Diabetic retinopathy

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A complete source of information intended for ophthalmologists. Includes everything from risk factors to pathophysiology to management.

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Diabetic retinopathy

  1. 1. DIABETIC RETINOPATHY PRESENTATION BY Dr. Sumeet Agrawal PG II Year
  2. 2. • Chronic retinal disorder characterized by gradually progressive alterations in the retinal microvasculature in patients with diabetes mellitus
  3. 3. OVERVIEW • EPIDEMIOLOGY • RISK FACTORS • PATHOGENESIS • PATHOLOGIC ENTITIES • DISEASE ENTITIES • DIFFERENTIAL DIAGNOSIS • MANAGEMENT • FOLLOW UP
  4. 4. EPIDEMIOLOGY
  5. 5. 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.
  6. 6. + [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
  7. 7. [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. [6] INDIANSTUDIES
  8. 8. 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—76 Klein 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—16 Vitale 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
  9. 9. RISK FACTORS
  10. 10. • DURATION OF DIABETES • GLYCEMIC CONTROL • HYPERTENSION • RENAL DYSFUNCTION • DYSLIPIDEMIA • PREGNANCY • OBESITY • ANEMIA
  11. 11. 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.
  12. 12. [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]
  13. 13. [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
  14. 14. 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
  15. 15. GlobalPrevalenceandMajorRiskFactorsofDiabeticRetinopathyEYE DISEASE(META-EYE)STUDYGROUPDiabetesCare2011;35:556–564.
  16. 16. • Duration of DM before puberty is not important.
  17. 17. 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%
  18. 18. Role of Blood Pressure UKPDS (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
  19. 19. 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
  20. 20. ‘Earliest’ in DR • Ophthalmoscopically detectable change • Histopathological change • Symptom • Electrophysiological abnormality
  21. 21. • 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
  22. 22. 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)
  23. 23. PATHOGENESIS
  24. 24. • 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
  25. 25. • 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
  26. 26. • Microvascular leakage • Microvascular occlusion
  27. 27. Microvascular leakage Degeneration and loss of pericytes Plasma leakage Hard exudate (Circinate pattern) Capillary wall weakening microaneurysm Retinal edema Intraretinal hemorrhage
  28. 28. Microvascular occlusion Neovascularization and fibrovascular proliferation VEGF Increased plasma viscosity Deformation of RBC Increased platelets stickiness Decreased capillary blood flow and perfusion Endothelial cell damage and proliferation Capillary basement membrane thickening Retinal hypoxia A-V shunt IRMA Cotton wool spots Proliferative retinopathy Rubeosis iridis
  29. 29. 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
  30. 30. • VASOACTIVE FACTORS – VEGF, – protein kinase C [PKC], – heparin, – angiotensin II, – PEDF, – biochemical pathways • VITREORETINAL INTERFACE
  31. 31. PATHOLOGIC ENTITIES
  32. 32. • MICROANEURYSM • CAPILLARY NON PERFUSION • INTRARETINAL HEMORRHAGES • HARD EXUDATES • COTTON WOOL SPOTS • VENOUS BEADING • INTRARETINAL MICROVASCULAR ABNORMALITIES (IRMA)
  33. 33. 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
  34. 34. • 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)
  35. 35. HARD EXUDATES • Outer plexiform layer • Accumulated lipoproteins • Circinate pattern • Centre usually contains a micro aneurysm • Differentiate from drusens
  36. 36. 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
  37. 37. VENOUS BEADING & LOOPS • Indicates sluggish retinal circulation • Nearly always adjacent to extensive areas of capillary nonperfusion • Focal vitreous traction
  38. 38. 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.
  39. 39. 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.)
  40. 40. • 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)
  41. 41. 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
  42. 42. 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
  43. 43. 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
  44. 44. DISEASE ENTITIES
  45. 45. • CLASSIFICATION – NPDR • Mild • Moderate • Severe – PDR – Advanced diabetic eye disease • DIABETIC MACULOPATHY • DIABETIC PAPILLOPATHY
  46. 46. MicroaneurysmsMild 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 NPDRVery severe NPDR
  47. 47. 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.
  48. 48. 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
  49. 49. 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.
  50. 50. Focal macular edema Diffuse macular edema
  51. 51. Macular ischemia
  52. 52. 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
  53. 53. Brian Y. Kim S, Scott D et al. Optical Coherence Tomographic Patterns of Diabetic Macular Edema .Am J Ophthalmol 2006;142:405–412.
  54. 54. • Sponge like Thickening – most common presentation – mostly in outer retinal layers while internal layers maintain their normal reflectivity – spongy appearance with increased retinal thickness
  55. 55. • 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
  56. 56. • 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
  57. 57. • 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
  58. 58. 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
  59. 59. 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
  60. 60. MANAGEMENT
  61. 61. METABOLIC CONTROL • SINGLE MOST IMPORTANT STEP – HbA1C < 7% – Lipid profile – Systoilc BP < 130 mmHg – KFTs – Proteinuria
  62. 62. MEDICAL THERAPY • ASPIRIN • TICLOPIDINE • PENTOXIFYLLINE • No significant role
  63. 63. LASER TREATMENT • 1959, first reported by Meyer-Schwickerath, who used a xenon arc photocoagulator • Goal – Cause regression of existing neovascular tissue – prevent progressive neovascularization.
  64. 64. 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.
  65. 65. 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
  66. 66. • 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.
  67. 67. • 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.
  68. 68. Under topical anesthesia Argon green (514 nm) Half to one burn width apart 500 u spot size with the Goldmann lens 200 u with the Rodenstock panfundoscopic or Volksuperquad lens Burn intensity : mild whitening of retina
  69. 69. 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.
  70. 70. • 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
  71. 71. • 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
  72. 72. • 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).
  73. 73. 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
  74. 74. ETDRS protocol
  75. 75. VEGF
  76. 76. 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
  77. 77. ANTI VEGF THERAPY
  78. 78. • 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
  79. 79. 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
  80. 80. • 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
  81. 81. 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
  82. 82. • Severe progressive fibrovascular proliferation • Anterior hyaloid fibrovascular proliferation • Intractable ghost cell glaucoma • Anterior segment neovascularisation with media opacities (PRP not possible) • Dense premacular hemorrhage
  83. 83. 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
  84. 84. • PVD induction is a major issue • Segmentation, • Delamination, and • en bloc delamination
  85. 85. 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)
  86. 86. PHARMACOLOGIC VITREOLYSIS • Ocriplasmin (JETREA) • Recombinant protease with activity against fibronectin and laminin • FDA approval on 17 October 2012
  87. 87. FOLLOW UP
  88. 88. • Diabetic retinopathy induces vision loss – Type 1 diabetes • proliferative retinopathy, – Type 2 diabetes, • macular edema, and proliferative retinopathy is relatively rare.

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