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The American Diabetes Association (ADA) position statement on diabetic retinopathy states that hyperglycemia has been the most consistently associated risk factor for retinopathy. A large and consistent set of observational studies and clinical trials confirms the association of poor glucose control and retinopathy.
The Diabetes Control and Complications Trial (DCCT), a randomized controlled clinical trial of intensive glycemic control vs conventional glycemic control in people with type 1 diabetes (T1D), demonstrated that intensive therapy reduced the development or progression of diabetic retinopathy by 34%-76%. The DCCT also demonstrated a definitive relationship between hyperglycemia and diabetic microvascular complications, including retinopathy. Early treatment with intensive therapy was effective.
The UK Prospective Diabetes Study (UKPDS) of patients with newly diagnosed T2D conclusively demonstrated that improved blood glucose control reduced the risk for retinopathy and nephropathy and, possibly, neuropathy. The overall microvascular complication rate was decreased by 25% in patients receiving intensive therapy vs conventional therapy. Epidemiologic analysis of the UKPDS data showed a continuous relationship between the risk for microvascular complications and glycemia, such that every percentage-point decrease in A1c (eg, 9% to 8%) was associated with a 35% reduction in the risk for microvascular complications.
More recently, the ACCORD trial of medical therapies demonstrated that intensive glycemic control reduced the risk for progression of diabetic retinopathy in people with T2D of 10 years' duration. This study included 2856 ACCORD participants enrolled in the ACCORD Eye Study and followed for 4 years.
The ADA recommends screening by an ophthalmologist for diabetic retinopathy within 5 years of the diagnosis of T1D and at the time of diagnosis of T2D. Women with preexisting diabetes who are planning pregnancy or who have become pregnant should be screened before pregnancy or in the first trimester.
While optimization of blood glucose, blood pressure, and serum lipid levels in conjunction with appropriately scheduled dilated eye examinations can substantially decrease the risk for vision loss from diabetic retinopathy, a significant proportion of those affected with diabetes develop diabetic macular edema or proliferative changes that require intervention. ADA treatment recommendations are:
• Refer patients with any level of macular edema, severe nonproliferative diabetic retinopathy (a precursor of proliferative diabetic retinopathy), or proliferative diabetic retinopathy to an ophthalmologist knowledgeable and experienced in the management and treatment of diabetic retinopathy.
• Laser photocoagulation therapy reduces the risk for vision loss in patients with high-risk proliferative diabetic retinopathy and, in some cases, severe nonproliferative diabetic retinopathy.
• Intravitreous injections of anti–vascular endothelial growth factor are indicated for central-involved diabetic macular edema, which occurs beneath the foveal center and may threaten reading vision.
Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia
Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
The American Diabetes Association (ADA) position statement on diabetic retinopathy states that hyperglycemia has been the most consistently associated risk factor for retinopathy. A large and consistent set of observational studies and clinical trials confirms the association of poor glucose control and retinopathy.
The Diabetes Control and Complications Trial (DCCT), a randomized controlled clinical trial of intensive glycemic control vs conventional glycemic control in people with type 1 diabetes (T1D), demonstrated that intensive therapy reduced the development or progression of diabetic retinopathy by 34%-76%. The DCCT also demonstrated a definitive relationship between hyperglycemia and diabetic microvascular complications, including retinopathy. Early treatment with intensive therapy was effective.
The UK Prospective Diabetes Study (UKPDS) of patients with newly diagnosed T2D conclusively demonstrated that improved blood glucose control reduced the risk for retinopathy and nephropathy and, possibly, neuropathy. The overall microvascular complication rate was decreased by 25% in patients receiving intensive therapy vs conventional therapy. Epidemiologic analysis of the UKPDS data showed a continuous relationship between the risk for microvascular complications and glycemia, such that every percentage-point decrease in A1c (eg, 9% to 8%) was associated with a 35% reduction in the risk for microvascular complications.
More recently, the ACCORD trial of medical therapies demonstrated that intensive glycemic control reduced the risk for progression of diabetic retinopathy in people with T2D of 10 years' duration. This study included 2856 ACCORD participants enrolled in the ACCORD Eye Study and followed for 4 years.
The ADA recommends screening by an ophthalmologist for diabetic retinopathy within 5 years of the diagnosis of T1D and at the time of diagnosis of T2D. Women with preexisting diabetes who are planning pregnancy or who have become pregnant should be screened before pregnancy or in the first trimester.
While optimization of blood glucose, blood pressure, and serum lipid levels in conjunction with appropriately scheduled dilated eye examinations can substantially decrease the risk for vision loss from diabetic retinopathy, a significant proportion of those affected with diabetes develop diabetic macular edema or proliferative changes that require intervention. ADA treatment recommendations are:
• Refer patients with any level of macular edema, severe nonproliferative diabetic retinopathy (a precursor of proliferative diabetic retinopathy), or proliferative diabetic retinopathy to an ophthalmologist knowledgeable and experienced in the management and treatment of diabetic retinopathy.
