Ординатура / Офтальмология / Английские материалы / Automated Image Detection of Retinal Pathology_Jelinek, Cree_2009
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Automated Image Detection of Retinal Pathology |
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2
Diabetic Retinopathy and Public Health
David Worsley and David Simmons
CONTENTS
2.1 |
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
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2.2 |
The Pandemic of Diabetes and Its Complications . . . . . . . . . . . . . . . . . . . . . . . . . . |
28 |
2.3 |
Retinal Structure and Function. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
29 |
2.4 |
Definition and Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
35 |
2.5 |
Classification of Diabetic Retinopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
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2.6 |
Differential Diagnosis of Diabetic Retinopathy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
40 |
2.7 |
Systemic Associations of Diabetic Retinopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
42 |
2.8 |
Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
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2.9 |
Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
45 |
2.10 |
Screening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
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2.11 |
Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
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|
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . |
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2.1Introduction
Diabetic retinopathy (DR) is the commonest complication of diabetes and is one of the leading causes of blindness [1]. Recent research has given a better understanding of the disease processes and is opening up new avenues for prevention and treatment. Very effective treatments are available and are optimally used when retinopathy is detected early, well before the patient is aware of symptoms. For this reason screening programs for early detection of retinopathy are an essential part of diabetes care and are in widespread use. Several screening modalities have been used, however, digital retinal photography is now considered the preferred screening tool. There is potential for automated image analysis to manage the large volume of images generated from screening the ever-increasing number of people with diabetes.
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Automated Image Detection of Retinal Pathology |
2.2The Pandemic of Diabetes and Its Complications
Diabetes mellitus is considered one of the major diseases of the 21st century, indeed it has been said that “What AIDS was in the last 20 years of the 20th century, diabetes is going to be in the first 20 years of this century” [2; 3]. Much of this growth is due to the increasing prevalence of type 2 diabetes, where insulin secretion from the beta cells of the pancreas is inadequate for daily demands [4]. Such demand depends upon a complex balance between various hormones, existing energy stores (e.g. as adipose tissue), physical activity, and resistance to insulin action in muscle, liver, and adipose tissue. Contemporary life in both the developed and developing world increasingly involves reductions in physical activity and increases in energy dense food, with a resulting energy imbalance leading to greater obesity, insulin resistance, and type 2 diabetes. There is now good evidence that the progression from lesser degrees of glucose intolerance (i.e., impaired fasting glucose and impaired glucose tolerance) to type 2 diabetes can be prevented, or at least delayed, through lifestyle change providing that substantial support is provided [5–7]. The other major group of patients have type 1 diabetes, where there is destruction of the beta cells through either auto-immune or other mechanisms. Type 1 diabetes is also increasing in prevalence [8]. Other rarer forms of diabetes mellitus exist including Maturity Onset Diabetes of Youth (MODY) and other inherited forms [9].
The epidemic of type 2 diabetes is not only associated with an increasing number of people with diabetes within a given age group, the mean age at which it is diagnosed (and presumably commences) is becoming younger [10]. Type 2 diabetes in youth and children is becoming more prevalent with type 2 diabetes now becoming as common as type 1 diabetes in pediatric diabetes clinics [11]. Of great concern is the growth in the number of women of child-bearing age with type 2 diabetes who become pregnant with poor glucose control with both immediate and long term teratogenic effects—the latter increasing the risk of diabetes in the offspring [12; 13].
Diabetes is associated with a range of acute and chronic complications, although the prevalence of these varies by ethnicity, country, and over time [14; 15]. Both type 1 and type 2 diabetes are associated with long term macrovascular complications such as ischemic heart disease, stroke, peripheral vascular disease, and heart failure, and microvascular complications such as nephropathy, neuropathy, and retinopathy. Other complications also continue to occur due to glycation such as cataract and cheiroarthropathy or with combined causes such as the diabetic foot.
