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DIABETIC RETINOPATHY-postgraduate teaching.pptx
- 1. DIABETIC RETINOPATHY PRESENTER:DR.MUGABI BARNABAS MODERATOR:DR.AMPAIREANNE MUSIKA 23RD/10/2023
- 2. OUTLINE • ETIOLOGY • ANATOMY •EPIDEMIOLOGY • PATHOPHYSIOLOGY • RISK FACTORS • CLASSIFICATION • DIABETIC MACULAR EDEMA • DIABETIC MACULOPATHY • CLINICAL PICTURE • IMAGING • TREATMENT
- 3. DIABETES MELLITUS • Diabetesmellitus is a group of metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both • The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.
- 4. Types of DM •Type 1 diabetes (β-cell destruction, usually leading to absolute insulin deficiency) • Type 2 diabetes ( insulin resistance with relative insulin deficiency )
- 5. OPHTHALMIC COMPLICATIONS OFDIABETES COMMON • RETINOPATHY • IRIDOPATHY • UNSTABLE REFRACTION. UNCOMMON • RECURRENT STYES • XANTHELASMA • ACCELERATED AGE-RELATED CATARACT • NEOVASCULAR GLAUCOMA (NVG) • OCULOMOTOR NERVE PALSIES. REDUCED CORNEAL • SENSITIVITY
- 6. • RARE • PAPILLOPATHY, •PUPILLARY LIGHT-NEAR DISSOCIATION • WOLFRAM SYNDROME • ACUTE- ONSET CATARACT • RHINO-ORBITAL MUCORMYCOSIS.
- 7. DEFINITION OF DIABETICRETINOPATHY • Diabetic retinopathy is a chronic progressive, potentially sight- threatening disease of the retinal microvasculature associated with the prolonged hyperglycaemia and other conditions linked to diabetes mellitus such as hypertension.
- 8. What is TheRetina? • The retina is a multilayered, light sensitive neural tissue lining the inner eye ball. Light is focused onto the retina and then transmitted to the brain through the optic nerve. • The macula is a highly sensitive area in the center of the retina, responsible for central vision.
- 11. PATHOPHYSIOLOGY • Diabetic Retinopathyis a microvasculopathy that causes: • Retinal capillary occlusion • Retinal capillary leakage
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- 14. RISK FACTORS • Nonmodifiable • Duration and age at onset • Puberty • Modifiable Risk Factors • Diabetic control/ HbA1c • Hypertension • Pregnancy • OTHERS : Hyperlipidemia, Smoking, Obesity
- 15. Risk factors DiabeticRetinopathy 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
- 16. Type 1 DM DURATION(YRS) DR PDR AFTER 5 YRS 25% AFTER 10 YRS 60% AFTER 15 YRS 80% AFTER 20-30 YRS 95% 30- 50%
- 17. Type 2 DM DURATION(YRS) DR PDR Yanko et al. 11-13 23% 3% ≥16 60% Klein et al. 10 67% 10% PDR will develop in 2% of patients if duration of DM is < 5 years and 25% if > 25 years
- 18. Puberty • Pre pubertalchildren (< 12 yrs) rarely develop complications of diabetes. • Puberty is a risk factor for developing retinopathy because of the physiological increased resistance to insulin. • Klein et al found that diabetes duration post menarche was associated with 30% increase risk or retinopathy compared with diabetes duration before menarche.
- 19. HbA1c DCCT showed inT1DM: Tight control had 76% reduction in rate of developments of DR ( primary prevention cohort) and 54% reduction in progression of established DR ( secondary intervention cohort) as compared to conventional treatment group
- 20. HbA1c • The DCCT: every 1% decrease in HbA1C level decrease the incidence of diabetic retinopathy by 28% . • Target HbA1c value of 6 - 7%
- 21. Hypertension • HTN iscommon in patients with T2DM. • Target BP <140/80 mm hg • Tight control appears to be particularly beneficial in T2DM with maculopathy.
- 22. Pregnancy • Gestational diabetesdoes not require an eye examination during pregnancy and does not increase the risk of diabetic retinopathy. • Diabetic retinopathy can worsen during pregnancy • Macular edema in pregnant patients can improve with delivery • Diabetic retinopathy in a pregnant patient is not a contraindication for natural vaginal delivery.
