STRUCTURAL CHANGES AND ROLE OF OCT IN DIABETIC RETINOPATHY

Suchismita Rout

DIABETIC RETINOPATHY DEFINITION•Progressive dysfunction of the retinal blood vessels caused by chronic hyperglycemia

•Initial stage of diabetic retinopathy marked by retinal edema, haemorrhage , exudates and capillary micro aneuryms, venous looping beading

RISK FACTORS Duration of diabetes (DM) •Diagnosis before the age of 30 years, the incidence of DR after 10 years is 50% and after 30 years 90%.Hypertension Poor blood sugar control (hyperglycemia)Poor lipids level( hyperlipidemia)Contribute to progression of DR

PATHOGENESIS OF DR

•Prolonged hyperglycemia is the major etiologic agent in all of the microvascular complications of diabetes, including diabetic retinopathy

•Diabetic Retinopathy is a micro vasculopathy that causes:

• Retinal capillary occlusion • Retinal capillary leakage

Capillary Oclussion caused by :

•Thickening of capillary basement membranes

•Breakdown of blood retinal barrier

•Damage of endothelial cells increased vascular permeability•Increased in retinal leukostasis

•Damage endothelial function•Vascular leakage•Capillary perfusion•angiogenseis

Microvascular leakage :

Structural changes in micro vessels • Impairment of endothelial tight junctions• Loss of pericytes• Weakening of capillary walls• Elevated levels of vascular endothelial growth factor (VEGF)

Chronic hyperglycemia

Loss of pericytes

Incresead VEGF

HEMATOLOGICAL ABNORMALITIESIncreased erythrocyte , red blood cell formation, platelet aggregation

Predispose to endothelial damage ,sluggish circulation , capillary occlusion

leads to Retinal ischemia triggers vasoproliferative growth factor , stimulates new vessels

ETDRS Classification of Diabetic Retinopathy

Diabetic retinopathy classified as •NPDR (non –proliferative diabetic retinopathy) Mild Moderate Severe Very severe•PDR (proliferative diabetic retinopathy)a) Early PDRb) High risk PDR

a)Mild NPDR :

•Characterised by

Microaneurysm only in one quadrant

Mild nonproliferative diabetic retinopathy

Microaneurysm

Moderate Non proliferative diabetic retinopathy

Characteristics•More than just microaneurysms but less than severe NPDR in two quadrants •Hard exudates

Moderate Nonproliferative Diabetic Retinopathy (NPDR)

Hard exudates

Flamed shaped hemorrhage

Microaneurysm

Severe non proliferative diabetic retinopathy

Any of the following: •More than 20 intraretinal hemorrhages in each of four quadrants •Definite venous beading in two or more quadrants •Prominent Intraretinal Microvascular Abnormalities (IRMA) in one or more quadrants •And no signs of proliferative retinopathy

neovascularization

neovascularization

Cotton-wool spot

Blot heammorahge

Hard exudates

Early Proliferative diabetic retinopathy • Non –high-risk PDR occurs when there are any new vessels on the surface of retina •These eyes should be followed every 2 to 3 months

HIGH-RISK-PROLIFERATIVE DIABETIC RETINOPATHY

•PDR with High risk characterized by one or more of the following:-NVD greater than one fourth to one third of the disk area.-Vitreous or preretinal hemorrhage associated with less extensive NVD or NVE one-half disk area or more in size.

Pathogenesis

• Primary feature is neovascularization caused by angiogenic growth factors elaborated by hypoxic retinal tissue in an attempt to re-vascularize hypoxic retina.•Clinically New vessels at the disc (NVD) New vessels elsewhere (NVE)• Leaks in FA

NVD

NVE

PDR -consequences

•Vitreous Haemorrhage •Tractional RD •Rubeosis Iridis and Neovascular Glaucoma (NVG)

TRACIONAL RETINAL DETACHMENT

Vitreous Hemorrhage (VH)

Diabetic maculopathy

•Diabetic maculopathy results from increased vascular permeability with or without intra retinal lipoprotein deposits (hard exudates) from ischemia due to closure of foveal capillaries • Involvement of the fovea by edema, hard exudates orischaemia..

FOCAL MACULOPATHY

• Associated with well circumscribed retinal thickening

• complete or incomplete rings of hard exudates

DIFFUSE MACULOAPTHY-

• diffuse retinal thickening, which may be associated with cystoid changes.

