Retinal Vascular Diseases Flashcards
Pathogenesis of Diabetic Retinopathy
Hyperglycaemia intiates microangiopathy where following events will take place in the retina,
• Degeneration and loss of pericytes, proliferation of endothelial cells, thickening of basement membrane and occlusion
• Leakage resulting in retinal oedema and hard exudates
• Decreased capillary flow
• Retinal Hypoxia cause IRMA and neovas
Signs of Diabetic Retinopathy
Microaneurysms, retinal haemorrhage, hard exudates, cotton wool spots, venous changes, intraretinal microvascular abnormalities, neovascularisation, pre-retinal haemorrhages, diabetic macular oedema, clinically significant macular oedema
Difference between dot and blot haemorrhages and flame-shaped haemorrhages
Dot and blot between INL and OPL
Flame shaped in NFL
Signs of Clinically Significant Macular Oedema
- Retinal oedema within 500um of the centre of macular
- Hard exudates within 500um of the centre of macular if adjacent retina thickens
- Retina oedema one disc area or larger
Severity of NPDR
Very mild: Microaneurysms
Mild: Microaneurysms, haemorrhages, etc but no IRMA
Moderate: Severe haemorrhages/ mild IRMA, venous beading in one quadrant, common cotton wool spots
Severe: 4-2-1, all haemorrhages, 2 venous beading, 1 moderate IRMA
Very Severe: 2 more of the criteria of severe
Managements for different severity of NPDR
advise to control diabetes and risk factors
mild: no treATMENT and annual review
moderate: monitor for CSMO
severe: laser therapy if followup not avail
intravitreal anti VEGF agents
Proliferative Diabetic Retinopathy Pathogenesis
Primary feature of PDR is neovascularisation which is caused by angiogenic growth factors released by hypoxic retinal tissue in an attempt to re-vascularise hypoxic retina
Angiogenic stimulators such as VEGF promote neovas on retina, ONH and on iris
Management for PDR and CSMO
Severe PDR: intra-vitreal anti-VEGF injection, Laser Pan-retinal photocoagulation, vitrectomy
CSMO: Macular grid laser to limit vision loss
Pathogenesis for Retinal Vein Occlusion
- Arteriolosclerosis is an important causative factor for branch and central retinal vein occlusion
- Because a retinal arteriole and its corresponding vein share an adventitial sheath, thickening the arteriole appears to compress the vein
- This causes occlusion of the veins and the elevation of venous and capillary pressure with stagnation of blood flow
- This causes hypoxia of the retina
Retinal Vein Occlusion risk factors
Advancing age, Hypertension, Hyperlipidaemia, Diabetes, Raised IOP, Oral contraceptive pill
Branch Retinal Vein Occlusion Signs
VA is variable, Dilation and tortuosity, flame-shaped, dot and blot haemorrhages, retinal oedema, cotton wool spots
Branch Retinal Vein Occlusion Course
Acute features takes 6-12 months to resolve and replaced with hard exudates, venous sheathing and sclerosis
Collaterals which may be local
Branch Retinal Vein Occlusion Prognosis
Reasonably good, in 6 months 50% va will better than 6/12
Branch Retinal Vein Occlusion Managements
Refer to ophthalmologist to monitor for sight threatening conditions. eg. macular oedema, neovas
Non-Ischaemic Central Retinal Vein Occlusion Signs
VA: moderate to severe reduction
APD: absent or mild
Tortuosity or dilation of all retinal veins
Dot and blot, flame shaped haemorrhages, disc and macular oedema, cotton wool spots
Non-Ischaemic Central Retinal Vein Occlusion Prognosis
Reasonably good, 50% to return to normal vision
Conversion to Ischaemic CRVO
Non-Ischaemic Central Retinal Vein Occlusion Management
Refer to ophthalmologist to monitor for conversion to ischaemic CRVO
Ischaemic Central Retinal Vein Occlusion Signs
VA: usually CF or worse
APD: Marked
Severe tortuosity and engorgment, dot and blot flame shaped haemorrhages, cotton wool spots
Ischaemic Central Retinal Vein Occlusion Prognosis
Acute signs resolves over 9-12 months
Extremely poor due to macular ischaemia
Rubeosis Iridis develop 50% of eyes in 2-4 months
Ischaemic Central Retinal Vein Occlusion Management
Refer to ophthalmologist urgently for eyes with rubeosis iridis for laser pan-retinal photocoagulation
Branch Retinal Artery Occlusion Signs
Narrowing of arteries and veins with sludging and segmentation of blood column
Cloudy white retina
Emboli
Branch Retinal Artery Occlusion prognosis
Poor unless obstruction can be relieved in few hours
VF defect is permanent and affected artery remains attenuated
Central Retinal Artery Occlusion Signs
VA: Severely reduced unless supplied by cilioretinal artery
APD: Profound or total
Fundus show similar changes to BRAO but more extensive
Cherry Red spot at fovea
Central Retinal Artery Occlusion Prognosis
Poor due to retinal infarctions, after a few weeks of retinal cloudiness, cherry red spots disappears
Permanent loss of useful vision
Cilioretinal Artery Occlusion signs
Cloudiness located to that part of the retina normally perfused by the vessel
REtinal Artery Occlusion Management
Refer to Emergency department immediately, ocular massage, anterior chamber parancentesis, intravenous acetazolamide
Hypertensive Retinopathy signs
Arteriolar narrowing, vascular leakage, hard exudates, cotton wool spots, optic disc swelling, arteriolosclerosis, changes at AV crossing
Arteriolosclerosis grading
Grade 1: sutble broadening of arteriolar light reflex
Grade 2: obvious broadening of arteriolar light reflex, deflection of veins at AV crossing (salus sign)
Grade 3: Copper wiring (bonnet sign) and tapering (gunn sign)
Grade 4: silver wiring w G3
Classification of Hypertensive Retinopathy
Grade I: narrowing of retinal arterioles, a/v ratio ≥ 1:2
Grade II: narrowing of retinal arterioles, a/v ratio <1:2
Grade III: soft exudates, flame shaped haemorrhages
Grade IV: Grade III + optic nerve oedema
Pathogenesis of Ischemic CRVO
rapid onset on venous obstruction that leads to reduced retinal perfusion, capillary closure and retinal hypoxia
profound vascular leakage results rubeosis iridis and neovascular glaucoma
fibrovascular membrane develops on retina, contracts progressively resulting in tractional RD.
BRAO symptoms
sudden, profound altitudinal or sectoral VF loss
CRAO presentation
sudden, painless, profound loss of vision
