Diabetic Diabetic RetinopathyRetinopathy Waseem Al-Zamil, MDWaseem Al-Zamil, MD..

the two main types of diabetes :the two main types of diabetes : Insulin-dependent diabetes Insulin-dependent diabetes

(IDD)(IDD)::

- known as type 1 .- known as type 1 .

- develops most frequently between - develops most frequently between 10 and 20 years of age .10 and 20 years of age .

Non-insulin-dependent diabetes Non-insulin-dependent diabetes (NIDD)(NIDD)::

- also known as type 2.- also known as type 2.

- develops most frequently between - develops most frequently between the ages of 50 and 70 years. the ages of 50 and 70 years.

PrevalencePrevalence

Diabetic retinopathy is a leading Diabetic retinopathy is a leading cause of new cases of blindness in cause of new cases of blindness in people aged 20 to 74 years .people aged 20 to 74 years .

It has a considerable impact on both It has a considerable impact on both the patient and the society because it the patient and the society because it typically affects individuals in their typically affects individuals in their most productive years .most productive years .

PrevalencePrevalence

Blindness is 25 more common in Blindness is 25 more common in diabetics than non diabetics.diabetics than non diabetics.

Prevalence of PDR is much more in Prevalence of PDR is much more in type I than type II.type I than type II.

Diabetic retinopathy more sever in Diabetic retinopathy more sever in type I than type II.type I than type II.

PrevalencePrevalence

Macular edema :Macular edema :

NPDR : 2 -6 %NPDR : 2 -6 %

PDR :PDR : 20-63 %20-63 % Macular edema :Macular edema :

20.1 % in younger onset group.20.1 % in younger onset group.

25.4 % in older onset group taking 25.4 % in older onset group taking insulininsulin

13.9 % in older onset group not taking 13.9 % in older onset group not taking insulininsulin

PrevalencePrevalence

The 25-year cumulative rate of The 25-year cumulative rate of progression of DR in Type I was:progression of DR in Type I was:

- progression of DR was 83%.- progression of DR was 83%.

- progression to PDR was 42%.- progression to PDR was 42%.

- macular edema was 26%.- macular edema was 26%.

( WESDR Ophthalmology. 2008 Nov;115(11):1859-68 ( WESDR Ophthalmology. 2008 Nov;115(11):1859-68 ((

RISK FACTORSRISK FACTORS

1.1. The duration of diabetesThe duration of diabetes : : is the most important factor. is the most important factor. In patients diagnosed as having In patients diagnosed as having

diabetes before the age of 30 years, diabetes before the age of 30 years, the incidence of DR : the incidence of DR :

- after 10 years is 50% - after 10 years is 50%

- after 30 years is 90% - after 30 years is 90%

RISK FACTORSRISK FACTORS

It is extremely rare for DR to It is extremely rare for DR to develop within 5 years of the onset develop within 5 years of the onset of diabetes.of diabetes.

about 5% of Type II have NPDR at about 5% of Type II have NPDR at presentation perhaps due to the lag presentation perhaps due to the lag between onset and diagnosis.between onset and diagnosis.

RISK FACTORSRISK FACTORS

2 . 2 . Glycemic control Glycemic control :: Good metabolic control of diabetes will Good metabolic control of diabetes will

not prevent DR, although it may delay its not prevent DR, although it may delay its development by a few years. development by a few years.

increased severity of diabetic retinopathy increased severity of diabetic retinopathy is associated with poorer glucose control.is associated with poorer glucose control.

insulin treatment is associated with a insulin treatment is associated with a decreased risk of either the development decreased risk of either the development or progression of diabetic retinopathy in or progression of diabetic retinopathy in patients with type 1 diabetes. patients with type 1 diabetes.

RISK FACTORSRISK FACTORS

With strict control of DM:With strict control of DM: - risk of developing retinopathy was - risk of developing retinopathy was

reduced by 75% . reduced by 75% . - 50% reduction in the rate of - 50% reduction in the rate of

progression of retinopathy in existing progression of retinopathy in existing retinopathy retinopathy

- early worsening of retinopathy is - early worsening of retinopathy is unlikely to threaten vision .unlikely to threaten vision .

