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- 2. • Retinal artery occlusions • Retinal vein occlusions • Diabetic retinopathy • Hypertensive retinopathy • Sickle cell retinopathy • Retinopathy of prematurity • Retinal telangiectasia 2
- 3. DIABETES MELLITUS Diabetes Mellitus is a group of diseases characterized by high blood glucose levels. Diabetes results from defects in the body's ability to produce and/or use insulin. • Type 1 diabetes is usually diagnosed in children and young adults. In type 1 diabetes, the body does not produce insulin. About 10% of people with diabetes have this form of the disease. • In Type 2 diabetes, either the body does not produce enough insulin or the cells ignore the insulin. This is the most common form of diabetes. 3
- 4. DIABETIC RETINOPATHY (DR) DEFINITION • Progressive dysfunction of the retinal blood vessels caused by chronic hyperglycemia. • DR can be a complication of type 1 or type 2 diabetes • Initially, DR is asymptomatic • If not treated, it can cause low vision and blindness. 4
- 5. DIABETIC RETINOPATHY EPIDEMIOLOGY • The total number of people with diabetes is projected to rise from 285 million in 2010 to 439 million in 2030. • Diabetic retinopathy is responsible for 1.8 million of the 37 million cases of blindness throughout the world . • Diabetic retinopathy (DR) is the leading cause of blindness in people of working age in industrialized countries. 5
- 6. RISK FACTORS FOR DIABETIC RETINOPATHY Duration of diabetes is a major risk factor associated with the development of diabetic retinopathy The severity of hyperglycemia is the key alterable risk factor associated with the development of diabetic retinopathy 6
- 7. DURATION OF DIABETES • The best predictor of diabetic retinopathy is duration of the disease • After 20 years of diabetes, more than 90% of patients with type 1 diabetes and 60% with type 2 have some degree on diabetic retinopathy • 33% of patients with diabetes have signs of diabetic retinopathy • People with diabetes are 25 times more likely to become blind than the general population. 7
- 8. OTHER RISK FACTORS 8 • Poor Blood Sugar control • Hypertension • Hyperlipidemia • Pregnancy • Nephropathy • Others: Smoking, Obesity, Anemia
- 9. 9
- 10. PATHOGENESIS OF DIABETIC MICRO ANGIOPATHY Diabetic Retinopathy is a microvasculopathy that causes: • Retinal capillary occlusion • Retinal capillary leakage Microvascular occlusion is caused by: • Thickening of capillary basement membranes • Abnormal proliferation of capillary endothelium • Increased platelet adhesion • Increased blood viscosity • Defective fibrinolysis Microvascular leakage is caused by: • Impairment of endothelial tight junctions • Loss of pericytes • Weakening of capillary walls • Elevated levels of vascular endothelial growth factor (VEGF) 10
- 11. Cotton – wool spots Neovascularization Ischemia Neovascula r glaucoma Microvascular Occlusion Fibrovascular bands Vitreous hemorrhage Increased VEGF Tractional retinal detachment Infarction 11
- 15. DIABETIC RETINOPATHY SYMPTOMS Asymptomatic in early stages of the disease As the disease progresses symptoms may include • Blurred vision • Floaters • Fluctuating vision • Distorted vision • Dark areas in the vision • Poor night vision • Impaired color vision • Partial or total loss of vision 15
- 16. Natural History of Diabetic Retinopathy • Mild nonproliferative diabetic retinopathy (NPDR) • Moderate NPDR • Severe NPDR • Very Severe NPDR • Proliferative diabetic retinopathy (PDR) 16
- 17. Findings Obsd International Clinical Diabetic Retinopathy Disease Severity Scale Proposed Disease Severity Level Findings Observable upon Dilated Ophthalmoscopy No apparent retinopathy No abnormalities Mild nonproliferative diabetic retinopathy Microaneurysms only Moderate nonproliferative diabetic retinopathy More than just microaneurysms but less than severe NPDR Severe nonproliferative diabetic retinopathy Any of the following: More than 20 intraretinal hemorrhages in each of four quadrants Definite venous beading in two or more quadrants Prominent IRMA in one or more quadrants and no signs of proliferative retinopathy. Proliferative diabetic retinopathy One or both of the following: Neovascularization Vitreous/preretinal hemorrhage 17
- 19. Histology of retina 1 RPE 2 Layers of Rods & Cones 3 External Limiting Membrane 4 Outer Nuclear layer 5 Outer Plexiform layer 6 Inner Nuclear layer 7 Inner Plexiform Layer 8 Ganglion Cell layer 9 Nerve Fibre layer 10 Internal limiting membrane 19
- 20. MICROANEURYSMS 20 • Focal dilatations of retinal capillaries • Appear as red dots. • Seen at the posterior pole, especially temporal to the fovea. • The first ophthalmoscopically detectable change in diabetic retinopathy.
