Transcript Sudden Painless Loss Of Vision

Sudden Painless
Loss Of Vision
By
Minal G. Birambole.
(internee)
G.A.M &R.C,
Shiroda,Goa
 Sudden loss of vision is alarming to both the patient
and the clinician alike.
 sudden & transient visual loss or obstruction may
simply be a symptom of dry eye or may herald the
onset of irreversible visual loss or stroke.
Causes of sudden loss of
vision
Central Retinal artery occlusion
Vitreous hemorrhage
Retinal detachment
Central Retinal vein occlusion
Optic neuritis
Methyl alcohol amblypia
Retinal artery occlusion
Etiology more common in
patients suffering from
hypertension.
 Thrombosis
 Embolism
 Retinal artritis
 Angiospasm
Central retinal artery occlusion
Clinical Features  More common in male
 Usually unilatral,rarely bilateral
 It is due to obstruction at the level of lamina
cribriosa.
Symptom –
Painless sudden loss of vision
Signs Direct pupilary reflex is absent.
 Retinal artery markly narrow.
 Retinal vein look normal.
 Retina become milky white.
 Chery red spot (central part of
macular area)
 Blood coloum is segmented.
 ERGs of CRAO
branch retinal artery occlusion
 Usually occurs
following lodgment of
embolus at bifercation.
 Retina distal to
occlusion become
odematous.
 Later on permanent
sectorial visual field
defect.
Management –
treatment is unsatisfactory as
retinal tissue can’t survive ischemia more than few
hours.
Emergency treatment Immediate lowering of intraocular pressure
by IV Mannitol
intermittent occular massage
paracentesis of anterior chamber
 Vasodilator & inhalation of mixture of 5%
carbon-di-oxide & 95% of water.
relive angiospasm
 Anticoagulant
 IV steroids
Complicationneovascular
glaucoma with
incidence varying
from 1% to 5%.
Retinal vein occlusion
Etiology  More common than artery occlusion
 Typically affects elderly patients in 6th or 7th
decade in life
 Pressure on the vein by sclerotic retinal artery
 Hyperviscocity of blood as in polycythemia
 Periphlebitis retinae(central or peripheral)
 Raised intraocular pressure,more common
in primary open angle glaucoma
 Local causeorbital cellulitis
facial erysipelas
cavernous sinus thrombosis
Central retinal vein occlusion
Non ischemic
 most common clinical variety
 Characterised by mild to
moderate visual loss.
Fundus
examination-
In early stage mild venous congesion
 Tortusity
 Few superficial flame shaped
haemorrhage more in periphery
than posterior.
 Mild papillodema
 Mild macular odema
In later stage-
 Sheathing arround main
vein
 Few cilioretinal collatrals
around disc
 Retinal haemorrhage
partly absorbed
 Macula shows chronic
cystoid odema.
Treatment Usually not required
 Condition resolve with
almost normal vision in
about 50% cases.
 No treatment is effective
for chronic cystoid
macular odema
 Course of oral steroids 812 weeks may be
effective.
IschemicRefers to acute complete occlusion of central retinal
vein
Characterised by marked Sudden loss of vision
Fundus examinationin early stage Massive engorgement
 Congestion
 Tortusity of veins
 Massive retinal
haemorrhage
 Papilloedema
 Macular area oedematous
in later stage Sheathing around vein &
collatrals seen around disc
 Neovascularisation at disc
 Macula-marked
pigmentary change
 Chronic cystoid oedema
Difference between ischemic from non
ischemic
Presence of relative afferent pupillary defect
Visual field defect
Reduced amplitude of b-wave of ERG.
Complication Rubiosis iridis
 Neovascular glaucoma in more than 50%
cases within 3 months
 Few develops vitreous hemorrhage
Treatment Panretinal
photocoagulation
 Cryo-application
 Photocoagulation
Above is carried out
when most of
interretinal blood is
absorbed.
Branch retinal vein occlusion
 More common than





central retinal vein
occlusion
Occur at following site
main branch at disc
margin
Major branch vein away
from disc
At A-V crossing causing
quadratic occlusion
Small macular occlusion
 Occlusion oedema &
haemorrhge are
limited to area drain
by affected vein.
