DIABETIC RETINOPATHY.pptx

This PPT is beneficial for undergraduate Medical students

1. DIABETIC RETINOPATHY Dr. Atul K umar Anand Senior Resident AIIMS Patna

2. Retinopathy Retina is frequently affected by systemic diseases & its manifestations are termed as retinopathy, e.g. – diabetic retinopathy, hypertensive retinopathy

3. Two main types of diabetes : Insulin-dependent diabetes (IDD) : - known as type 1 . - develops most frequently between 10 and 20 years of age . Non-insulin-dependent diabetes (NIDD) : - also known as type 2. - develops most frequently between the ages of 50 and 70 years.

4. Prevalence Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years It has a considerable impact on both the patient and the society because it typically affects individuals in their most productive years

5. Prevalence Blindness is 25 % more common in diabetics than non diabetics. Prevalence of PDR is much more in type I than type II. Diabetic retinopathy more severe in type I than type II.

6. RISK FACTORS The duration of diabetes : the most important factor. 5-10 yrs of diabetes – 27% >10yrs – 71-90% 20-30 yrs – 95% ( 30-50 % PDR)

7. RISK FACTORS It is extremely rare for DR to develop within 5 years of the onset of diabetes. about 5% of Type II have NPDR at presentation perhaps due to the lag between onset and diagnosis.

8. RISK FACTORS 2 . Glycemic control : 2 nd important risk factor the only important modifiable factor Although good metabolic control of diabetes will not prevent DR, but it may delay its development & progression by a few years. increased severity of diabetic retinopathy is associated with poorer glucose control. insulin treatment is associated with a decreased risk of either the development or progression of diabetic retinopathy in patients with type 1 diabetes.

9. RISK FACTORS With strict control of DM: - risk of developing retinopathy was reduced by 75% . - 50% reduction in the rate of progression of retinopathy in existing retinopathy Diabetes Control and Complications Trial (DCCT) Research Group N Engl J Med 1993; 329:977-986.

10. RISK FACTORS 3 . Miscellaneous factors : - pregnancy (Hormonal changes) – 10% new onset and 4% NPDR to PDR - systemic hypertension – independent risk factor - renal diseases - anaemia .( ↓oxygen ) - elevated serum lipid. - smoking - Alcohol. ( ? ) - Obesity.

11. Ocular Risk Factors PVD : complete PVD may prevent the development of PDR because the hyaloid is needed as a scaffold for retinal neovascularization . attached posterior hyaloid has also been associated with an increased risk for DME

12. Ocular Risk Factors High myopia : choroidal degeneration and extensive old chorioretinopathy protect against DR. believed to act in the same manner as pan retinal photocoagulation by reducing the metabolic needs of the retina

13. Ocular Risk Factors Removal of cataract : DR may progress after cataract surgery. If the cataract preclude retina evaluation and treatment, prompt postoperative retinal evaluation and treatment should considered.

14. 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 .(severe NPDR-PDR)

15. Microvascular leakage Microvascular leakage is caused by: Loss of pericytes The pericytes are wrapped around the capillaries and are thought to be responsible for the structural integrity of the vessel wall. Impairment of endothelial tight junctions Weakening of capillary walls Elevated levels of vascular endothelial growth factor (VEGF)

16. PATHOGENESIS Loss pericytes Microvascular leakage haemorrhage retinal oedema Diffuse Localized Microanurysm ” ”

17. PATHOGENESIS Microvascular occlusion : caused by thickening of the capillary basement membrane. capillary endothelial cell damage and proliferation. changes in red blood cells leading to defective oxygen transport, and increased stickiness and aggregation of platelets

18. Cotton – wool spot Neovascularization Ischemia Neovascular glaucoma Microvascular Occlusion Fibrovascular bands Vitreous hemorrhage Increased VEFG Tractional retinal detachment Infarction

19. New vessel proliferation Fibrous glial tissue proliferaion Tractional RD RD IRMA

20. CLINICAL FEATURES - SYMPTOMS Diabetic retinopathy is asymptomatic in early stages of the disease As the disease progresses symptoms may include Blurred vision Floaters Fluctuating vision( Flactuating refractive error & cataract) Distorted vision Dark areas in the vision Poor night vision Impaired color vision Partial or total loss of vision

21. CLINICAL FEATURES - SIGNS Microaneurysms : - located in the inner nuclear layer . - the first clinically detectable lesions . - small round dots .(20-200 μ ) - mostly located near and temporal to the macula. - When coated with blood they may be indistinguishable from dot haemorrhages .

