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Retinal Vascular Disease Don Simpson, O.D. St. Louis VA Medical Center.

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Presentation on theme: "Retinal Vascular Disease Don Simpson, O.D. St. Louis VA Medical Center."— Presentation transcript:

1 Retinal Vascular Disease Don Simpson, O.D. St. Louis VA Medical Center

2 WELCOME TO MID-TOWN 915 N GRAND BLVD 2 BLOCKS N OF THE FOX THEATER St. Louis VAMC - John Cochran Division

3 St. Louis VA Rotation 2 divisions John Cochran – mid town Jefferson Barracks- south county Equal time both divisions

4 Case # 1 71 yo male pt presents for routine eye exam No remarkable findings until Fundus examination Med hx remarkable for htn, ateriosclerosis Rt eye reveals following:

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6 Diagnosis Retinal embolus- Hollenhorst plaque What now?

7 Return to history Anterior circulation TIA SX ? Amaurosis fugax Unilateral motor disturbance Unilateral numbness, tingling Slurred speech Momentary confusion 50-75% of stroke patients have TIAs

8 Return to examination Additional tests Auscultation of carotid arteries What if normal? What if bruit?

9 Management ? TIA sx present TIA sx absent

10 No TIA Sx Primary care provider, Neurology Antiplatelet meds if on none, ASA contraindications 81 mg qd Carotid ultrasound Echocardiogram

11 TIA SX Urgent care Primary care provider Neurology ER

12 St Louis VA Neurology Heading of Neuro consult work sheet at St. Louis VA “ TRANSIENT ISCHEMIC ATTACK IS A MEDICAL EMERGENCY. If TIA is suspected, please refer the patient to the ER or page the Neuro resident on call for an immediate assessment. TIA should also mean: TAKE IMMEDIATE ACTION “

13 Additional signs carotid insufficiency Hypo-perfusion retinopathy Ocular ischemic syndrome

14 Hypo-perfusion retinopathy Peripheral retinal hemorrhages associated with decreased retinal artery perfusion pressure

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19 Ocular ischemic syndrome NVI Retinal neovascularization Neovascular glaucoma

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22 Surgical management carotid disease Carotid angiogram Gold standard to evaluate stenosis Invasive procedure Carotid endarterectomy

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25 Cardiac sources of emboli Mitral valve disease Arrhythmias- a fib, vent tach Valve replacement thrombi Sbe

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27 Retinal Emboli and Stroke Beaver Dam study- population based Looked at risk of CVA with retinal emboli Results published in Archives of Ophth Vol 117; Aug 99. [ ]

28 Findings in Beaver Dam Study Emboli prevalence 1.3% [3.1%>75yo] Emboli not present at follow up 90% of the time With emboli 3x greater risk of fatal CVA in 8 years than if no emboli present

29 TMVL & HTIA Transient monocular vision loss Hemispheric TIA Stroke risk lower if only tmvl v htia sx based on large trials NASCET, ECST 3yr risk CVA with med tx 10% tmvl 3yr risk CVA with med tx 20% htia Why risk different?

30 6 RISK FACTORS FOR STROKE IN TMVL MALE 75yo or > Hx htia or stroke Hx intermittent claudication Internal carotid stenosis of 80-94% Absence of collateral vessels on angiogram 3 of these risk factors with TMVL carotid endarterectomy beneficial

31 ASYMPTOMATIC HOLLENHORST PLAQUE No evidence to suggest that carotid endarterectomy is of benefit

32 Prevalence of Stroke by Age and Sex NHANES: Source: CDC/NCHS and NHLBI.

33 Estimated Direct and Indirect Costs of Cardiovascular Diseases and Stroke United States: 2005 Source: Heart Disease and Stroke Statistics – 2005 Update.

34 Percentage Breakdown of Deaths From Cardiovascular Diseases United States:2002 Preliminary Source: CDC/NCHS.

35 Case 2 Sudden vision loss right eye few days duration 65 yo male Ocular hx unremarkable Med hx hypertension, diabetes

36 Examination Best corrected vision - 10/400 Right afferent pupillary defect

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38 DIAGNOSIS CRVO 2 types Ischemic vs non ischemic likely ischemic

39 Ischemic CRVO VA less than 20/200 APD Numerous CWS > 10 disc areas of capillary nonpefusion 30% of all CRVO % develop NVG NVG 3-4 months [90 day glaucoma]

40 Nonischemic CRVO VA usually better than 20/200 or better No APD Few cotton wool spots May progress to ischemic CRVO

41 Uncommon Etiologies of CRVO Polycythemia Plasma cell dyscrasias

42 Polycythemia Increased RBC and blood volume Polycythemia vera- idiopathic Secondary polycythemia- erythrocytosis Erythrocytosis can be due to hypoxia or condition causing increased stimulating factor

43 Plasma Cell Dyscrasias Multiple myeloma Waldenstrom’s macroglobulinemia Malignant production of immunoglobulins Increased serum viscosity

44 Homocystinemia Elevated homocystine levels associated with atherosclerosis and CRVO Normal homocystine metabolism, but elevated levels of the amino acid

