DIABETIC RETINOPATHY

PRESENTATION BYDr. Sumeet Agrawal

PG II Year

• Chronic retinal disorder characterized by gradually progressive alterations in the retinal microvasculature in patients with diabetes mellitus

OVE

RVIE

W• EPIDEMIOLOGY• RISK FACTORS• PATHOGENESIS• PATHOLOGIC ENTITIES• DISEASE ENTITIES• DIFFERENTIAL DIAGNOSIS• MANAGEMENT• FOLLOW UP

EPIDEMIOLOGY

EPIDEMIOLOGY• 31.7 million diabetic subjects in • Largest number of diabetics in any single country.• 12. 5 % of urban population & 4 % of the rural

population • Expected to increase to 79.4 million by 2030• Type 2 diabetes in Indians differs from that in

western population :– onset is at a younger age,– obesity is less common,– genetic factors appear to be stronger.Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes, estimates for the year 2000 and projections for 2030. Diabetes Care.

2004;27:1047–1053.Mohan V, Ramachandran A, Snehalatha C, Mohan R, Bharani G, Viswanathan M. High prevalence of maturity onset diabetes of the young

(MODY) among Indians. Diabetes Care. 1985;8:371–374.Joshi SR. Metabolic syndrome: emerging clusters of the Indian phenotype. J Assoc Physicians India. 2003;51:445– 456.

+[1]

[1] Rema M et al. Prevalence of Diabetic Retinopathy in Urban India: The Chennai Urban Rural Epidemiology Study (CURES) Eye Study, I.Invest. Ophthalmol. Vis. Sci;

July 2005 vol. 46: 328-333

[6]R Piyush et al.Prevalence of Diabetic Retinopathy in Western Indian Type 2 Diabetic Population: A Hospital – based Cross – Sectional StudyJournal of Clinical and Diagnostic Research. 2013 Jul, Vol-7(7): 1387-1390

[7] Agrawal RP, Ranka M, Beniwal R, Gothwal SR, Jain GC, Kochar DK et al. Prevalence of diabetic retinopathy in type 2 diabetes in relation to risk factors: Hospital based study. Int J Diab Dev Countries. 2003;23:16-19.

[8] Rema M, Premkumar S, Anitha B, Deepa R, Pradeepa R, Mohan V. Prevalence of diabetic retinopathy in urban India: The Chennai Urban Rural Epidemiology Study (CURES) Eye Study, I. Invest Ophthalmol Vis Sci. 2005; 46 : 2328-33.

[11] Rema M, Ponnaiya M, Mohan V. Prevalence of retinopathy in non insulin dependent diabetes mellitus at a diabetes centre in southern India. Diabetes Res Clin Pract.1996; 34: 29-36.

[12] Narendran V, John RK, Raghuram A, Ravindran RD, Nirmalan PK, Thulasiraj RD. Diabetic retinopathy among self reported diabetics in southern India: a population based assessment. Br J Ophthalmol. 2002;86:1014–18.

[13] Mahesh G, Giridhar A, Saikumar SJ, Anna Elisa, Ramkumar, Bhat S. Prevalence of Diabetic Retinopathy in a Rural Population of South ndia. AIOC PROCEEDINGS. 2009; community/social opthalmology session: 142-45.

[6]INDIAN

STUDIES

Epidemiology of DME• 10-year incidence of DME

– 20.1% among patients diagnosed before age 30 years (younger onset)

– 39.3% among patients diagnosed after age 30 (older onset) • Diabetes Control and Complications Trial (DCCT)

– 27% of patients develop macular edema within 9 years of diabetes• 3% in eyes with mild nonproliferative diabetic retinopathy

(NPDR), • 38% with moderate to severe NPDR, and • 71% with proliferative diabetic retinopathy (PDR) develop DME• Older onset diabetics are at a higher risk

Anderson JM, Itallie CMV. Tight junctions and the molecular basis for regulation of paracellular permeability. Am J Physiol. 1995;269:G467—76Klein R, Klein BEK, Moss SE. Th e epidemiology of ocular problems in diabetes mellitus. in SS F (ed): Ocular problems in diabetes mellitus. Boston, Blackwell Scientifi c Publications, 1991, p. 1--51

Klein R, Klein BEK, Moss SE, Cruickshanks KJ. Th e Wisconsin epidemiologic study of diabetic retinopathy. XV. Th e long term incidence of macular edema. Ophthalmology. 1995;102:7—16Vitale S, Maguire MG, Murphy RP, et al. Clinically signifi cant macular edema in Type 1 diabetes. Incidence and risk factors. Ophthalmology. 1995;102. 117--6.

