Endocrinology

Diabetic Retinopathy song

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Diabetic Retinopathy

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Key points in this song10

Diabetic retinopathy is the leading cause of blindness in working-age adults in the United States, caused by chronic hyperglycemia damaging retinal microvasculature.
The earliest finding is microaneurysms (outpouchings of weakened capillary walls), appearing as small red dots on fundoscopy.
Non-proliferative diabetic retinopathy (NPDR) features include microaneurysms, dot-and-blot hemorrhages, hard exudates (lipid deposits), cotton-wool spots (nerve fiber layer infarcts), and venous beading.
Proliferative diabetic retinopathy (PDR) is defined by neovascularization driven by VEGF release in response to retinal ischemia, and is the stage at risk for vitreous hemorrhage and traction retinal detachment.
Diabetic macular edema (DME) is the most common cause of vision loss in diabetic retinopathy and can occur at any stage; it results from breakdown of the inner blood-retinal barrier.
All Type 1 diabetics should have their first dilated eye exam 5 years after diagnosis; Type 2 diabetics require screening at the time of diagnosis due to often delayed recognition of disease onset.
Hypertension and poor glycemic control (elevated HbA1c) are the two most important modifiable risk factors that accelerate progression of diabetic retinopathy.
Intravitreal anti-VEGF agents (e.g., ranibizumab, bevacizumab) are first-line treatment for diabetic macular edema and high-risk proliferative diabetic retinopathy.
Panretinal photocoagulation (PRP) is indicated for high-risk PDR to destroy ischemic retina and reduce VEGF-driven neovascularization.
Intensive glycemic control (DCCT and UKPDS trials) significantly reduces the risk of developing and progressing diabetic retinopathy in both Type 1 and Type 2 diabetes.