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Classification of severity of diabetic retinopathy Lesions presentSeverity Nonproliferative No retinal lesionsNo retinopathy No lesions other than microaneurysmsMicroaneurysms.

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Presentation on theme: "Classification of severity of diabetic retinopathy Lesions presentSeverity Nonproliferative No retinal lesionsNo retinopathy No lesions other than microaneurysmsMicroaneurysms."— Presentation transcript:

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3 Classification of severity of diabetic retinopathy Lesions presentSeverity Nonproliferative No retinal lesionsNo retinopathy No lesions other than microaneurysmsMicroaneurysms only Microaneurysms plus retinal hemorrhage,hard exudate Mild NPDR,venous loops, or both Mild NPDR plus cottonwool spots and/or IRMAModerate NPDR Presence of one of the following features:microaneurysms plus venous beading and/or H/MA ≥ Standard photograph 2A in four quadrants,or marked venous beading in two or more quadrants, or moderate IRMA(standard photograph 8A in one or more quadrants) Severe NPDR Two or more of the above features described in severe NPDRVery severe NPDR Proliferative New vessels and/or fibrous proliferations;or preretinal and/or vitreous hemorrhagePDR without HRC NVD≥standard photograph 10A;or less extensive NVD,if vitreous or preretinal hemorrhage is present;or NVE≥half disc area,if vitreous or preretinal hemorrhage is present PDR with HRC Extensive vitreous hemorrahage precluding grading,retinal detachment involving the macula,or phthisis bulbi or enucleation secondary to a complication of diabetic retinopathy Advanced PDR

4 SIMPLIFIED CLASSIFICATION OF DIABETIC RETINOPATHY ln an attempt to improve communication between the ophthalmologists and the primary care physicians caring for patients with diabetes and between clinicians worldwide, a recent international classification of diabetic retinopathy and macular edema was developed. This classification is based on the data collected in the clinical trials and epidemiologic studies of diabetic retinopathy and it simplifies the ETDRS classification of diabetic retinopathy for clinical. With the introduction of this new simplified scale, it is hoped that these systems will be valuable in improving both screening of individuals with diabetes and communication and discussion among individuals caring for these patients. ln an attempt to improve communication between the ophthalmologists and the primary care physicians caring for patients with diabetes and between clinicians worldwide, a recent international classification of diabetic retinopathy and macular edema was developed. This classification is based on the data collected in the clinical trials and epidemiologic studies of diabetic retinopathy and it simplifies the ETDRS classification of diabetic retinopathy for clinical. With the introduction of this new simplified scale, it is hoped that these systems will be valuable in improving both screening of individuals with diabetes and communication and discussion among individuals caring for these patients.

5 EPIDEMIOLOGY OF DIABETES AND DIABETIC RETINOPATHY The Centers for Disease Control estimate that 18.2 million American have diabetes and 5.2 million don't know they have it. Type 2 diabetes accounts for up to 95% of aIl diabetes cases,affecting 8% of the population aged 20 and older. Among the population 60 years and older, 18.6% are affected with diabetes. The prevalence of type 2 diabetes has tripled in the last 30 years, much of it due to an increase in obesity.

6 Among the estimated 10.2 million individuals in the USA older than 40 years of age and with known diabetes, the prevalence rates of diabetic retinopathy and vision-threatening diabetic retinopathy were 40.3% and 82%, respectively. This translates to 4.1 million adults over the age of 40 years having diabetic retinopathy; one in every 12 known persons with diabetes has severe visionthreatening diabetic retinopathy.

7 Data from population-based studies such as the Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) provide valuable information regarding both the prevalence and the risk factors associated with the development of diabetic retinopathy.

8 ln the younger-onset group, which consists of patients whose age at diagnosis of diabetes was less than 30 years and who were taking insulin at the time of the examination (presumably those with type 1 diabetes), retinopathy, either proliferative or nonproliferative, was seen in 13% of patients with less than a 5-year duration of diabetes and in 90% of patients with a duration of 10 to 15 years. ln the younger-onset group, which consists of patients whose age at diagnosis of diabetes was less than 30 years and who were taking insulin at the time of the examination (presumably those with type 1 diabetes), retinopathy, either proliferative or nonproliferative, was seen in 13% of patients with less than a 5-year duration of diabetes and in 90% of patients with a duration of 10 to 15 years.