- 21. RETINAL HAEMORRHAGES 21 Dot haemorrhages • In the inner nuclear layer or outer plexiform layer • Bright red dots (same size as large microaneurysms). Dark Blot/ round haemorrhages • Larger lesions • Located within the mid retina • Extent – marker for neovascularization Flame Shaped haemorrhages • Superficial and in the nerve fiber layer
- 22. Non-proliferative diabetic retinopathy (NPDR) 22
- 23. Non-proliferative diabetic retinopathy (NPDR) 23
- 24. HARD EXUDATES ( INTRA-RETINAL LIPID EXUDATES ) 24 • Yellowish waxy looking patches with distinct margins • Outer plexiform layer • Surrounding capillaries and microaneurysms, in a circinate pattern.
- 25. Hard exudates ( Intra-retinal lipid exudates ) 25
- 26. COTTON WOOL SPOTS 26 • Occlusion of retinal pre-capillary arterioles supplying the nerve fibre layer with concomitant swelling of local nerve fibre axons. • “Soft exudates" or "nerve fibre layer infarctions" • White, fluffy lesions in the nerve fibre layer.
- 28. LATE NON PROLIFERATIVE CHANGES Intra-retinal microvascular abnormalities (IRMA) • Represent intraretinal arteriolar-venular shunts which have not breached the internal limiting membrane of the retina. • Indicate severe non-proliferative diabetic retinopathy that may rapidly progress to proliferative retinopathy. Venous beading • Focal narrowing and sausage-shaped dilatation of the retinal veins. • Sign of severe non proliferative diabetic retinopathy. 28
- 29. Late non proliferative changes 29
- 30. 30 Clinical Findings • Microaneurysms • Management/Treatment • Annual follow-up MILD NONPROLIFERATIVE DIABETIC RETINOPATHY
- 32. 32 • Clinical Findings • Microaneurysms/ medium to large Intraretinal haemorrhages in 1- 3 quadrants • Mild Intraretinal Microvascular Abnormalities (IRMA’s) • Venous beading in not more than 1 quadrant • Cotton wool spots • Management/Treatment • 6-12 month follow-up without CSME • Color fundus photography Moderate Nonproliferative Diabetic Retinopathy (NPDR)
- 33. Moderate Nonproliferative Diabetic Retinopathy (NPDR) Hard exudates Flamed shaped hemorrhage Microaneurysm 33
- 34. SEVERE NONPROLIFERATIVE DIABETIC RETINOPATHY (NPDR) 34 Clinical Findings Any of the following: (4-2-1 Rule) • More than 20 intraretinal hemorrhages in each of four quadrants • Definite venous beading in two or more quadrants • Prominent Intraretinal Microvascular Abnormalities (IRMA) in one or more quadrants • And no signs of proliferative retinopathy
- 35. SEVERE NONPROLIFERATIVE DIABETIC RETINOPATHY (NPDR) Management/Treatment • 3-4 month follow-up • Color fundus photography • Possible panretinal photocoagulation • CSME present: color fundus photography, fluorescein angiography, focal photocoagulation, 3-4 month follow-up 35
- 36. Severe Nonproliferative Diabetic Retinopathy (NPDR) Venous beading 36
- 37. 37 • Clinical Findings • Ischemia induced neovascularization • at the optic disk (NVD) • elsewhere in the retina (NVE) • New vessels on the iris (NVI) • Vitreous hemorrhage/Pre-retinal haemorrhage • Retinal traction, tears, and detachment Proliferative Diabetic Retinopathy (PDR)
- 38. PROLIFERATIVE DIABETIC RETINOPATHY (PDR) 38 • Management/Treatment –2-4 month follow-up –Color fundus photography –Panretinal photocoagulation (3-4 month follow-up) –Vitrectomy
