diabetic retinopathy:  the 5 findings you can not afford to overlook

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Disclosures. The content of this COPE Accredited CE activity was prepared independently without input from members of the ophthalmic community.I have no direct financial or proprietary interest in any companies, products or services mentioned in this presentation. The content and format of this course is presented without commercial bias and does not claim superiority of any commercial product or service..

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diabetic retinopathy: the 5 findings you can not afford to overlook

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1. Diabetic Retinopathy: The 5 Findings You Can Not Afford to Overlook! Kyle Cheatham, OD, FAAO Heartland Eye Consultants, Omaha, NE. FCO Student Chapter Coordinator

2. Disclosures The content of this COPE Accredited CE activity was prepared independently without input from members of the ophthalmic community. I have no direct financial or proprietary interest in any companies, products or services mentioned in this presentation. The content and format of this course is presented without commercial bias and does not claim superiority of any commercial product or service. Heartland Eye Consultants

3. Understanding the Fundamentals for DM is Important for ….. Our patients…. Diabetes is the leading cause of blindness in the U.S. for patients within the ages of 20-74. Our practice…. Thoroughly understanding this condition gives you confidence on when and why to refer for consultation. The profession…. No other systemic health condition allows us a better opportunity to coordinate care with primary care physicians. Heartland Eye Consultants

4. Goals of This Course Quickly overview epidemiology, pathophysiology and terminology associated with the condition. Discuss diabetic findings with an emphasis on “threats to vision” associated with the condition. Utilize evidence based medicine to understand how to properly monitor and manage the threats to vision. Heartland Eye Consultants

5. Pathophysiology of Retinopathy Diabetes leads to microvascular disease and damage to pericytes of the blood retinal barrier. Theories: Hyperglycemia causes production of toxic metabolites Byproducts of glucose metabolism cause alteration  in cell signaling pathways Heartland Eye Consultants

6. Overview of Terminology Nonproliferative diabetic retinopathy (NPDR) is also called background diabetic retinopathy (BDR). Proliferative diabetic retinopathy (PDR) indicates the presence of neovascularization; it is always associated with a worse prognosis. Clinically significant macular edema (CSME) is the leading cause of legal blindness in diabetes. Do not confuse CSME with cystoid macular edema (CME). Heartland Eye Consultants

7. Epidemiology of Diabetic Retinopathy Overview of Type 1 DM: Believed to be autoimmune in nature (pancreatic destruction); weak genetic component, strong concern for diabetic ketoacidosis. At diagnosis: no BDR is expected After 5 years duration - 25% have retinopathy, PDR is rare. After 20 years duration: 98% have BDR, 60% have PDR, 30% have CSME. Duration is disease is strongest risk factor for determining what IDDM patients will have retinopathy. Heartland Eye Consultants

8. Epidemiology of Diabetic Retinopathy Overview of Type 2 DM: Results from insulin-resistant receptor cells or abnormal B-cell production of insulin; strong genetic component, high association with obesity. Statistics for NIDDM Type 2 Diabetics: At diagnosis: 20% have BDR After 5 years duration: 30% have BDR, 2% have PDR. After 20 years duration: 50% have BDR, 10% have PDR, 20% have CSME. 15-19 year duration: 84% on insulin, 53% non-insulin dependent have retinopathy Heartland Eye Consultants

9. Epidemiology of Diabetic Retinopathy Statistics for IDDM Type 2 Diabetics: At diagnosis: 30% have BDR After 5 years duration: 40% have BDR, 2% have PDR. After 20 years duration: 90% have BDR, 25% have PDR, 40% have CSME. Heartland Eye Consultants

10. ADA Guidelines for DM Exams Type 1 should have a DFE within 5 years of diagnosis Type 2 shortly after diagnosis Exams should be done annually unless  retinopathy is progressing then they should  be more frequent. Less frequent exams (q2- 3 years) at the discretion of the doctor if exams are normal and HA1C is controlled. Heartland Eye Consultants

11. What are Our Best Predictors for Vision Loss in DM Retinopathy? Overview of mild, moderate, severe NPDR. Determining risk of progression from NPDR to PDR (The 4-2-1 rule): Severe retinal hemorrhages in 4 quadrants Venous beading in 2 quadrants IRMA in 1 quadrant Heartland Eye Consultants

12. Threats to Vision in DM Macular Disease Macular Ischemia Macular Edema Proliferative Disease Tractional Retinal Detachment Neovascular Glaucoma Preretinal/Vitreous Hemorrhage Heartland Eye Consultants

13. Macular Disease Key points regarding Macular Ischemia: Macular can appear normal or thickened Also referred to as macular non-perfusion Fluorescein angiography will reveal capillary non-perfusion larger than normal area of approximately 1 disc diameter in size. No treatment for this condition. Heartland Eye Consultants