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11 These rates increase to 84% and 53%, respectively, with an increased diabetes duration of 15 to 19 years. PDR develops in 2% of patients with type 2 diabetes and a duration less than 5 years and 25% of patients with a duration of 25 or more years of diabetes. These rates increase to 84% and 53%, respectively, with an increased diabetes duration of 15 to 19 years. PDR develops in 2% of patients with type 2 diabetes and a duration less than 5 years and 25% of patients with a duration of 25 or more years of diabetes.

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13 Severity of retinopathy As retinopathy progresses from the mild to moderate to severe and then very severe stages, the risk of developing PDR or visualloss also increases.

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16 For patients with bilateral moderate NPDR, the 4-year risk of progression to PDR was increased by 40-fold when compared with patients who had microaneurysms in only one eye.

17 Diabetic retinopathy disease severity scale Proposed disease severity level Finding 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 nonproliferative diabeticretinopathy Severe nonproliferative diabetic retinopathy Any of the following: More than 20 intraretinal hemorrhages in each of four quadrants Definite venous beading in more than two quadrants Prominent intrartinal microvascular abnormalities in more than one quadrant and no signs of proliferative retinopathy Proliferative diabetic retinopathy One or more of the following: Neovascularization Vitreous/preretinal hemorrhage Diabetic macular edema disease severity scale Proposed disease severity level Finding observable upon dilated ophthalmoscopy Diabetic macular edema apparently absent No apparent retinal thickening or hard exudates in posterior pole Diabetic macular edema apparently present Some apparent retinal thickening or hard exudates in posterior pole If diabetic macular edema is present,it can be categorized as follows: Proposed disease severity level Finding observable upon dilated ophthalmoscopy Diabetic macular edema present Mild diabetic macular edema Some retinal thickening or hard exudates in posterior pole but distant from the center of the macula Moderate diabetic macular edema Retinal thickening or hard exudates approaching the center of the macula but not involving the center Severe diabetic macular edema Retinal thickening or hard exudates involving the center of the macula

18 Glycemic control The relationship of glucose control and the chronic complications of diabetes has been extensively studied in observational studies. These studies all demonstrated that increased severity of diabetic retinopathy is associated with poorer glucose contral.

19 Randomized, controlled clinical trials of glycemic control were designed to address the causal role of glucose control in diabetic complications. ln the Diabetes Control and Complications Trial (DCCT),1441 patients with type 1 diabetes were randomly assigned to either conventional or intensive insulin treatment and followed for a period of 4 to 9 years.

20 Conventional treatment was characterized by one or two daily insulin injections, daily self- monitoring of urine or blood glucose, and diet and exercise education. Hemoglobin A 1c (HbA 1c ) values were not used to guide treatment, unless an upper limit of 13% was exceeded.

21 Intensive treatment consisted of insulin administered three or more times daily by injection or an external pump, with dose adjusted according to self-monitored blood glucose results performed at least four times per clay, as weIl as anticipated dietary intake and exercise, and with the goal of lowering HbA 1 c (measured monthly) to within the nondiabetic range (< 6.05%). Intensive treatment consisted of insulin administered three or more times daily by injection or an external pump, with dose adjusted according to self-monitored blood glucose results performed at least four times per clay, as weIl as anticipated dietary intake and exercise, and with the goal of lowering HbA 1 c (measured monthly) to within the nondiabetic range (< 6.05%).

22 The DCCT demonstrated that intensive insulin treatment is associated with a decreased risk of either the development or progression of diabetic retinopathy in patients with type 1 diabetes.

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24 The benefit of the strict control was also evident in patients with existing retinopathy (50% reduction in the rate of progression of retinopathy compared with controls). At 6- and 12-month visits, a small adverse effect of intensive treatment on retinopathy progression was seen, similar to that described in other trials of glucose control.

25 However, in eyes with little or no retinopathy at the time of initiating intensive glucose control, this early worsening of retinopathy is unlikely to threaten vision. When the DCCT results were stratified by hemoglobin A 1 C (HbA 1 C) levels, there was a 35% to 40% reduction in the risk of retinopathy progression for every 10% decrease in HbA 1 C (e.g., from 8% to 7.2%).

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27 With an additional 7 more years of foIlow-up when the HbA 1 Cs in both treatment groups were not statistically significant (8.1 % versus 8.2%, P = 0.09), the rate of progression of retinopathy remained statistically significantly less in those treated with the intensive therapy than in the conventional therapy.

28 The intensive glycemic control over a period of 6.5 years conferred benefits weIl beyond the period of treatment. These data have resulted in recommendations for achieving intense control with HbA 1 C level below 7% as soon as the diagnosis of diabetes is made.