- 23. Pregnancy PREGNANT DIABETIC WOMENRISK OF DEVELOPMENT REMARKS WITHOUT DR NPDR 10% NPDR PDR 4% UNTREATED PDR REQUIRE - PAN RETINAL PHOTOCOAGULATION (PRP) TREATED PDR USUALLY DOES NOT WORSEN
- 24. ETDRS NSE SDRGSAAO INTERNATIONAL None R0 none R0 none No apparent retinopathy Microaneurysm only R1 background R1 mild background Mild NPDR Mild NPDR Mod NPDR Moderate NPDR R2 preproliferative R2 moderate BDR Moderately severe NPDR Severe NPDR R3 severe BDR Severe NPDR Very severe NPDR
- 25. NO DR • DESCRIPTION Noevidence of retinal vascular disease • FOLLOW-UP Yearly with dilated funduscopic exams
- 26. MILD NPDR • DESCRIPTION •ETDRS: ≥ 1 microaneurysm with no other findings • Kanski:Any or all : microaneurysms, retinal hemorrhages, exudates, cotton wool spots, up to the level of moderate NPDR with no IRMAs or venous beading • FOLLOW-UP 6-12 months with dilated funduscopic exam There are a few cotton-wool spots and intraretinal hemorrhages in this photograph, which doesn't really fit the ETDRS/International classification for true mild NPDR. Might still mild NPDR, because while there are multiple hemorrhages and cotton-wool spots, there are still < 20 per quadrant. Published in: Community Eye Health Journal Vol. 24, No. 75, September 2011
- 28. MODERATE NPDR DESCRIPTION • Anyof the following: • ≥ 20 intraretinal hemorrhages in 1-3 quadrants • Venous beading in no more than 1 quadrant • Presence of mild intraretinal microvascular abnormalities (IRMAs) in no more than 1 quadrant • Cotton-wool spots commonly present. • FOLLOW-UP • 6 months with dilated funduscopic exam • PROGNOSIS • PDR in up to 26% and high risk PDR in up to 8% within a year.
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- 32. Cotton-wool spots Fig :Cotton-wool spots and IRMA,
- 33. SEVERE NPDR DESCRIPTION • Oneof the following (4-2-1 rule): 4 quadrants of ≥ 20 hemorrhages ≥ 2 quadrants of venous beading ≥ 1 quadrant of IRMAs FOLLOW-UP 4 months with dilated funduscopic exam PROGNOSIS PDR in up to 50% and high risk PDR in up to 15% within a year.
- 34. VERY SEVERE NPDR •DESCRIPTION • ≥ 2 of the 4-2-1 criteria • FOLLOW-UP • 2-3 months with dilated funduscopic exam • PROGNOSIS • High-risk PDR in up to 45% within a year. cotton-wool, spots, IRMA, and venous beading
- 35. PROLIFERATIVE DIABETIC RETINOPATHY •Proliferative diabetic retinopathy (PDR) is characterized by neovascularization arising from the optic disc and retina, which may cause preretinal and vitreous hemorrhage.
- 36. Proliferative diabetic retinopathy Mild– moderate PDR • NVD <1/3 disc area • NVE <1/2 disc area • (NVD or NVE :insufficient to meet high risk criteria) High risk PDR • NVD > 1/3 disc area • Any NVD with vitreous haemorrhage • NVE > 1/2 disc area with vitreous haemorrhage
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- 41. ADVANCED DIABETIC EYEDISEASE • Hemorrhage : • Preretinal hemorrhage ( retrohyaloid), • Intragel haemorrhage or • Both • Tractional retinal detachment • Rubeosis iridis
- 42. ADVANCED DIABETIC EYEDISEASE
- 43. 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.
- 45. Why is Diabeticmacular edema so important? • 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.