Diabetes Control and Complications Trial Research Group N Engl J Med 1993; Diabetes Control and Complications Trial Research Group N Engl J Med 1993; 329:977-986. 329:977-986.

RISK FACTORSRISK FACTORS

3 . 3 . Miscellaneous factorsMiscellaneous factors : :

- pregnancy. (Hormonal changes )- pregnancy. (Hormonal changes )

- systemic hypertension. - systemic hypertension.

- renal disease .- renal disease .

- anaemia.( ↓oxygen )- anaemia.( ↓oxygen )

- elevated serum lipid.- elevated serum lipid.

- carotid artery occlusive disease. - carotid artery occlusive disease.

- Alcohol. ( ? )- Alcohol. ( ? )

- Obesity.- Obesity.

Ocular Risk FactorsOcular Risk Factors

PVD :PVD :• due to degenerative changes in the due to degenerative changes in the

vitreous.vitreous.• significantly more common in diabetic significantly more common in diabetic

subjects.subjects.• complete PVD may prevent the development complete PVD may prevent the development

of PDR because the hyaloid is needed as a of PDR because the hyaloid is needed as a scaffold for retinal neovascularization.scaffold for retinal neovascularization.

• attached posterior hyaloid has also been attached posterior hyaloid has also been associated with an increased risk for DMEassociated with an increased risk for DME

Ocular Risk FactorsOcular Risk Factors

High myopia :High myopia :• choroidal degeneration and choroidal degeneration and

extensive old chorioretinopathy extensive old chorioretinopathy protect against DR.protect against DR.

• believed to act in the same manner believed to act in the same manner as pan retinal photocoagulation by as pan retinal photocoagulation by reducing the metabolic needs of the reducing the metabolic needs of the retinaretina

Ocular Risk FactorsOcular Risk Factors Removal of cataract Removal of cataract ::• DR may progress after cataract DR may progress after cataract

surgery.surgery.• Patient who have CSME, SNPDR or Patient who have CSME, SNPDR or

PDR should undergo photocoagulation PDR should undergo photocoagulation if the media is sufficiently clear.if the media is sufficiently clear.

• If the cataract preclude retina If the cataract preclude retina evaluation and treatment, prompt evaluation and treatment, prompt postoperative retinal evaluation and postoperative retinal evaluation and treatment should considered.treatment should considered.

PATHOGENESISPATHOGENESIS

Diabetic retinopathy is a microangiopathy Diabetic retinopathy is a microangiopathy affecting the retinal precapillary affecting the retinal precapillary arterioles, capillaries and venules .arterioles, capillaries and venules .

Retinopathy has features of both:Retinopathy has features of both:

- microvascular leakage. (mild- mod - microvascular leakage. (mild- mod NPDR)NPDR)

- microvascular occlusion .(sever NPDR-- microvascular occlusion .(sever NPDR-PDR)PDR)

PATHOGENESISPATHOGENESIS

Microvascular occlusion :Microvascular occlusion :

1.1. thickening of the capillary thickening of the capillary basement membrane.basement membrane.

2.2. capillary endothelial cell damage capillary endothelial cell damage and proliferation.and proliferation.

3.3. changes in red blood cells leading changes in red blood cells leading to defective oxygen transport, and to defective oxygen transport, and increased stickiness and increased stickiness and aggregation of plateletsaggregation of platelets

PATHOGENESISPATHOGENESIS

Microvascular Microvascular occlusionocclusion

retinal ischaemiaretinal ischaemia

retinal hypoxiaretinal hypoxia

Arteriovenous shunts

(IRMA)

Neovascularization Fibrous glial cellFibrous glial cell

proliferationproliferation

New vessel proliferation

Fibrous glial tissue proliferaion

Tractional RD RD

IRMA

PATHOGENESISPATHOGENESIS Microvascular leakageMicrovascular leakage : :

- due to reduction in the number of - due to reduction in the number of pericytes .pericytes .

- The pericytes are wrapped around the - The pericytes are wrapped around the capillaries and are thought to be capillaries and are thought to be responsible for the structural integrity of responsible for the structural integrity of the vessel wall. the vessel wall.

