- •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 |
57 |
|
|
Fig. 3.2 Global estimates of number of persons with diabetes mellitus in 2000 compared with projected numbers for the year 2030 in three age groups. Reprinted
with permission from Wild et al.27
Table 3.1 Estimated numbers of people with diabetes mellitus in selected countries in 2000 and projections for 2030
|
2000 |
|
2030 |
|
|
Ranking |
Country |
People with diabetes (millions) |
|
Country |
People with diabetes (millions) |
|
|
|
|
|
|
1 |
India |
31.7 |
India |
79.4 |
|
2 |
China |
20.8 |
China |
42.3 |
|
3 |
US |
17.7 |
US |
30.3 |
|
4 |
Indonesia |
8.4 |
|
Indonesia |
21.3 |
5 |
Japan |
6.8 |
|
Pakistan |
13.9 |
6 |
Pakistan |
5.2 |
|
Brazil |
11.3 |
7 |
Russian Federation |
4.6 |
Bangladesh |
11.1 |
|
8 |
Brazil |
4.6 |
|
Japan |
8.9 |
9 |
Italy |
4.3 |
|
Philippines |
7.8 |
10 |
Bangladesh |
3.2 |
|
Egypt |
6.7 |
Reprinted with permission from Wild et al.27 List of countries with the highest numbers of estimated cases of diabetes for the years 2000 and 2030.
3.3Factors Influencing the Prevalence of Diabetes Mellitus
Age strongly influences the prevalence of diabetes (Fig. 3.1).31,34,26 In most studies prevalence increases with age in both genders.14,21,28,34,37 Not all studies
have supported this consensus.21 The third National Health and Nutrition Examination Study (NHANES III) in the United States showed a peak prevalence for diabetes of 13.2% in those 75 years.28 As a consequence, the prevalence of diabetes is high in residents of nursing and retirement homes.37,38
Ethnicity may influence the prevalence of diabetes, although the effects of confounding variables
are difficult to unravel. In Indonesia, the prevalence rate of diabetes is lowest (1.7%).30 In European and in the US white populations, prevalence rates are 2–10%, whereas in Arab, Israeli, Indian, black,
and Hispanic American populations, the rates are 14–20%.21,30 Among Pacific Islanders of Nauru
and among Pima Indians in the United States, the prevalence rate is 50%.30,37 In the United Kingdom,
Asian men were shown to have a prevalence four times than that of white men and Asian women were shown to have a prevalence two times than that of white women.39 In the United States, the NHANES III study demonstrated that non-Hispanic blacks had a 1.6 times higher prevalence of diabetes than non-Hispanic whites and Hispanic Americans had a
58 |
A.R. Bhavsar et al. |
|
|
Fig. 3.3 The prevalence of diabetes in India is increasing with time and is increasing more rapidly in urban than in rural areas. A rural–urban gradient in prevalence of diabetes is a consistent finding over time. Reprinted with permission from Gupta and Kumar30
1.9 times higher prevalence.28 The diversity in prevalence rates has been attributed in part to gene– environment interaction. Populations that have been relatively protected from periodic famines (e.g., white Europeans) for 15–20 generations have been hypothesized to have adapted to high-caloric diets and to have low insulin resistance, whereas populations exposed until more recently to regular periodic famines (e.g., Pacific Islanders, Native Americans, Australian Aboriginal peoples, natives of middle eastern desert regions) have retained high insulin resistance and develop DM when exposed to obesogenic environments (Table 3.2).30,40
Socioeconomic status has an inconsistent relationship with prevalence of diabetes mellitus. Lower status has been associated with higher diabetes prevalence in some studies and higher status has been associated with higher diabetes prevalence in others.26,37 The inconsistency does not appear to be
haphazard, however. Across the world, as socioeconomic status increases, so does body mass index (BMI), up to approximately 10,000–15,000 international dollars per person gross domestic product.41 As income rises further, BMI falls. In South Asia, most persons are on the rising limb of this relationship such that rising status correlates with rising obesity and more prevalent diabetes.30 In contrast, in developed countries most people are on the descending limb of income–BMI relationship such that increasing poverty is associated with obesity and secondarily an increased prevalence of diabetes.
