Diabetic retinopathy

DIABETICRETINOPATHY

RIYAZ KAHN7TH Semster MBBSNGMC, KOHALPUR

Monday, May 1, 2023

Normal Retina• Innermost tunic of the

eyeball• A thin, delicate &

transparent membrane• Most highly developed

tissue of the eye.• Purplish-red due to

visual purple of the rods & underlying vascular choroid.

Diabetic Retinopathy

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INTRODUCTION:

Diabetic Retinopathy is a chronic gradually progressive sight-threatening disease of retinal microvasculature associated with prolonged hyperglycaemia & other conditions linked to diabetes.


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INCIDENCE

• Incidence is more in Female (F:M=4:3)• Higher in patients with type1 DM .• Almost all patients with type 1 DM develop DR in

about 15 years. • However, type II DM also contributes to a

significant proportion of DR as type II DM is much more common than type I DM.


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RISK FACTORS

• DURATION OF DIABETES• POOR GLYCEMIC

CONTROL• UNCONTROLLED

HYPERTENSION• RENAL DYSFUNCTION• DYSLIPIDEMIA

• PREGNANCY• OBESITY• ANEMIA• CATARACT SURGERY


RISK FACTORSDuration of disease:

It is the most important risk factor. It is worth noting that it is the duration of disease after the onset of puberty, which acts as risk factor. For example, the risk of retinopathy is roughly same for two 25 years old patients, of whom one developed DM at 12 years(onset of puberty) and other at the age of 6 years because both have same duration( 13yrs) of disease after the onset of puberty. The risk of retinopathy in children diagnosed prior to the age of 2 years have a negligible risk of retinopathy for the first 10 yrs. So, age of onset also acts as a risk factor. However, after onset of puberty, age of onset is not a risk factor.

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PATHOGENESIS

• Diabetic retinopathy is a microangiopathy affecting the retinal precapillary arterioles, capillaries and venules .• Retinopathy has features of both: - microvascular leakage. (mild- mod NPDR) - microvascular occlusion .(sever NPDR-PDR)


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Microvascular occlusion Microvascular leakage

PATHOGENESIS


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PATHOGENESIS Microvascular leakage

Degeneration and loss of pericytes

Plasma leakage

Hard exudate(Circinate pattern)

Capillary wall weakening

microaneurysm

Retinal edema

Intraretinal hemorrhage


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PATHOGENESIS Microvascular occlusion

Neovascularizationand fibrovascular proliferation

VEGF

Increased plasma viscosityDeformation of RBCIncreased platelets stickiness

Decreased capillary blood flowand perfusion

Endothelial cell damage and proliferationCapillary basement membrane thickening

Retinal Ischemia

A-V shuntIRMA

Proliferative retinopathy

Rubeosis iridis


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SYMPTOMS

1 Blurred vision2. Floaters and

flashes3. Fluctuating vision4. Distorted vision5. Dark areas in the

vision6. Poor night vision7. Impaired color

vision8. Partial or total loss

of vision

DR is aymptomatic in early stages of the disease. Symptoms depend upon the retinal changes.


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SYMPTOMS


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CLINICAL FEATURES

1. Microaneurysms2. Intraretinal Hemorrhages3. HARD EXUDATES4. Macular Edema5. VENOUS Loop & BEADING6. INTRARETINAL

MICROVASCULAR ABNORMALITIES (IRMA)

7. Neovascularization8. Fibrous Glial proliferation 9. Lipaemia Retinalis


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CLINICAL FEATURES1. Microaneurysms - located in the inner nuclear layer . -mostly near and temporal to the macula - the first clinically detectable lesions in

NPDR. - small round red dots .(20-200 μ) - When coated with blood they may be

indistinguishable from dot haemorrhages.


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CLINICAL FEATURES

2. Intra-retinal HaemorrhagesIf the hemorrhage is deep (i.e., in the inner nuclear layer or outer plexiform layer), it usually is round or oval ("dot or blot")Dot haemorrhages appear as bright red dots and are the same size as large microaneurysms Blot haemorrhages are larger lesions they are located within the mid retina and often within or surrounding areas of ischaemia.


