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Diabetic Retinopathy Steven Sanislo, M.D. Assistant Professor Stanford University Department of Ophthalmology.

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Presentation on theme: "Diabetic Retinopathy Steven Sanislo, M.D. Assistant Professor Stanford University Department of Ophthalmology."— Presentation transcript:

1 Diabetic Retinopathy Steven Sanislo, M.D. Assistant Professor Stanford University Department of Ophthalmology

2 Diabetic Retinopathy Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years in the USA Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years in the USA Many of the complications of diabetic retinopathy can be prevented or delayed by blood glucose control and timely intervention. Many of the complications of diabetic retinopathy can be prevented or delayed by blood glucose control and timely intervention.

3 Ocular Anatomy

4 Retinal Anatomy

5 Retinal Histology Sclera Choroid RPE Photoreceptor outer segments Photoreceptor inner segment Outer Plexiform layer Bipolar cells Inner plexiform layer Ganglion cells Nerve fiber layer

6 Retinal Diagnostic Tests Fundus Photography Fundus Photography Fluorescein Angiography (FA) Fluorescein Angiography (FA) Optical Coherence Tomography (OCT) Optical Coherence Tomography (OCT) Ocular Ultrasonography Ocular Ultrasonography Electroretinography (ERG) Electroretinography (ERG)

7 Fundus Photos and FA

8 Fundus Photography

9 Normal FA

10 Optical Coherence Tomography (OCT)

11 Normal OCT

12 B-scan Ultrasound

13 Normal Ultrasound

14 Pathogenesis of DR Prolonged hyperglycemia is the major etiologic agent in all of the microvascular complications of diabetes, including diabetic retinopathy. Prolonged hyperglycemia is the major etiologic agent in all of the microvascular complications of diabetes, including diabetic retinopathy. The cellular mechanisms through which hyperglycemia acts currently remain unclear The cellular mechanisms through which hyperglycemia acts currently remain unclear

15 Pathogenesis of DR Mechanisms that have been proposed are: 1. hyperglycemia may alter the expression of one or more genes, leading to increased (or decreased) amounts of certain gene products that can alter cellular functions. 1. hyperglycemia may alter the expression of one or more genes, leading to increased (or decreased) amounts of certain gene products that can alter cellular functions. 2. Glycosylated proteins can undergo a series of reactions, leading to considerable alteration of proteins. 2. Glycosylated proteins can undergo a series of reactions, leading to considerable alteration of proteins. 3. Chronic hyperglycemia may produce oxidative stress in cells, leading to the formation of an excess of "toxic end products of oxidation" including peroxides, superoxides, nitric oxide, and oxygen free radicals. 3. Chronic hyperglycemia may produce oxidative stress in cells, leading to the formation of an excess of "toxic end products of oxidation" including peroxides, superoxides, nitric oxide, and oxygen free radicals.

16 VEGF and DR Vascular Endothelial Growth Factor Vascular Endothelial Growth Factor Promotes vascular growth and permeability Promotes vascular growth and permeability Elevated levels of circulating VEGF in conditions with retinal ischemia Elevated levels of circulating VEGF in conditions with retinal ischemia

17 Anatomic Changes Microanerysms Damage to endothelial cells leads to dilated capillaries and venules Damage to endothelial cells leads to dilated capillaries and venules These altered vessels allow serum and blood to leak into the retina These altered vessels allow serum and blood to leak into the retina

18 NPDR

19 NPDR FA

20 NPDR OCT

21 Retinal Ischemia

22 PDR

23 PDR

24 PDR FA

25 Vitreous Hemorrhage (VH) Vitreous Hemorrhage (VH)

26 VH ultrasound

27 TRD ultrasound

28 Epiretinal Membrane

29 PDR Retinal Detachment

30 Iris Neovascularization

31 Mechanisms of Vision Loss Retinal ischemia Retinal ischemia Macular edema Macular edema Vitreous hemorrhage Vitreous hemorrhage Epiretinal membrane formation Epiretinal membrane formation Retinal detachment Retinal detachment Neovascular glaucoma Neovascular glaucoma

32 Prevention Prospective controlled interventional studies have shown that strict control of blood glucose and blood pressure significantly reduces and delays the onset and severity of diabetic retinopathy. Prospective controlled interventional studies have shown that strict control of blood glucose and blood pressure significantly reduces and delays the onset and severity of diabetic retinopathy.

33 Screening Type 1 diabetics: First screen 5 years after onset, then annually. Type 2 diabetics: First screen upon diagnosis and then annually.

34 Treatment NPDR without macular edema - NPDR without macular edema - Observe Observe Macular edema - Macular edema - 1. Focal/Grid laser photocoagulation 1. Focal/Grid laser photocoagulation 2. Vitrectomy with membrane peeling 2. Vitrectomy with membrane peeling 3. Intraocular Steroid* 3. Intraocular Steroid* 4. Intraocular VEGF inhibitor* 4. Intraocular VEGF inhibitor* * Off-label use, contraversial

35 DME laser treatment

36 * * * * * * * * * * * *

37 Treatment Vitreous Hemorrhage - Vitreous Hemorrhage - 1. Pan-retinal photocoagulation 1. Pan-retinal photocoagulation 2. Vitrectomy with laser photocoagulation 2. Vitrectomy with laser photocoagulation 3. Intraocular VEGF inhibitor* 3. Intraocular VEGF inhibitor* Traction Retinal Detachment - Traction Retinal Detachment - 1. Observation if not involving the macula 1. Observation if not involving the macula 2. Vitrectomy with membrane dissection 2. Vitrectomy with membrane dissection * Off-label use, contraversial

38 Pan-retinal Photocoagulation

39 Vitrectomy

40 http://www.youtube.com/watch?v=iOwpEa4KB5c http://www.youtube.com/watch?v=iOwpEa4KB5c


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