Diabetic Retinopathy

(OVERVIEW)

PROF. MD SHAMSUL HAQUE

 Introduction
•37 million blind people worldwide
•4.8% due to DR (about 1.7 million)
•Prevalence of DM(diabetes mellitus )—28%(type-2,more
common)
•Prevalence of DR–18%(more common in type -1, 40% than
type-2, 20%)
•PDR more common in type—1 (about 5 to 10%)
Applied anatomy of the retina
Applied anatomy of the retina(cont.)

Ultra-microscopic structures of human retina

 Objectives

We want to learn
•Define diabetic retinopathy
•Classify diabetic retinopathy
•Symptoms and signs of diabetic retinopathy with
interpretation
•Diagnosis
•Available treatment options
•When to refer
 What is diabetic retinopathy?

It is a progressive microangiopathy characterised by

increased capillary permeability , leakage and occlusion
due to persistent hyperglycemia
Risk factors for diabetic retinopathy (DR)

•Age of patient and duration of diabetes

•Poor control of diabetes
•Hypertension
•Hyperlipidemia
•Nephropathy
•Obesity
•Anaemia
•Pregnancy
•Cataract surgery
•Smoking
PATHOGENESIS OF DR
 A-V-shunt

VEGF
Hypoxic retina

Rubiosis iridis
PDR
A

D
 Signs of DR retinopathy

Microaneurysms
• Localized out pouching of capillary
• Focal dilatation of the capillary wall
• Fusion of two arms of the capillary loop

Location: inner nuclear layer

FFA: hyperfluorescent dots due to

leakage
 Retinal haemorrhage
3 types
1.Dot haemorrhage –Red ,small dot like located in inner nuclear
layer/outer plexiform layer
2.Blot haemorrhage– Red, larger in size located in inner nuclear
layer/outer plexiform layer
3.Superficial NFL hge—flame shaped hge located in the nerve fibre
layer, similar in hypertensive retinopathy , so check BP

Source of hge –microaneurysm, capillary rupture

FFA--- blocked fluorescence
Hard exudate and cotton wool spot
Hard exudate –consists of
liporotein and lipid filled
macrophage
Waxy –yellow lesions arranged in
the form of ring or clumps
Location—outer plexiform layer

FFA ---blocked fluorescence

Cotton wool spot—dead opaque

nerve fibre due to ischaemia

FFA– blocked fluorescence

 Venous beading/looping and IRMA

•Indicate sluggish retinal circulation

•Present near the area of capillary non-perfusion

IRMA

Venous looping
Ischaemic fundus producing VEGF
 New vessels formation
•Always superficial in location
•New vessels grow along the path of least resistance
•Easily grow on the disc due to absent of ILM
•Associated with fibrous proliferation
•Location: Disc , retinal surface , interface and vitreous,iris,angle
•FFA: Profuse leakage of dye
NPDR– Nonproliferative diabetic retinopathy
 Mild nonproliferative diabetic retinopathy –Mild NPDR
•Presence of microaneurysm only
•Number of microaneurysm be one or more, dot hge may be present
•All other signs are absent

CFP FFA
 Moderate NPDR
•Mild NPDR plus
•Dot and blot hge
•Hard exudate
•Cotton wool spot
 Moderate NPDR

CFP FFA
 Severe NPDR
Moderate NPDR +Presence of any one of the following features

•4 quadrants—intra-retinal hge and microaneurysms

•2 quadrants—venous changes
•1 quadrant---IRMA
4:2:1 rule
•Very severe NPDR
•Presence of any two of the
following features
•4 quadrants—intra-retinal
hge and
microaneurysms
•2 quadrants—venous changes
•1 quadrant---IRMA
•4:2:1 rule
mild+moderate+severe
+ venous changes
IRMA
Severe NPDR with VMT
Proliferative diabetic retinopathy (PDR)
(Hallmark is new vessel formation)

A.Early
NVD—less than 1/3rd of the disc area or NVE –less than ½
of the disc area

B.High risk
• NVD more than 1/3rd of the disc area
• Any NVD with vitreous hge or pre-retinal hge
• NVE more than ½ disc area with vitreous hge or pre-
retinal hge
Early PDR

NVD
Early PDR
A.

