Describe the retinal vascular occlusions with their management.

Central Retinal Artery Occlusion

• Central retinal artery occlusion (CRAO) is a stroke OF the eye, and must be managed as such. It presents with sudden, painless, profound loss of vision, to counting fingers or worse
• Signs — a relative afferent pupillary defect, which appears within seconds and is the most reliable early sign; a pale, oedematous retina from infarction of the inner layers; a cherry-red spot at the fovea; attenuated arterioles; and "cattle-trucking" or box-carring — segmentation of the blood column into discrete boluses within the vessels
• The cherry-red spot is not a red lesion. It is normal choroid seen through the thin foveola, contrasted against the white infarcted retina around it — which is why it fades over the following weeks as the oedema resolves, leaving optic atrophy and attenuated vessels

Central Retinal Vein Occlusion

• Central retinal vein occlusion (CRVO) is thrombosis of the vein at or behind the lamina cribrosa, where artery and vein share a common adventitial sheath and a rigid channel
• The classical appearance is the "blood and thunder" fundus — widespread flame and dot haemorrhages in all four quadrants, dilated and tortuous veins, disc swelling, cotton-wool spots and macular oedema
• The essential division IS ischaemic versus non-ischaemic, because it determines the risk of neovascular glaucoma and therefore the follow-up:
• Ischaemic — vision worse than 6/60; a relative afferent pupillary defect; numerous cotton-wool spots; and more than 10 disc areas of capillary non-perfusion on fluorescein angiography. Carries a substantial risk of neovascular glaucoma at 3 months — "90-day glaucoma"
• Non-ischaemic — better vision, no afferent defect, fewer haemorrhages; but up to a third convert to the ischaemic form, so it cannot be discharged
• Risk factors — hypertension, which is the commonest; diabetes; hyperlipidaemia; glaucoma and raised intraocular pressure, which is an important and often forgotten association — so the pressure must be measured in both eyes; smoking; and, in a patient under 50, hyperviscosity, thrombophilia, oral contraceptives, vasculitis and hyperhomocysteinaemia, which warrant a full haematological screen
• Complications — macular oedema, which is the commonest cause of visual loss; neovascularisation of the iris and angle with neovascular glaucoma; disc and retinal new vessels with vitreous haemorrhage; and macular ischaemia.
• Treatment — anti-VEGF injection is first-line for macular oedema and has transformed the outcome; an intravitreal dexamethasone implant is an alternative, particularly in pseudophakic eyes; and panretinal photocoagulation is given for neovascularisation of the iris, angle or retina — but is not given prophylactically in ischaemic occlusion, since the CVOS showed no benefit from treating before new vessels appear
• Follow-UP is the critical intervention — monthly review with undilated iris examination and gonioscopy for at least 6 months in ischaemic occlusion, since new vessels appear in the angle before the iris and this is the stage at which the eye can still be saved

Branch Retinal Vein Occlusion and Other Occlusions

• Branch retinal vein occlusion (BRVO) occurs at an arteriovenous crossing, where the artery and vein share a common adventitial sheath and the thickened arteriosclerotic artery compresses the vein. This anatomy is why hypertension is the dominant risk factor
• The superotemporal quadrant is much the commonest site, because it has the greatest number of crossings — and because the resulting inferior field defect and macular involvement bring the patient in
• Appearance — a wedge of flame haemorrhages, oedema and cotton-wool spots with its apex at the crossing point and fanning peripherally, respecting the horizontal midline
• Complications — macular oedema (the commonest cause of visual loss); retinal neovascularisation with vitreous haemorrhage, which occurs in ischaemic cases; and rarely tractional detachment. Neovascular glaucoma is uncommon in branch occlusion, unlike central occlusion
• Collateral vessels develop across the horizontal raphe and are a sign of chronicity, not of activity
• Treatment — anti-VEGF or a steroid implant for macular oedema; sectoral laser to the ischaemic quadrant for neovascularisation; and management of hypertension and other risk factors