Diabetic retinopathy

Diabetic retinopathy

1. PRESENTED BY: D r . Kawshik Nag MS Resident Phase A (Ophthalmology ) Chittagong Medical College Diabetic Retinopathy

2. Retinopathy is the most important ocular complication of diabetes . DR is more common in type 1 DM than type 2 DM. Proliferative Diabetic Retinopathy (PDR) affects 5-10% of diabetic population. Type 1 Diabetes are at particular risks, with an incidence of upto 90% after 30 years.

3. RISK FACTORS of DR Duration of diabetes -Most important Patient diagnosed before age 30 years 50 % DR after 10 years 90 % DR after 30 years Poor metabolic control Less important, but relevant to development and progression of DR Increased HbA1c associated with increased risk.

4. Pregnancy Associated with rapid progression of DR Predicating factors : poor pre-pregnancy control of DM, too rapid control during the early stages of pregnancy, pre- eclampsia and fluid imbalance. Hypertension Very common in patients with DM type 2 Should strictly control (<140/80 mmHg)

5. Nephropathy Associated with worsening of DR Renal transplantation may be ass with improvement of DR and better response to photocoagulation Other Obesity , increased BMI, high waist-to-hip ratio Hyperlipidemia Anemia

6. Pathogenesis Here microangiopathy occurs and it leads to: Microvascular occlusion Microvascular leakage

7. Hyperglycemia Intracellular sorbitol accumulation Free radicals Glycated end products Disruption of ion channel function Protein kinase C activation Direct effect Microangiopathy Hematological & on retinal cells (damage to capillary wall ) Rheological changes Intra retinal Edema Microvascular Occlusion causes Hemorrhages Exudates Ischemia IRMA Neovascularization hemorrhage Fibrosis Traction

8. SYMPTOMS Diabetic retinopathy is asymptomatic in early stages of the disease. As the disease progresses symptoms may include – Blurred vision Floaters and flashes Distorted vision Dark areas in the vision Poor night vision Impaired color vision Partial or total loss of vision

9. SIGNS OF DIABETIC RETINOPATHY Microaeurysm Retinal hemorrhage Hard exudates Cotton wool spot Venous beading Intraretinal microvascular abnormalities (IRMA) Macular oedema

10. Microaneurysm Localized saccular outpouchings of capillary wall red dots Focal dilatation of capillary wall where pericytes are absent Fusion of 2 arms of capillary loop Usually seen in relation to areas of capillary non-perfusion at the posterior pole in temporal to fovea It is the earliest signs of DR

11. Scattered hyperfluorescent Microaneurysms may leak plasma constituents into the retina

12. Retinal Hemorrhage Capillary or microaneurysm is weakened rupture intraretinal hemorrhages Dot & blot hemorrhages Deep hemorrhage - inner nuclear layer or outer plexiform layer Usually round or oval Dot hemorrhages - bright red dots (same size as large microaneurysms ) Blot hemorrhages - larger lesions Flame-shape or splinter hemorrhages More superficial - in nerve fiber layer Absorbed slowly after several weeks Indistinguishable from hemorrhage in hypertensive retinopathy May have co-existence of systemic hypertension BP must be checked

13. Dot & blot VS splinter hemorrhage

14. Hard exudate Intra-retinal lipid exudates Yellow deposits of lipid and protein within the retina Accumulations of lipids leak from surrounding capillaries and microaneuryisms May form a circinate pattern Hyperlipidemia may correlate with the development of hard exudates

15. Cotton Wool Spot White fluffy lesions in nerve fiber layer Result from occlusion of retinal pre-capillary arterioles supplying the nerve fiber layer with concomitant swelling of local nerve fiber axons Also called "soft exudates" or "nerve fiber layer infarctions“ Fluorescein angiography shows no capillary perfusion in the area of the soft exudate Very common in DR, specially if patient with hypertension.

16. Hard Exudate VS Cotton Wool Spot

17. Venous beading Dilatation and beading of retinal vein Appearance resembling sausage-shaped dilatation of the retinal veins Sign of severe NPDR

18. Intraretinal microvascular abnormalities ( IRMA) Abnormal dilated retinal capillaries or may represent intraretinal neovacularization which has not breached the internal limiting membrane of the retina. Severe NPDR indicate rapidly progress to PDR

19. Diabetic maculopathy Macular ischemia Retinal capillary non-perfusion Progressive NPDR Macular edema Focal or diffuse or mixed Increased retinal vascular permeability Seen in both NPDR and PDR Cause of visual loss in DR Important in planning for treatment

20. Focal macular edema Diffuse macular edema

21. Macular ischemia

22. Clinical Significant Macular Edema ( CSME) Retinal edema within 500 microns of centre fovea Hard exudates within 500 microns of fovea if ass with adjacent retinal thickening Retinal edema > 1 disc diameter, any part is within 1 disc diameter of centre of fovea

23. CLASSIFICATION Non-proliferative Diabetic Retinopathy (NPDR) : No DR Very Mild NPDR Mild NPDR Moderate NPDR Severe NPDR Very Severe NPDR Proliferative Diabetic Retinopathy (PDR): Mild to Moderate PDR High Risk PDR

24. Nonproliferative diabetic retinopathy Very Mild : Indicated by the presence of at least 1 micro aneurysm. Mild : Microaneurysms , retinal haemorrhage , exudates, cotton wool spots.