- Development of retinal edema requires - Development of retinal edema requires accumulation of fluid which occurs if :accumulation of fluid which occurs if :

Leakage: Absorption:

-Microanurerysms. -Incompetent

capillaries

-Uptake from adjusent capillaries

-Healthy RPE cells

PATHOGENESISPATHOGENESIS

Loss pericytes

Microvascular leakage

haemorrhage retinal oedema

Diffuse Localized

Microanurysm” ”

CLINICAL FEATURES

MicroaneurysmsMicroaneurysms : :

- located in the inner nuclear layer .- located in the inner nuclear layer .

- the first clinically detectable lesions .- the first clinically detectable lesions .

- small round dots .(20-200 - small round dots .(20-200 μμ))

- mostly located near and temporal to the - mostly located near and temporal to the macula.macula.

- When coated with blood they may be - When coated with blood they may be indistinguishable from dot indistinguishable from dot haemorrhages. haemorrhages.

CLINICAL FEATURES

HaemorrhagesHaemorrhages : :

The clinical appearance depending on locationThe clinical appearance depending on location

- - 'dot' and 'blot' 'dot' and 'blot' ::

* originating from the venous end of the * originating from the venous end of the capillaries. *located in the compact middle capillaries. *located in the compact middle layers of the retina .layers of the retina .

- - Flame-shaped Flame-shaped : :

* originate from the more superficial * originate from the more superficial precapillary arterioles, follow the course of precapillary arterioles, follow the course of the retinal nerve fibre layer. (liner disribution)the retinal nerve fibre layer. (liner disribution)

CLINICAL FEATURES

Hard exudatesHard exudates : :

- located between the inner plexiform and - located between the inner plexiform and inner nuclear layers of the retina. (OPL)inner nuclear layers of the retina. (OPL)

- They are often distributed in a (circinate - They are often distributed in a (circinate pattern) .pattern) .

- The centres of rings of hard exudates - The centres of rings of hard exudates usually contain microaneurysms . usually contain microaneurysms .

- Made up of accumulated lipoproteins .- Made up of accumulated lipoproteins .

CLINICAL FEATURES

Retinal oedemaRetinal oedema : :- located between the outer plexiform located between the outer plexiform

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

plexiform and nerve fibre layers, until plexiform and nerve fibre layers, until eventually the entire thickness of the eventually the entire thickness of the retina may become oedematous. retina may become oedematous.

- with further accumulation of fluid, the with further accumulation of fluid, the fovea assumes a cystoid appearance .fovea assumes a cystoid appearance .

Macular edema types: (FFA + Macular edema types: (FFA + Clinical)Clinical)

1.1. Focal ME Focal ME :which has identifiable :which has identifiable leakage source.leakage source.

2.2. Diffuse MEDiffuse ME: which has multiple : which has multiple unidentifiable source of leakage.unidentifiable source of leakage.

3.3. Cystoid MECystoid ME: in which fluid : in which fluid accumulate in OPL and INL to form accumulate in OPL and INL to form cystoid spaces.cystoid spaces.

Optical coherence Optical coherence tomographic patterns of tomographic patterns of diabetic macular edemadiabetic macular edema

(1) spongelike (1) spongelike retinal swelling.retinal swelling.

(2) cystoid macular (2) cystoid macular edema (CME).edema (CME).

(3) serous retinal (3) serous retinal detachment (SRD). detachment (SRD).

Kim BY, Smith SD, Kaiser PK: Optical coherence tomographic patterns of diabetic macular edema. Am J Ophthalmol 142(3):405-412, 2006

CLINICAL FEATURES

Vascular changesVascular changes : :- venous changes :in the form of 'beading', venous changes :in the form of 'beading',

'looping' and 'sausage-like' segmentation.'looping' and 'sausage-like' segmentation.- It represent endothelial cell proliferation.It represent endothelial cell proliferation.- arterioles may also be narrowed and arterioles may also be narrowed and

even obliterated, resembling a BRAO .even obliterated, resembling a BRAO .

- The most powerful predictors for - The most powerful predictors for development of PDR.development of PDR.

