DIABETIC RETINOPATHY

Dr Samuel Ponraj

RISK FACTORS

• Duration of Diabetes• Poor control of Diabetes• Pregnancy• Systemic diseases –

Hypertension,Nephropathy,Hyperlipidemia, Anemia, Obesity• Family History

Pathogenesis

• Capillaropathy• Aldose Reductase• Vasoproliferative factors

• Capillaropathy:

Loss of Pericytes

Thickening of Capillary basement membrane

Endothelial cell damage

Haematological changes –abnormalities of [erythrocytes and

leucocytes] , increased platelet stickiness, and increased plasma viscosity

Capillary leakage,occlusion,microaneurysm

• Aldose reductase:

GLUCOSE SORBITOL

-Can not diffuse out easily-Intracellular Concentration rises

Osmotic diffusion of water - Electrolyte imbalance

• Vasoproliferative factors:

Capillary Non - Perfusion

Retinal Hypoxia

VEGF induced Neovascularisation

ClassificationProposed disease severity level Findings on Ophthalmoscopy

No apparent retinopathy No abnormalities

Very Mild NPDR Few Microaneurysms only

Mild NPDR Few microaneurysms ,Retinal haemorrhage, hard exudates in 1 or 2 quadrants

Moderate NPDR Above findings seen in 2 or 3 quadrants

Severe NPDR Above findings in all quadrants & atleast of the following plus signs• Cotton wool spots• > 20 intraretinal hemorrhages in each of 4 quadrants•Venous beeding in 2 or more quadrants•IRMA in 1 or more quadrants

PDR One or more of following:Extraretinal neovascularisationVitreous /preretinal hemorrhages

Clinically significant macular oedema

• Retinal thickening within 500 µm of the centre of the macula

• Exudates within 500 µm of the centre of the macula, if associated with retinal thickening (which may be outside the 500 µm .

• Retinal thickening one disc area (1500 µm) or larger, any part of which is within one disc diameter of the centre of the macula.

Diabetic macular edema

Due to increased retinal capillary permeability/leakage & localised edema

- Most common cause of visual impairment in DM

1.Focal DME: - Well circumscribed retinal thickening - Hard exudates [circinate pattern] F/A : HF - leakage , good macular perfusion

• Diffuse DME: - Diffuse thickening ,edema Cystoid spaces F/A : HF Diffuse leakage – Flower petal look

• Ischaemic DME: - Due to microvascular blockage F/A: HF Capillary non perfusion @ FAZ.

HIGH RISK CHARACTERISTICS

• NVD - 1/4 TO 1/3 DISC area with or without VH or PRH• NVD – ¼ DISC area with VH or PRH• NVE - > ½ DISC area with VH or PRH

Signs: • Microaneurysms - localized out-pouchings - focal dilatation of the capillary wall - fusion of two arms of capillary loop inner capillary plexus (inner nuclear layer) F/A : Tiny HF dots due to leakage

• Retinal Haemorrhages : - Superficial NFL Haemorrhages – flame shaped [Precapillary arteriole] -Intraretinal [nuclear]Haemorrhages - Dot & blot Haemorrhages [Venous end of capillaries]

• Hard Exudates: -composed of lipoprotein and lipid-filled

macrophages located mainly within the outer plexiform layer [chronic localized retinal oedema]

-Waxy yellow lesions – ring/clumps. F/A: HF - blockage of background choroidal

and retinal capillary fluorescence.

• Cotton wool Spots /Soft exudates/ NFL infarcts - Local ischaemia ,axoplasmic flow block swollen ends -cytoid bodies ,neuronal debris.- Small, whitish, fluffy superficial lesions - focal HF due to blockage of background

choroidal fluorescence

• Venous anomalies : -seen in ischaemia ,Sluggish retinal circulation - generalized dilatation and tortuosity, - ‘looping’ ‘beading’ ‘sausage-like’

segmentation

• IRMA: - Arteriolar-venular shunts - bypassing the

capillary bed [Collaterals] - Fine, irregular, red intraretinal linesF/A : HF ,no leakage.

Investigations

• Complete blood picture• Routine & microscopic urine analysis• Blood sugar fasting & post prandial• Glycosylated hemoglobin [HbA1C]• Lipid ,thyroid & renal profile• Fundus Fluorescein Angiography• OCT

OCT

• Dense material within neurosensory retina [Hard exudates]

NORMAL DME

Medical Therapy :

Antiplatelet therapy : Ticlopidine ,Aspirin reduces stroke ,CVS

morbidity by inhibiting Platelet aggregation.

Anti hypertensive agents : ACE inhibitors/B- blockers – tight blood

pressure control ,

• Antiangiogenesis: Intravitreal Anti – VEGF to suppress retinal

neovascularization.• Blood sugar control.

Pan retinal Photocoagulation

• Aim: To destroy ischaemic areas ,decrease production of vasoproliferative factors , stimulates release of antiangiogenic factors from RPE.

• Regression of Neovascularization.• Use of Argon laser.• 1200 -2000 burns , 500 um spot size, 0.1 sec• Scatter pattern over periphery retina.

Peripheral retinal Cryotherapy

• Done for anterior retina – inadequate visualization of fundus due to opaque media.

• Focal laser therapy: - 500–3000 µm from the centre of the macula. - Spot size -50-100 um, 0.1 sec

• Grid therapy: - more than 500 µm from the centre of the macula

and 500 µm from the temporal margin of the optic disc.

-Spot size -100 um ,0.1 sec

Pars plana vitrectomy

• Indications: - Non clearing Vitreous haemorrhage - Macular threatening traction retinal detachment - Macular edema with thickened taut posterior

hyaloid - Severe preretinal macular haemorrhage

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