- •Diabetic Retinopathy
- •Preface
- •Acknowledgments
- •Contents
- •Contributors
- •Pathophysiology of Diabetic Retinopathy
- •1.1 Retinal Anatomy
- •1.1.1 History
- •1.1.2 Anatomy
- •1.1.3 Microanatomy of the Retina Neurons
- •1.1.4 Intercellular Spaces
- •1.1.5 Internal Limiting Membrane
- •1.1.6 Circulation
- •1.1.7 Arteries
- •1.1.8 Veins
- •1.1.9 Capillaries
- •1.2 Hemodynamics, Macular Edema, and Starling’s Law
- •1.3 Biochemical Basis for Diabetic Retinopathy
- •1.3.1 Increased Polyol Pathway Flux
- •1.3.2 Advanced Glycation End Products (AGEs)
- •1.3.3 Activation of Protein Kinase C (PKC)
- •1.3.4 Increased Hexosamine Pathway Flux
- •1.4 Macular Edema
- •1.5 Development of Proliferative Diabetic Retinopathy
- •1.6 Summary of Key Points
- •1.7 Future Directions
- •References
- •Genetics and Diabetic Retinopathy
- •2.1 Background for Clinical Genetics
- •2.2 The Role of Polymorphisms in Genetic Studies
- •2.3 Types of Genetic Study Design
- •2.4 Studies of the Genetics of Diabetic Retinopathy
- •2.4.1 Clinical Studies
- •2.4.2 Molecular Genetic Studies
- •2.4.3 EPO Promoter
- •2.4.4 Aldose Reductase Gene
- •2.4.5 VEGF Gene
- •2.5 Genes in or Near the HLA Locus
- •2.6 Receptor for Advanced Glycation End Products (RAGE) Genes
- •2.7 Endothelial NOS2 and NOS3 Genes
- •2.9 Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 1 Gene (SLC2A1)
- •2.11 Potential Value of Identifying Genetic Associations with Diabetic Retinopathy
- •2.12 Summary of Key Points
- •2.13 Future Directions
- •Glossary
- •References
- •Epidemiology of Diabetic Retinopathy
- •3.1 Introduction and Definitions
- •3.2 Epidemiology of Diabetes Mellitus
- •3.3 Factors Influencing the Prevalence of Diabetes Mellitus
- •3.4 Epidemiology of Diabetic Retinopathy
- •3.5 Diabetes and Visual Loss
- •3.6 Prevalence and Incidence of Diabetic Retinopathy
- •3.7 By Diabetes Type
- •3.8 By Insulin Use
- •3.10 By Duration of Diabetes Mellitus
- •3.11 By Ethnicity
- •3.12 Gender
- •3.13 Age at Onset of Diabetes
- •3.14 Socioeconomic Status and Educational Level
- •3.15 Family History of Diabetes
- •3.16 Changes Over Time
- •3.17 Epidemiology of Diabetic Macular Edema (DME)
- •3.18 Epidemiology of Proliferative Diabetic Retinopathy (PDR)
- •3.19 Socioeconomic Impact of Diabetes
- •3.20 Socioeconomic Impact of Diabetic Retinopathy
- •3.21 Summary of Key Points
- •3.22 Future Directions
- •References
- •Systemic and Ocular Factors Influencing Diabetic Retinopathy
- •4.1 Introduction
- •4.2 Systemic Factors
- •4.2.1 Glycemic Control
- •4.2.1.1 Type 1 Diabetes Mellitus
- •4.2.1.2 Type 2 Diabetes Mellitus
- •4.2.1.3 Rapidity of Improvement in Glycemic Control
- •4.2.2 Glycemic Variability
- •4.2.3 Insulin Use in Type 2 Diabetes
- •4.2.5 Blood Pressure
- •4.2.6 Serum Lipids
- •4.2.7 Anemia
- •4.2.8 Nephropathy
- •4.2.9 Pregnancy
- •4.2.10 Other Systemic Factors
- •4.2.11 Influence on Visual Loss
- •4.3 Effects of Systemic Drugs
- •4.3.1 Diuretics
- •4.3.3 Aldose Reductase Inhibitors
- •4.3.4 Drugs That Target Platelets
- •4.3.5 Statins
- •4.3.6 Protein Kinase C Inhibitors
- •4.3.7 Thiazolidinediones (Glitazones)
- •4.3.8 Miscellaneous Drugs
- •4.4 Ocular Factors Influencing Diabetic Retinopathy