NVE
High risk PDR

NVD

NVE
 Early PDR

NVD

NVE

High risk PDR

NVD

NVE
 Diabetic maculopathy

•Focal

•Diffuse

•Ischaemic

•Mixed

•CSME

•CMO
Focal maculopathy

Multifocal maculopathy
Diffuse maculopathy with
CSME
Diffuse maculopathy
Diffuse maculopathy
Diffuse maculopathy with cystic change
Ischaemic maculopathy
Ischaemic maculopathy
Ischaemic maculopathy
Mixed maculopathy
Mixed maculopathy
Pathogenesis of diabetic macular oedema

VEGF is released from endothelium,

pericyte and RPE of ischaemic
retina
As a result,
•Tight junctions between
endothelial cell is impaired
•RPE function is impaired
•Both cause macular oedema
Cystoid macular oedema
Clinically significant macular oedema
 Advanced diabetic eye disease(ADED)

Actually , these are serious vision threatening

complications of diabetic retinopathy which includes

•Persistent vitreous haemorrhage

•TRD
•Rhegmatogenous RD
•Combined detachment(rhegmatogenous+TRD )
•Retinoschisis
•Neovascular glaucoma

Advice: Refd to V—R Surgeon

ADED
 Vit. hge

Tractional RD

ADED
ADED
Burned out case, ADED
This is a separate entity
Diabetic papillopathy
D/D of diabetic retinopathy
 Differences between diabetic and
hypertensive retinopathy(clinical)

Diabetic retinopathy Hypertensive retinopathy

1.Usually retina wet 1.Usually retina dry

2.Retinal hge more 2.Retinal hge less
3.Dots blots hge common 3.Usually not seen
4.Numerous microaneurysms 4.Very rare microaneurysm
5.Flame shaped hge uncommon 5.Common
6.Cotton wool spots uncommon 6.Common
7.Hard exudate common 7.Uncommon
8.BRVO,CRVO less common 8.More common
9.Vascular sclerotic changes uncommon 9. Common
10.Diabetic pt 10.Hypertensive pt
 Management of diabetic retinopathy

Components
•History
•Examination
•Investigations
•Diagnosis
•Treatment and follow up
 History

•Duration of DM
•Control of DM (ask for Hb A1c)
•Type of medication
•Nature of work
•Weight in relation to height
•Hypertension
•Renal disease
•Pregnancy
•Systemic diseases(related)
•Ocular history
 Examinations

A.General examination(in short)

B.Ocular examination
C.Systemic examination(related)

A. Ocular examination
•VA
•IOP
•Gonioscopy
•S/L—Exam
•Ophthalmoscopy – both direct and
indirect

B. Systemic examination(related)
 Ophthalmic investigations

Imaging

•CFP
•FFA
•OCT
•B-Scan
 Lab. Investigations

•Blood sugar
•HbA1c
•Hb%
•Lipid profile
•Serum creatinine
•CBC
•Urine –R/E
 Treatment modalities

•Control of risk factors

•Laser

•Intra-vitreal anti- VGEF

•Intra-vitreal steroid

•ACE –inhibitor

•Anti- oxidant

•PPV
 Control of risk
factors

Age of pt and duration of

diabetes

•DR rarely develop before puberty

100%

•At diagnosis –20%

80%

•10 years after diagnosis—40 to 50%

60%

•20 years after diagnosis

Type—1 , 100% 40%
Type—2 , 60%
20%

0%
Type-1 Type 2
Prevention –no prevention for type–1 but for
type-2

•Primary prevention
•Secondary prevention
•Tertiary prevention
 Hyperlipidemia and DR

•Increased intake lipids/ ↑endogenous production

•Increased serum lipids

•Increased extra-vasation of lipid in retina

•Hard exudates in the retina

•Impairment of vision

Suggestions:
• Low intake of lipid
•Start lipid lowering agents
 Diabetic nephropathy(DN) and DR

•Diabetic nephropathy accelerates DR

•Diabetic nephropathy increases macular oedema

•Gross proteinuria usually associated with PDR

•Presence of DR suggests detail renal evaluation

•DR is resistant to treatment in presence of gross nephropathy

•Visual prognosis is better if renal transplantation is done rather than

dialysis
 Pregnancy and DR
•Pregnancy increases the progression of DR by about 1.5 fold

•Diabetic women having no DR, if she wants pregnancy , there

is a 10% chance of developing DR

•DR pregnant women with poorly controlled diabetes should

not strictly control DM suddenly , as there is a serious
deterioration of DR

Advice:
•Consultation and motivation
 Anaemia and DR

•Anaemia is directly related to the development of

high risk PDR

•If Hb level is less than 12mg /dl , the risk of

development of DR is double

•Anaemic pt with mild DR , there is 5-fold risk of

developing severe retinopathy

Advice:
•Appropriate correction of anaemia
Puberty and DR
Ocular risk factor-cataract surgery in DR pt

