No TIA Sx Primary care provider, Neurology Antiplatelet meds if on none, ASA contraindications 81 mg qd Carotid ultrasound Echocardiogram
TIA SX Urgent care Primary care provider Neurology ER
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 “
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. [1063-68]
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
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?
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
ASYMPTOMATIC HOLLENHORST PLAQUE No evidence to suggest that carotid endarterectomy is of benefit
Prevalence of Stroke by Age and Sex NHANES: 1999-2002 Source: CDC/NCHS and NHLBI.
Estimated Direct and Indirect Costs of Cardiovascular Diseases and Stroke United States: 2005 Source: Heart Disease and Stroke Statistics – 2005 Update.
Percentage Breakdown of Deaths From Cardiovascular Diseases United States:2002 Preliminary Source: CDC/NCHS.
Case 2 Sudden vision loss right eye few days duration 65 yo male Ocular hx unremarkable Med hx hypertension, diabetes
Examination Best corrected vision - 10/400 Right afferent pupillary defect
DIAGNOSIS CRVO 2 types Ischemic vs non ischemic likely ischemic
Ischemic CRVO VA less than 20/200 APD Numerous CWS > 10 disc areas of capillary nonpefusion 30% of all CRVO- 50-60% develop NVG NVG 3-4 months [90 day glaucoma]
Nonischemic CRVO VA usually better than 20/200 or better No APD Few cotton wool spots May progress to ischemic CRVO
Uncommon Etiologies of CRVO Polycythemia Plasma cell dyscrasias
Polycythemia Increased RBC and blood volume Polycythemia vera- idiopathic Secondary polycythemia- erythrocytosis Erythrocytosis can be due to hypoxia or condition causing increased stimulating factor
Plasma Cell Dyscrasias Multiple myeloma Waldenstrom’s macroglobulinemia Malignant production of immunoglobulins Increased serum viscosity
Homocystinemia Elevated homocystine levels associated with atherosclerosis and CRVO Normal homocystine metabolism, but elevated levels of the amino acid
Neovascular glaucoma Response to ischemia Difficult to manage Intractable pain/ enucleation
Clinical Management and Natural History of CRVO Arch Ophth Vol 115, Apr 97, 486-91 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
Follow up CRVO based on Initial Visual Acuity >20/40 q 1-2 months for 6 months 20/50-200 q 1-2 months for 6 months <20/200 q 1 month for 6 months
CRVO Treatment PRP if ischemic Intravitreal triamcinolone injection as tx for non-ischemic occlusion, likely not effective for ischemic occlusion
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
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
CRAO Treatment AC paracentisis if <24 hours old IV diamox Ocular massage Inspiration of high concentration of oxygen and carbon dioxide
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
Examination findings Best corrected vision 20/20;20/40 Perrla – no afferent defect Confrontation field superior defect OS SLEx and IOP unrmarkable Fundus examination
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
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
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