A sedentary lifestyle is associated with a higher prevalence of diabetes. Lifestyle changes that occur when groups move from rural to urban environments has been shown to increase prevalence rates in Native Americans, Australian Aborigines, Polynesian Pacific Islanders, South Asian Indians, and East Indians (Fig. 3.3).30,37 Urban–rural gradients
Table 3.2 Prevalences of diabetes mellitus by population
Population |
Prevalence (%) |
Age range (years) |
References |
|
|
|
|
|
|
20; 40 |
|
28 |
|
8 |
|
Hispanic USA |
9.3; 22.9 |
Harris et al.,28 |
|
Varma et al. |
|||
Non-Hispanic white USA |
4.8 |
20 |
Harris et al.28 |
|
|
|
|
Non-Hispanic black USA |
8.2 |
20 |
Harris et al. 29 |
|
|||
Spain |
5–6.8 |
NG |
Mundet et al. |
|
|
|
|
Barbados black |
19.4 |
40–84 |
Leske et al.21 |
|
|
|
|
South Asian Indian |
10.3*; 28.2 |
20; 40 |
|
Kumar,30 Raman et al.31 |
|||
Singapore Malay |
23.1 |
Gupta and 1 |
|
|
|
||
40–80 |
Wong et al. |
|
|
|
|||
Australia |
7; 9.9 |
49 |
al.25, Mitchell et al.32 |
||||
Taiwan |
4.9; 6.2 |
Cugati et |
33 |
Chou et al.34 |
|||
China |
3.2; 6.9; 12.9 |
40; 30 |
Chen et al. |
35,20, |
36 |
||
20; 30; 40 |
Wang et al., |
|
|
Xie et al. |
|||
*Median value of 21 epidemiologic studies. NG = not given. Selected prevalences of diabetes mellitus in various populations.
3 Epidemiology of Diabetic Retinopathy |
59 |
|
|
of diabetes prevalence seem to be diminishing in south Asia over time.30
Obesity is an independent risk factor for diabetes, presumably through its effect of increasing insulin resistance of peripheral tissues.37 In the NHANES III study, increasing obesity was associated with increasing prevalence of diabetes after adjusting for other variables.42 Central obesity, in particular, is associated with DM. The associations of a high-fat
diet and sedentary lifestyle with prevalence of diabetes probably occur through effects on BMI.37,43
3.4Epidemiology of Diabetic Retinopathy
Diabetic retinopathy is the most common microvascular complication of diabetes mellitus and the leading cause of blindness in persons from age 20 to 74 in
the United States with 12,000–24,000 new cases of blindness per year.24,44 Data from WESDR indicate
that 1.07 and 1.3% of persons with diabetes develop, respectively, PDR and DME annually, almost all in patients older than 20 years.5 Based on the estimated US diabetic population over age 20 in 2008 of 14,456,000, an estimated 154,679 new cases of PDR and 187,928 new cases of DME will develop annually. Similar facts and estimates apply to other developed countries.19 In the United States in the year 2000, the numbers of persons with DR and vision-threatening DR were 4.1 million and 0.9 million, respectively.2 These numbers are expected to triple by the year 2050 and for those over age of 65 to quadruple.2 The primary factors responsible include increasing numbers of diabetics, increasing longevity of diabetics, and disproportionate increases in growth rates of Hispanics, in whom prevalence of DR is higher than in non-Hispanic whites and blacks.2
The Wisconsin Epidemiologic Study of Diabetes
A disproportionate fraction of the epidemiologic literature of diabetic retinopathy stems from WESDR, thus some background on this study is warranted. Over a 1-year period from 1979 to 1980, diabetic patients were identified from 452 of the 457 primary care practices for diabetics in an 11-county area of Wisconsin.45,46 After removing patients with incorrect diagnoses, patients who
had died or moved, and patients confined to nursing homes, 9,283 patients were identified. Of these, 1,396 were <30 years old at diagnosis and 5,431 were 30 years old at diagnosis.45,46 In the younger
onset group, 1,210 were taking insulin and all were examined for the study. From the older onset group, a random sample of 1,370 patients spread over three subgroups stratified by diabetes duration were chosen for study. The older group was further categorized by insulin use or not. Many baseline variables including retinal photography variables were obtained and then the patients were followed over time. The older onset patients were studied over 10 years and the younger onset patients over 25 years. Over 200 reports arising from analyses of this data set have been published, and those results comprise a large portion of the information reviewed in this chapter.47
3.5 Diabetes and Visual Loss
Diabetes mellitus is associated with increased levels of all cause visual impairment after adjusting for the
effects of age, sex, race, educational level, blood pressure, smoking, and body mass index.9,48 The
relative risk of blindness in persons with diabetes has been reported to be 5.2 times the risk of those without diabetes.48 The prevalences of visual
impairment in adults with and without diabetes vary from 3.8 to 13% and from 1.4 to 2%, respectively.5,8,9 The prevalence rates of visual impairment by diabetes type from WESDR are shown in Table 3.3. The annual incidence of blindness was 3.3 per 100,000 population.5
Incidence rates of loss of vision were obtained in WESDR. Two categories of visual loss examined were doubling of the visual angle and blindness. There were relatively few events for the blindness