Klein R, Klein BEK, Moss SE. Visual impairment in diabetes. Ophthalmology 1984; 91:1-8

RISK FACTORS

• DURATION OF DIABETES• GLYCEMIC CONTROL• HYPERTENSION• RENAL DYSFUNCTION• DYSLIPIDEMIA• PREGNANCY• OBESITY• ANEMIA

RISK FACTORS• DURATION OF DIABETES– Single most important risk factor

DURATION OF DM

PREVALANCE OF DR

DURATION OF DM

PREVALANCE OF DR

> 5 yrs. very low 11 – 13 yrs. 23 %

5 – 10 yrs. 27 % 13 – 16 yrs. 44 %

TYPE 1 10 – 20 yrs. 71 – 90 % TYPE 2 16 – 20 yrs. 60 %

> 20 yrs. 95 % [20-30% PDR]

20 – 30 yrs. 77 %

> 30 yrs 96 %

Klein R., Klein B., Moss S., et al: The Wisconsin epidemiologic study of diabetic retinopathy. XIV. Ten-year incidence and progression of diabetic retinopathy. Arch Ophthalmol 1994; 112:1217-1228.

Yanko L., Goldbourt U., Michaelson C., et al: Prevalence and 15-year incidence of retinopathy and associated characteristics in middle-aged and elderly diabetic men. Br J Ophthalmol 1983; 67:759-765.

Kostraba J.N., Dorman J.S., Orchard T.J., et al: Contribution of diabetes duration before puberty to the development of microvascular complications in IDDM subjects. Diabetes Care 1989; 12:686-693.

[1] Rema M et al. Prevalence of Diabetic Retinopathy in Urban India: The Chennai Urban Rural Epidemiology Study (CURES) Eye Study, I.Invest. Ophthalmol. Vis. Sci;

July 2005 vol. 46: 328-333

[1]

[6]R Piyush et al.Prevalence of Diabetic Retinopathy in Western Indian Type 2 Diabetic Population: A Hospital – based Cross – Sectional Study Journal of Clinical and Diagnostic

Research. 2013 Jul, Vol-7(7): 1387-1390

PREVALENCE OF DIABETIC RETINOPATHY IN TYPE 2 DIABETES IN RELATION TO RISK FACTORS: HOSPITAL BASED STUDY. A Raghav et al. INT. J. DIAB. DEV. COUNTRIES. 2003; 23: 16-9

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• Duration of DM before puberty is not important.

Role of Glycemic Control

DCCT (1993)• 1441 subjects with

IDDM followed for 6.5yrs

• Randomized into strict and conventional t/t

• Strict control group had average HbA1c 7.2%– Conventional: 8.8%

• Strict control resulted in…– Reduced risk of retinopathy by 76%– Reduced risk of progression by 54%

Role of Blood PressureUKPDS (1998)• 1148 hypertensive type-2 diabetics randomized into

tight and less-tight BP control and followed for 8.4 yrs

• Average BP:– Tight: 144/82– Less tight: 154/87

• Tighter BP control resulted in…– 34% reduction in

progression of DR– 47% reduced risk of loss of 3 lines VA

Role of Cholesterol

• WESDR (1991): Higher serum cholesterol increased risk of hard exudates in type-1 DM

• ETDRS (1996): Higher serum lipids increased risk of hard exudates and loss of VA

• Elevated lipids may increase the morbidity of diabetic macular edema

‘Earliest’ in DR

• Ophthalmoscopically detectable change• Histopathological change• Symptom• Electrophysiological abnormality

• Poor night vision (dark adaptation) • Poor recovery from bright lights (photo stress)

• Diminution of the amplitude of the oscillatory potentials (OP's) of the electroretinogram at a time when both the a- and b-waves are normal

• Ischemia in the inner nuclear layer • Predictor of progression • Severity inversely proportional to the amplitude of the

b-wave

Color vision assessment:

Acquired blue-Yellow defect (patients would be unable to accurately match self – monitored color - dependent urine or blood-glucose tests)

NOTE : Macular disorders : Blue-yellow defects (Exceptions : Cone dystrophy, Stargardt’s disease

Optic nerve disorders : Red-green defects (Exceptions : glaucoma, autosomal dominant optic neuropathy)

PATHOGENESIS

• ALDOSE REDUCTASE– Converts sugars, when present in high concentration, into alcohols.

