Abstract
Introduction
About 5% of retinal artery occlusions are cilioretinal artery occlusions (CLRAO). It was found to be mostly unilateral (70.30% to 93.65%) and temporal in location (80.77% to 100%).
Etiopathogenesis
Risk factors for CLRAO include emboli from various atheromas, vasculitis, collagen vascular disorders, hypertensive vascular changes, hemoglobinopathies, hypercholesterolemia, hypercoagulable conditions, arrhythmias, migraine etc.
Clinical presentation
Cilioretinal artery occlusion may present in three different scenarios: i) Isolated ii) with central retinal vein occlusion (CRVO) iii) in combination with Ischemic optic neuropathy.
Imaging features
FFA shows slow filling of cilioretinal artery. SD OCT may reveal hyperreflectivity of inner retinal layers. OCTA will show non perfusion of CLRA along with compromised perfusion of superficial and deep retinal capillary plexus and hyper reflective inner retinal layers. Perimetry shows paracentral scotoma which may be persistent in many cases. Association of paracentral acute middle maculopathy (PAMM) with isolated CLRAO causing paracentral scotomas, has been reported. Type 1 PAMM lesions affect layers above outer plexiform layer (OPL) and Type 2 PAMM involve layers below OPL.
Management
Time period for active intervention is between 4.5 to 12 h. Meta-analysis reports suggest administration of thrombolytic agents before 4.5 h for better outcome. Hyperbaric oxygen (HBO) therapy is another modality. Reduction of intraocular pressure need to be achieved. Methyl prednisolone is advisable in CLRAO associated with Giant cell arteritis and other vasculitis. American Heart Association suggests administration of intravenous or intraarterial tissue Plasminogen Activator (tPA) as a viable option.
Conclusion
CLRAO and its management still has the potential for further research and trials.
Keywords
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