• landmarks are obliterated by severe edema which may render localization of the fovea impossible

FOCAL MACULOPATHY

DIFFUSE MACULOPATHY

ISCHEMIC MACULOPATHY

•The signs are variable and the macula may look relatively normal • Despite reduced visual acuity. • FA shows capillary non-perfusion at the fovea and

frequently other.• Areas of capillary non-perfusion at the posterior

pole .

Normal macula and ischemic maculopathy

OPTICAL COHERENCE TOMOGRAPHYIN DIABETIC RETINOPATHY

Principles of operation and technology:

OCT is a diagnostic imaging technique to examine living tissue non –invasively by means of high –resoluiton tomographic cross -sections of retina.

produces reliable, reproducible and objective retinal images

It enhances the ability to exactly diagnose diabetic macular edema, epi retinal membranes, vitreomacular or vitroretinal traction.

also brings new insights into morphological changes of the retina in diabetic retinopathy.

•OCT based on principle interferometry, involves interference between reflected light and reference mirror.

H e a l t h y M a c u l aH e a l t h y M a c u l a

O SO SI S / O SI S / O SE L ME L M R P ER P EI SI S

N F L : N e r v e F i b e r L a y e r O P L : O u t e r P l e x i f o r m L a y e r I S / O S : J u n c t i o n o f i n n e r a n d o u t e rI L M : I n n e r L i m i t i n g M e m b r a n e O N L : O u t e r N u c l e a r L a y e r p h o t o r e c e p t o r s e g m e n t sG C L : G a n g l i o n C e l l L a y e r E L M : E x t e r n a l l i m i t i n g m e m b r a n e O S : P h o t o r e c e p t o r O u t e r S e g m e n t I P L : I n n e r P l e x i f o r m L a y e r I S : P h o t o r e c e p t o r I n n e r S e g m e n t R P E : R e t i n a l P i g m e n t E p i t h e l i u mI N L : I n n e r N u c l e a r L a y e r

I L MI L M G C LG C LN F LN F L

C h o r o i dC h o r o i d

I P LI P L I N LI N L O P LO P L O N LO N L

L o g R e f l e c t i o n

OCT INTERPRETATION

2 modes of interpretationQualitative analysis: •Includes morphological changes of retinal layer, •Anomalous changes in pre/epi/sub retinal membrane•allows differentiates hypo-reflectivity, hyper-reflectivity .•Quantitaive analysis allows thickness, volumes and shadows area

Hyper-rlefective•Hard exudates •Cotton –wool spotsHypo-reflective•Intra retinal edema •Cystoid macular edema•Exudative retinal detachmentShadow effect•Heamorrhage •Retinal vesselsREFLECTIVITY means ability of the analyzed structures to reflect the light waves. Yellow, orange and red for high reflectivity and blue ,green and black for low reflectivity

NORMAL RETINA

•RNFL - high reflective (red)•IPL & OPL - moderate back scattering(yellow)•Nuclear layers - scattering (green)•Photoreceptors - dark layer•RPE & choriocapillaries - high reflective(red)•Choroid & sclera - low reflectivity

APPLICATIONS

• detachments of neurosensory retina and RPE• operculum, posterior hyaloid, ERM• Deformation in the foveal profile• Staging macular holes• Evaluating vitreo-retinal interface• Quantifying retinal thickness • RNFL thickness in glaucoma• post laser ,post surgery follow-up and monitoring

MACULAR HOLE

•Macular hole ,stage 1(no depression ,cyst present)•Stage 2( partial rupture of retina, increased thickness)•Macula hole ,stage 3(hole extends to RPE, increased thickness, some fluid)

•Macular hole ,stage 4(complete hole, edema at margin, complete PVD)

NORMAL FOVEAL PROFILE

DIABETIC RETINOPATHY

NPDR• Macular edema• cystoid macular edema• sponge-like swelling• neurosensory detachment(serous )• Hard exudatesPDR (TRD - sub-retinal fibrosis)

CENTRAL SEROUS RETINOPATHY

•Serous detachment •PED(pigment epithelial detachment)

PIGMENT EPITHELIAL DETACHMENT

GEOGRAPHY ATROPHY