(glucose to sorbitol) – Sorbitol cannot easily diffuse out of cells, – Osmotic forces draw water into the cells resulting in electrolyte

imbalance. – Retinal pericytes and Schwann cells,

• VASOPROLIFERATIVE FACTORS– Vascular endothelial growth factor (VEGF), – In the vitreous of patients with diabetic retinopathy – Decreases after PRP

• GROWTH HORMONE– Reversal of florid diabetic retinopathy in women who had postpartum

hemorrhagic necrosis of the pituitary gland– Growth hormone deficiency was found to be somewhat protective

against retinopathy

• PLATELETS AND BLOOD VISCOSITY– Platelets in diabetic patients are “stickier” than

platelets of patients without diabetes– Diabetic platelets are especially sensitive to

thromboxane and to other aggregating agents such as epinephrine.

– Focal capillary occlusion and focal areas of ischemia in the retina

• Microvascular leakage• Microvascular occlusion

Microvascular leakage

Degeneration and loss of pericytes

Plasma leakage

Hard exudate(Circinate pattern)

Capillary wall weakening

microaneurysm

Retinal edema

Intraretinal hemorrhage

Microvascular occlusion

Neovascularizationand fibrovascular proliferation

VEGF

Increased plasma viscosityDeformation of RBCIncreased platelets stickiness

Decreased capillary blood flowand perfusion

Endothelial cell damage and proliferation

Capillary basement membrane thickening

Retinal hypoxia

A-V shuntIRMA

Cotton wool spots

Proliferative retinopathy

Rubeosis iridis

PATHOGENESIS OF DME• BREAKDOWN OF BLOOD RETINAL BARRIER– changes in the tight junctions, – pericyte loss,– endothelial cell loss,– retinal vessel leukostasis, – up-regulation of vesicular transport, – increased permeability of the surface membranes of

retinal vascular endothelium and RPE cells,– activation of the AGE receptor, – downregulation of glial-cell,– derived neurotropic factor (GDNF),

– retinal vessel dilation

• VASOACTIVE FACTORS– VEGF, – protein kinase C [PKC], – heparin, – angiotensin II, – PEDF,– biochemical pathways

• VITREORETINAL INTERFACE

PATHOLOGIC ENTITIES

• MICROANEURYSM• CAPILLARY NON PERFUSION• INTRARETINAL HEMORRHAGES• HARD EXUDATES• COTTON WOOL SPOTS• VENOUS BEADING• INTRARETINAL MICROVASCULAR

ABNORMALITIES (IRMA)

MICRO ANEURYSMS• Pericytes : Mesothelial cells• Surround and support the capillary endothelium• 1:1• Weakens the capillaries => thin-walled

dilatations• Endothelial cells proliferate • Layers of basement membrane material• Fibrin &/or erythrocytes, may occlude the

lumen• Small red dots; 20-200 μ; OPL/INL• Temporal to the fovea• Venous side => arterial side• Permeable to lipid and fluid

• FFA differentiates– Patent micro aneurysms and dot hemorrhages– Cannot if it is filled with clotted blood– Many more seen in FFA than ophthalmoscopically

• Rupture => intra retinal hemorrhage– Deep (OPL/INL) :

• Dot (venous end of the capillaries), • blot (superficial precapillary arterioles; larger)

– Superficial (NFL) : flame shaped, splinter (hypertensives)

HARD EXUDATES

• Outer plexiform layer• Accumulated lipoproteins• Circinate pattern• Centre usually contains a micro aneurysm• Differentiate from drusens

COTTON WOOL SPOTS

• White fluffy lesions in nerve fibre layer• Occlusion of retinal pre-capillary arterioles• Swelling of local nerve fibre axons• “Soft exudates" or "nerve fibre layer infarctions" • FFA – no capillary perfusion in the area of the soft exudate

• Very common in DR with concomitant hypertension

VENOUS BEADING & LOOPS

• Indicates sluggish retinal circulation • Nearly always adjacent to extensive areas of

capillary nonperfusion• Focal vitreous traction

INTRA RETINAL MICROVASCULAR ABNORMALITIES (IRMA) :

• Dilated, tortuous retinal capillaries• Shunt between arterioles and venules.• Adjacent to areas of capillary closure.