22. MICROANEURYSM

23. CLINICAL FEATURES Haemorrhages : The clinical appearance depending on location - 'dot' and 'blot' : originating from the venous end of the capillaries. located in the compact middle layers of the retina . - Flame-shaped : originate from the more superficial precapillary arterioles, follow the course of the retinal nerve fibre layer. (linear disrtibution )

24. CLINICAL FEATURES Hard exudates : - located between the outer plexiform and inner nuclear layers of the retina. - They are often distributed in a ( circinate pattern) . - The centres of rings of hard exudates usually contain microaneurysms . - Made up of accumulated lipoproteins .

25. Hard exudates

26. CLINICAL FEATURES Retinal 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. with further accumulation of fluid, the fovea assumes a cystoid appearance .

27. Macular edema types: (FFA + Clinical) Focal ME :which has identifiable leakage source. Diffuse ME : which has multiple unidentifiable source of leakage. Cystoid ME : in which fluid accumulate in OPL and INL to form cystoid spaces.

28. CLINICAL FEATURES Vascular changes : venous changes :in the form of 'beading', 'looping' and 'sausage-like' segmentation. It represent endothelial cell proliferation. arterioles may also be narrowed and even obliterated, resembling a BRAO . - The most powerful predictors for development of PDR.

29. CLINICAL FEATURES Cotton-wool spots : (Soft exudates ) - Nerve fiber layer infarction. - caused by capillary occlusion in the retinal nerve fibre layer. The interruption of axoplasmic flow caused by the ischaemia , and subsequent build-up of transported material within the nerve axons, is responsible for the white and opaque appearance of these lesions. Disappear within weeks to months.

30. HARD AND SOFT EXUDATES

31. CLINICAL FEATURES Intraretinal microvascular abnormalities ( lRMA ) : Dilated, tortous retinal capillaries that act as a shunt between arterioles and venules . frequently seen adjacent to areas of capillary closure. IRMA may resemble focal areas of flat NVE . But in IRMA : intraretinal location. absence of profuse leakage on fluorescein angiography. failure to cross over major retinal blood vessels.

32. IRMA- Intraretinal microvascular anomalies

33. CLINICAL FEATURES New Vessels: 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 .

34. NVD:

35. NVE:

36. Classification of DR (ETDRS) Non-proliferative DR (NPDR) Mild Moderate Severe Very severe Proliferative DR (PDR) Early PDR PDR with HRC Advanced diabetic eye disease III. Clinically significant macular edema (CSME) - May exist by itself or along with NPDR and PDR

37. Mild NPDR At least one microaneurysm - earliest clinically detectable lesion Retinal hemorrhages Hard exudates

38. Moderate NPDR Microaneurysms and/or dot and blot hemorrhages in at least 1 quadrant Soft exudates (Cotton wool spots)

39. Mild and Moderate Non- proliferative DR was previously known as Background DR

40. Severe NPDR Any one of the following 3 features is present Severe hemorrhages in all 4 quadrants Significant venous beading in 2 or more quadrants Moderate IRMA in at least 1 quadrant Known as the 4-2-1 rule

41. Very Severe NPDR Any two of the features of the 4-2-1 rule is present

42. Severe and Very severe Non-proliferative DR was known as the Pre-proliferative

43. Proliferative DR(PDR ) Characterized by Proliferation of new vessels from retinal veins New vessels on the optic disc or within 1 disc diameter(NVD) New vessels elsewhere on the retina (NVE)

44. Proliferative DR

45. Clinically significant macular edema (CSME) defined as the presence of one or more of the following features: Retinal oedema within 500 µ m of the centre of the fovea . Hard exudates within 500 µ m of the fovea, if associated with adjacent retinal thickening (which may be outside the 500 µ m limit) . Retinal oedema that is one disc area (1500 µ m) or larger, any part of which is within one disc diameter of the centre of the fovea.

46. CLASSIFICATION Background DR(BDR): have microaneurysm , haemorrhage , & exudates Diabetic Maculopathy : presence of any retinopathy at macula Pre proliferative DR(PPDR): featutes of BDR + IRMA, venous changes. Indicates progressive retinal ischemia with a heightened risk of progression to retinal neovascularization

47. PDR: have neovascularization ( NVD/NVE) Advanced diabetic eye disease(ADED): have tractional RD, persistant VH, NVG

48. ADVANCED DIABETIC EYE DISEASE TRD Rubeosis C. Preretinal and vitreous haemorrhage a b c

49. Classification of severity of diabetic retinopathy Nonproliferative DRP : Microaneurysms , retinal hemorrhage and hard exudate Mild NPDR Mild NPDR plus cotton wool spots . Moderate NPDR Moderate NPDR plus one of : Intraretinal Hges in four quadrants . marked venous beading in two or more quadrants IRMA one or more quadrants. Severe NPDR Two or more of the above features described in severe NPDR Very severe NPDR 4 : 2 : 1 Rule