The biochemical criteria for diabetes were originally defined by their ability to predict microvascular disease, particularly diabetic retinopathy, over time [16]. Indeed, diabetic retinopathy was considered such a specific diabetes-related complication that studies predicted the length of time between development and diagnosis of diabetes by backward linear regression [17]. In the first AusDiab study, however, using linear regression between duration and prevalence of retinopathy, the clinical diagnosis of diabetes was thought to have been made at the same time as diabetes developed [18]. AusDiab also showed that retinopathy (defined as the presence of
Diabetic Retinopathy and Public Health |
29 |
at least one definite retinal hemorrhage and/or microaneurysm) was present before overt diabetes was detected: 6.7% (5.3% to 8.4%) in impaired fasting glucose and impaired glucose tolerance with a comparable prevalence in newly diagnosed diabetes 6.2% (4.0% to 9.2%) and in those without diabetes 5.8% (3.7% to 8.5%) [18]. Similar prevalences were found in the Blue Mountains Eye Study [19].
Diabetic retinopathy is a leading cause of visual loss in working-age adults worldwide [20]. Severe vision loss is primarily from diabetic macular edema (DME) and proliferative diabetic retinopathy (PDR). As DME is more common than PDR in type 2 diabetes, and 90% of diabetics are type 2, DME is the leading cause of visual loss in diabetic retinopathy [21].
The prevalence of diabetic retinopathy has recently been thoroughly reviewed by Williams et al. [22]. Tables 2.1a, 2.1b, 2.2a, 2.2b, and 2.2c show the prevalence and incidence respectively of diabetic retinopathy by retinopathy grade and type of diabetes (type 1, type 2 diabetes, and mixtures of both) across countries, ethnic groups, and over time. There are clearly major differences in prevalence and incidence between studies depending on when and where they were undertaken and depending on the methods used for assessing retinopathy. There are likely to be ethnic differences in diabetic retinopathy as there are in nephropathy, but these remain inconsistent [22].
The most significant predictor of the prevalence of DR is duration of diabetes. In view of the importance of diabetic retinopathy and its contribution to blindness, as well as its utility in providing a window on the natural history of diabetes in individuals and populations, this chapter will focus on how diabetic retinopathy is defined and classified, the pathophysiology, the epidemiology, its prevention through optimizing metabolic control and associated health care issues, and screening for early changes.
2.3Retinal Structure and Function
The retina is a transparent layer of vascularized neural tissue lining the inner layer of the back wall of the eye, between the retinal pigment epithelium on the outer and the vitreous on the inner side. The retina captures photons and converts these to photochemical and electrical energy, integrates the signals, and transmits the resultant signal to the visual cortex of the brain via the optic nerve, tracts, and radiations.
The retinal architecture is lamellar. Within this there are major cell types performing sensory, nutritional, regulatory, immunomodulatory, and structural functions. The retina is uniquely partitioned from the vascular system by the blood-retinal barrier and blood-aqueous barrier. The blood supply is dual; to the inner retina it is by the retinal circulation lying within the inner retina (the inner blood-retinal barrier) and to the outer retina it is by the choroidal circulation, a thick vascular layer lying outside of the retinal pigment epithelium (the outer blood-retinal barrier). The retinal pigment epithelium and the choroid are critical to retinal function.