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CLINICAL FEATURES


INTRARETINAL HEMORRHAGES

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CLINICAL FEATURES 3. Hard Exudates•Yellowish-white waxy-looking patches arranged in clumps or in circinate pattern.•Located between the inner plexiform and inner nuclear layers of the retina. (OPL) •The centres of rings of hard exudates usually contain microaneurysms . • Made up of accumulated lipoproteins .


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CLINICAL FEATURES


Hard Exudates

CLINICAL FEATURES

4. Macular Oedema :- located between the outer plexiform and inner

nuclear layers. - Later it may involve the inner plexiform and nerve

fibre layers, until eventually the entire thickness of the retina may become oedematous. • Seen in both NPDR and PDR• Most common cause of visual loss in DR


CLINICAL FEATURES

• Macular edema types: (FFA + Clinical)1. Focal ME :which has identifiable leakage source.2. Diffuse ME: which has multiple unidentifiable

source of leakage.3. Cystoid ME: in which fluid accumulate in OPL and

INL to form cystoid spaces.


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Focal macular edema

Diffuse macular edema


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CLINICAL FEATURES5. VENOUS LOOPS & BEADING•Indicates sluggish retinal circulation •Nearly always adjacent to extensive areas of capillary nonperfusion•Focal vitreous traction•The most powerful predictors for development of PDR.


CLINICAL FEATURES

6. Intraretinal microvascular abnormalities (lRMA) :

- Dilated, tortous retinal capillaries that act as a shunt between arterioles and venules.

- Seen as fine irregular red lines connecting arterioles with venules

- frequently seen adjacent to areas of capillary closure.


CLINICAL FEATURES

7. Neovascularisation- Unlike IRMA, they arise on the retinal surface and

may extend or be pulled into the vitreous cavity.- NVD : NV appears on or within one DD of disc

margin .- NVE : any other location .


CLINICAL FEATURES

8. Fibrous Glial proliferation :- Accompanied growth of new vessels.- It is proliferation between the posterior vitreous gel

and the ILM(internal limiting membrane).- Derived from retinal glial cells and fibrocytes.


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CLINICAL FEATURES

9. Lipaemia Retinalis• A peculiar feature • Occurs especially in young patient when the

triglyceride concentration in the blood exceeds 2000mg/100ml.• Retinal vessels contain fluid which looks like

milk, the arteries being pale red and the veins having slight violet tint.


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CLASSIFICATION by ETDRS

1. NON-PROLIFERATIVE DIABETIC RETINOPATHY ( NPDR)I. MILD NPDRII. MODERATE NPDRIII. SEVERE NPDR IV. VERY SEVERE NPDR

2. PROLIFERATIVE DIABETIC RETINOPATHY3. DIABETIC MACULOPATHY4. ADVANCED DIABETIC EYE DISEASE (ADED)


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CLASSIFICATIONOnly Microaneurysms Mild NPDR

Mild NPDR plus hemorrhages, hard exudates Moderate NPDR

Moderate NPDR plus one of :1. Intraretinal Hges in four quadrants .2. Marked venous beading in two quadrants 3. IRMA in one quadrants.

Severe NPDR (4-2-1 rule)

Two or more of the above features described in severe NPDR

Very severe NPDR


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CLASSIFICATIONNew vessels and/or fibrous proliferations; or preretinal

and/or vitreous hemorrhage Early PDR

1. NVD > 1/3 of DD.2. NVD <1/4 DD, with vitreous or preretinal

hemorrhage 3. NVE > ½ DD, with vitreous or preretinal

hemorrhage

PDR with High Risk

Characteristics

1. Persistent Vitreous hemorrhage2. Tractional retinal detachment3. Neovascular glaucome

Advanced Diabetic Eye

Disease

Approximately 50% of patients with severe NPDR progress to proliferative retinopathy with high-risk characteristics within 1 year.


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CLASSIFICATION


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CLASSIFICATION

Diabetic MaculopathyClinically Significant Macular Edema (CSME)

1.Retinal edema within 500 µm of the center of the fovea .

2.Hard exudates within 500 µm of the fovea, if associated with adjacent retinal thickening (which may be outside the 500 µm limit) .

3.Retinal edema that is one disc area (1500 µm) or larger, any part of which is within one disc diameter of the center of the fovea.


