W. Intravitreal bevacizumab for the treatment of neovascular glaucoma associated with central retinal artery occlusion. Korean J Ophthalmol. 2009; 23:215–218.

3. Hayreh SS, Podhajsky P. Ocular neovascularization with retinal vascular occlusion. II: Occurrence in central and branch retinal ar tery occlusion. Arch Ophthalmol. 1982; 100:1585–1596.

4. Rudkin AK, Lee AW, Chen CS. Ocular neovascularization following central retinal artery occlusion: prevalence and timing of onset. Eur J Ophthalmol. 2010; 20:1042–1046.

5. Duker JS, Sivalingam A, Brown GC, Reber R. A prospective study of acute central retinal artery obstruction: the incidence of secondary ocular neovascularization. Arch Ophthalmol. 1991; 109:339–342.

6. Ahn SJ, Kim JM, Hong JH, et al. Efficacy and safety of intra-arterial thrombolysis in central retinal artery occlusion. Invest Ophthalmol Vis Sci. 2013; 54:7746–7755.

7. Sivak-Callcott JA, O'Day DM, Gass JD, Tsai JC. Evidence-based recommendations for the diagnosis and treatment of neovascular glaucoma. Ophthalmology. 2001; 108:1767–1776.

8. Hayreh SS, Podhajsky PA, Zimmerman MB. Retinal artery occlusion: associated systemic and ophthalmic abnormalities. Ophthalmology. 2009; 116:1928–1936.

9. Mendrinos E, Machinis TG, Pournaras CJ. Ocular ischemic syndrome. Surv Ophthalmol. 2010; 55:2–34.

10. Aiello LP, Avery RL, Arrigg PG, et al. Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. N Engl J Med. 1994; 331:1480–1487.

11. Duker JS, Brown GC. The efficacy of panretinal photocoagulation for neovascularization of the iris after central retinal artery obstruction. Ophthalmology. 1989; 96:92–95.

12. Natural history and clinical management of central retinal vein occlusion: the Central Vein Occlusion Study Group. Arch Ophthalmol. 1997; 115:486–491.