- •4.6 Economic Consequences
- •4.7 Summary of Key Points
- •4.8 Future Directions
- •References
- •Defining Diabetic Retinopathy Severity
- •5.1 Summary of Key Points
- •5.2 Future Directions
- •5.3 Practice Exercises
- •References
- •6.1 Optical Coherence Tomography (OCT)
- •6.2 Heidelberg Retinal Tomograph (HRT)
- •6.3 Retinal Thickness Analyzer (RTA)
- •6.4 Microperimetry
- •6.5 Color Fundus Photography
- •6.6 Fluorescein Angiography
- •6.7 Ultrasonography
- •6.8 Multifocal ERG
- •6.9 Miscellaneous Modalities
- •6.10 Summary of Key Points
- •6.11 Future Directions
- •6.12 Practice Exercises
- •References
- •Diabetic Macular Edema
- •7.1 Epidemiology and Risk Factors
- •7.2 Pathophysiology and Pathoanatomy
- •7.2.1 Anatomy
- •7.3 Physiology
- •7.4 Clinical Definitions
- •7.5 Focal and Diffuse Diabetic Macular Edema
- •7.6 Subclinical Diabetic Macular Edema
- •7.7 Refractory Diabetic Macular Edema
- •7.8 Regressed Diabetic Macular Edema
- •7.9 Recurrent Diabetic Macular Edema
- •7.10 Methods of Detection of Diabetic Macular Edema
- •7.11 Case Report 1
- •7.12 Case Report 2
- •7.13 Other Ancillary Studies in Diabetic Macular Edema
- •7.14 Natural History
- •7.15 Treatments
- •7.15.1 Metabolic Control and Effects of Drugs
- •7.16 Focal/Grid Laser Photocoagulation
- •7.16.1 ETDRS Treatment of CSME
- •7.17 Evolution in Focal/Grid Laser Treatment Since the ETDRS
- •7.18 Macular Thickness Outcomes After Focal/Grid Photocoagulation
- •7.19 Resolution of Lipid Exudates After Focal/Grid Laser Photocoagulation
- •7.20 Inconsistency in Defining Refractory Diabetic Macular Edema
- •7.21 Alternative Forms of Laser Treatment for Diabetic Macular Edema
- •7.22 Peribulbar Triamcinolone Injection
- •7.23 Intravitreal Triamcinolone Injection
- •7.24 Intravitreal Dexamethasone Delivery System
- •7.27 Combined Intravitreal and Peribulbar Triamcinolone and Focal Laser Therapy
- •7.28 Vitrectomy
- •7.29 Supplemental Oxygen and Hyperbaric Oxygenation
- •7.30 Resection of Subfoveal Hard Exudates
- •7.31 Subclinical Diabetic Macular Edema
- •7.32 Cases with Simultaneous Indications for Focal and Scatter Laser Photocoagulation
- •7.34 Factors Influencing Treatment of Diabetic Macular Edema
- •7.35 Sequence of Therapy
- •7.36 Interaction of Cataract Surgery and Diabetic Macular Edema
- •7.37 Summary of Key Points
- •7.38 Future Directions
- •References
- •Diabetic Macular Ischemia
- •8.1 Introduction
- •8.2 Pathogenesis, Anatomy, and Physiology
- •8.3 Natural History
- •8.4 Clinical Evaluation
- •8.5 Clinical Significance of Diabetic Macular Ischemia
- •8.6 Controversies and Conundrums
- •8.7 Summary of Key Points
- •8.8 Future Directions
- •References
- •Treatment of Proliferative Diabetic Retinopathy
- •9.1 Introduction
- •9.2 Laser Photocoagulation
- •9.2.1 Indications
- •9.2.2 PRP Technique
- •9.2.3 Complications
- •9.2.4 Outcome
- •9.3 Intraocular Pharmacological Therapy
- •9.4 Vitreoretinal Surgery
- •9.4.1 Indications
- •9.4.2 Preoperative Management
- •9.4.3 Instrumentation
- •9.4.4 Techniques
- •9.4.5 Postoperative Management
- •9.4.6 Complications
- •9.4.7 General Outcome
- •9.5 Follow-Up Considerations in PDR
- •9.6.1 Cataract and PDR