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INVESTIGATIONS

• Urine Examination• Blood sugar estimation• 24 hour urinary protein• Renal fuction tests• Lipid profile• Haemogram• Opthalmological examination


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INVESTIGATIONS


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Ocular Changes In DiabetesLIDS Xanthelesma, Recurrent StyeConjuctiva

Microaneurysms, Sub conjuctival hemorrhages

Iris Deposition of glycogen in iris stroma causing sluggish pupillary reactionRubeosis Iridis

LENS Diabetic CataractEarly maturity of senile cataract

Vitreous HemorrhageRetinitis proliferenceRetinal Detachment


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Ocular Changes In Diabetes

Retina Diabetic RetinopathyLipaemia Retinalis

Optic N Optic neuritis, atrophy, 3rd N palsyRefraction Early presbyopia

During hyperglycemia there is myopia & in reversible hypermetropia


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Vision loss in Diabetic Patients( Source:evidence based medicine care)

• Retinopathy and cataract are complications of Diabetes that may lead to visual impairment and blindness.

1)Cataract: it is the most common cause of severe visual loss in people with type II DM( NIDDM or maturity onset), and second to proliferative retinopathy in type I DM. Cataract causes gradual progressive loss of vision.


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Vision loss in Diabetic Patients( Source:evidence based medicine care)2. Diabetic Retinopathy: causes of vision loss in

diabetic retinopathy are:i) Macular Edema( maculopathy: It is the most

common causee of vision loss in DR overall and in patient with NPDR. Though macular edema may cause sudden painless loss of vision, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive, and there is gradual loss of vision.


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Vision loss in Diabetic Patients( Source:evidence based medicine care)ii) Vitreous Hemorrhage: It is the most common cause of vision loss in PDR and is the most common cause of sudden painless loss of vision. Patient typically gives history of sudden onset of floaters followed immediately by severe vision loss.

iii) Retinal detachment: Tractional retinal detachment is the 2nd most common cause of sudden painless loss of vision in PDR ( after vitreous hemorrhage). If central retina is not involved, vision loss may be gradual.


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TREATMENT

1. Metabolic control of DM and associated risk factors.

2. Laser Therapy3. Intravitreal Anti-VEGF drugs4. Intravitreal Steroids5. Pars Plana vitrectomy


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TREATMENT Laser Therapy

• Laser photocoagulation causes a retinal burn which is visible on fundoscopy.• Retinal and optic disc

neovascularization can regress with the use of retinal laser photocoagulation


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TREATMENT

• Panretinal Laser Photocoagulation

Indications:i) PDR with HRCsii) Neovascularisation of Irisiii) Sever NPDR associated with

i) Poor compliance for follow upii) Before cataract surgeryiii) Renal Failure

iv) Pregnancy


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Macular photocoagulation1. Focal photocoagulation

treatment of choice for focal DME not involving the centre of fovea

2. Grid photocoagulationto treat the cases of

diffuse DME not responding to Anti-VEGFs and intravitreal steroids.


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Anti VEGF

Vascular endothelial growth factor (VEGF)

oBevacizumab (Avastin) (1.25 mg)oRanibizumab (Lucentis) (0.5 mg)

• It should be preferred over laser therapy• Treatment of macular oedeme, PDR


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INTRAVITREAL STEROIDS

• Intravitreal Triamcinolone Acetonide (20mg)


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VITRECTOMY IN DIABETIC PATIENTS• Vitrectomy, plays a vital role

in the management of severe complications of diabetic retinopathy.• The major indications are

non-clearing vitreous hemorrhage, traction retinal detachment, and combined traction /hegmatogenous retinal detachment. • Pars Plana Vitrectomy


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Screening

The American Academy of Ophthalmology has recommended screening for diabetic retinopathy

5 years after the diagnosis in patients with type I DM and

at the time of diagnosis in patients with type II DM


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Follow up

Suggested follow-up Retinal FindingAnnually NormalEvery 9 months Mild NPDREvery 6 months Moderate NPDREvery 4 months Sever NPDREvery 2- 4 months CSMEEvery 2-3 months PDR


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THANK YOU

Diabetic retinopathy

Health & Medicine

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