CLINICAL FEATURES Cotton-wool spotsCotton-wool spots : (Soft exudates ) : (Soft exudates )

- Nerve fiber layer infarction.- Nerve fiber layer infarction.

- caused by capillary occlusion in the - caused by capillary occlusion in the retinal nerve fibre layer. retinal nerve fibre layer.

- The interruption of axoplasmic flow The interruption of axoplasmic flow caused by the ischaemia, and subsequent caused by the ischaemia, and subsequent build-up of transported material within build-up of transported material within the nerve axons, is responsible for the the nerve axons, is responsible for the white and opaque appearance of these white and opaque appearance of these lesions. lesions.

- Disappear within weeks to months.Disappear within weeks to months.

CLINICAL FEATURES Intraretinal microvascular abnormalitiesIntraretinal microvascular abnormalities

(lRMA) :(lRMA) :- Dilated, tortous retinal capillaries that act as a Dilated, tortous retinal capillaries that act as a

shunt between arterioles and venules.shunt between arterioles and venules.- frequently seen adjacent to areas of capillary frequently seen adjacent to areas of capillary

closure. closure. - IRMA may resemble focal areas of flat NVE . IRMA may resemble focal areas of flat NVE .

But in IRMA : But in IRMA : 1.1. intraretinal location.intraretinal location.2.2. absence of profuse leakage on fluorescein absence of profuse leakage on fluorescein

angiography.angiography.3.3. failure to cross over major retinal blood vessels. failure to cross over major retinal blood vessels.

CLINICAL FEATURES

New Vessels:New Vessels:- Unlike IRMA, they arise on the Unlike IRMA, they arise on the

retinal surface and may extend or be retinal surface and may extend or be pulled into the vitreous cavity.pulled into the vitreous cavity.

- NVD : NV appears on or within one NVD : NV appears on or within one DD of disc margin .DD of disc margin .

- NVE : any other location .NVE : any other location .

CLINICAL FEATURES

Fibrous Glial proliferation :Fibrous Glial proliferation :- Accompained growth of new vessels.Accompained growth of new vessels.- It is proliferation between the It is proliferation between the

posterior vitreous gel and the ILM.posterior vitreous gel and the ILM.- Derived from retinal glial cells and Derived from retinal glial cells and

fibrocytes. fibrocytes.

Classification of severity of Classification of severity of diabetic retinopathydiabetic retinopathy

NonproliferativeNonproliferative DRP :DRP : Mild NPDRMild NPDRMicroaneurysms, retinal hemorrhage Microaneurysms, retinal hemorrhage

and hard exudate and hard exudate

Moderate Moderate NPDR NPDR

Mild NPDR plus cotton wool spots .Mild NPDR plus cotton wool spots .

Severe Severe NPDR NPDR

Moderate NPDR plus one of :Moderate NPDR plus one of :

1.1. Intraretinal Hges in four quadrants .Intraretinal Hges in four quadrants .

2.2. marked venous beading in two or marked venous beading in two or more quadrants more quadrants

3.3. IRMA one or more quadrants. IRMA one or more quadrants.

Very severe Very severe NPDR NPDR

Two or more of the above features Two or more of the above features described in severe NPDR described in severe NPDR

4 : 2 : 1

Rule

Classification of severity of Classification of severity of diabetic retinopathydiabetic retinopathy

ProliferativeProliferative DRP :DRP :

Early PDREarly PDRNew vessels and/or fibrous New vessels and/or fibrous proliferations; or preretinal and/or proliferations; or preretinal and/or vitreous hemorrhagevitreous hemorrhage

PDR with PDR with HRC HRC

1.1. NVD ≥ 1/3 of DD.NVD ≥ 1/3 of DD.

2.2. less extensive NVD, if vitreous or less extensive NVD, if vitreous or preretinal hemorrhage is present .preretinal hemorrhage is present .

3.3. NVE ≥ half disc area, if vitreous or NVE ≥ half disc area, if vitreous or preretinal hemorrhage is present preretinal hemorrhage is present

Advanced Advanced PDR PDR

1.1. Extensive vitreous hemorrhage Extensive vitreous hemorrhage precluding grading.precluding grading.

2.2. retinal detachment involving the retinal detachment involving the macula.macula.