• Laser photocoagulation therapy reduces the risk for vision loss in patients with high-risk proliferative diabetic retinopathy and, in some cases, severe nonproliferative diabetic retinopathy.
• Intravitreous injections of anti–vascular endothelial growth factor are indicated for central-involved diabetic macular edema, which occurs beneath the foveal center and may threaten reading vision.
Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia
Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
The American Diabetes Association (ADA) position statement on diabetic retinopathy states that hyperglycemia has been the most consistently associated risk factor for retinopathy. A large and consistent set of observational studies and clinical trials confirms the association of poor glucose control and retinopathy.
The Diabetes Control and Complications Trial (DCCT), a randomized controlled clinical trial of intensive glycemic control vs conventional glycemic control in people with type 1 diabetes (T1D), demonstrated that intensive therapy reduced the development or progression of diabetic retinopathy by 34%-76%. The DCCT also demonstrated a definitive relationship between hyperglycemia and diabetic microvascular complications, including retinopathy. Early treatment with intensive therapy was effective.
The UK Prospective Diabetes Study (UKPDS) of patients with newly diagnosed T2D conclusively demonstrated that improved blood glucose control reduced the risk for retinopathy and nephropathy and, possibly, neuropathy. The overall microvascular complication rate was decreased by 25% in patients receiving intensive therapy vs conventional therapy. Epidemiologic analysis of the UKPDS data showed a continuous relationship between the risk for microvascular complications and glycemia, such that every percentage-point decrease in A1c (eg, 9% to 8%) was associated with a 35% reduction in the risk for microvascular complications.
More recently, the ACCORD trial of medical therapies demonstrated that intensive glycemic control reduced the risk for progression of diabetic retinopathy in people with T2D of 10 years' duration. This study included 2856 ACCORD participants enrolled in the ACCORD Eye Study and followed for 4 years.
The ADA recommends screening by an ophthalmologist for diabetic retinopathy within 5 years of the diagnosis of T1D and at the time of diagnosis of T2D. Women with preexisting diabetes who are planning pregnancy or who have become pregnant should be screened before pregnancy or in the first trimester.
While optimization of blood glucose, blood pressure, and serum lipid levels in conjunction with appropriately scheduled dilated eye examinations can substantially decrease the risk for vision loss from diabetic retinopathy, a significant proportion of those affected with diabetes develop diabetic macular edema or proliferative changes that require intervention. ADA treatment recommendations are:
• Refer patients with any level of macular edema, severe nonproliferative diabetic retinopathy (a precursor of proliferative diabetic retinopathy), or proliferative diabetic retinopathy to an ophthalmologist knowledgeable and experienced in the management and treatment of diabetic retinopathy.
• Laser photocoagulation therapy reduces the risk for vision loss in patients with high-risk proliferative diabetic retinopathy and, in some cases, severe nonproliferative diabetic retinopathy.
• Intravitreous injections of anti–vascular endothelial growth factor are indicated for central-involved diabetic macular edema, which occurs beneath the foveal center and may threaten reading vision.
Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia
Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
A 48-year-old Black man with type 2 diabetes (T2D) presented with complaints of a "flickering" sensation and a decrease in brightness of colors in both eyes as well as floaters in his left eye for several weeks. He reported that his symptoms fluctuate with changes in his blood glucose levels. His last eye examination was 2 years ago and his ocular history was unremarkable. His medical history was significant with a history of hypertension and T2D requiring insulin. His most recent glycated hemoglobin (A1c), 2 months ago, was 8.4%. His BMI was 31.2. The patient's medications were dulaglutide 0.75 mg injection pen, glargine insulin 42 units, losartan 100 mg, and amlodipine 10 mg.
On examination, his best-corrected visual acuity was 20/20 in the right eye and 20/30 in the left eye. Confrontation fields were intact, extraocular movements were full and extensive, and both pupils were equal, round, and reactive to light without afferent pupillary defects. Anterior segment examination was unremarkable in both eyes, without iris neovascularization. Intraocular pressures were 17 mm Hg in the right eye and 16 mm Hg in the left eye. On dilated fundus examination, the cup-to-disc ratio was 0.45 horizontally and vertically, with the presence of 1/4 disc diameters of neovascularization of the disc in the right eye and 2/3 disc diameters of neovascularization of the disc in the left eye.
Posterior segment findings were significant for scattered microaneurysms and dot/blot hemorrhages in the maculae. In the periphery of both eyes, there were tortuous vessels, scatter microaneurysms with dot/blot hemorrhages, and multiple areas of neovascularization elsewhere, with several foci of vitreous traction. There was no vitreous hemorrhage or tractional retinal detachment of either eye.
Spectral domain optical coherence tomography revealed an epiretinal membrane in the right eye and a blunted foveal contour with parafoveal cystic spaces, probably secondary to vitreomacular contraction. The left eye also had an epiretinal membrane and blunted foveal contour secondary to vitreomacular adhesion. The patient was diagnosed with bilateral high-risk proliferative diabetic retinopathy.
