Dr Saquib DIABETIC RETINOPATHY UG

1. RETINA - DIABETIC RETINOPATHY 14th May2020 May
2020AL KERATITIS
DR M SAQUIB
MBBS,MS , FSCEH DELHI,FHVDESAI PUNE,
EX REGISTRARA JNMCH,AMU
CONSULTANT OPHTHALMOLOGIST
HOD D/O OPHTHALMOLOGY
G.S .MEDICAL COLLEGE
Founder sec: MEDICS India , www.medicsngo.org
Mail-dms2k5@gmail.com , 9634123800

2. • The global prevalence of DR and DME, for the
period 2015 to 2019 were 27.0% for any DR
comprising of 25.2%, NPDR, 1.4% PDR and
4.6% DME. The lowest prevalence was in
Europe at 20.6% and South East Asia at 12.5%

4. Risk Factors
• Duration
• Age of Onset
• Gender - F:M . 4:3
• Poor Metabolic Control
• Heredity
• Pregnancy
• Hypertension
• Smoking
• Obesity
• Anaemia
• Hyperlipidaemia

5. Pathogenesis
Microangiopathies
Pre capillary arterioles
Capillary & Venules
Retina
Vascular Endothelium Damage
Loss of Pericytes
Capillary Basement Membrane Thickening
Haematological and Biochemical
Platelet Adhesion
Blood Viscosity RBC Deformation
Serum Lipid Altered
Leukostasis
Fibrinolysis
Lose Laminar Blood Flow
Weakened Capillary Wall
Microaneurysm,Haemorhage
Microvascular Blood Retinal Barrier Break
Oedema,Haemorhage ,Lipid Leak( Hard
Exudates )
Microvascular Occlusion
Ischemia ,A V Shunt
Hyperglycemia –Induced Oxidative Stress
Proangiogenic Factor
VEGF, PDGF, HGF
Deletetion of Anti Angiogenic Factor

13. D

14. Non-p Non-proliferative diabetic retinopathy (NPDR Non proliferative diabetic
retinopathy (NPDR)

16. Cotton Wool Spots
Cotton wool spots result from occlusion of retinal pre-
capillary arterioles supplying the nerve fibre layer with
concomitant swelling of local nerve fibre axons. Also
called "soft exudates" or "nerve fibre layer infarctions"
they are white, fluffy lesions in the nerve fibre layer.
Fluorescein angiography shows no capillary perfusion in
the area of the soft exudate. They are very common in
DR, especially if the patient is also hypertensive.

17. Hard exudates ( Intra-retinal lipid exudates )
• Accumulations of lipids
leak from surrounding
capillaries and
microaneuryisms, they
may form a circinate
pattern.

18. Characteristics of Clinically Significant Macular (O)Edema
( CSME )
• The leading cause of visual loss amongst diabetics. Diagnosed by
stereoscopic assessment of retinal thickening, usually by slit lamp
biomicroscopy.
•
• Defined as the presence of one or more of the following, ( Modified Airlie
-House Criteria )
•
• Retinal oedema within 500 microns of the centre fovea.
•
• Hard exudates within 500 microns of fovea if associated with adjacent
retinal thickening
•
• Retinal oedema that is one disc diameter or larger, any part of which is
within one disc diameter of the centre of the fovea.
•
• Laser grid photocoagulation reduces the risk of visual loss by 50% at 2
years

20. Proliferative Diabetic Retinopathy
• More than 50% cases after 25 years diabtic age
• Juvenile onset DM Common
• NEOVASCULARISATION - /PDR
• NVD /NVE
• Fibrovascular Epiretinal Membrane
• Vitreous Detachment / Vitreous Haemorhage

25. Ischaemic Maculopathy
• Maculopathy in type 1 diabetics is often due to drop out
of the perifoveal capillaries with non perfusion and the
consequent development of an ischaemic maculopathy.
• Enlargement of the foveal avascular zone (FAZ) is
frequently seen on fluorescein angiography. Ischaemic
maculopathy is not uncommon in type 2 diabetics,
maculopathy in this group may show both changes due to
ischaemia but also retinal thickening.

26. Ischaemic Maculopathy

27. Proliferative diabetic retinopathy

28. Late Disease
• Contraction of associated fibrous tissue formed
by proliferative disease tissue can result in
deformation of the retina and tractional retinal
detachment

31. PDR
• High Risk Characteristics ( HRCs)by Diabetic
Retinopathy Group .
• 1.Early NVD/NVE PDR without HRCs
• 2. PDR with HRCs
NVD ¼ TO 1/3 of Disc area with or without VH OR PRH
NVD less ¼ disc area with VH or PRH
NVE more than ½ disc area with VH or PRH
-

33. Clinico-Angiographic Classification
• Focal Exudative Maculopathy :FFA – Focal leakage
with adequate macular perfusion
• Micro aneurysm ,Haemorhages,macular edema,hard exudates
• Diffuse Exudative Maculopathy: FFA – Diffuse
leakage at posterior pole ,
• Diffuse Retinal Edema and thickening posterior pole
• Ischemic Maculopathy :FFA-Non perfusion ,faz increases
,Capillary drop out, Arteriole Blocked
• Micro Vascular Block Marked Visual loss with microaneurysm
,haemorhage
• Mixed

35. OCT Classification of Diabetic Macular Oedema
Non Traction DME Traction DME
a.Spongy Thickness of Macula
b.Cystoid Macular Oedema
c.Neurosensory detachment with
or witjout a or b
Treatment – Conservative
a. Vitro foveal Traction
b. Taut /Thickened Posterior
Hyaloid Membrane
Treatment – Surgical /Pars Plana
Vitrectomy

37. Management
• SCREENING – First Examination
• Every Year
• Every 6 month
• Every 3 month
• INVESTIGATION – BS –F/PP,HB,HBA1C,
RFT , 24 Hr ,Urinary Protein
FFA, OCT
• TREATMENT - Metabolic control /Associated risk factors
• Intravitreal Anti VEGF
• Intravitreal Steroid
• Laser therapy

39. ETDRS
Focal DME ( Not involving centre of fovea) -
Focal LASER
Diffuse DME---------------Grid LASER
( Not Responding anti VEGF /Intravit
Steroid)
MOA LASER --- Stimulate RPE Pump
VEGF Release
LASER – ARGON GREEN /Double
frequency YAG 532 nm
Anti VEGF Indication
Focal CME Involving center of fovea
Diffuse DME
Diabetic CME
DME with Neurosensory detachment
Before PRP in case of PDR & Diffuse DME
4 weekly
Frequent Injection
Macular Photocoagulation is
CONTRAINDICATED in Ischemic
Maculopathy and Tractional DME

40. PANRETINAL PHOTO PHOTOCOAGULATION (PRP)
1200-1600 Spots ,500 um size ,0.1 sec duration
• Indication
• PDR with HRC
• NEOVASCULARISATION OF IRIS ( NVI)
• Severe NPDR associated with poor compliance for
followup
• Before Cataract surgery /YAG CAP
• Renal Failure
• Single shot Anti VEGF ( AVASTIN/LUCENTIS) may
protect Macula or Reduce Vitreous Haemorrhage.