25. Moderate: Includes the presence of hemorrhages (1-3 quadrants) , micro - aneurysms , hard exudates and Cotton wool spot. Microaneurysm Exudate Cotton wool

26. Severe: The (4-2-1) rule; one or more of: H emorrhages and microaneurysms in 4 quadrants. V enous beading in at least 2 quadrants. I ntraretinal microvascular abnormalities in at least 1 quadrant IRMA Beading

27. Proliferative diabetic retinopathy 5% of DM pt . Findings- Neovascularization : NVD, NVE Vitreous changes Advanced diabetic eye disease Final stage of Uncontrolled PRD Glaucoma (neovascularization) Blindness from persistent vitreous hemorrhage,t ractional retinal detachment , opaque membrane formation.

28. Rubeosis iridis ( neovascularisation of the iris) Neovascular glaucoma

29. Diagnostic Testing Fundus Fluorescein Angiography : T o guide treatment of CSME T o identify Ischemic maculopathy Intraretinal microvascular abnormalities vs Neovascularization It can be evaluation in hazy media It is not a screening modality It is not a routine investigation

30. Fundus Photography: For documentation purpose

31. Optical Coherence Tomography(OCT): N on contact N on invasive M icron resolution C ross-sectional study of retina C orrelates very well with the retinal histology

32. Optical Coherence Tomography(OCT) Qualitative analysis : D escription by location D escription of form and structure Identification of anomalous structures O bservation of the reflective qualities of the retina Quantitative analysis: R etinal thickness and volume N erve fiber layer thickness .

33. Retinal Anatomy Compared to OCT The vitreous - black space on the top of the image F ovea - normal depression U mbo- central hyper reflective dot within foveola The nerve fiber layer (NFL) and the retinal pigment epithelium (RPE) highly reflective than the other layers of the retina ( red – yellow ) Retinal nerve fiber layer – thicker on nasal side of macula Areas of minimal signals ( blue – black) Outer nuclear layer – thickest portion

34. Ultrasonography ( B- scan) : When opaque media preclude retinal examination. Useful in ruling out- Retinal detachment Traction threatening macular detachment Vitreous hemorrhage.

35. Diabetic retinopathy Normal Comparison between Normal Retina & DR

36. Screening for DR Patients withType 1 diabetes should have an ophthalmologic examination within 5 years after onset. Patients with Type 2 DM should have an ophthalmologic examination at the time of the diabetes diagnosis. If there is no DR then one annual examination required. If any level of DR, progression and sight threatening, then examination will be required more frequently

37. Screening for DR Women with pre existing type 1 or type 2 DM who are planning pregnancy or pregnant should be counseled on risk of development &/ or progression of DR. Eye examinations should be started from 1 st trimster and monitored every trimster and for 1 year of postpartum period .

38. Management Medical treatment . Observation. Laser therapy . Anti VEGF Agents Vitrectomy.

39. Medical treatment: G lucose control : controlling diabetes. maintaining the HbA1C level in the 6-7% range. Level of activity : M aint a ini n g a health y lifestyl e wit h regular e x ercise can help reduce the complication of diabetes and DR. Blood pressure control. Lipid-lowering therapy .

40. Laser therapy Panretinal photocoagulation (PRP) High-risk PDR (3/4) Vitreous or preretinal hemorrhage New vessels on optic disc or within 1,500 microns from optic disc rim Large new vessels Iris or angle neovascularization CSME

41. Focal or Grid laser CSME in both NPDR and PDR Inducing involution of new vessels Preventing vitreous hemorrhage and preventing visual loss Limitations : Patient must have clear lens and vitreous If cataract treat before laser PRP If vitreous hemorrhage vitrectomy + laser photocoagulation

42. (a) before and (b) after focal laser photocoagulation.   (b) (a)

43. Focal laser Before After

44. Intravitreal Anti VEGF Agents Bevacizumab Ranibizumab Aflibercept

45. Surgery P ars plana vitrectomy (PPV ) Inications - Severe persistent vitreous hemorrhage Progressive tractional RD (threatening or involving macula ) Combined tractional and rhegmatogenous RD Premacular subhyaloid hemorrhage Recurrent vitreous hemorrhage after laser PRP

46. Vitrectomy : Removes blood Removes Traction Allows PRP

47. Vitrectomy

48. Aspirin in diabetic eye Aspirin use did not alter progression of diabetic retinopathy. Aspirin use did not increase risk of vitreous hemorrhage. Aspirin use did not affect visual acuity. Aspirin reduce s risk of cardiovascular morbidity and mortality.

49. Follow up: Retinal finding Suggested follow-up Normal Annually Mild NPDR 1 year Moderate NPDR 6 months - 1year or refer to ophthalmologist. Sever NPDR Every 4 months DME Every 2-4 months PDR Every 2-3 months