- •9.6.2 Dense Vitreous Hemorrhage and Untreated PDR
- •9.6.3 Untreated PDR with Diabetic Macular Edema
- •9.6.4 PDR with Severe Fibrovascular Proliferation/Traction Retinal Detachment
- •9.6.5 PDR with Neovascular Glaucoma
- •9.6.6 Conditions Altering the Clinical Course of PDR
- •9.7 Summary of Key Points
- •9.8 Future Directions
- •References
- •Cataract Surgery and Diabetic Retinopathy
- •10.1 Scope of the Problem of Diabetic Retinopathy Concomitant with Surgical Cataract
- •10.2 Visual Outcomes After Cataract Surgery in Patients with Diabetic Retinopathy
- •10.3 Postoperative Course and Special Considerations After Cataract Surgery in Patients with Diabetic Retinopathy
- •10.4 The Influence of Cataract Surgery on Diabetic Retinopathy
- •10.5 The Role of Ancillary Testing in Managing Cataract Surgery in Eyes with Diabetic Retinopathy
- •10.6 Candidate Risk and Protective Factors for Diabetic Macular Edema Induction or Exacerbation Following Cataract Surgery and Suggested Management Actions
- •10.7 The Problem of Adherence to Preferred Practice Guidelines
- •10.8 Management of the Diabetic Eye Without Macular Edema About to Undergo Cataract Surgery
- •10.9 Treatment of Diabetic Macular Edema Detected Before Cataract Surgery When the Macular View Is Clear
- •10.10 Management When Cataract Sufficient to Obscure the Macular View and DME Coexist or When Refractory DME and Cataract Coexist
- •10.11 Patients with Simultaneous Indications for Panretinal Photocoagulation and Cataract Surgery
- •10.12 Management of Cataract in Patients with Diabetic Retinopathy Undergoing Vitrectomy
- •10.13 Influence of Vitrectomy Surgery on Cataract Formation
- •10.15 Postoperative Endophthalmitis in Patients with Diabetic Retinopathy
- •10.16 Summary of Key Points
- •10.17 Future Directions
- •References
- •The Relationship of Diabetic Retinopathy and Glaucoma
- •11.1 Interaction of Diabetes and Glaucoma
- •11.2 Iris and Angle Neovascularization Pathoanatomy and Pathophysiology
- •11.3 Epidemiology
- •11.4 Clinical Detection
- •11.5 Classification
- •11.6 Risk Factors for Iris Neovascularization
- •11.7 Entry Site Neovascularization After Pars Plana Vitrectomy
- •11.8 Anterior Hyaloidal Fibrovascular Proliferation
- •11.9 Treatments for Iris Neovascularization
- •11.10 Modifiers of Behavior of Iris Neovascularization
- •11.11 Management of Neovascular Glaucoma
- •11.12 Summary of Key Points
- •11.13 Future Directions
- •References
- •The Cornea in Diabetes Mellitus
- •12.1 Introduction
- •12.2 Pathophysiology
- •12.3 Anatomy and Morphological Changes
- •12.4 Clinical Manifestations
- •12.5 Ocular Surgery
- •12.6 Treatment of Corneal Disease in Diabetes Mellitus
- •12.7 Conclusion
- •12.8 Summary of Key Points
- •12.9 Future Directions
- •References
- •Optic Nerve Disease in Diabetes Mellitus
- •13.1 Relevant Normal Optic Nerve Anatomy and Physiology
- •13.2 The Effect of Diabetes on the Optic Nerve
- •13.3 Nonarteritic Anterior Ischemic Optic Neuropathy and Diabetes
- •13.4 Diabetic Papillopathy
- •13.5 Disk Edema Associated with Vitreous Traction
- •13.6 Superior Segmental Optic Hypoplasia (Topless Optic Disk Syndrome)
- •13.7 Wolfram Syndrome
- •13.8 Summary of Key Points