3.3. phthisis bulbi .phthisis bulbi .

Diagnostic TestingDiagnostic Testing

Fluorescein Angiography :Fluorescein Angiography :- Not needed to identify CSME or PDR.Not needed to identify CSME or PDR.- But :But :

1.1. As a guide during CSME treatment.As a guide during CSME treatment.

2.2. Identify macular capillary nonperfusion.Identify macular capillary nonperfusion.

3.3. Identify subtle areas of NV causing Identify subtle areas of NV causing recurrent vitreous hemorrhage despite recurrent vitreous hemorrhage despite full PRP.full PRP.

Diagnostic TestingDiagnostic Testing Color Fundus photography :Color Fundus photography :- For Documentation purpose .For Documentation purpose .

Ultrasonography :Ultrasonography :- When opaque media preclude retinal When opaque media preclude retinal

examination.examination.- Useful in ruling out :Useful in ruling out :

1.1. RD.RD.

2.2. Traction threatening macular detachment.Traction threatening macular detachment.

Diagnostic TestingDiagnostic Testing

Color vision assessment:Color vision assessment:- DM associated with acquired blue-DM associated with acquired blue-

Yellow defect caused by diabetes it Yellow defect caused by diabetes it self and macular edema. (patients self and macular edema. (patients unable accurately match in self –unable accurately match in self –monitored color-dependant urine or monitored color-dependant urine or blood-glucose tests)blood-glucose tests)

Diagnostic TestingDiagnostic Testing

Visual Felid:Visual Felid:- Diabetic individuals often Diabetic individuals often

complaining of night vision loss and complaining of night vision loss and felid constriction due to:felid constriction due to:

1.1. Retinopathy.Retinopathy.

2.2. Retinal non perfusion.Retinal non perfusion.

3.3. Laser surgery.Laser surgery.

- Higher risk of developing glaucoma. - Higher risk of developing glaucoma.

Complications of Complications of proliferative diabetic proliferative diabetic

retinopathyretinopathy1.1. Persistent vitreous Persistent vitreous

haemorrhagehaemorrhage . .

2.2. Retinal detachmentRetinal detachment . .

3.3. Opaque membranesOpaque membranes . .

4.4. Rubeosis iridisRubeosis iridis . .

MANAGEMENT OF MANAGEMENT OF DIABETIC DIABETIC

RETINOPATHYRETINOPATHY Medical Therapy :Medical Therapy :• Glycemic control :Glycemic control :

DCCT , Tight control decrease risk DCCT , Tight control decrease risk of progression of retinopathy , of progression of retinopathy , nephropathy and neuropathy.nephropathy and neuropathy.

• Blood pressure control.Blood pressure control.• Blood lipids control.Blood lipids control.

MANAGEMENT OF MANAGEMENT OF DIABETIC RETINOPATHYDIABETIC RETINOPATHY

Laser surgery :Laser surgery :

The treatment of depends on the The treatment of depends on the severity of retinopathy and the severity of retinopathy and the presence or absence of CSME, presence or absence of CSME, which may be present at any stage .which may be present at any stage .

Macular oedemaMacular oedema

defined as the presence of any defined as the presence of any retinal thickening or hard exudates retinal thickening or hard exudates within one disc diameter (i.e. 1500 within one disc diameter (i.e. 1500 µµm) of the centre of the fovea. m) of the centre of the fovea.

clinically insignificant macular clinically insignificant macular oedema do not require treatment, oedema do not require treatment, only should be followed up at 6 only should be followed up at 6 monthly intervals. monthly intervals.

Clinically significant Clinically significant macular oedemamacular oedema (CSMO) (CSMO)

defined as the presence of one or more of defined as the presence of one or more of the following features: the following features:

1.1. Retinal oedema within 500 Retinal oedema within 500 µµm of the m of the centre of the fovea .centre of the fovea .

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

3.3. Retinal oedema that is one disc area Retinal oedema that is one disc area (1500 (1500 µµm) or larger, any part of which is m) or larger, any part of which is within one disc diameter of the centre of within one disc diameter of the centre of the fovea.the fovea.