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30 Findings in a study of Japanese patients with type 2 diabetes have shown that multiple insulin-injection treatment reduced the onset of retinopathy from 32% to 8% and reduced a two- step progression retinopathy from 44% to 19%, compared with people receiving conventional insulin treatments over 6 years.

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32 After 6 years of follow-up,a smaller proportion of patients in the intensive treatment group than in the conventional group had a two-step progression(worsening) in.diabetic retinopathy(P<0.01).

33 Epidemiologic analysis of the UKPDS data showed a continuous relationship between the risk of microvascular complications and glycemia,so for every percentage point decrease in HbA 1 C (e.g., 9% to 8%), there was a 35% reduction in the risk of microvascular complications.

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35 The findings of observational studies assessing the importance of blood pressure in the progressing of NPDR are inconsistent. Hypertension

36 However, in the UKPDS a randomized comparison of more intensive blood pressure control versus less intensive blood pressure control in persons with type 2 diabetes demonstrated that intensive blood pressure control was associated with a decreased risk of retinopathy progression

37 Tight blood pressure control resulted in a 37% reduction in microvascular diseases, predominantly reduced risk of retinal photocoagulation, when compared to less tight control.

38 A previously published study of blood pressure medication in diabetic retinopathy suggested that there might be a specific benefit of angiotensin-converting enzyme (ACE) inhibition and blood pressure reduction, even in normotensive persons, on the progression of diabetic retinopathy.

39 The UKPDS included a randomized comparison of beta- blockers and ACE inhibitors in the tight blood pressure control arm of that study. Benefits from tight blood pressure control were present in both the beta- blocker and ACE inhibitor treatment groups, with no statistically significant difference between them.

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41 The WESDR, a population-based study, and the ETDRS found that elevated levels of serum cholesterol were associated with increased severity of retinal hard exudate. Elevated serum lipid levels

42 ln dependent of the accompanying macular edema, the severity of retinal hard exudate at baseline was associated with decreased visual acuity in the ETDRS. The severity of retinal hard exudate was also a significant risk factor for moderate visual loss (15 letters or more loss) during the course of the study.

43 More recently, the DCCT investigators also evaluated the association of severity of retinopathy and retinal hard exudates with serum lipids.

44 They found that the severity of retinopathy was associated with increasing triglycerides and inversely associated with high-density lipoprotein cholesterol.

45 The NMR-LSP results showed an increasing severity of retinopathy with small and medium very-low- density lipoprotein and inversely with very-low- density lipoprotein size. These data support the potential role for dyslipoproteinemia in the pathogenesis of diabetic retinopathy.

46 Elevated serum triglyceride levels were also associated with a greater risk of developing high-risk PDR in the ETDRS patients.

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48 Although these are all observational findings, the data are compelling to recommend lowering elevated serum lipids in patients with diabetic retinopathy to reduce the risk of visual loss.

49 ln addition to reducing the risk of cardiovascular disease, reducing the risk of visual loss should be another motivating factor for patients to lower elevated serum lipids.

50 Pregnancy and diabetic retinopathy Diabetic retinopathy may be accelerated during pregnancy because of the pregnancy itself or the changes in metabolic control.

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52 Ideally, patients who are planning to become pregnant should have their eyes examined before they attempt to conceive and should make every attempt to lower their blood glucose levels to as near normal as possible for the health of the fetus, as well as their own health.

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54 Pregnant women with less than severe NPDR should be examined every 3 months, whereas those with more severe stages should be seen every 1 to 3 months, as recommended by the American Academy of Ophthalmology Preferred Practice Pattern.

55 Other systemic risk factors Diabetic nephropathy, as measured by albuminuria, proteinuria,or renal failure, is found to be a risk factor associated with progression of retinopathy in some, but not aIl, studies.

56 Anemia has also been reported tobe associated with progression ofdiabetic retinopathy in two smallcase series and two epidemiologicstudies.

57 There was a progressive increase in the risk of development of high-risk PDR with decreasing hematocrit in an adjusted multivariate model in the ETDRS.

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59 History of diabetic neuropathy and cardiovascular autonomic neuropathy have also been suggested to be associated with increased risk of progression of Retinopathy.