- •13.9 Future Directions
- •References
- •Screening for Diabetic Retinopathy
- •14.1 Introduction
- •14.2 Who Does Not Need to Be Screened
- •14.5 Screening with Dilated Ophthalmoscopy by Ophthalmic Technicians or Optometrists
- •14.6 Screening with Dilated Ophthalmoscopy by Ophthalmologists
- •14.7 Screening with Dilated Ophthalmoscopy by Retina Specialists
- •14.8 Photographic Screening
- •14.9 Nonmydriatic Photography
- •14.10 Mydriatic Photography
- •14.11 Risk Factors for Ungradable Photographs
- •14.12 Number of Photographic Fields
- •14.13 Criteria for Referral
- •14.14 Obstacles to the Use of Teleophthalmic Screening Methods
- •14.15 Combination Methods of Screening
- •14.16 Case Yield Rates
- •14.17 Compliance with Recommendation to Be Seen by an Ophthalmologist
- •14.18 Intravenous Fluorescein Angiography and Oral Fluorescein Angioscopy
- •14.19 Automated Fundus Image Interpretation
- •14.20 Subgroups Needing Enhanced Screening Efforts
- •14.21 Screening in Pregnancy
- •14.22 Economic Considerations
- •14.23 Comparisons of the Screening Methods
- •14.24 Accountability of Screening Programs
- •14.25 Summary of Key Points
- •14.26 Future Directions
- •References
- •Practical Concerns with Ethical Dimensions in the Management of Diabetic Retinopathy
- •15.1 Incorporating Ancillary Testing in the Management of Patients with Diabetic Retinopathy
- •15.2.1 Case 1
- •15.2.2 Case 2
- •15.4 Working in a Managed Care Environment (Capitation)
- •15.5 Interactions with Medical Industry
- •15.7 Comanagement of Patients
- •15.9 Summary of Key Points
- •15.10 Future Directions
- •References
- •Clinical Examples in Managing Diabetic Retinopathy
- •16.1.1 Discussion
- •16.2 Case 2: Bilateral Proliferative Diabetic Retinopathy with Acute Vitreous Hemorrhage in One Eye and a Chronic Traction Retinal Detachment in the Other Eye
- •16.2.1 Discussion
- •16.2.2 Opinion 1
- •16.2.3 Opinion 2
- •16.2.4 Opinion 3
- •16.3 Case 3: Sight Threatening Diabetic Retinopathy in a Patient with Concomitant Medical and Socioeconomic Problems
- •16.3.1 Discussion
- •16.4 Case 4: Asymptomatic Retinal Detachment Following Vitrectomy in a Patient Who Has Had Panretinal Laser Photocoagulation
- •16.4.1 Discussion
- •16.5 Case 5: Management of Progressive Vitreous Hemorrhage Following Scatter Photocoagulation for Proliferative Diabetic Retinopathy
- •16.5.1 Discussion
- •16.6.1 Discussion
- •16.7 Case 7: Proliferative Diabetic Retinopathy with Macular Traction and Ischemia
- •16.7.1 Discussion
- •16.8 Case 8: What Is Maximal Focal/Grid Laser Photocoagulation for Diabetic Macular Edema?
- •16.8.1 Definition of the Problem
- •16.8.2 Discussion
- •16.9 Case 9: What Independent Information Does Macular Perfusion Add to Patient Management in Diabetic Retinopathy?
- •16.9.1 Discussion
- •16.10 Case 10: Macular Edema Following Panretinal Photocoagulation for Proliferative Diabetic Retinopathy
- •16.10.1 Discussion
- •16.11 Case 11: Diabetic Macular Edema with a Subfoveal Scar
- •16.11.1 Discussion
- •16.12.1 Definition of the Problem
- •16.12.2 Discussion
- •16.13.1 Definition of the Problem
- •16.13.2 Discussion
- •16.14 Case 14: How Is Diabetic Macular Ischemia Related to Visual Acuity?