Focal laser Focal laser photocoagulationphotocoagulation

All eyes with CSMO should be All eyes with CSMO should be considered for treatment with laser considered for treatment with laser photocoagulation irrespective of the photocoagulation irrespective of the level of visual acuity because level of visual acuity because treatment reduces the risk of visual treatment reduces the risk of visual loss by 50%.loss by 50%.

Focal laser Focal laser photocoagulationphotocoagulation

Poor visual outcome after focal Poor visual outcome after focal laser associated with :laser associated with :

1.1. Macular ischemia .Macular ischemia .

2.2. Hard exudates deposit in the fovea.Hard exudates deposit in the fovea.

3.3. Marked cystoid macular edema.Marked cystoid macular edema.

4.4. Diffuse fluorescin leakage .Diffuse fluorescin leakage .

Direct treatmentDirect treatment

involves applying laser burns to involves applying laser burns to microaneurysms and microvascular lesions in microaneurysms and microvascular lesions in the centre of rings of hard exudates located the centre of rings of hard exudates located between 500 and 3000 between 500 and 3000 µµm (two disc diameters) m (two disc diameters) from the centre of the fovea.from the centre of the fovea.

- The spot size is : 50-100 - The spot size is : 50-100 µµm .m .

- The duration of : 0.10 second or less.- The duration of : 0.10 second or less.

- The power : sufficient power to obtain a - The power : sufficient power to obtain a gentle whitening or darkening of the gentle whitening or darkening of the microaneurysm.microaneurysm.

- Wave length : green - Wave length : green –– yallow Argon yallow Argon

1500 mirco

500 micro

3000 micro

Direct treatmentDirect treatment

Treatment of lesions between 300 Treatment of lesions between 300 and 500 and 500 µµm from the centre of the m from the centre of the fovea should be considered if CSMO fovea should be considered if CSMO persists, in spite of previous persists, in spite of previous treatment and, if visual acuity is less treatment and, if visual acuity is less than 6/12.than 6/12.

Grid treatmentGrid treatment

used for areas of diffuse retinal used for areas of diffuse retinal thickening located more than 500 thickening located more than 500 µµm m from the centre of the fovea and 500 from the centre of the fovea and 500 µµm m from the temporal margin of the optic from the temporal margin of the optic disc.disc.

- The spot size is : 50 - 100- The spot size is : 50 - 100µµm .m . - The exposure time : 0.10 second.- The exposure time : 0.10 second. - The burns should be of very light - The burns should be of very light

intensity and one burn width apart. intensity and one burn width apart. - Wave length : green - Wave length : green –– yallow Argon . yallow Argon .

Macular oedema Macular oedema treatmenttreatment

It should be emphasized that the It should be emphasized that the main aim of treatment is to preserve main aim of treatment is to preserve the patient's current visual level.the patient's current visual level.

Only about 15% of eyes show Only about 15% of eyes show improvement. improvement.

It may take up to 4 months for the It may take up to 4 months for the oedema to resolve, re-treatment oedema to resolve, re-treatment should not be considered should not be considered prematurely .prematurely .

Focal Laser Side EffectsFocal Laser Side Effects

1.1. Paracentral scotoma.Paracentral scotoma.

2.2. Transient increased edema and Transient increased edema and decresed vision.decresed vision.

3.3. Choroidal neovascularization.Choroidal neovascularization.

4.4. Subretinal fibrosis.Subretinal fibrosis.

5.5. Scar expansion.Scar expansion.

6.6. Foveolar burns.Foveolar burns.

Anti-VGEF & Macular Anti-VGEF & Macular EdemaEdema

Anti-VGEF & Macular Anti-VGEF & Macular EdemaEdema

Algorithm for panretinal scatter Algorithm for panretinal scatter

coagulation of the retinacoagulation of the retina

laser photocoagulationlaser photocoagulation

The following are the clinical features of The following are the clinical features of eyes at high risk PDR:eyes at high risk PDR:

NVD or neovascularization within one disc NVD or neovascularization within one disc diameter of the optic disc more than one-diameter of the optic disc more than one-quarter disc in area .quarter disc in area .

