Retinal Vascular Diseases

Question 1

Pathogenesis of Diabetic Retinopathy

Answer 1

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

Question 2

Signs of Diabetic Retinopathy

Answer 2

Microaneurysms, retinal haemorrhage, hard exudates, cotton wool spots, venous changes, intraretinal microvascular abnormalities, neovascularisation, pre-retinal haemorrhages, diabetic macular oedema, clinically significant macular oedema

Question 3

Difference between dot and blot haemorrhages and flame-shaped haemorrhages

Answer 3

Dot and blot between INL and OPL

Flame shaped in NFL

Question 4

Signs of Clinically Significant Macular Oedema

Answer 4

• 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

Question 5

Severity of NPDR

Answer 5

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

Question 6

Managements for different severity of NPDR

Answer 6

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

Question 7

Proliferative Diabetic Retinopathy Pathogenesis

Answer 7

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

Question 8

Management for PDR and CSMO

Answer 8

Severe PDR: intra-vitreal anti-VEGF injection, Laser Pan-retinal photocoagulation, vitrectomy
CSMO: Macular grid laser to limit vision loss

Question 9

Pathogenesis for Retinal Vein Occlusion

Answer 9

• 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

Question 10

Retinal Vein Occlusion risk factors

Answer 10

Advancing age, Hypertension, Hyperlipidaemia, Diabetes, Raised IOP, Oral contraceptive pill

Question 11

Branch Retinal Vein Occlusion Signs

Answer 11

VA is variable, Dilation and tortuosity, flame-shaped, dot and blot haemorrhages, retinal oedema, cotton wool spots

Question 12

Branch Retinal Vein Occlusion Course

Answer 12

Acute features takes 6-12 months to resolve and replaced with hard exudates, venous sheathing and sclerosis
Collaterals which may be local

Question 13

Branch Retinal Vein Occlusion Prognosis

Answer 13

Reasonably good, in 6 months 50% va will better than 6/12

Question 14

Branch Retinal Vein Occlusion Managements

Answer 14

Refer to ophthalmologist to monitor for sight threatening conditions. eg. macular oedema, neovas

Question 15

Non-Ischaemic Central Retinal Vein Occlusion Signs

Answer 15

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

Question 16

Non-Ischaemic Central Retinal Vein Occlusion Prognosis

Answer 16

Reasonably good, 50% to return to normal vision

Conversion to Ischaemic CRVO

Question 17

Non-Ischaemic Central Retinal Vein Occlusion Management

Answer 17

Refer to ophthalmologist to monitor for conversion to ischaemic CRVO

Question 18

Ischaemic Central Retinal Vein Occlusion Signs

Answer 18

VA: usually CF or worse
APD: Marked
Severe tortuosity and engorgment, dot and blot flame shaped haemorrhages, cotton wool spots

Question 19

Ischaemic Central Retinal Vein Occlusion Prognosis

Answer 19

Acute signs resolves over 9-12 months
Extremely poor due to macular ischaemia
Rubeosis Iridis develop 50% of eyes in 2-4 months

Question 20

Ischaemic Central Retinal Vein Occlusion Management

Answer 20

Refer to ophthalmologist urgently for eyes with rubeosis iridis for laser pan-retinal photocoagulation

Question 21

Branch Retinal Artery Occlusion Signs

Answer 21

Narrowing of arteries and veins with sludging and segmentation of blood column
Cloudy white retina
Emboli

Question 22

Branch Retinal Artery Occlusion prognosis

Answer 22

Poor unless obstruction can be relieved in few hours

VF defect is permanent and affected artery remains attenuated

Question 23

Central Retinal Artery Occlusion Signs

Answer 23

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

Question 24

Central Retinal Artery Occlusion Prognosis

Answer 24

Poor due to retinal infarctions, after a few weeks of retinal cloudiness, cherry red spots disappears
Permanent loss of useful vision

Question 25

Cilioretinal Artery Occlusion signs

Answer 25

Cloudiness located to that part of the retina normally perfused by the vessel

Question 26

REtinal Artery Occlusion Management

Answer 26

Refer to Emergency department immediately, ocular massage, anterior chamber parancentesis, intravenous acetazolamide

Question 27

Hypertensive Retinopathy signs

Answer 27

Arteriolar narrowing, vascular leakage, hard exudates, cotton wool spots, optic disc swelling, arteriolosclerosis, changes at AV crossing

Question 28

Arteriolosclerosis grading

Answer 28

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

Question 29

Classification of Hypertensive Retinopathy

Answer 29

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

Question 30

Pathogenesis of Ischemic CRVO

Answer 30

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.

Question 31

BRAO symptoms

Answer 31

sudden, profound altitudinal or sectoral VF loss

Question 32

CRAO presentation

Answer 32

sudden, painless, profound loss of vision