retinal vascular disease don simpson, o.d. st. louis va medical center
TRANSCRIPT
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Retinal Vascular Disease
Don Simpson, O.D.
St. Louis VA Medical Center
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WELCOME TO MID-TOWN 915 N GRAND BLVD2 BLOCKS N OF THE FOX THEATER
St. Louis VAMC - John Cochran Division
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St. Louis VA Rotation
2 divisions John Cochran – mid town Jefferson Barracks- south county Equal time both divisions
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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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Diagnosis
Retinal embolus- Hollenhorst plaque What now?
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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
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Return to examination
Additional tests Auscultation of carotid arteries What if normal? What if bruit?
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Management
? TIA sx present TIA sx absent
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No TIA Sx
Primary care provider, Neurology Antiplatelet meds if on none, ASA contraindications 81 mg qd Carotid ultrasound Echocardiogram
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TIA SX
Urgent care Primary care provider Neurology ER
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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 “
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Additional signs carotid insufficiency
Hypo-perfusion retinopathy Ocular ischemic syndrome
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Hypo-perfusion retinopathy
Peripheral retinal hemorrhages associated with decreased retinal artery perfusion pressure
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Ocular ischemic syndrome
NVI Retinal neovascularization Neovascular glaucoma
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Surgical management carotid disease
Carotid angiogram Gold standard to evaluate stenosis Invasive procedure Carotid endarterectomy
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Cardiac sources of emboli
Mitral valve disease Arrhythmias- a fib , vent tach Valve replacement thrombi Sbe
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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]
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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
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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?
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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
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ASYMPTOMATIC HOLLENHORST PLAQUE
No evidence to suggest that carotid endarterectomy is of benefit
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Prevalence of Stroke by Age and Sex
NHANES: 1999-2002
Source: CDC/NCHS and NHLBI.
1.1
3.1
6.6
11.5
0.41.2
12.0
0.3 0.82.1
3.0
6.3
0
2
4
6
8
10
12
14
20-34 35-44 45-54 55-64 65-74 75+
Ages
Per
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f P
op
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Men Women
`
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Estimated Direct and Indirect Costs of Cardiovascular Diseases and StrokeUnited States: 2005
Source: Heart Disease and Stroke Statistics – 2005 Update.
254.8
142.1
56.8 59.727.9
393.5
050
100150200250300350400450
Hea
rtD
isea
se
Cor
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Percentage Breakdown of Deaths From Cardiovascular DiseasesUnited States:2002 Preliminary
Source: CDC/NCHS.
18%
6%
5%
4%0%0%
13%
53%
Coronary Heart Disease
Stroke
Congestive Heart Failure
High Blood Pressure
Diseases of the Arteries
Rheumatic Fever/RheumaticHeart Disease
Congenital CardiovascularDefects
Other
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Case 2
Sudden vision loss right eye few days duration
65 yo male Ocular hx unremarkable Med hx hypertension, diabetes
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Examination
Best corrected vision - 10/400 Right afferent pupillary defect
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DIAGNOSIS
CRVO 2 types Ischemic vs non ischemic likely ischemic
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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]
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Nonischemic CRVO
VA usually better than 20/200 or better No APD Few cotton wool spots May progress to ischemic CRVO
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Uncommon Etiologies of CRVO
Polycythemia Plasma cell dyscrasias
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Polycythemia
Increased RBC and blood volume Polycythemia vera- idiopathic Secondary polycythemia- erythrocytosis Erythrocytosis can be due to hypoxia or
condition causing increased stimulating factor
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Plasma Cell Dyscrasias
Multiple myeloma Waldenstrom’s macroglobulinemia Malignant production of immunoglobulins Increased serum viscosity
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Homocystinemia
Elevated homocystine levels associated with atherosclerosis and CRVO
Normal homocystine metabolism, but elevated levels of the amino acid
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Neovascular glaucoma
Response to ischemia Difficult to manage Intractable pain/ enucleation
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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
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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
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CRVO Treatment
PRP if ischemic Intravitreal triamcinolone injection as tx for
non-ischemic occlusion, likely not effective for ischemic occlusion
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Vision Limiting Complications of BVO Macular edema- 1/3 spontaneously regain
vision Macular nonperfusion, no vision improvement Vitreous heme- NVE, NVD
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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
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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
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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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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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Right fundus
diagnois CRAO Other questions Duration < 24 hr management
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Duration < 24 hr
AC paracentisis IV diamox Ocular massage Inspiration of high concentration of oxygen
and carbon dioxide
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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
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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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Disposition after GCA ruled out
Work up for other associated systemic conditions, emergent
Need medical work up for associated systemic conditions
Internest, cardiology, neurology
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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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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
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CRAO Treatment
AC paracentisis if <24 hours old IV diamox Ocular massage Inspiration of high concentration of oxygen
and carbon dioxide
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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
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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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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
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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
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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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Management
Diagnosis Retinal arterial macroaneurysm Additional tests FA Prognosis
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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
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Retinal Arterial Macroaneurysms
Distinct entity from Coats, Lebers, Eales Temporal retina within 1st 3 bifurcations M:F ratio 1:2 usually < 60 years old 75% have HTN, atherosclerosis
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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
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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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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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