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Automated Image Detection of Retinal Pathology |
Table 2.1a: Summary of the Range of Global Prevalence Estimates in Type 1, Type 2, and Mixed Cohort Diabetic Patients
Population |
Grade |
Type 1 |
|
Type 2 |
Mixed Cohort |
|
Retinopathy |
|
|
|
|
United States |
Any DR |
0–84% (97.5% |
7–55% |
37–61.1% |
|
|
|
415 years |
DM |
|
|
|
|
duration) |
|
|
|
|
PDR |
3.8–25% |
(70% |
0.9–5% |
|
|
|
430 years |
DM |
|
|
|
|
duration) |
|
|
|
|
CSMO |
6% |
|
2–4% |
|
United |
Any DR |
33.6–36.7% |
21–52% |
16.5–41% |
|
Kingdom |
PDR |
1.1–2.0% |
|
1.1–4% |
1.1–8% |
|
CSMO |
2.3–6.4% |
|
|
6.4–6.8% |
Australian |
Any DR |
42% |
|
13–59.7% |
29.1% (10% at 5 |
|
|
|
|
|
years and |
|
|
|
|
|
80% 435 years |
|
|
|
|
|
DM duration) |
|
PDR |
|
|
|
1.6–7% |
|
CSMO |
|
|
|
4.3–10% |
European |
Any DR |
16.6–76.5% |
32.6–61.8% |
26.2% |
|
|
PDR |
7.3–17% |
|
3.1–15.9% |
1.8% |
|
CSMO |
|
|
5.4% |
|
Scandinavian |
Any DR |
10.8–68.3% |
18.8–65.9% |
13.8–75.1% |
|
|
|
(90% 420 years |
|
|
|
|
|
DM duration) |
|
|
|
|
PDR |
2.6–28.4% |
|
4.2–14.5% |
1.7–2.4% |
|
CSMO |
16% |
|
0.6–26.1% |
8% |
|
Blindness |
1.4% |
|
|
|
African |
Any DR |
63.9% |
|
26.5–31.4% |
28.5% |
American |
PDR |
18.9% |
|
0.9–1.5% |
0.9% |
|
CSMO |
|
|
8.6% |
8.6% |
|
Blindness |
3.1% |
|
|
|
Hispanic |
Any DR |
|
|
33.4–45% |
48% |
American |
PDR |
|
|
5.6–6.0% |
|
|
CSMO |
|
|
|
|
American |
Any DR |
19.7– 20.9% |
19–49.3% |
1.7% (total pop.) |
|
Indian |
PDR |
|
|
5.1–7% |
|
|
CSMO |
|
|
|
|
|
|
|
|
|
|
CSMO, clinically significant macular edema; DM, diabetes mellitus, DR, diabetic retinopathy; PDR, proliferative DR.
Adapted from Williams et al., Eye, 18, 963, 2004, Ref. [22]. With permission.
Diabetic Retinopathy and Public Health |
31 |
Table 2.1b: Summary of the Range of Global Prevalence Estimates in Type 1, Type 2, and Mixed Cohort Diabetic Patients (continued)
Population |
Grade |
Type 1 |
Type 2 |
Mixed Cohort |
|
Retinopathy |
|
|
|
NZ European |
Any DR |
|
37.3% |
|
|
PDR |
|
2.7% |
|
|
CSMO |
|
8.7% |
|
NZ Maori |
Any DR |
|
40.7% |
|
|
PDR |
|
5.0% |
|
|
CSMO |
|
8.6% |
|
NZ Pacific |
Any DR |
|
43.8% |
|
|
PDR |
|
6.2% |
|
|
CSMO |
|
13.0% |
|
South Asia |
Any DR |
13.6% |
6.7–34.1% |
|
|
PDR |
1.9% |
0.7–10.3% |
|
|
CSMO |
|
6.4–13.3% |
|
|
Blindness |
|
4.1% |
|
UK South Asians |
Any DR |
|
11.6% |
|
|
PDR |
|
|
|
|
CSMO |
|
|
|
Japanese |
Any DR |
|
31.6–38% |
|
|
PDR |
|
2.8–10% |
|
|
CSMO |
|
|
|
|
Blindness |
|
2.9% |
|
Chinese |
Any DR |
|
19–42% |
28–45.2% |
|
PDR |
|
0.4–12.7% |
2.2% |
|
CSMO |
|
2.7% |
|
|
Blindness |
|
0.3% |
|
African |
Any DR |
26–43% |
30.5–43% |
12.7–42.4% |
|
PDR |
|
|
12.8% |
|
CSMO |
|
|
|
South American |
Any DR |
|
54–51.2% |
|
|
PDR |
|
3.4–5.5% |
|
|
CSMO |
|
4.7–8.2% |
|
|
|
|
|
|
CSMO, clinically significant macular edema; DM, diabetes mellitus, DR, diabetic retinopathy; PDR, proliferative DR.
Adapted from Williams et al., Eye, 18, 963, 2004, Ref. [22]. With permission. NZ data from ref. [23]