• May resemble focal areas of flat NVE . – In IRMA : • Intraretinal location• Absence of profuse leakage on FFA• Failure to cross over major retinal blood vessels.

PROLIFERATIVE DIABETIC RETINOPATHY

• Usually arise from veins• NVD: within 1 disc diameter of the optic disc• NVE: further than 1 disc diameter away• Capillary non-perfusion is more extensive in

NVD• More often in younger patients (<40 yrs.)

• Vessels grow along the path of least resistance– Absent ILM over the optic disc– Posterior hyaloid face

• Associated with fibrous proliferation– Vascular (into the vitreous cavity, surface of

retina/disc)– Avascular (thickening of the posterior hyaloid)

PDR and the Vitreous

• PVD in diabetics leads to shrinkage of the entire vitreous

• New vessels are pulled into the vitreous by it’s contracting forces

• Vitreous hemorrhage, breaks and RD• Vitrectomy inhibits neovascularisation

Hemorrhage in PDR

• Location:– Subhyaloid: settles down and absorbed faster– Into the vitreous: very slow clearing– Sub-ILM: round/oval/boat shaped• Increased progression to RD

DIABETIC RD

• TRACTION ALONE (Non-rhegmatogenous)– Confined to the posterior pole (rarely beyond 2/3rd

distance to the equator– Taut and shiny surface– Concave towards the pupil– No shifting/subretinal fluid

DISEASE ENTITIES

• CLASSIFICATION– NPDR• Mild• Moderate• Severe

– PDR– Advanced diabetic eye disease

• DIABETIC MACULOPATHY• DIABETIC PAPILLOPATHY

Microaneurysms Mild NPDR

Mild NPDR plus hemorrhages, hard exudates, cotton wool spots .

Moderate NPDR

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

Severe NPDR (4-2-1 rule)

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

New vessels and/or fibrous proliferations; or preretinal and/or vitreous hemorrhage

Early PDR

1. NVD ≥ 1/3 of DD.2. less extensive NVD, if vitreous or preretinal

hemorrhage is present .3. NVE ≥ half disc area, if vitreous or preretinal

hemorrhage is present

PDR with High Risk

Characteristics

1. Extensive vitreous hemorrhage precluding grading.2. Retinal detachment involving the macula.3. Phthisis bulbi .

Advanced Diabetic Eye

Disease

Early Treatment Diabetic Retinopathy Study Research Group: Early Photocoagulation for diabetic retinopathy. ETDRS Report Number 9. Ophthalmology 98:766, 1991

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

Diabetic Maculopathy

• Macular ischemia– Retinal capillary non-perfusion– Progressive NPDR

• Macular edema– Increased retinal vascular permeability– Seen in both NPDR and PDR– Most common cause of visual loss in DR

Clinically 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.

Focal macular edema

Diffuse macular edema

Macular ischemia

DIAGNOSING DME

• Slit lamp biomicroscopy– Contact lens– 78 D / 90 D

• FFA– leakage on the FA does not equate to clinical retinal thickening or

edema– focal leakage: well-defined focal area of leakage from

microaneurysms or dilated capillaries – diffuse leakage: presence of widespread leakage from IRMA, retinal

capillary bed– diffuse cystoid leakage: diffuse leakage and pooling of dye in the

cystic spaces of the macula in the late phase of the angiogram– Macular ischemia

Brian Y. Kim S, Scott D et al. Optical Coherence Tomographic Patterns of Diabetic Macular Edema .Am J Ophthalmol 2006;142:405–412.

• Sponge like Thickening – most common presentation– mostly in outer retinal layers while internal layers

maintain their normal reflectivity– spongy appearance with increased retinal

thickness

• Cystoid Spaces – second most common pattern– intra-retinal cystoid spaces– involves variable depth of retina

and has intervening septa in between

– progresses gradually to involve the whole of retinal thickness

• Serous Detachment – Seen as a hypo-reflective area between neurosensory retina

and RPE• Taut Posterior Hyaloid Membrane – Taut, thickened, shiny, glistening hyper-reflective membrane– Striations on retina over the posterior pole – Attachment to the disc and the top of the elevated macular

surface– Retinal thickness is greatly increased – Intra-retinal hyporeflective cyst like cavities (corresponding to

fluid accumulation) – Foveal detachment

• Atypical form of nonarteritic anterior ischemic optic neuropathy (NAION)