60 A.R. Bhavsar et al.
Table 3.3 Prevalence of different levels of visual impairment in diabetes mellitus by the visual acuity in the better seeing eye
Group (N) |
>20/40 (%) |
20/40–20/160 (%) |
20/200 (%)* |
Younger onset (996) |
91.7 |
4.7 |
3.6 |
Older onset, taking insulin (674) |
81.6 |
15.7 |
2.7 |
Older onset, not taking insulin (696) |
87.5 |
10.0 |
0.3 |
|
|
|
|
*Includes patients in whom visual acuity could not be measured.
Adapted with permission from Klein et al.49 The percentages refer to the number of diabetics of each type (N) shown in the left column. Younger onset = almost all type 1 diabetes. Older onset, taking insulin = a mixture of patients with type 1 and type 2 diabetes. Older onset, not taking insulin = type 2 diabetes.
outcome and many for the doubling of visual angle outcome, thus for statistical reasons associations between risk factors and outcomes were explored for doubling of the visual angle and not for blindness. The most important results are presented in Tables 3.4 and 3.5. The incidence rates for vision loss are higher for the older onset groups than for the younger onset group. The risk factor analysis is complicated as Table 3.5 illustrates. The most salient point is that increasing age is a risk factor for visual loss in all types of diabetes. In a separate study of African Americans with type 1 diabetes, 6-year incidence rates for doubling of the visual angle and blindness were 13.5 and 0.6%, respectively; increased age was the only demographic risk factor for visual loss.50
WESDR provides information of a population that is predominantly white. In black type 1 diabetics, similar data have been reported. The 6-year incidences of doubling of visual angle and blindness were 9.8 and 0.6%, respectively.50 The risk factors were similar as well, with older age at baseline the strongest demographic predictive variable.50
3.6Prevalence and Incidence of Diabetic Retinopathy
Estimates of the prevalence of diabetic retinopathy need to be understood within the context that
retinopathy occurs in a proportion of persons who have no diabetes mellitus under various definitions of the term. Associations with such fundus changes include hypertension, serum glucose levels within the normal range, BMI, and aging. Estimates of the proportions of persons with this status range from 0.6 to 9.8% depending on
methods of retinopathy detection (higher with photographs than clinical examination).21,51–53
Fiveand ten-year incidences of retinopathy in persons without diabetes have been reported to be 6.0–10% and 6.5% in independent studies, respectively.53–55
Some studies do not distinguish DR by diabetes type. In a population-based study of this type in adults over the age of 49 from Australia, prevalence and 5-year incidence of any DR were reported to be 35.3 and 22.2%, respectively.53 In this study, duration of DM was the only demographic baseline factor associated with risk for retinopathy progression.53 In the Barbados Eye Study of blacks aged 40–84, the prevalence and
4-year incidence of any DR were 28.5 and 30.1%, respectively.21,56 There were no important demo-
graphic risk factors associated with incidence of retinopathy.56
retinopathy indistinguishable from diabetic
Table 3.4 Incidence of vision loss outcomes in WESDR
|
|
Doubling of visual angle |
Blindness |
|
|||
|
|
|
|
|
|
|
|
|
|
10-year incidence, |
14-year incidence, |
10-year incidence, |
14-year incidence, |
||
Type of diabetes |
|
% (N) |
% (N) |
% (N) |
% (N) |
||
Younger onset |
9.2 |
(880) |
14.2 (880) |
1.8 (868) |
2.4 (868) |
||
Older onset, taking insulin |
32.8 |
(472) |
|
4.0 (465) |
|
||
Older onset, not taking insulin |
21.4 |
(494) |
|
4.8 (490) |
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All data from Moss et al.22,44 Data for visual impairment are similar to data for doubling of visual angle for each group. Too many patients in the older onset groups had died by the 14-year follow-up study, thus only data for the younger onset group were reported.