- •16.14.1 Definition of the Problem
- •16.14.2 Discussion
- •References
- •Subject Index
3 Epidemiology of Diabetic Retinopathy |
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Table 3.10 Estimates of prevalence of forms of diabetic retinopathy by gender |
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Any DR (F%/M%) |
DME (F%/M%) |
PDR (F%/M%) |
References |
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42.8/22.9 |
8.4/1.6 |
6.9/2.0 |
Wong et al.1 |
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44.8/49.6 |
10.8/9.8 |
6.4/5.6 |
Varma et al.8 |
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35.5/38 |
27.9/32.1 |
3.1/1.3 |
Chou et al.34 |
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46.5/56.5 |
8.5/10.6 |
5.4/5.9 |
Villalpando et al.67 |
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14.6/21.3 |
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Rema et al.60 |
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14.6/21.1 |
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Raman et al.31 |
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45.1/44.4 |
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Wang et al.20 |
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13.9/24.7 |
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Al-Maskari and El-Sadig58 |
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Data from selected references on the effect of gender on prevalence of DR. F=female, M=male. DR = diabetic retinopathy. DME = diabetic macular edema. PDR = proliferative diabetic retinopathy.
There may be an interaction between the effect of gender and the type of diabetes. In type 1 diabetes, being female has been associated with higher prevalence of retinopathy; however, men had a higher prevalence of more severe retinopathy.23,45 Similarly, for younger onset diabetes, the 10-year incidence rate of improvement was higher and rate of progression was lower for females than for males.10 There was no gender difference in 10-year incidence rates of any DR, improvement in DR severity, or progression in DR severity for older onset diabetics taking insulin. Females had a higher 10-year incidence rate of improvement of retinopathy in the older onset, not taking insulin group, but gender did not influence incidence rates for any DR or progression of DR.10 The WESDR 25-year analysis in this same cohort demonstrated that being male was significantly associated with progression of retinopathy with a hazard ratio of 1.30 (95% CI 1.11–1.54, p = 0.0002). Being male was also associated with less improvement in diabetic retinopathy.
3.13 Age at Onset of Diabetes
Diabetic retinopathy is associated with age at onset of diabetes.36,45,46 In WESDR, the presence of any
retinopathy, proliferative retinopathy, and macular edema were most frequently encountered in younger onset individuals diagnosed prior to 30 years of age, while they were least frequently
encountered in older onset individuals diagnosed after 30 years of age who did not require insulin.45,46
Other studies support the conclusion that earlier age of onset of type 2 diabetes is a risk factor for increased prevalence and severity of DR independent of other traditional risk factors.71
3.14Socioeconomic Status and Educational Level
The reported influence of socioeconomic status on prevalence, incidence, and severity of diabetic retinopathy has been inconsistent. Associations
between lower socioeconomic status and worse retinopathy have been reported.72–74 Other studies have not found such associations.75,26 Lower educa-
tion has been associated with higher prevalence of DR and lower prevalence of DR.36,65
3.15 Family History of Diabetes
No association of family history of diabetes with
presence of diabetic retinopathy has been reported across multiple studies.26,32,61
3.16 Changes Over Time
Trends over time in diabetic retinopathy endpoints are shown in Table 3.11. Based on Medicare claims data, in elderly persons with diabetes over the period 1994–2004, there are lower rates of prevalence and incidence of NPDR, PDR, and DME within 1
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A.R. Bhavsar et al. |
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Table 3.11 Estimated annual incidence of vision loss endpoints in patients with diabetes by diabetes type over time |
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Younger |
Older onset, |
Older onset, not |
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Endpoint |
Period |
onset (%) |
taking insulin (%) |
taking insulin (%) |
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Blindness |
1980(2)–1984(6) |
0.38 |
0.82 |
0.67 |
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1984(6)–1990(2) |