- 46. International Clinical DiabeticMacular Edema Disease Severity Scale Proposed disease severity level Findings observable upon dilated ophthalmoscopy DME apparently absent No apparent retinal thickening or hard exudates in posterior pole DME apparently present Some apparent retinal thickening or hard DME present exudates in posterior pole Mild DME (some retinal thickening or hard exudates in posterior pole but distant from the center of the macula) Moderate DME (retinal thickening or hard exudates approaching the center of the macula but not involving the center) Severe DME (retinal thickening or hard exudates involving the center of the macula)
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- 48. Clinically Significant MacularEdema • Retinal thickening located at or within 500 μm of the center of the macula • Hard exudates at or within 500 μm of the center if associated with thickening of adjacent retina • A zone of thickening larger than 1 disc area (1500 μm) if located within 1 disc diameter of the center of the macula
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- 50. DIABETIC MACULOPATHY (DM) DMis further classified as: • Focal maculopathy • Diffuse maculopathy • Ischaemic maculopathy • Mixed
- 51. Focal maculopathy DESCRIPTION • Wellcircumscribed • Retinal thickening • Complete/incomplete ring of • FA : • Late, focal hyperfluorescence • Good macular perfusion
- 53. Diffuse maculopathy DESCRIPTION: • Diffuse •Retinal thickening • Cystoid changes • Scattered microaneurysms • Small hemorrhages FA : • Mid to Late, diffuse hyperfluorescence
- 55. Ischaemic maculopathy • DESCRIPTION •Macula may look relatively normal • Reduced visual acuity • PPDR may be present • FA : Capillary non-perfusion at fovea, posterior pole and periphery
- 56. RECOMMENDED EYE EXAMINATION SCHEDULE DiabetesType Recommended Initial Evaluation Recommended Followup* Type 1 5 years after diagnosis Yearly Type 2 At time of diagnosis Yearly pregnancy (type 1 or type 2) Soon after conception and early in the first trimester No retinopathy-mild or moderate NPDR: every 3-12 months Severe NPDR or worse: every 1-3 months Abnormal findings may dictate more frequent follow-up examinations
- 57. SYMPTOMS • Asymptomatic • Decreasedvision • Floaters • Metamorphopsia • Symptoms of retinal detachment
- 58. OCULAR EXAMINATION • Visualacuity • Intraocular pressure • Slit lamp biomicroscopy • Gonioscopy before dilating pupils • Funduscopic examination of the posterior pole under dilated pupil • Examination of peripheral retina and vitreous under dilated pupil
- 59. IMAGING • Digital photography •Fluorescein angiography • optical coherence tomography (oct)
- 60. TREATMENT OF DIABETICRETINOPATHY • Effective in 90% of cases to prevent severe visual loss • Good glycemic control • Adequate control of hypertension • Encourage changes in lifestyles • Treatment options Laser therapy Anti-VEGF drugs (ranibizumab, aflibercept, bevacizumab) Surgery
- 61. Treatment of diabeticretinopathy • HbA1c target (6.5-7.5%). • NPDR with T2DM : Add fenofibrate with statin • Macular edema : No pioglitazone • Systolic BP ≤130mmHg : Retinopathy and/or nephropathy • Systolic BP < 140mmHg : Without retinopathy, • Pregnancy : No statin • (Diabetic patients planning pregnancy should be informed on the need for assessment of diabetic retinopathy before and during pregnancy; Tropicamide alone should be used if mydriasis is required during pregnancy )
- 62. Treatment of diabeticretinopathy DIABETIC PREGNANT WOMEN 1ST ANTENATAL VISIT 2ND VISIT AT (FOLLOW UP) NO DR 28 WEEKS DR 16-20 WEEKS PPDR DURING PREGNANCY AT LEAST 6 MONTHS FOLLOWING DELIVERY (Macular edema in pregnant patients can improve with delivery, no intravitreal anti-VEGF is recommended. Consider intravitreal steroids.)
- 63. Treatment of diabeticmacular edema • Laser Therapy • Focal laser : FDA approved based on ETDRS findings Micropulse laser • Anti-VEGF Drugs • Aflibercept • Ranibizumab • Bevacizumab *Anti-VEGF injections are considered the new gold standard of therapy for eyes with centre- involving macular oedema and reduced vision
- 64. Treatment of diabeticmacular edema • Steroids Intravitreal Injections Intravitreal implants Ozurdex (Dexamethasone) Iluvien (FlucinoloneAcetonide) • Surgery Consider in cases of vitreomacular traction Tractional retinal detachment
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