60 Eye examination schedule Routine minimum follow - up Recommended time for first examination Time of onset of diabetes mellitus Annually5 years after onset Less than 30 years of age AnnuallyAt time of diagnosisAge 30 and older At least every 3 months Before or soon after conception Before pregnancy

61 Recommended follow-up schedule Status of retinopathyFollow-up(months) No retinopathy or microaneurysms only 12 Mild/moderate NPDR without macular edema6-12 Mild/moderate NPDR with macular edema that is not clinically significant4-6 Mild /moderate NPDR with clinically significant macular edema 3-4 Severe/very severe NPDR3-4

62 Diabetes Control and Complication trial: rates of progression from nonproliferative diabetic retinopathy to proliferative diabetic retinopathy and crude relative risks (RRs),by follow-up time period Time period (years) Conventional(C) rate (cases/person-years)* Intensive(I)rate (cases/person-years)* Crude RR,I:C (3/351)0.55(2/362) (11/688)1.41(10/711) (12/646)0.88(6.681) (20/504)0.69(4/580)0.17 Modified from Diabetes Control and Complications Trial Research Group. The effect of intensive diabetes treatment on the progression of diabetic retinopathy in insulindependent diabetes mellitus. Arch Ophthalmol1995; 113: *Rates in cases per 100 person-years at risk.

63 Early* worsening(EW) in Diabetes Control and Complications Trial patients assigned to intensive treatment Clinically important EW‡CWS/IRMA EW† Baseline retinopathy severity No. (%) with EWNo. of patientsNo. (%) with EWNo. of patients 0(0.0)3484(1.1)348No retinopathy 0(0.0)14014(10.0)140MA only, one eye 2(1.8)10924(22.0)109MA only, both eyes 6(7.3)8229(48.3)60Mild NPDR 6(18.8)32NANA§Moderate NPDR Modified from Diabetes Control and Complications Trial Research Group. Early worsening of diabetic retinopathy in the diabetes control and complications trial. Arch Ophthalmol1998; 116: CWS, Cottonwool spot; IRMA, intraretinal microvascular abnormalities; MA, microaneurysms; NPDR, nonproliferative diabetic retinopathy. *Within 6 to 12 months of beginning intensive treatment. †Cottonwool spots or intraretinal microvascular abnormalities. ‡Development of macular edams or of proliferative diabetic retinopathy or severe NPDR. §Not applicable; CWS/lRMA at baseline..

64 Indications for photocoagulation Treatment should be carried out promptly in most eyes with PDR that have well-established NVD or vitreous or preretinal hemorrhage. Treatment is particularly urgent when localized fresh vitreous or preretinal hemorrhage is present because of the risk that dispersion of the hemorrhage throughout the vitreous or recurrent bleeding may soon make treatment more difficult or impossible.

65 When visible or suspected new vessels seem insufficient to explain the hemorrhage, special consideration should be given to other possible causes, such as fresh retinal tears, partially avulsed retinal veins, or small patches of new vessels that have been completely avulsed from the disc or retina.

66 Complete avulsion of a small new vessel patch from its connections to the disc or retina should be considered as a possible explanation of a recent vitreous hemorrhage when the detached posterior vitreous surface can be seen anterior to the disc or retina and contains a subtle opacity, suggesting a small patch of empty new vessels. This occurrence is uncommon, but not rare, and has a good prognosis. Usually no trace can be seen on the disc or retina of the previous new vessel patch and no treatment is necessary.

67 Progressive contraction of fibrous proliferations leading to displacement or detachment of the macula sometimes follows scatter photocoagulation for high-risk characteristics in eyes with extensive fibrous proliferations.

68 Few such eyes were included in the DRS, but analyses of them indicated that outcome was better with photocoagulation than without it and suggested that it is only excessively heavy treatment that should be avoided.

69 When high-risk characteristics are definitely present, scatter photocoagulation should usually be carried out, despite the presence of fibrous proliferations or localized traction retinal detachment. Areas of fibrous proliferations and retinal detachment should be avoided, and treatment strength should be mild to moderate. It may be desirable to divide treatment between several episodes.

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71 Extensive neovascularization in the anterior chamber angle is a strong indication for scatter photocoagulation, if it is feasible, regardless of the presence of high-risk characteristics. Remarkable regression of these new vessels often occurs soon after scatter photocoagulation; if this treatment is carried out before extensive closure of the angle has occurred, full-blown neovascular glaucoma can be prevented.

72 When opacities of the media preclude retinal photocoagulation, cryoapplications or vitrectomy with endophotocoagulation may be used, with or without additional direct photocoagulation of the new vessels in the anterior chamber angle.

73 The presence of extensive retinal hemorrhage, IRMAs, venous beading, and opaque small arteriolar branches, often accompanied by prominent soft exudates, suggests rapidly progressive closure of the retinal capillary bed and severe retinal ischemia. New vessels are usually present in such eyes but may be relatively unimpressive. Severe retinal ischemia increases the urgency to initiate scatter photocoagulation, whether or not DRS high-risk characteristics are present, since eyes so affected appear to be at greater risk of anterior segment neovascularization.

