Case 3

1. Rayos, K.- Rodas, F. Case 3

2. Case 3 • 21 year old student • CC: Loss of vision OS and eye aches associated with movement.    • PMH: Similar episode in the OD three years ago with spontaneous resolution. Also, a history of right sided numbness made better with ‘hilot’.  • Vision: Right 20/20-2Left 20/40-1    • IOP: OU 15mm Hg (Normal IOP: 15.5 mmHg with fluctuations of 2.75)

3. What is your working diagnosis? • Hypertensive Retinopathy

4. Hypertensive Retinopathy • Characterized by a variety of retinal vascular signs in individuals with elevated BP • Causes blurring of vision • Bilateral, symmetrical • End organ manifestation

5. Hypertensive Retinopathy • Funduscopic findings: • Focal attentuation of a major retinal arteriole • Broadening of the arteriolar light reflex • Arteriovenous crossing changes • Hemorrhages • Retinal infarcts (Cotton-wool spots) • Choroidal infarcts (Elschnig’s spots) • Serous dettachment of the retina • Severe disk edema

6. Arteriosclerotic Changes • Arteriolar narrowing that is almost always bilateral • Grade I - 3/4 normal caliber • Grade II - 1/2 normal caliber • Grade III - 1/3 normal caliber • Grade IV - thread-like or invisible • Arterio-venous crossing changes (aka “AV nicking") with venous constriction and banking • Arteriolar color changes • Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width of the arteriole. • Silver wire arterioles are those arterioles in which the central light reflex occupies all of the width of the arteriole.

7. Stages of Hypertensive Retinopathy • Grade 1 – general narrowing of arterioles • Grade 2- Narrowing of arterioles plus arteriolar spasm • Grade 3 – Grade 2 changes plus hemorrhage and exudates - Flame-shaped (splinter hemorrhages)- seen in the nerve fiber layer - Cotton wool spots – result of microinfarction of NFL which produces aggregates of Cytoid bodies - Hard waxy exudates may be seen (lipophilic exudates located in Outer plexiform Inner Nuclear layer)

8. Stages of Hypertensive Retinopathy • Grade 4- All grade 3 changes with optic disc edema, necrosis, thinning, clumping and proliferation of Retinal pigment epithelium • May also occur as a result of obliterative changes in the choriocapillary in malignant hypertension .

9. Vascular Changes • Arteriolar narrowing • A:V- 2:3 • AV crossing changes • Grading • I- Leakage • II- Blood and hemorrhage • III- Cotton wool spots • IV- Optic disc swelling, subretinal exudates

10. What are your differentials? Other retinopathies that are known complications of high blood pressure are called: • Diabetic retinopathy • Ischemic optic neuropathy • Retinal artery occlusion • Retinal emboli • Retinal vein occlusion

11. Diabetic RetinopathyNon-proliferative Type • Capillaries develop: • Microaneurysms • Thickening of the BM • Dec # of pericytes • Classification based on severity: • Mild • Atleast 1 microaneurysm • Moderate • Extensive microaneurysm • Intraretinal hemorrhages • Venous beading • Cotton wool spots • Severe • Cotton wool spots • Venous beading • Intraretinalmicrovascular abnormalities (IRMA)

12. Diabetic RetinopathyProliferative Type • Presence of neovascularization on optic disk • Bleeding of vessels • Massive vitreous hemorrhage • Sudden visual loss

13. Ischemic Optic Neuropathy • Age: older age groups • Nonarteritic: late 40s and older • Arteritic: >50 y/o • Gender predilection: F>M • History: painless visual loss upon awakening • Early: malaise, weight loss, fever, vague abdominal or GI pains, and anorexia • Late: abdominal aortic aneurysm • Clinical Findings: • Nonarteritic: visual loss and field loss, small cup disc ratio, sectorial disc edema, pale and swollen optic disc • Arteritic: chalky white, pale, and swollen optic disc; quite prominent, ropey, and tender temporal arteries; oral, tongue, or scalp ulcer

14. Retinal Artery Occlusion • Age: Mean: early in the 7th decade • Gender predilection: M>F • History: Acute persistent painless loss of vision, complete/sectional visual field defect, history of hypertension or diabetes mellitus, other medical problems (atrial fibrillation), prolonged direct pressure or drug-induced • Clinical Findings: • Fundoscopy: afferent pupillary defect, cherry red spot and a ground-glass retina, emboli, whitening of the retina and Boxcar segmentation (BRAO) • PE: can have murmurs, carotid bruits, or other signs of cardiovascular disease

