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diabetic_retinopathy.ppt
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- 2. Acknowledgement ◦ Photographs inthis presentation are courtesy of Dr.J J Kanski ( Kanski JJ et al: Retinal vascular disease. In: Kanski JJ et al, eds: Synopsis of Clinical Ophthalmology. 3rd ed. Philadelphia, PA: Saunders; 2013:241-65.) 2
- 3. Diabetes and eyedisease – Learning Objectives ◦ At the end of the class, students shall be able to ◦ Recognize the importance of diabetic retinopathy as a public health problem ◦ Identify the risk factors for diabetic retinopathy ◦ Describe and distinguish between the stages of diabetic retinopathy ◦ Understand the role of risk factor control and annual dilated eye examinations in the prevention of vision loss 3
- 4. Diabetes Mellitus Diabetes Mellitusis 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. 4
- 5. Diabetic Retinopathy (DR) Definition ◦Progressivedysfunction 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. 5
- 6. Diabetic Retinopathy Epidemiology ◦The totalnumber 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. 6
- 7. Risk factors forDiabetic Retinopathy 7
- 8. 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. 8
- 9. Other Risk factors 9 •Poor Blood Sugar control • Hypertension • Hyperlipidemia • Pregnancy • Nephropathy • Others: Smoking, Obesity, Anemia
- 10. Pathogenesis of DiabeticMicro 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 rglaucoma Microvascular Occlusion Fibrovascular bands Vitreous hemorrhage Increased VEGF Tractional retinal detachment Infarction 11
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- 15. Diabetic retinopathy symptoms Asymptomatic inearly 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 ofDiabetic Retinopathy ◦Mild nonproliferative diabetic retinopathy (NPDR) ◦Moderate NPDR ◦Severe NPDR ◦Very Severe NPDR ◦Proliferative diabetic retinopathy (PDR) 16
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- 19. Histology of retina 19 1RPE 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
- 20. Microaneurysms 20 • Focal dilatationsof 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
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- 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 •Occlusionof 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.
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- 28. Late non proliferativechanges 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 proliferativechanges 29
- 30. 30 Clinical Findings ◦Microaneurysms ◦Management/Treatment ◦Annual follow-up MILDNONPROLIFERATIVE DIABETIC RETINOPATHY
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- 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) 33 Hard exudates Flamed shaped hemorrhage Microaneurysm
- 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 DiabeticRetinopathy (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) 36 Venous beading
- 37. 37 ◦Clinical Findings ◦Ischemia inducedneovascularization ◦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
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- 41. High-Risk Proliferative diabeticretinopathy 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 andreview on the effect on bevacizumab in diabetic macular edema Graefes Arch Clin Exp Ophthalmol(2011) 249:15-27
- 44. Why is Diabeticmacular 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 Diabeticmacular 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 disc area or larger, within 1 disc diameter of the center of 46
- 47. 47 Imaging of macularedema with optical coherence tomography
- 48. Ischaemic Maculopathy • Maculopathyin 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. 48
- 49. Advanced diabetic eyeDisease • Persistent vitreous haemorrhage • Diabetic tractional retinal detachment • Neovascular Glaucoma 49
- 50. Clinical Stages ofRetinopathy Vitreous hemorrhage
- 51. Late Complications 51 TRACTIONAL RETINALDETACHMENT
- 52. Clinical Stages ofRetinopathy New vessel growth
- 53. Diabetic Eye Disease KeyPoints •Treatments exist but work best before vision is lost 53 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
- 54. Screening for diabeticeye 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 54
- 55. PREVENTION http://www.aao.org/newsroom/release/20091030.cfm 55 90 percent ofdiabetic eye disease can be prevented simply by proper regular examinations, treatment and by controlling blood sugar.
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- 57. DIABETIC RETINOPATHY TREATMENT Thebest measure for prevention of loss of vision from diabetic retinopathy is strict glycemic control 57
- 58. Laser Photocoagulation Laser Photocoagulationis recommended for eyes with: ◦ Clinical significant macular edema CSME ◦ High risk Proliferative diabetic retinopathy 58
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- 62. VITRECTOMY •Remove vitreous hemorrhage •Repair retinal detachment •Allowtreatment with PRP
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- 64. CONCLUSIONS Diabetic Retinopathy is preventablethrough strict glycemic control and annual dilated eye examination by an ophthalmologist. 64