74 Patients should be aware of this risk and the risk of a sudden decrease in central vision, which may occur with occlusion of the remaining arterioles supplying the macula. The clinical impression that scatter photocoagulation may precipitate such an occlusion has led to the suggestion that initial scatter treatment be divided between three or four episodes in the hope of reducing this risk.

75 The ETDRS recommended that scatter, treatment not be used in eyes with mild to moderate NPOR but that it be considered for eyes approaching the high-risk stage (i.e., eyes with very severe NPDR or moderate PDR) and that it usually should not be delayed when the high-risk stage is present. The ETDRS recommended that scatter, treatment not be used in eyes with mild to moderate NPDR but that it be considered for eyes approaching the high-risk stage (i.e., eyes with very severe NPDR or moderate PDR) and that it usually should not be delayed when the high-risk stage is present.

76 A policy of continued observation would be expected to spare only a minority of eyes from the risks of treatment, while increasing the risk that rapid progression might occur between follow-up visits and that entry into the high-risk stage might be marked by occurrence of a large vitreous hemorrhage, making satisfactory treatment difficult. In choosing between prompt treatment and deferral, the commitment of the patient to careful follow-up and the state of the fellow eye are important factors.

77 If visual function decreased in the fellow eye after scatter photocoagulation, deferral of treatment in the second eye may be desirable. On the other band, in a patient whose first eye had an unfortunate outcome without photocoagulation or one with photocoagulation only after PDR was advanced, prompt treatment may be preferable, particularly if close follow-up will be difficult.

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79 In the type 2 group, the 5-year rate of severe visual loss or vitrectomy was about 5% in eyes assigned to early photocoagulation versus 13% in eyes assigned to deferral, whereas in the type 1 group the rates were about 8% in both treatment groups.

80 Greater responsiveness to photocoagulation in older versus younger patients has also been observed in other studies.

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82 If photocoagulation is deferred until high-risk characteristics develop, and this occurs in the later stages of pregnancy or when renal transplantation or dialysis is required, these more pressing problems may make it difficult to complete photocoagulation according to a schedule considered optimal from the ophthalmologic point of view. As already mentioned.

83 Scatter photocoagulation and macular edema Macular edema sometimes increases, at least temporarily, after scatter photocoagulation, and this may be followed by transient or persistent reduction of visual acuity.

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85 If a delay of scatter treatment seems undesirable, the ETDRS protocol can be used, combining focal/grid treatment for macular edema with scatter treatment in the nasal quadrants at the first episode of photocoagulation and adding scatter in the temporal quadrants at one or more subsequent episodes.

86 Certainly, scatter treatment should not be delayed when the risks of vitreous hemorrhage or neovascular glaucoma seem high, regardless of the status of the macula.

87 Number of episodes used for scatter treatment The new technique of optical coherence tomography was used in a recent study comparing shorter versus longer spacing between episodes of scatter photocoagulation.

88 Among the techniques currently in use, the number of episodes in which initial scatter treatment is carried out varies from one to four or more. Those techniques using a smaller number of larger burns tend toward a single episode with retrobulbar anesthesia, whereas those using a larger number of smaller burns nearly always divide treatment into two or more episode.

89 Multiple episodes make it easier to avoid retrobulbar anesthesia and its occasional complications, but they may cause delays and inconvenience for patients who must travel Iong distances for treatment. Angle-closure glaucoma secondary to serous detachment of the peripheral choroid and ciliary body is less common when scatter treatment is carried out in two or more sessions over a period of 1 or 2 weeks, and some observers believe that small losses in visual acuity may also be less common.

90 Thirty-six patients with severe nonproliferative or early proliferative retinopathy and 20/20 vision in each eye at baseline received scatter photocoagulation in the following manner: in one eye, one quadrant was treated every week for 4 weeks and in the other eye, one quadrant was treated every other week for 8 weeks.

91 OCT assessment of macular thickness was performed at baseline, before each session of photocoagulation, and at 16 weeks, the end of the follow-up period. Four of 36 eyes in the weekly treatment group and 3 of 36 in the biweekly group developed center-involved macular edema with decreased visual acuity (from 20/40 to 20/200), which was treated with photocoagulation.

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93 The increase was less after the biweekly treatments and at 16 weeks was closer to, but had not reached, the baseline value. There was little change in retinal thickness outside the central zone with either treatment technique.

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