15. Retinal Emboli • Most commonly arise from carotid artery disease • In patients younger than 40, a cardiac origin such as atrial fibrillation, mitral valve prolapse or subacuteendocarditis is considered Three types: 1. Cholesterol emboli • Also called Hollenhorst plaques • Usually arise from an atheromatous plaque in the carotid artery and consist of cholesterol and fibrin • Lodge at the bifurcation of the retinal arterioles, are refractile and appear larger than the vessel that contains them

16. Retinal Emboli 2. Calcific emboli • Originates from damaged cardiac valves producing complete occlusion and infarction of the distal retina • Solid and calcified and usually occur in younger patients 3. Platelet fibrin emboli • Account for most cases of amaurosisfugax • Due to the transit of platelet aggregates through the retinal and choroidal circulations • May be reduced by drugs that reduce platelet aggregation like aspirin

17. Central Retinal Vein Occlusion • Increased incidence in smokers, hypertension, diabetes mellitus, hyperlipidemia,collagen-vascular disease, chronic renal failure and hyperviscosity syndromes • Fundoscopy shows • Dilated tortuous veins with retinal and macular edema • Hemorrhages all over the posterior pole • Cotton wool spots

18. Diagnostic Examinations • Get patient’s Blood Pressure • Ophthalmoscopy • Flourescein angiography

19. Sphygmomanometry • Used to monitor the blood pressure of the patient Source: Table 241-1. Harrison’s Principles of Internal Medicine 17thed.

20. Ophthalmoscopy • Ophthalmoscope has long been regarded as part of the standard evaluation of persons with hypertension • Ophthalmoscope has been shown to have high rates of interobserver variability (20 to 42 percent)and intraobserver variability (10 to 33 percent) when used inpersons with mild hypertension • few studies have demonstrated associationsbetween hypertensive retinopathy and specific cardiovascularoutcomes (e.g., incident stroke and coronary heart disease)or have adequately controlled for relevant confounding factors(e.g., hyperlipidemia and cigarette smoking) http://content.nejm.org/cgi/content/full/351/22/2310

21. Mild Hypertensive Retinopathy – Opthalmoscopy Mild Hypertensive Retinopathy – Opthalmoscopy Figure 1. Examples of Mild Hypertensive Retinopathy. Panel A shows arteriovenous nicking (black arrow) and focal narrowing (white arrow). Panel B shows arteriovenous nicking (black arrows) and widening or accentuation ("copper wiring") of the central light reflex of the arterioles (white arrows).

22. Moderate Hypertensive Retinopathy – Opthalmoscopy Panel A shows retinal hemorrhages (black arrows) and a cotton-wool spot (white arrow). Panel B shows cotton-wool spots (white arrows) and arteriovenous nicking (black arrows).

23. Moderate Hypertensive Retinopathy – Opthalmoscopy Multiple cotton-wool spots (white arrows), retinal hemorrhages (black arrows), and swelling of the optic disk are visible

25. Fluorescein angiography • Technique for examining the circulation of the retina using the dye tracing method • Involves injection of sodium fluorescein into the systemic circulation, and then an angiogram is obtained by photographing the fluorescence emitted after illumination of the retina with blue light at a wavelength of 490 nanometers • Can detect diabetic retinopathy, vein occlusions, retinal artery occlusions, edema of the optic disc, and tumors.

26. Causes of hyperfluorescence: Causes of hypofluorescence: blocking defect (i.e. blood) filling defect (capillary blockage) • leaking defects (i.e. capillary leakage, aneurysm, neovascularization) pooling defects staining transmission (filling) defects abnormal vasculature

27. Treatment • Control hypertension • Other vision- threatening conditions should also be controlled • Laser • Intravitreal injection of corticosteroids • Anti-vascular endothelial growth factor drugs • monoclonal antibodies such as bevacizumab (Avastin), • antibody derivatives such as ranibizumab (Lucentis), or • orally-available small molecules that inhibit the tyrosine kinases stimulated by VEGF: • lapatinib(Tykerb), sunitinib (Sutent), sorafenib (Nexavar), axitinib, and pazopanib Merck manual online medical library

28. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cardio&part=A379&rendertype=table&id=A433http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cardio&part=A379&rendertype=table&id=A433

29. Thank you!