•Cataract surgery accelerate pre-existing macular edema and DR

•First evaluate retina by doing ophthalmoscopy. FFA and OCT

•Treat retina first then do cataract surgery after about 2 to 4 wks

•If media is hazy enough to evaluate retina then do cataract

surgery first

•After one week of cataract surgery , evaluate retina and treat

accordingly
 Laser treatment in diabetic retinopathy
How does laser work?
•The aim of laser is to make the hypoxic retina to anoxic
retina
•Laser causes photocoagulation of treated portion of the
retinal tissue
•Treated portion of the retina forms scar which is thinner
than rest of the retinal tissue
•These thinning scars permit increased oxygenation from
choroidal circulation to the inner layers of the retina
•Vascular auto-regulatory response of the retina improves
•Destroys highly metabolically active outer retinal cells,
reducing retinal oxygen consumption
•Increase in vasoinhibitors
Indications of laser treatment
DF-YAG LASER PROCEDURE IN DR TREATMENT

1. Focal
• Few burns in a small specific area
• Indication– focal diabetic maculopathy

2. Multifocal
• Few burns in multiple small specific area
• Indication—multifocal diabetic maculopathy

3. Macular grid
• Burns are applied in the macular area in grid pattern
sparing the fovea
• Indication—diffuse diabetic maculopathy
 Cont.
4. Sectoral
• Burns are applied in a large specific area
• Indication– large ischaemic zone to make anoxic zone in DR
5. Multi-sectoral
• Like sectoral but more than one area
• Indication– ischaemic DR
6. PRP
• Usually done in two separate days , burns are applied over
the whole retina sparing the macula
•PRP—1
•PRP—2 , usually after two weeks
•Indication –PDR , Very severe NPDR
Laser machine for laser treatment of DR

Two types of laser machine are in use in Bangladesh

•Double frequency YAG laser machine
•Pascal laser machine
Pascal laser
PRP Guideline
Side effects of PRP
 Side effects of PRP
Cont.
Anti-VEGF(vascular endothelial growth factor )
Three anti-VEGF are currently in use

1. Ranibizumab (lucentis)– is a antibody

•Mode of action– binds to VEGF receptors and

decreases vascular permeability

•Dose –0.5mg /0.05ml – every 4 wks –intra-vitreal

•
•Peak action – two weeks

•Duration of action- 4 to 6 wks

 Cont.
2. Bevacizumab (avastin)-- is a
antibody
•Mode of action- binds to VEGF
receptors and decreases vascular
permeability
•Dose –1.25mg/0.05ml—every 4 wks
–intra-vitreal
• Peak action– after two weeks
•Duration of action– 4 to 6 wks

3.Pegaptanib(macugen)—not available in our

country
Intra-vitreal triamcinolone acetonide(IVTA ) in DR
•IVTA improves visual acuity by
reducing macular oedema
•Mode of action: Reduces vascular
permeability
•Dose – 2mg /0.05ml
•Peak action –after 1 week
•Duration of action– 3 to 6 months

Side effects:
Raised IOP(30 to 40%)
Cataract
 Indications of anti-VEGF or IVTA

• In DME - before focal or grid laser if CRT ≥ 300 µ.

• Persistent macular edema after adequate laser

• Hard exudates in the centre of the fovea.

• In PDR with mild vitreous hemorrhage

• In PDR before vitrectomy

• Neovascular glaucoma with vitreous hemorrhage

 Formalities for intra-vitreal injection

•Patient assessment
•Prophylactic topical antibiotic
•Counseling of the patient
•Informed written consent
•Strict aseptic precaution
•Must be given in operation theatre

Side effects of intra-vitreal injection

•Lens injury
•Choroidal haemrrhage
•Retinal tear
•Endophthalmitis
•CVD
•MI
 Focal
DME

Before IVB After IVB

After laser,CFP After laser,FFA

 Diffuse
Diabetic
Maculopathy

Before IVB After IVB

After laser ,CFP After laser , FFA

Laser treatment of diffuse DME, CRT <300 micron
•Type of laser: DF –YAG laser

•Procedure: Macular grid

•Power: 100 to 110 Mw

•Spot size: 100 micron

•Duration: 100 Ms

•No. of spot: 324

•Next plan--

Macular grid
PRP
PRP
 PDR with diffuse maculopathy
Treatment: IVB two injections followed by PRP
Next plan : Fill in laser
IDEAL PRP
Incomplete PRP
Plan: Fill in laser
 Follow up of DR Patients
•No DR ---- Every year
•
•Mild NPDR--- Every 9 months

•Moderate NPDR--- Every 6 months

•CSME ---- Every 6 months

•Severe NPDR --- Every 4 months

•Very severe NPDR--- Every 2 to 3 months

•
•Early PDR---- Every 2 to 3 months

•High risk PDR --- Every 2 months

Thanks