14. Macular Edema Macular edema is excessive fluid WITHIN the layers of the retina, distinct from the accumulation of fluid under or between the retinal layers (subsensory fluid, serous retinal detachment).  Results from excessive leakage from capillaries within the macular region that overwhelms normal homeostasis mechanisms (i.e. RPE pumps). Can occur in NPDR or PDR. Heartland Eye Consultants

15. Diabetic Macular Edema Macula will always appear thickened in macular edema. Tips for finding macular edema…. Is macular edema always treated? Heartland Eye Consultants

16. Clinically Significant Macular Edema (CSME) Criteria for CSME and subsequent treatment with focal/grid laser photocoagulation. Exudate within 1/3 DD of the fovea with associated retinal thickening. Retinal thickening within 1/3 DD of the fovea. Retinal thickening within 1 DD of the fovea that is 1DD in size.  Heartland Eye Consultants

17. Cystoid Macular Edema (CME) Not the same as clinically significant macular edema (CSME) #1 cause of CME is post-cataract extraction, which is believed to be prostaglandin mediated. Occasionally, in diabetes, CME can accompany diabetic macular edema. Classic clinical appearance of fluid-filled, cystoid spaces in the macular region. Heartland Eye Consultants

18. Cystoid Macular Edema Heartland Eye Consultants

19. Diabetic Macular Edema Heartland Eye Consultants

20. Proliferative Diabetic Retinopathy Heartland Eye Consultants

21. Preretinal / Vitreous Hemorrhage Quick review of various types of hemorrhages (vitreous, preretinal, intraretinal, subretinal hemorrhages) with emphasis on differentiating preretinal and vitreous hemes. Etiology of preretinal/vitreous hemorrhages – leakage of blood from neovascularization into vitreous (neo vessel breaks due to vitreous traction) Management – B-scan ultrasonography and considerations of vitrectomy Heartland Eye Consultants

22. Tractional Retinal Detachment Etiology – retinal detachment results from vitreous traction on preretinal neovascularization. Management –Cryo laser, vitrectomy, scleral buckle Heartland Eye Consultants

23. Neovascular Glaucoma Etiology – VEGF release results from insufficient oxygen supply and can perculate to anterior segment and result in fibrovascularization, thereby blocking the trabecular meshwork and decreasing outflow. When is gonioscopy appropriate (compare to CRVO). Management - Standard of care is PRP. Temporary improvements may be possible with intermittent, repeated anti-VEGF medications (i.e. Avastin, Lucentis, Macugen). Heartland Eye Consultants

24. PRP Treatment in Proliferative Disease Are all cases of neovascularization treated? Treatment for proliferative disease is recommended when patient has high risk characteristics (HRC’s), which include either of the following criteria: NVD >1/4  DD Any NVD/NVE with associated preretinal or vitreous hemorrhage Heartland Eye Consultants

25. Effectiveness of PRP Patients with HRC’s: Treatment Group: 10% reached severe vision loss (SVL) (5/200) Observation Group: 28% reached SVL Clinical Significance: 18% absolute risk reduction of SVL, which means approximately 1 out of 5 patients receive benefit from the treatment. Patients with Proliferative disease, but no HRC’s: Treatment Group: 5-10% reached SVL Observation Group: 2-5% reached SVL Patients with Very severe NPDR, but no HRC’s: Treatment Group: 3-4% reached SVL Observation Group: 1-2% reached SVL Overall Summary Point: Only  patients with HRC’s are treated! Heartland Eye Consultants

26. Other Diabetic Findings Cranial Nerve Palsies Review of history, signs, symptoms, pathophysiology and diagnosis of CN III, IV and CN VI palsies. Management: review of when diagnostic imaging is appropriate. Heartland Eye Consultants

27. Other Diabetic Findings NAION Etiology: Ischemia to anterior portion of optic disc with exact causal mechanism unknown Epidemiology: most prominent in patients > 50, no gender predilection Risk factors (HTN, DM, disc at risk) Prominent symptoms (vision loss classically occurs in morning, altitudinal visual field defect, etc) Testing (normal ESR, CRP, etc) Heartland Eye Consultants

28. Other Diabetic Findings Cataracts – review of pathophysiology Beware of hypertension/diabetic combination leading to increased microvascular damage. Heartland Eye Consultants

29. Lecture Summary Two broad categories (macula and proliferative disease) with five overall concerns: Macular edema Macular ischemia Preretinal/Vitreous hemorrhage Tractional Retinal Detachment Neovascular Glaucoma Heartland Eye Consultants

30. Thank You! Any Questions? Heartland Eye Consultants

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