Central retinal artery occlusion Central retinal vein occlusion

Central retinal artery occlusion Central retinal vein occlusion Hypertensive retinopathy Dr. Soujanya K Assistant Professor, YMCH

CENTRAL RETINAL ARTERY OCCLUSION

Pathogenesis

Obstruction by an embolus – secondary to a plaque of atheroma situated at the bifurcation of the common carotid artery Embolus from diseased mitral or aortic valve

Central retinal artery occlusion is nearly always at the lamina cribrosa, where the vessels normally become slightly narrowed.

Sudden and complete retinal ischaemia

Symptoms • Sudden painless loss of vision

Signs • Direct pupillary light reflex is absent

NORMAL RETINA CRAO

Arteries: Narrowed cherry-red spot Retina becomes milky white due to oedema Veins: segmented (cattle trucking)

After a few weeks: • Oedema subsides, • Grossly attenuated thread-like arteries • Optic atrophy

Management • Retinal tissue – cannot survive ischemia more than few hours • EMERGENCY TREATMENT

Management • Immediate lowering of intraocular pressure: – intravenous mannitol – intermittent ocular massage – paracentesis of anterior chamber

Management • Vasodilators (Amyl nitrite) and inhalation of a mixture of 5% CO 2 and 95% O 2.

Complication • Neovascular glaucoma: 1% to 5%,

CENTRAL RETINAL VEIN OCCLUSION

Classification Vein occlusions CRVO – Central retinal vein occlusion BRVO- Branch retinal vein occlusion Ischaemic CRVO Non-ischaemic

Pathogenesis • Arteriosclerosis

Sclerotic retinal artery presses on the Retinal vein where the two share a common adventitial sheath Lamina cribrosa

AV Crossing

Normal Vs Arteriosclerosis

AV Crossing

Elevation of venous and capillary pressure.

Stagnation of blood flow.

Hypoxia

Extravasation of blood constituents

Increased tissue pressure

Venous occlusion Venous pressure stagnation Hypoxia Damage to capillary endothelium Extravasation of blood constituents Tissue pressure

Venous congestion + tortuosity Mild disc oedema Superficial h’ge

• Extensive haemorrhages • Soft exudates • Disc oedema • Macular oedma • RAPD

Macular oedema

Complications

Complications

Management • Screening monthly- for 6 months : to detect anterior segment neovascularisation

Management • Neovascularisation: q Pan retinal photocoagulation • Macular oedema: q. Focal LASER q Intra-Vitreal Bevacizumab q Intra-Vitreal steroid

HYPERTENSIVE RETINOPATHY

Pathogenesis Elevated BP Microvascular damage Vasoconstrictio n

Pathogenesis • Primary response: vasoconstriction Hypertension In young In old Hypertensive narrowing Involutional sclerosis- prevents the same degree of narrowing seen in young individuals

Sustained Hypertension Inner blood– retinal barrier is disrupted Increased vascular permeability.

Signs 1. Arteriolar narrowing: Focal or generalised

FOCAL NARROWING

GENERALISED NARROWING

Signs - Cotton wool spots

Signs- Vascular leakage

• Flame-shaped retinal haemorrhages • Retinal oedema • hard exudates around the fovea (Macular star) • Disc Oedema

Arteriolosclerosis involves thickening of the vessel wall Grade 1 Grade 2 Grade 3 Grading of arteriosclerosis Grade 4

NORMAL ATERIES AND VEINS

• Subtle broadening of the arteriolar light reflex, Grade 1 • Mild generalized arteriolar attenuation

• obvious broadening of the arteriolar light reflex Grade • deflection of veins at arteriovenous crossings (Salus sign) 2

• ‘Copper-wiring’ of arterioles • Banking of veins distal to arteriovenous crossings (Bonnet sign). Grade 3 • Tapering of veins on both sides of the crossings (Gunn sign) and right-angled deflection of veins

Normal Vs Arteriosclerosis

Grade 4 • Silver-wiring’ of arterioles associated with grade 3 changes.

Grading of hypertensive retinopathy (Keith and Wegner) Grade • Mild generalised arteriolar narrowing 1 • Marked generalised + focal arteriolar narrowing Grade • Salu’s sign 2 • Grade 2 + copper wiring, Bonnet’s sign, Gunn’s sign Grade • Flame shaped haemorrhages, cottonwool spots, hard exudates 3 Grade • Grade 3 + silver wiring+ disc oedema 4

Summary

Questions • 1. Describe pathogenesis and clinical features of CRAO • 2. Enumerate the treatment modalities of CRAO • 3. Enumerate the clinical features and management of CRVO • 4. Differentiate between ischaemic and non ischaemic CRVO • 5. Describe grading of hypertensive retinopathy