Umi Kalthum Md Noh, Sin Yee Fang and Norshamsiah Md Din
A 73-year-old gentleman with diabetes mellitus was found to have impending central retinal vein occlusion (CRVO), on routine eye check-up. Despite initiation of anti-platelet agent, he developed ischaemic CRVO two months later, with severe macula oedema. His systemic investigations showed good diabetic control, no blood dyscrasia/hypercoagulable state, normal lipid profile and inflammatory markers. Echocardiogram was normal. A month later, arteriolar attenuation was noted with rubeosis irides, and fluorescein angiogram study confirmed central retinal artery occlusion (CRAO). After ruling out the systemic risk factors, we postulate two possible anatomical related patho-mechanism of CRAO following CRVO: 1, CRVO converts the retinal circulation into a closed loop, results in complete hemodynamic block of the retinal circulation, and hence secondary CRAO; 2, swollen retinal nerve fibres at the optic nerve head secondary to CRVO cause compression to the retinal artery at the level of the lamina cribrosa, this compression is further aggravated by the increased in intraocular pressure (IOP), and hence secondary CRAO.