Less extensive NVD associated with Less extensive NVD associated with vitreous or preretinal haemorrhage.vitreous or preretinal haemorrhage.

NVE more than one-half disc in area in NVE more than one-half disc in area in association with vitreous or preretinal association with vitreous or preretinal haemorrhage. haemorrhage.

laser photocoagulationlaser photocoagulation

The aim of treatment is to:The aim of treatment is to:

1.1. induce involution of new vessels .induce involution of new vessels .

2.2. prevent vitreous haemorrhage. prevent vitreous haemorrhage. Initial treatment involves the Initial treatment involves the

placement of about 2000-3000 burns placement of about 2000-3000 burns in a scatter pattern, extending from in a scatter pattern, extending from the posterior fundus to cover the the posterior fundus to cover the peripheral retina in one or more peripheral retina in one or more sessions. sessions.

laser photocoagulationlaser photocoagulation

The technique of PRP is as follows: The technique of PRP is as follows:

1.1. Topical corneal anaesthesia is adequate Topical corneal anaesthesia is adequate in most patients.in most patients.

2.2. - - The spot sizeThe spot size :depends on which :depends on which contact lens is being used. (500 - 200 contact lens is being used. (500 - 200 µµm). m).

- - The durationThe duration : between 0.10 and 0.05 : between 0.10 and 0.05 secondsecond

- - The power levelThe power level : produces a gentle : produces a gentle burnburn

laser photocoagulationlaser photocoagulation

3.3. burns spaced about one half burn apart. burns spaced about one half burn apart.

4.4. the power is increased by 50 mW increments the power is increased by 50 mW increments until a grey-white burn of gentle intensity is until a grey-white burn of gentle intensity is produced .produced .

Follow-upFollow-up : :

- is after an interval of 4-8 weeks.- is after an interval of 4-8 weeks.

- In eyes with severe NVD, several treatment - In eyes with severe NVD, several treatment sessions with 5000 or more burns may be sessions with 5000 or more burns may be required. - the most important required. - the most important cause of persistent neovascularization is cause of persistent neovascularization is inadequate treatment. inadequate treatment.

laser photocoagulationlaser photocoagulation

Signs of involution :Signs of involution :

1.1. regression of neovascularization leaving regression of neovascularization leaving only 'ghost' vessels or fibrous tissue.only 'ghost' vessels or fibrous tissue.

2.2. decrease in venous dilatation.decrease in venous dilatation.

3.3. absorption of retinal haemorrhages .absorption of retinal haemorrhages .

4.4. disc pallor .disc pallor . Treatment of recurrenceTreatment of recurrence : :

Further argon laser PRP filling in any Further argon laser PRP filling in any gaps between previous laser scars. gaps between previous laser scars.

PARS PLANA VITRECTOMY PARS PLANA VITRECTOMY INDICATIONSINDICATIONS

1.1. Severe persistent vitreous Severe persistent vitreous haemorrhagehaemorrhage . .

2.2. Tractional retinal detachment Tractional retinal detachment involving the macula. involving the macula.

3.3. Combined tractional and Combined tractional and rhegmatogenous retinal detachmentrhegmatogenous retinal detachment ..