- 41. HIGH-RISK PROLIFERATIVE DIABETIC RETINOPATHY At risk for serious vision loss Any combination of three of the following four findings • NVD <1/4 disc area with vitreous or preretinal hemorrhage. • NVE > 1/2 disc area with vitreous or preretinal hemorrhage. • NVD 1/4 to 1/3 disc area with or without vitreous or preretinal hemorrhage. 41
- 42. DIABETIC MACULAR EDEMA • Diabetic macular edema is the leading cause of legal blindness in diabetics. • Diabetic macular edema can be present at any stage of the disease, but is more common in patients with proliferative diabetic retinopathy. 42
- 43. 43 Meta analysis and review on the effect on bevacizumab in diabetic macular edema Graefes Arch Clin Exp Ophthalmol(2011) 249:15-27
- 44. WHY IS DIABETIC MACULAR EDEMA SO IMPORTANT? 44 • The macula is responsible for central vision. • Diabetic macular edema may be asymptomatic at first. • As the edema moves in to the fovea (the center of the macula) the patient will notice blurry central vision. • The ability to read and recognize faces will be compromised. Macula Fovea
- 45. 45 • Normal • Macular Edema
- 46. CLINICALLY SIGNIFICANT DIABETIC MACULAR EDEMA (CSDME) • Thickening of the retina at or within 500 µm of the center of the macula. • Hard exudates at or within 500 µm of the center of the macula, if associated with thickening of the adjacent retina. • Area of retinal thickening 1 46
- 47. 47 Imaging of macular edema with optical coherence tomography
- 48. 48 OCT BASED CLASSIFICATION OF DME
- 49. 49
- 50. ISCHAEMIC MACULOPATHY • Maculopathy in type 1 diabetics is often due to drop out of the perifoveal capillaries with non perfusion. • Enlargement of the foveal avascular zone (FAZ) is frequently seen on fluorescein angiography. • Ischaemic maculopathy is not uncommon in type 2 diabetics • Maculopathy in this group may show both changes due to ischaemia and retinal thickening. 50
- 51. ADVANCED DIABETIC EYE DISEASE • Persistent vitreous haemorrhage • Diabetic tractional retinal detachment • Neovascular Glaucoma 51
- 52. Clinical Stages of Retinopathy Vitreous hemorrhage
- 53. LATE COMPLICATIONS 53 TRACTIONAL RETINAL DETACHMENT
- 54. Clinical Stages of Retinopathy New vessel growth
- 55. DIABETIC EYE DISEASE KEY POINTS • Treatments exist but work best before vision is lost 55 RECOMMENDED EYE EXAMINATION SCHEDULE Diabetes Type Recommended Time of First Examination Recommended Follow- up* Type 1 3-5 years after diagnosis Yearly Type 2 At time of diagnosis Yearly Prior to pregnancy (type 1 or type 2) Prior to conception and early in the first trimester No retinopathy to mild moderate NPDR every 3-12 months Severe NPDR or worse every 1-3 months. *Abnormal findings may dictate more frequent follow-up examinations h ttp://one.aao.org/CE/PracticeGuidelines/PPP_Content.aspx?cid=d0c853d3-219f-487b-a524-326ab3cecd9a
- 56. SCREENING FOR DIABETIC EYE PROBLEMS SHOULD IDEALLY INCLUDE THE FOLLOWING • The history of any visual symptoms or changes in vision • Measurement of visual acuity • Iris examination by slit lamp biomicroscopy prior to pupil mydriasis. • Pupil mydriasis. ( tropicamide 0.5 % • Patients should be accompanied by a relative and instructed not to drive home. • Examination of the crystalline lens • Fundus examination 56
- 57. PREVENTION http://www.aao.org/newsroom/release/20091030.cfm 57 90 percent of diabetic eye disease can be prevented simply by proper regular examinations, treatment and by controlling blood sugar.