0.05 |
0.14 |
0.37 |
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1990(2)–1995(6) |
0.18 |
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Doubling of visual angle |
1980(2)–1984(6) |
1.51 |
3.62 |
1.87 |
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1984(6)–1990(2) |
0.52 |
3.31 |
2.50 |
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1990(2)–1995(6) |
0.85 |
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PDR |
1980(2)–1984(6) |
2.71 |
1.98 |
0.53 |
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1984(6)–1990(2) |
3.97 |
3.17 |
1.34 |
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1990(2)–1994(6) |
2.8% |
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1994(6)–2005(7) |
1.6% |
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Data from WESDR.59,10 |
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year after diagnosis and during 6 years of follow-up more recently.76 In type 1 diabetics in WESDR, the same trend has been noted in incidence of PDR (Table 3.11).59Analogous trends have been noted
in other studies from Europe and the United States.57,77 It is possible that these data reflect
improvements in primary care of diabetes mellitus over time. Independent population-based studies have not reported decreased rates of blindness due
to diabetes during a time when the rates of PDR and DME have been declining.78,79 The discordance
may reflect a lag phase between improvement in management and decline in some but not all ocular late complications.78
3.17Epidemiology of Diabetic Macular Edema (DME)
In WESDR, the prevalence rates of DME in younger onset, older onset taking insulin, and
older onset not taking insulin groups were 6, 12, and 4%, respectively.45,46 The 4-, 10-, and 25-year
incidence rates of DME are shown in Table 3.12. Persons taking insulin have higher rates than those not taking insulin. The association between insulin use and higher incidence of DME may reflect the increased severity of diabetes in insulin users rather than a causal relationship between insulin use and DME. The annual incidence rates of DME show a decrease in the most recent period compared to earlier periods. In WESDR, for the periods from 1990–1992 to 1994–1996 and from 1994–1996 to
2005–2007, the annual rates of incidence were 2.3 and 0.9%, respectively.80 Similarly, in Denmark, the 20-year cumulative incidence of DME in type 1 diabetics decreased from 18.6% in a cohort diagnosed from 1965 to 1969 to 7.4% for the cohort diagnosed from 1979 to 1984, presumably reflecting better glycemic control in the latter era.81 The annual incidence of DME in studies in which annual examinations were performed is higher, presumably because some eyes develop and then resolve DME and are not counted in study designs such as WESDR without annual examinations. For example, the annual incidence of DME in type 1 diabetics examined annually with diabetes of duration from 10 to 20 years is 6.7%, approximately three times the rate calculated from WESDR data from a similar era.13
Studies consistently report that DME depends on duration of diabetes.80,8,16,20,82 Prevalence rates
of DME vary in younger onset diabetics from 0% in patients whose duration of diabetes is less than 5 years to 29% in patients whose duration of diabetes is 20 or more years.83 In older onset diabetics, the prevalence varies from 3% in patients whose duration of diabetes is less than 5 years to 28% in patients whose duration of diabetes is 20 or more years. Incidence rates also depend on duration of diabetes. Figures 3.4 and 3.5 show the parabolic relationship of 10-year incidence of DME to duration of diabetes in younger onset and older onset diabetes. In younger onset diabetes, the 10-year incidence of DME on average rises from 7% in a newly diagnosed patient to 27% in a patient who has had diabetes for 12 years and thereafter drops.
3 Epidemiology of Diabetic Retinopathy |
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Table 3.12 Various incidence rates of diabetic macular edema by diabetes type |
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Diabetes type |
4-year incidence (%) |
10-year incidence (%) |
25-year incidence (%) |
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Younger onset |
8.2 |
20.1 |
29 |
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Older onset, taking insulin |
8.4 |
25.4 |
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Older onset, taking no insulin |
2.9 |
13.9 |
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Data from Klein et al.16,80,82 The 25-year incidence is not available for the older onset groups because too many of these persons had died by the 25-year follow-up time.
