Diabetic retinopathy

SamPonraj 7,500 views 31 slides Jul 14, 2013
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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

C lassification Proposed 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 neovascularisation Vitreous / 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 lines F/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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