50. Classification of severity of diabetic retinopathy Proliferative DRP : New vessels and/or fibrous proliferations; or preretinal and/or vitreous hemorrhage Early PDR NVD ≥ 1/3 of DD. less extensive NVD, if vitreous or preretinal hemorrhage is present . NVE ≥ half disc area, if vitreous or preretinal hemorrhage is present PDR with HRC Extensive vitreous hemorrhage precluding grading. retinal detachment involving the macula. phthisis bulbi . Advanced PDR

51. Retinopathy Screening Type 1 diabetes - screen within 3-5 years of diagnosis after age 10 Type 2 diabetes - screen at time of diagnosis Pregnancy - women with preexisting diabetes should be screened prior to conception and during first trimester

52. Diagnostic Testing Fluorescein Angiography : Not needed to identify CSME or PDR. But : As a guide during CSME treatment. Identify macular capillary nonperfusion

53. Diagnostic Testing Color Fundus photography : For Documentation purpose . Ultrasonography : When opaque media preclude retinal examination. Useful in ruling out : RD. Traction threatening macular detachment.

54. MANAGEMENT OF DIABETIC RETINOPATHY Medical Therapy : Glycemic control : Tight control decrease risk of progression of retinopathy , nephropathy and neuropathy as well. Blood pressure control. Blood lipids control.

55. MANAGEMENT OF DIABETIC RETINOPATHY Laser : The treatment of depends on the severity of retinopathy and the presence or absence of CSME, which may be present at any stage .

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

57. Treatment of clinically significant macular oedema For microaneurysms in centre of hard exudate rings located 500-3000 m from centre of fovea Focal treatment Gentle whitening or darkening of microaneurysm (100-200 m , 0.10 sec) For diffuse retinal thickening located more than 500 m from centre of fovea and 500 m from temporal margin of disc Grid treatment Gentle burns (100-200 m , 0.10 sec), one burn width apart

58. Focal or Grid CSME in both NPDR and PDR Panretinal (PRP) PDR PHOTOCOAGULATION

59. laser photocoagulation(PRP) The aim of treatment is to: induce involution of new vessels . prevent vitreous haemorrhage. Initial treatment involves the placement of about 2000-3000 burns in a scatter pattern, extending from the posterior fundus to cover the peripheral retina in one or more sessions.

60. laser photocoagulation The technique of PRP is as follows: Topical corneal anaesthesia is adequate in most patients. - The spot size :depends on which contact lens is being used. (500 - 200 µ m). - The duration : between 0.10 and 0.05 second - The power level : produces a gentle burn

61. Indications for treatment of proliferative diabetic retinopathy NVD > 1/3 disc in area Less extensive NVD + haemorrhage NVE > 1/2 disc in area + haemorrhage

62. Spot size (200-500 m ) depends on contact lens magnification Gentle intensity burn (0.10-0.05 sec) Follow-up 4 to 8 weeks Area covered by complete PRP Initial treatment is 2000-3000 burns Laser panretinal photocoagulation

63. Algorithm for panretinal scatter coagulation of the retina

64. Anti-VGEF & Macular Edema Intra vitreal injection of bevacizumab ( avastin ) or ranibizumamb ( lucentis ) Intra vitreal injection of steroid: triamcinolone acetonide (IVTA)

65. OZURDEX sustain-released dexamethasone intravitreal implant 22 G needle last 6 mths FDA approved for BRVO/CRVO associated ME non-infectious uveitis NEW COMERS

66. OZURDEX NEW COMERS

67. Indications for vitreoretinal surgery: PPV Retinal detachment involving macula Severe persistent vitreous haemorrhage Dense, persistent premacular haemorrhage Progressive proliferation despite laser therapy

68. DR Management : Summery Strict glycemic control along with control of blood pressure & blood lipid CSME/PDR: laser(focal or grid or PRP){argon, krypton, diode, frequency doubled YAG} DME: anti VEGF, IVTA, ozurdex ADED: surgery(PPV) Follow up

69. Follow up Suggested follow-up Retinal Finding Annually Normal Every 9 months Mild NPDR Every 6 months Moderate NPDR Every 4 months Sever NPDR Every 2- 4 months CSME Every 6 months CNSME Every 2-3 months PDR

70. Simulation of defective vision as experienced by a Diabetic whose vision has been affected by Diabetic retinopathy Normal Defective