Case Presentation

1. Case Presentation

2. CC: “Can’t see out of right eye” History of Present Illness • 68 yo African American male presents with sudden painless vision loss in right eye. • Describes flashes of light in peripheral vision before vision loss • Then states that felt that a curtain was being drawn down over his right eye. • Notes that vision has been slowly getting worse in both eyes “over the years.”

3. History • Past Ocular Hx: myopia (near-sighted), decrease in visual acuity over past several years at near and distance, told has slight cataracts, no ocular medications, no eye surgeries or trauma, mother lost vision when in her late 70’s • Past Medical Hx: HTN, diabetes mellitus • Past Surgical Hx: cholecystectomy at age 57

4. History • Allergies: KNDA • Social Hx: smokes 1 PPD, occasional alcohol, no drugs • Family Hx: mother with myopia, no family history of any other ocular conditions, no cancers run in family, hx of diabetes • Review of systems: notes frequent nighttime urination, burring in feet

5. Exam • Vital Signs: T 98.6, HR 80, RR 16, BP 142/90 • General: No acute distress, alert and oriented x3, obese • Head, ear, nose, throat: atraumaticand normocephalic, no rhinorrea or epistaxis, no pharyngeal erythema or lesions • Lymph: no swollen glands • Cardiovascular: regular rate and rhythm, 2/6 systolic murmur over left sternal boarder, 1+ lower extremity edema • Respiratory: clear to auscultation bilaterally, no wheezes, rales, or rhonchi

6. What is the differential for a patient with sudden painless vision loss?

7. Differential Diagnosis of Painless Sudden Vision Loss • Retinal detachment • Retinal artery occlusion • Retinal vein occlusion • Vitreous hemorrhage • Temporal Arteritis • What other exams or tests should be done?

8. Tests/Imaging • Dilated fundus exam • B- scan ultrasonography • Optical Coherence Tomography (OCT): able to visualize the retina in cross-section • Fluorescein angiography (if cause still uncertain or to further evaluate retinal vasculature)

9. Ophthalmic Exam • Visual Acuity with correction • RE: no light perception • LE: 20/60 • External exam • Pupils: relative afferent pupillary defect on right • Intraocular pressure: normal (~15 mm hg) bilaterally • Dilated fundus exam: • RE: only able to get portion of retina in focus • LE: a few small hemorrhages and hard exudates present

10. Dilated Fundus Exam RE (Retinal Detachment) http://www.floridalionsfoundation.org/Retinal%20Detachment.htm

11. Dialated Fundus Exam LE (proliferative diabetic retinopathy) Increased blood vessels http://www.aao.org/theeyeshaveit/acquired/early-retinopathy.cfm

12. Diabetic Retinopathy

13. Normal Fundus Exams Normal Right Eye Normal Left Eye http://en.wikipedia.org/wiki/Fundus_photography

14. http://www.geteyesmart.org/eyesmart/diseases/detached-torn-retina.cfmhttp://www.geteyesmart.org/eyesmart/diseases/detached-torn-retina.cfm

15. Right Eye B-scan Ultrasonography Total retinal detachment and vitreous hemorrhage http://emedicine.medscape.com/article/1228865-overview#a30

16. Diagnosis • Retinal detachment in RE • Need to assess whether affects the macula. If the macula is detached then the vision will not be able to be restored. • Diabetic Retinopathy (proliferative diabetic retinopathy)

17. Type 2 Diabetes • Presentation: • Polyuria and polydipsia • End organ damage (described latter) • Hyperosmolar hyperglycemic state • Plasma glucose often >600 mg/dL with dehydration but no ketonuria • Asymptomatic and discovered with screening • Closely linked to an increase in in weight • Overweight: BMI ≥85th % and <95th % • Obese: BMI ≥95th % • Other risk factors: family hx, female gender, ethnicity (Native American, Hispanic, Asian-American, and Pacific Islander), other insulin resistant states (ex. Polycystic ovary syndrome) • Much of damage from diabetes results from vascular complications

18. Pathogenesis of Type 2 DM • Increased obesity leads to increased peripheral resistance to insulin-mediated glucose uptake. Initial beta cells of pancreas can produce increased insulin to counteract resistance. But can only up regulate production so much. Eventually, the beta cells burn out and insulin production falls leading to even worse glucose control.

19. Diagnosing Type 2 Diabetes • Fasting plasma glucose ≥126 mg/dL • Symptoms of hyperglycemia and random plasma glucose of ≥200 mg/dL • Abnormal oral glucose tolerance test (OGTT): plasma glucose ≥200 mg/dLmeasured 2 hours after glucose load of 1.75 g/kg • Hemoglobin A1C ≥6.5% • Unless unequivocal hyperglycemia is present, the diagnosis should be confirmed by repeat testing on a subsequent day.

20. Small Vessel Damage Accumulation of advanced glycosylation end products in the plasma contributes to microvasculardisease. Improved glycemic control improves the risk of microvascular complications. • Nephropathy: microalbuminuria (30-300 mg/day) is earliest stage. Screening for microalbuminuria with microalbumin-to-creatinine ratio in random urine sample • Retinopathy: ophthalmic screening at time of diagnosis of type 2 DM. Subsequent follow-up by ophthalmologist • Neuropathy: affects autonomic and peripheral nerves. Screen for with yearly foot exams with a monofilament.

21. Large Vessel Damage • Macrovascular complications • Coronary artery disease • Peripheral vascular disease • Cerebral vascular disease • Association between glycemic control and risk of complications not as clearly established as with microvascular complications. A large prospective study (United Kingdom Prospective Diabetes Study) did find a benefit from better control.

22. Comorbidities • Hypertension • Dyslipidemia • Nonalcoholic fatty liver disease

23. Regulating Blood Sugars Individualized A1C goals for patients, but a value of <7% is often appropriate • Non-pharmacologic: • Dietary modification • Weight loss • Increased physical activity

24. Pharmacologic management • Metformin: often initial pharmacologic choice • Sulfonylureas (eg. glipizide): can cause hypoglycemia • Thiazolidinediones “TZDs” (rosiglitazone and pioglitazone): increase insulin sensitivity. Infrequently used due to concerns over hepatotoxicity/MI • Meglitinides(repanglinide and neteglinide) • DPP-4 Inhibitors (sitagliptin and saxagliptin) • Glucagon-like peptide 1 “GLP-1” agonists (exenatide and liraglutide) • Alpha-glucosidase inhibitors (acarbose and miglitol) • Insulin

25. Management • Macrovascular risk factor management • Smoking cessation • Aspirin • Blood pressure control • Reduction in serum lipids • Diet/exercise