- 58. Primary prevention Strict glycemic control Blood pressure control Secondary prevention Annual eye examination examination Tertiary prevention Retinal Laser photocoagulation Intravitreal Injections of Anti- VEGF Vitrectomy 58
- 59. DIABETIC RETINOPATHY TREATMENT 59 The best measure for prevention of loss of vision from diabetic retinopathy is strict glycemic control
- 60. LASER PHOTOCOAGULATION Laser Photocoagulation is recommended for eyes with: • Clinical significant macular edema CSME • High risk Proliferative diabetic retinopathy 60
- 61. Treatment
- 64. VITRECTOMY • Remove vitreous hemorrhage • Repair retinal detachment • Allow treatment with PRP
- 65. Treatment
- 66. CONCLUSIONS 66 Diabetic Retinopathy is preventable through strict glycemic control and annual dilated eye examination by an ophthalmologist.
- 67. HYPERTENSIVE RETINOPATHY • Hypertensive retinopathy refers to fundus changes occurring in patients suffering from systemic hypertension. 67
- 68. PATHOGENESIS 1.Vasoconstriction: It is the primary response of retinal arterioles to raised blood pressure. It reflects the severity of hypertension. 2.Atherosclerosis: It mainly occurs in older patients. It reflects the duration of hypertension. 3.Increased vascular permeability: It results from hypoxia and may result in retinal edema, exudates and hemorrhages 68
- 69. KEITH AND WEGNER GRADING (1939) • GRADE 1 : Tortuosity (twisting) of retinal arteries with increased reflectiveness (silver wiring) • GRADE 2 : Grade 1 + Arteriovenous napping (thickened retinal arteries pass over retinal veins) • GRADE 3 : Grade 2 + flamed shape haemorrhage and cotton wool exudates(due to small infarcts) • GRADE 4: Grade 3 + Papilledema (blurring of the optic disc due to swelling ) 69
- 70. 70
- 71. CLINICAL TYPES • Hypertension with involutionary (senile) sclerosis: In old age patients • Hypertension without sclerosis: In young patients exposed to raised BP for a short duration • Hypertension with compensatory arteriolar sclerosis: In young patients exposed to benign hypertension for a long duration (usually associated with benign nephrosclerosis; thus called renal retinopathy) • Malignant hypertension: Rapidly progressive and severe changes in fundus (marked vasoconstriction, papilloedema, flame shaped hemorrhage, cotton wool spots is seen; but papilloedema is an essential feature). 71
- 72. • Acute malignant hypertension will cause patients to complain of eye pain, headaches or reduced visual acuity. • Chronic arteriosclerotic changes from hypertension will not cause any symptoms alone. 72
- 73. DIAGNOSIS • Diagnosis is by history (duration and severity of hypertension) and fundoscopy. Sometimes, fluorescein angiography may be required. 73
- 74. MANAGEMENT • By itself, chronic hypertensive retinopathy rarely, if ever, results in significant loss of vision. Treatment of the underlying systemic condition can halt the progress of the retinal changes, but arteriolar narrowing and arteriovenous nicking usually are permanent. • Treatment of malignant hypertensive retinopathy consists of lowering blood pressure in a slow, deliberate, controlled fashion to prevent end-organ damage. • Too rapid a decline can lead to ischemia of the optic nerve head, brain and other vital organs, resulting in permanent damage. 74
- 75. MANAGEMENT • Drugs that are commonly used in the outpatient setting to reduce blood pressure include: • Angiotensin converting enzyme inhibitors, • Calcium channel blockers, v Diuretics, and V B-adrenergic blockers. • Very rarely, If vision loss occurs, treatment of the retinal edema with laser or with intravitreal injection of corticosteroids or antivascular endothelial growth factor drugs (eg, ranibizumab, pegaptanib, bevacizumab) may be useful. 75
- 76. THANK YOU ! 76