- 1.
How is diabetic retinopathy classified? What fundus features are characteristic of each category?
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Nonproliferative diabetic retinopathy (NPDR): This form is arbitrarily divided into three categories based on severity: mild, moderate, and severe. Features of mild and moderate nonproliferative retinopathy result predominantly from loss of capillary integrity (i.e., microaneurysms, dot-and-blot hemorrhages, hard yellow exudates, and macular edema) ( Fig. 45-1 ). Cotton-wool spots are also seen. Features of more severe NPDR are related to early signs of ischemia. In addition to the features found in mild nonproliferative disease, the fundus shows venous beading and intraretinal microvascular abnormalities (IRMAs) as well as more extensive intraretinal hemorrhages ( Fig. 45-2 ).
Figure 45-1
Nonproliferative diabetic retinopathy with exudates, hemorrhages, and edema.
Figure 45-2
Severe nonproliferative retinopathy with venous beading and intraretinal microvascular abnormalities.
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Proliferative diabetic retinopathy (PDR): Typical features are related to the consequences of extensive retinal capillary nonperfusion. Fundus findings include those of NPDR as well as the development of neovascularization of the disc (NVD; Fig. 45-3 ), neovascularization elsewhere in the retina (NVE), preretinal and/or vitreous hemorrhage, and vitreoretinal traction with tractional retinal detachment.
Figure 45-3
Neovascularization of the disc in proliferative retinopathy.
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- 2.
What is the most common cause of vision loss in diabetic retinopathy?
The most common cause of vision loss in diabetic retinopathy is macular edema.
- 3.
Who is at risk for the development of diabetic retinopathy?
All patients with diabetes mellitus are at risk for diabetic retinopathy. Relative risk factors include the following:
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Duration of diabetes: The longer diabetes has been present, the greater the risk of some manifestation of diabetic retinopathy. After 10 to 15 years, more than 75% of patients show some signs of retinopathy.
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Age: Diabetic retinopathy is uncommon before puberty even in patients who were diagnosed shortly after birth. NPDR appears sooner in patients diagnosed with diabetes after the age of 40. This may be related to duration of disease before diagnosis.
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Diabetic control: The Diabetic Control and Complications Trial (DCCT) clearly demonstrated a correlation between poor long-term glucose control and subsequent development of diabetic retinopathy as well as other complications of diabetes.
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Renal disease: Proteinuria is a particularly good marker for the development of diabetic retinopathy. This association may not be causal, but a patient with renal dysfunction should be followed more closely.
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Systemic hypertension: Again, the causal nature of the relationship is not certain.
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Pregnancy: Diabetic retinopathy may progress rapidly in patients who are pregnant. Patients with preexisting retinopathy are at particular risk.
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- 1.
Macular edema
- 2.
Macular ischemia
- 3.
Vitreous hemorrhage
- 4.
Macular traction detachment
- 5.
Combined rhegmatogenous/tractional retinal detachment
- 4.
What is the significance of the hemoglobin A 1 C? What is its correlation with the development of diabetic retinopathy?
Hemoglobin A 1 C is serum glycosylated hemoglobin. It is an indicator of the average level of serum glucose for the preceding 3 months. Thus it provides a report card of the adequacy of glucose control for the preceding 3 months without identifying peaks, valleys, or timing of glucose fluctuation. The hemoglobin A 1 C has been found to correlate most closely with the development of diabetic retinopathy. Nondiabetic patients typically have a level of 6 or less. The DCCT demonstrated that hemoglobin A 1 C of less than 8 was associated with a significantly reduced risk of retinopathy compared with a value greater than 8.
- 5.
What is the recommendation for screening patients with diabetes?
Patients with juvenile insulin-dependent diabetes should have a dilated ophthalmologic examination 5 years after diagnosis. Patients with type II adult-onset diabetes should be examined at diagnosis. All diabetic patients should have an annual dilated funduscopic examination; more frequent examinations depend on the findings.
- 6.
What are the fluorescein angiographic features of nonproliferative and proliferative diabetic retinopathy?
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In mild-to-moderate nonproliferative retinopathy the large vessels fill normally. Pinpoint areas of early hyperfluorescence correspond to microaneurysms, whereas dot-and-blot hemorrhages are hypofluorescent. Microaneurysms leak in the later frames with blurring of margins and diffusion of fluorescein dye, whereas hemorrhages remain hypofluorescent throughout the study. Telangiectasis hyperfluoresces with late leakage. Hard yellow exudate generally does not appear on a fluorescein angiogram unless it is extremely thick, in which case it is hypofluorescent. Macular edema usually is apparent as fluorescein leaks into the retina as the angiogram progresses ( Figs. 45-4 and 45-5 ).
Figure 45-4
Early phase fluorescein angiogram shows pinpoint hyperfluorescence corresponding to microaneurysms.
Figure 45-5
Later phase fluorescein angiogram shows leakage with diffusion of dye and blurring of the microaneurysms.
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More severe nonproliferative retinopathy has the features noted above as well as evidence of retinal capillary loss. Cotton-wool spots are usually hypofluorescent, sometimes with late hyperfluorescence along the margins. Areas of capillary dropout appear as smooth, hypofluorescent “ground-glass” patches, with staining at the margins in the later frames of the angiogram. IRMAs fill in the arterial phase of the angiogram and does not leak significantly in the later frames ( Fig. 45-6 ).
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