• No visual symptom• Non-specific minimal visual disturbance such as painless

mild blurring or distortion• Visual acuity is usually normal or mildly diminished, except

coexisting diabetic maculopathy occurs• Usually resolves within 2-10 months with residual mild optic

atrophy

DIABETIC PAPILLOPATHY

DIFFERENTIAL DIAGNOSIS

• Radiation retinopathy • Hypertensive retinopathy • Retinal venous obstruction (central retinal vein occlusion

(CRVO), branch retinal vein occlusion (BRVO)) • Ocular ischemic syndrome • Anemia • Leukemia • Coats’ disease • Idiopathic juxtafoveal retinal telangiectasia • Sickle cell retinopathy

ASYMMETRIC DR

• CAUSES– Myopia ≥5 D, – Anisometropia >1 D, – Amblyopia, – Unilateral elevated intraocular pressure, – Complete posterior vitreous detachment, – Unilateral carotid artery stenosis, – Ocular ischemic syndrome, and – Chorioretinal scarring

MANAGEMENT

METABOLIC CONTROL

• SINGLE MOST IMPORTANT STEP– HbA1C < 7%– Lipid profile– Systoilc BP < 130 mmHg– KFTs– Proteinuria

MEDICAL THERAPY

• ASPIRIN• TICLOPIDINE• PENTOXIFYLLINE

• No significant role

LASER TREATMENT

• 1959, first reported by Meyer-Schwickerath, who used a xenon arc photocoagulator

• Goal – Cause regression of existing neovascular tissue– prevent progressive neovascularization.

LASER TREATMENT• Neovascularisation with high risk characteristics• Severe NPDR in both eyes• One-eyed patient with severe NPDR- other eye lost

because of complications of PDR• Pregnant ladies with severe NPDR• Diabetics with severe NPDR likely to undergo

cataract surgery in near future• Unlikely to follow-up regularly• Significant areas of capillary nonperfusion and

leakage.

MECHANISM OF ACTION• Increase in oxygenation from the choroid to the inner retina through

the laser scars due to the thinning of the retina in the treated area

• Autoregulatory response to breathing pure oxygen improves

• Decreases choroidal circulation in the midperiphery, which in turn shunts blood flow centrally, (“reverse choroidal steal”)

• Hypoxic retina to anoxic

• Destroys highly metabolically active outer retinal cells, reducing retinal oxygen consumption

• Increase in vasoinhibitors

• DRS – 50% reduction in severe visual loss in eyes with severe

NPDR or PDR – Visual acuity of 20/100 or better that had– Risk of severe visual loss with PDR at the 2-year follow-up

• 6% in the treated eyes compared• 16% in the control group

• High-risk characteristics,– 11% in the treated eyes– 26% in the control group.

• Macular edema should be treated first• Treat the inferior quadrant first• Limits:– Posteriorly : Superiorly & Inferiorly - temporal vascular

arcades– Nasally - ½ DD from disc– Temporally - 2 DD from foveal center

• Avoid the horizontal meridians• Avoid in areas of prominent fibrovascular

membranes, vitreoretinal traction and tractional retinal detachment

• Green, red or diode laser photocoagulation may be used when vitreous hemorrhage or cataract prevents the use of an argon laser.

Under topical anesthesiaArgon green (514 nm)

Half to one burn width apart500 u spot size with the Goldmann lens

200 u with the Rodenstock panfundoscopic or Volksuperquad lensBurn intensity : mild whitening of retina

SIDE EFFECTS• Pain during the treatment• Decrease in night vision,• Impaired colour vision, • Impaired peripheral vision (5%),• Loss of 1 or 2 lines of visual acuity (3%),• Mydriasis,• Glare, • Temporary loss of accommodation,• Photopsias,• Macular edema may be aggravated,• Exudative retinal detachment,• Retinal breks, • Ciliochoroidal effusion, • Elevated intraocular pressure, • Angle-closure glaucoma, • Subretinal or epiretinal fibrosis• Damage to cornea/iris/lens

Stoltz RA, Brucker AJ: Lasers in diabetes; in Fankhauser F, Kwasniewska S (eds): Lasers in Ophthalmology. The Hague, Karger Publications, 2003, pp 229–240.