45 Neovascular glaucoma Response to ischemia Difficult to manage Intractable pain/ enucleation

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49 Clinical Management and Natural History of CRVO Arch Ophth Vol 115, Apr 97, Prognostic value of initial visual acuity 20/40 or better- likely good outcome 20/50-20/200- variable prognosis 20/200 or worse- poor prognosis, likely ischemic, high risk NVI, ANV 56% of <20/200 had NVI and ANV at one month

50 Follow up CRVO based on Initial Visual Acuity >20/40 q 1-2 months for 6 months 20/ q 1-2 months for 6 months <20/200 q 1 month for 6 months

51 CRVO Treatment PRP if ischemic Intravitreal triamcinolone injection as tx for non-ischemic occlusion, likely not effective for ischemic occlusion

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54 Vision Limiting Complications of BVO Macular edema- 1/3 spontaneously regain vision Macular nonperfusion, no vision improvement Vitreous heme- NVE, NVD

55 Clinical Features of BVO NV if capillary nonperfusion > 5 disc areas NVE/D most likely 6-12 months up to 3 years Close f/u until heme resolves

56 PC Criterion BVO Study FA proven macular edema No residual heme in center of fovea 3-18 month duration No DM retinopathy VA less than 20/40 Grid tx to leaking area- no closer than FAZ

57 Management of BVO if VA<20/40 Watch for 3-6 months FA, ME vs macular nonperfusion Grid PC if <20/40 / IVK More than 5 disc areas of retina involved FA watch for NV

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59 I can’t see out of my right eye Sudden vision loss rt eye BCVA= 20/ LP; 20/20 Rt afferent pupillary defect Med hx aterioro sclerosis, htn, type 2 diabetes Slex and iop normal Fundus examination OS normal Rt eye

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61 Right fundus diagnois CRAO Other questions Duration < 24 hr management

62 Duration < 24 hr AC paracentisis IV diamox Ocular massage Inspiration of high concentration of oxygen and carbon dioxide

63 Additional Hx Physical sx Important questions Stat Lab tests? ESR, C-RP Essential condition to rule in / rule out GCA What tx? Steroids / bx later Why critical ? Bilateral blindness

64 Giant Cell Arteritis Fever, malaise, weight loss, scalp tenderness Need STAT ESR&C-RP in evaluating CRAO Temporal artery biopsy PO steroids Risk of bilateral blindness within hours if no treatment

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66 Disposition after GCA ruled out Work up for other associated systemic conditions, emergent Need medical work up for associated systemic conditions Internest, cardiology, neurology

67 Systemic Conditions Associated with CRAO Carotid stenosis Cardiac valvular disease, MVP, Rheumatic Coagulopathies, sickle cell disease, platelet and factor abnormality Optic nerve drusen Elevated intraocular pressure Collagen vascular disease, SLE, Giant cell arteritis

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71 Clinical Features of CRAO APD Cherry red spot in macula due to nerve fiber layer thinning at fovea Acutely arteries are attenuated Emboli visible 20% of cases NVG 15-20% of cases Need systemic work up

72 CRAO Treatment AC paracentisis if <24 hours old IV diamox Ocular massage Inspiration of high concentration of oxygen and carbon dioxide

73 There is a curtain in my vision Phone call/ walk in visit Initial differential Happened less than 3 hours ago Sudden loss of vision superior field left eye 64 yo male hx hypertension

74 Examination findings Best corrected vision 20/20;20/40 Perrla – no afferent defect Confrontation field superior defect OS SLEx and IOP unrmarkable Fundus examination

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76 Diagnosis ? Branch retinal artery occlusion Emergent/invasive measures for vision preservation ?Y/N Next Urgent / emergent medical evaluation? Y/N Work up for source of embolus

77 BRAO Features 90% on temporal vessels Permanent field defect 80% cases final VA >20/40 Similar etiologies as CRAO Ocular therapeutic measures generally not undertaken

78 There is a dark spot in my vision Inferior field left eye Present for 2 weeks Normal vision OU Normal fundus examination OD

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81 Management Diagnosis Retinal arterial macroaneurysm Additional tests FA Prognosis

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83 Management of Macroaneurysms FA helpful in dx, ddx Spontaneous resolution in 12 months Observation if no macular involvement Photo-coagulation in some cases with macular involvment

84 Retinal Arterial Macroaneurysms Distinct entity from Coats, Lebers, Eales Temporal retina within 1 st 3 bifurcations M:F ratio 1:2 usually < 60 years old 75% have HTN, atherosclerosis

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88 Sickle cell disease Patients of African descent Hemoglobinopathy, abnl amino acid Sickle shaped RBC trapped in small vessels- hypoxia, necrosis Different genotypes, least severe systemically has most ocular complications and vice versa

89 Ocular Findings in Sickle Cell Comma shaped conj capillaried Iris atrophy, synechia Salmon patch retinal hemorrhages Black sunbursts in retina Peripheral retinal sea fans, neovascularization Scatter PC to reduce ischemia

90 Stages of Sickle Cell Retinopathy 1. Peripheral arterial occlusions 2. Peripheral arterio-venous anastomosis 3. Neovascularization 4. Vitreous hemorrhage 5. Retinal detachment

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