4.4. Progressive fibrovascular Progressive fibrovascular proliferationproliferation . .

5.5. Rubeosis iridis associated with Rubeosis iridis associated with vitreous haemorrhagevitreous haemorrhage..

PARS PLANA VITRECTOMY PARS PLANA VITRECTOMY INDICATIONSINDICATIONS

6.6. Dense, persistent, premacular, Dense, persistent, premacular, subhyaloid haemorrhagesubhyaloid haemorrhage . .

7.7. Red Blood Cell-induced Red Blood Cell-induced glaucoma.glaucoma.

8.8. Bilateral vitreous haemorrhage Bilateral vitreous haemorrhage ..

9.9. Dense cataract associated with Dense cataract associated with vitreous haemorrhage .vitreous haemorrhage .

Follow upFollow up

Retinal Retinal FindingFinding

Suggested follow-upSuggested follow-up

NormalNormalAnnuallyAnnually

Mild NPDRMild NPDREvery 9 monthsEvery 9 months

Moderate NPDRModerate NPDREvery 6 monthsEvery 6 months

Sever NPDRSever NPDREvery 4 monthsEvery 4 months

CSMECSMEEvery 2- 4 monthsEvery 2- 4 months

CNSMECNSMEEvery 6 monthsEvery 6 months

PDRPDREvery 2-3 monthsEvery 2-3 months

Aspirin & DRPAspirin & DRP

Is Aspirin effective in preventing Is Aspirin effective in preventing progression of diabetic retinopathy ?progression of diabetic retinopathy ?

1.1. Aspirin use did not alter progression Aspirin use did not alter progression of diabetic retinopathy .of diabetic retinopathy .

2.2. Aspirin use did not increase the risk Aspirin use did not increase the risk of vitreous hemorrhage .of vitreous hemorrhage .

3.3. Aspirin use did not effect visual acuity.Aspirin use did not effect visual acuity.4.4. Aspirin use reduce the cardiovascular Aspirin use reduce the cardiovascular

morbidity and mortality .morbidity and mortality .

Sorbinil & DRPSorbinil & DRP Sorbinil is an aldose reductase inhibitor.Sorbinil is an aldose reductase inhibitor. Sorbinil does not affect the progression of Sorbinil does not affect the progression of

DRP or Diabetic neuropathy.DRP or Diabetic neuropathy.

Practical PointsPractical Points

Pregnancy :Pregnancy :• DR accelerate during pregnancy and DR accelerate during pregnancy and

improve postpartum.improve postpartum.• Do not hesitate to treat with laser Do not hesitate to treat with laser

when indicated.when indicated.• FFA should be avoided in all but the FFA should be avoided in all but the

most difficult cases of macular most difficult cases of macular edema.edema.

Practical PointsPractical Points

PRPPRP::• Three-mirror lens can be used for Three-mirror lens can be used for

both focal laser and PRP.both focal laser and PRP.• Do not forget lens magnification , in Do not forget lens magnification , in

most lenses use 200most lenses use 200μμm to produce m to produce 500500 μ μm spot in the retina.m spot in the retina.

• Do not count the spots but fill up an Do not count the spots but fill up an appropriate region of retina .appropriate region of retina .

Practical PointsPractical Points

• Usually PRP performed in 2 sessions Usually PRP performed in 2 sessions spaced 2-4 weeks apart.spaced 2-4 weeks apart.

• If possible start with inferior retina.If possible start with inferior retina.• If patient discomfortable during PRP:If patient discomfortable during PRP:- Reassure the patient it is expected and Reassure the patient it is expected and

the treatment going well.the treatment going well.- Decrease the duration to about 0.05 s.Decrease the duration to about 0.05 s.- Do it in more but shorter sessions.Do it in more but shorter sessions.- Retrobulbar anesthetic can be used.Retrobulbar anesthetic can be used.

Practical PointsPractical Points

• Major reason for under treatment is Major reason for under treatment is not well dilated pupil.not well dilated pupil.

• If NV recur after complete PRP :If NV recur after complete PRP :- Add more PRP in the periphery or Add more PRP in the periphery or

between previous laser burns.between previous laser burns.- Vitrectomy .Vitrectomy .

Practical PointsPractical Points

CSME + Capillary non perfusion :CSME + Capillary non perfusion :• Some recommend doing grid laser for Some recommend doing grid laser for

area with capillary non perfusion area with capillary non perfusion (decrease possibility of NV )(decrease possibility of NV )

Lowering serum lipid and ME :Lowering serum lipid and ME :• Clofibrate (in several British study)Clofibrate (in several British study)• Reduce amount of hard exudate but Reduce amount of hard exudate but

macular edema edema persist with macular edema edema persist with only modest improvement in VA .only modest improvement in VA .

RememberRemember

Argon blue : 488 nm.Argon blue : 488 nm. Argon green : 514 nm.Argon green : 514 nm. Dye yellow : 577 nm.Dye yellow : 577 nm. Krypton red : 647 nm.Krypton red : 647 nm.