• Topical non-steroidal anti-inflammatory drops• 2 weeks and 4 weeks (to see for any untoward

complications),• Follow-up visits at 3-month • Additional laser is needed in at least 30% of

patients• Between prior laser scars • Peripheral retina

• Signs of a good successful laser:– Reduced number of exudates and hemorrhages,– Stabilization / sometimes improvement of visual

acuity,– Reduction in the angry look of NVD / NVE, – Appearance of fibrous component in the areas of

previous new vessels,– Reduced caliber of retinal vessels

• The Early Treatment Diabetic Retinopathy Study (ETDRS) set the guidelines for treatment of DME : – Glycemic control

(DCCT), – O ptimal BP control

(UKPDS) and – Macular focal/grid

photocoagulation reducing the risk of moderate vision loss by 50% (from 24% to 12% after 3 years).

LASER THERAPY FOR DME

• FOCAL TREATMENT (leaking microaneurysm 500 – 3000 u from center)– Aim : closure of leak

• GRID TREATMENT (diffuse leak 500 u away form center)– Aim : stimulate retinochoroidal pump

ETDRS protocol

VEGF

ANTI VEGF THERAPY• Bevacizumab (Avastin)

– monoclonal antibody to VEGF which binds to and neutralize all the active forms of the VEGF molecule

– 4 to 6 weekly injections• Ranibizumab (Lucentis)

– humanized, antigen-binding fragment (Fab) of a second-generation, recombinant monoclonal antibody directed against VEGF

• Aflibercept (Eylea)– recombinant fusion protein consisting of vascular endothelial

growth factor (VEGF)-binding portions from the extracellular domains of human VEGF receptors 1 and 2, that are fused to the Fc portion of the human IgG1 immunoglobulin

– 8 weekly injections

ANTI VEGF THERAPY

• DA VINCI (2008)– VEGF Trap Eye Vs laser in DME– Change in BCVA at 24 and 52 weeks– VEGF Trap eye significantly better

• VISTA DME (2011)– VEGF Trap Eye in center involving DME

STEROIDS• Intravitreal Triamcinolone Acetonide– 4mg/0.1 mL

• Flucinolone acetonide implant– low-dose (0.23 micrograms/day) or high-dose (0.45

micrograms/day) insert that lasts for 36 or 24 months respectively

– FAME trial (2011)• Ozurdex• Posurdex

• Frequent side effects

• Diabetic Retinopathy Clinical Research Network (drcr.net), – 150 clinical centers and – 500 physicians in United States, – 840 eyes, intravitreal TA (1 mg or 4 mg) was compared

with focal/grid photocoagulation in patients with DME. • After a two-year period, – photocoagulation produced superior visual acuity and

retinal thickness measurements and had fewer side-effects than TA

SURGICAL MANAGEMENT

• INDICATIONS OF PPV:– Dense, non-clearing vitreous hemorrhage (6

months)– TRD involving/threatening the macula– Combined TRD and RRD– Diffuse DME with posterior hyaloid traction– Significant recurrent vitreous hemorrhage despite

maximal PRP

• Severe progressive fibrovascular proliferation• Anterior hyaloid fibrovascular proliferation• Intractable ghost cell glaucoma• Anterior segment neovascularisation with

media opacities (PRP not possible)• Dense premacular hemorrhage

Objectives of Vitrectomy in DR

• Removal of axial opacities• Relief of anteroposterior and tangential traction• Segmenting or peeling of epiretinal membranes• Endolaser treatment• Effecting hemostasis• Closure of all retinal breaks• Treatment and prophylaxis of complications

• PVD induction is a major issue

• Segmentation, • Delamination, and • en bloc delamination

DRVS STUDY

• Vitrectomy 1 to 4 months after the onset of severe vitreous hemorrhage for type 1 diabetics yields final vision greater than or equal to 20/40 in 36% of this sub-group as compared to only 12% with conventional management (p =.001)

PHARMACOLOGIC VITREOLYSIS

• Ocriplasmin (JETREA)• Recombinant protease with activity against

fibronectin and laminin• FDA approval on 17 October 2012

FOLLOW UP

• Diabetic retinopathy induces vision loss – Type 1 diabetes • proliferative retinopathy,

– Type 2 diabetes, • macular edema, and proliferative retinopathy is

relatively rare.