CRVO -
2003/09/16
pathophys-
caused by
thrombus
eval - hx:
dm, htn, cv dz
exam: ?
evidence of glc, NVI/NVA (gonio crucial, usually happens in 3-4 months) - may
see qmonth x 6 months
when to do
more extensive work-up:
no htn, dm
or cv dz
young
patients <50 yrs
family hx of
thrombophilia
w/u for
young pt with crvo:
cbc (c diff
and platelet count)
resistance
to activated protein c in whites
hgb
electrophoresis in blacks
if neg,
consider:
antiphospholipid
antibody, lupus anticoagulant, anticardiolipin antibody
homocysteine
level, spep, protin c, s, and atIII
management:
optimize
control of htn, dm (for other eye)
if have
perfused crvo (no rapd, intermediate to good Va)
- control
iop
- monthly
f/u for progression to non-perfused status (1/3 convert over 3 yeas)
if
non-perfused crvo (rapd, intermediate to poor va)
- monthly
f/u for nv
- PRP for
any NV
lessons from
CVO study
1/3 of
perfused crvos convert over 3 years
initial va
is good predictor for final va except when in intermediate range
nvi/nva
develop in 35% of nonperfused eyes
prophylactic
PRP not effective (but consider if pt is non-compliant)
unlike in
brvo, grid laser for macular edema not effective (trend toward beneficial effect
in younger pts)
BRVO
what looks
like:
sx - sudden
or gradual loss of vision (mild or severe) - may be preceded by transient loss
of vision
localized
intraretinal hemorrhage (often pie-shaped)
sometimes:
macular
edema (persistent in 1/3)
cotton-wool
spots
vitreous
hemorrhage
old BVOs:
scattered HE, MAs, fibrosis, sheathing, cysts, holes, pigmentary changes
pathophys:
thrombus
formation at a-v crossing, where artery is anterior to vein
stasis,
hypoxia, endothelial cell loss
eval:
hx: htn, cv
dz, obesity (dm not strong independent risk factor)
exam: evid
of glc, uveitis, toxoplasmosis, Coat's disease
when to do
more extensive w/u: same as crvo, rarely necessary
management
(BVOS)
- grid laser
for perfused macular edema
va must be
20/40 or worse
wait 3
months for spontaneous improvement
fa used to
determine status of macular perfusion
wait for
blood to clear for adequate fa (no sense in getting fa acutely)
65% vs 37%
rate of improvement with and without grid laser
- segmental
scatter photocoagulation for NV
other
treatments - sheathotomy at a-v crossing
CRAO
looks like:
sx - abrupt
loss of vision (cf to lp in 90%)
may be
preceded by transient loss of vision
opacified
retina assumes a yellow-white appearance
- cherry red
spot
- may take
hours to become apparent
- limited to
the posterior pole
- resolves
over 6-8 weeks
RAPD c pale
disc - see very often
cilioretinal
artery in 25%
looks like:
visible
emboli in 20-40%
-yellow
cholesterol plaques usually from carotid
-calcific
emboli less common - cardiac valves
-qualitative
assessment should not influence work-up
rubeosis
iridis in 20%
-develop
faster than in CRVO (mean 4-5 weeks)
NVD in 2-3%
pathophys
crao caused
by
-emboli
-thrombus
due to: atherosclerotic plaque, vasculitis, spasm, dissecting aneurysm, htn
arterial necrosis
50% have
structural cardiac pathology
45% have
carotid atherosclerosis
-18%
hemodynamically significant
MUST FIND
SOURCE IN CRAO
eval:
hx: htn in
2/3, dm in 1/4, heart disease (sbe, rheumatic dz, valvular dz, congenital
defects, recent MI)
IVDA
exam:
prepaillary
arterial loops
disc drusen
auscultation
eval:
ancillary
tests
fa not
necessary but can distinguish ophthalmic artery occlusion vs. crao
carotid u/s
esr on
>55 years old, carotid u/s
younger pts
need hypercoag workup
management:
irreversible
damage after 90-100 minutes in primate model
modalities:
ocular
massage, O2 100% - gives nl pO2 at inner retina
CO2 -
vasodilator, causes increased retinal blood flow - carbogen
anteior
chamber paracentesis
thrombolytic
therapy - systemic complications, gen not used
vasodilators
- ntg, papaverine
laser to
emboli
can f/u
qmonth x 6 months
BRAO
sx: blurred
vision or field defect
localized
superficial retinal whitening
eval: same
as crao
management:
observation
unless perifoveal capillaries involved
prognosis
much better than CRAO, 20/40 or better in 80%