Fig. 3.4 The peak 10-year incidence of DME in younger onset diabetes as assessed from the fitted curve would be at approximately 12 years duration. Data from Klein et al.82
10 Year Incidence of DME in Younger Onset Dlabetics by Duration
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(%) |
35 |
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30 |
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Incidence |
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25 |
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20 |
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y = –0.6207x2 |
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15 |
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+ 8.378x – 0.6776 |
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Year |
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10 |
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10 |
5 |
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0 |
3 |
5 |
7 |
9 |
11 |
13 |
15 |
22 |
27 |
35 |
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1 |
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Duration (Years)
Fig. 3.5 The peak 10-year incidence of DME in older onset diabetes as assessed from the fitted curve would be at approximately 10 years
duration. Data from Klein et al.82
10 Year Incidence of DME in Older Onset Diabetes by Duration
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40 |
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(%) |
35 |
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30 |
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Incidence |
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25 |
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20 |
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15 |
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10 Year |
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y = –0.649x2 |
+ 7.0019x + 5.5095 |
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10 |
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5 |
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0 |
3 |
5 |
7 |
9 |
11 |
13 |
15 |
22 |
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1 |
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Duration (Years)
In older onset diabetes, the 10-year incidence of DME on average rises from 12% in a newly diagnosed patient to 25% in a patient who has had diabetes for 10 years and thereafter begins to drop.
Prevalence rates of DME reported for various populations and ethnic groups studied according to diabetes type are shown in Table 3.13. According
to the Multiethnic Study of Atherosclerosis (MESA), the prevalence of DME was higher in blacks (11.1%), Hispanics (10.7%), and Chinese (8.9%) than whites (2.7%).84 In the Atherosclerosis Risk in Communities Study, DME was also more prevalent in blacks than whites.14 However, race may not be an independent risk factor. When
68 |
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A.R. Bhavsar et al. |
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Table 3.13 Prevalence of diabetic macular edema by type of diabetes and population |
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|
Population |
Type I (%) |
Type II (%) |
Mixed cohort (%) |
References |
USA Caucasian |
6 |
2–4 |
|
Williams et al.19 |
USA biracial (blacks, whites) |
|
|
1.6 |
Klein et al.14 |
UK Caucasian |
2.3–6.4 |
|
6.4–6.8 |
Williams et al.19 |
Australian Caucasian |
|
|
4.3–10 |
Williams et al.,19 Mitchell et al.32 |
European Caucasian |
|
5.4 |
|
Williams et al.19 |
Scandinavian Caucasian |
16 |
0.6–26.1 |
8 |
Williams et al.19 |
African American |
|
8.6 |
8.6 |
Williams et al.,19 Leske et al.21 |
Hispanic American |
|
|
10.4 |
Varma et al.,8 Williams et al.19 |
South Asian |
|
6.4–13.3 |
|
Williams et al.19 |
Indian |
|
|
1.4 |
Raman et al.26 |
Chinese |
|
2.7–5.2 |
|
Williams et al.,19 Wang et al.20 |
South American |
|
4.7–6.2 |
|
Williams et al.19 |
Wide ranges among studies partially reflect variations in other factors such as duration of diabetes mellitus in addition to ethnic variations.
Adapted and expanded from Williams et al.19
adjusted for other baseline variables, ethnicity was not associated with prevalence of vision-threatening retinopathy (primarily DME).84 The 9-year incidence rate of DME for blacks in the Barbados Eye Study was 8.7%, lower than the 10-year incidence rate of 13.9% reported for the older onset, not taking insulin group in the predominantly white WESDR from an earlier era.85
Age at diagnosis influenced incidence of DME in WESDR (Fig. 3.6). The relation of 10-year incidence of DME and age at baseline examination was nonlinear with a peak value at approximately
30 years in younger onset diabetics and at approximately 50 years in older onset diabetics. This relationship did not hold when 25-year incidence of DME was examined with adjustment for other baseline variables.80
With control of other baseline variables gender, occupation, income, marital status, educational level, and health insurance status have not been associated
with the 25-year incidence of DME in younger onset diabetics.80,84 The 10-year incidence of DME in both
younger onset and older onset diabetics was not associated with gender in WESDR.82
Fig. 3.6 The solid line represents data from younger onset diabetics and the dashed line from older onset diabetics. Ten year incidence of diabetic macular edema versus age at baseline examination. Reprinted with
permission from Klein et al.82