 Vision is affected
when macular area is
involve.
Treatment Grid
photocoagulationsin chronic
macular odema
 Scatter
photocoagulationsin
neovascularisation
Vitreous haemorrhage
Usually occur from retinal vessels
Pre retinal
haemorrhage
intrageal
haemorrhage
Etiology Associated with PVD
 Trauma to eye
 Inflamatory disease like
chorioretinitis,periphlebiti
s retinae
 Vascular disoders like
HTN retinopathy
 Metabolic disease like
DM retinopathy
 Neoplasm
 idiopathic
Clinical featuresSign Distant direct opthalmoscopyblack shadow against the
red glow in small haemorrhage.
 Direct & indirect
opthalmoscopypresence of blood in
vitreous cavity
 Ultrasonography with B-scanit help in diagnosis.
Symptoms In less haemorrhage-
sudden development
of floaters.
 In more haemorrhage-
of vision
sudden painless loss
Treatment Conservative treatmentbed rest
elevation of
patients head
bilateral eye
patches
 Treatment of causemanagement
of retinal break, phlebitis,
proliferative retinopathy.
 Vitrectomy-
by pars plana
route, if haemorrhage
is not absorb after 3
months.
Retinal detachment
Separation of neurosensory retina proper from
the pigment epithelium.
Classification1. Primary retinal detachment
2. Secondary retinal detachment
Primary retinal detachment
Usually associated with retinal break
Sub retinal fluid seeps
Separate the sensory retina from pigmentary
epithelium
Etiology Most common in 40-60
yrs.
 More in males
 40% cases are myopic
 More common in aphakes
 Retinal degenaration
 Trauma
 Senile post.vitreous
detachment
PathogenesisSenile acute
predisposing
Post.vitreous
retinal
Detachment
degenaration
Retinal break
aphakia
trauma
Degenarated fluid seeps through retinal breaks
Retinal detachment
Clinical featuresProdromal symptomdark spot in
front of the eye
photopsia
Symptoms loss in field of vision which
progress total loss when
detachment progress to macular
area.
 Sudden painless loss of vision
A view from person having retinal detachment.
Sign External examinationeye is usually normal
 Intraoccular pressure
is low
 Plain mirror
examinationan altered red reflex
in pupilary area.
 Opthlmoscopy Detach retina gives
grey reflex & raised
anteriorly.
 it thrown in to folds
which oscilate with
the movement of eye
 Total detachment of
retina funnel shaped,
being attached only at
disc & ora serrata
 Retinal vessels
appear dark tortuous.
 Electroretinographysubnormal or
absent
 Ultrasonographyconfirm the
diagnosis
Complicationproliferative vitreoretinopathy
complicated cataract
uvelitis
phthisis bulbi
Proliferative vitreoretinopathy
Uveitis
Pthisis bulbi
Treatment Sealing of retinal breaksby producing aseptic chorioretinitis,
cyocoagulation,
photocoagulation
 Scleral bucklingTo bring the sclrochoroid & retina near to each
other
 Drainage of SRF
chororetinitis
 Internal tamponade by
SF6 gas or silicon oil
 Pars plana vitrectomy
Solid retinal detachment
Occurs due to retina being pushed sway by neoplasm
or accumulation of fluid beneath the retina.
Etiology Systemic diseasetoxaemia in pregnancy
renal HTN
blood dyscrasias
polyarthritis nodosa
 Occular disease Inflammation like the Harada’s disease,
posterior scleritis,orbital cellulitis
 Vascular disease like central serous
retinopathy & exudative retinopathy
 Neoplasm like malignant melanoma of
choroids
Clinical featuresCan be differentiate from simple
1. Absence of photopsia
2. Holes or tears
3. Folds
4. Undulation
5. Smooth & convex detachment
6. At summit of tumour,it usually rounded &
fixed
7. Pattern of retinal vessel is disturbed
Treatment Absorption of fluid
 Treatment of causative
factor
 If tumour-enucleation
Optic neuritis
Includes inflammatory &
demyelinating disorder of
optic nerve
Etiology Idiopathic
 Hereditary optic neuritis
 Demyelinating disordersmultiple sclerosis
neuromyelitis
optica
Clinical featuresClassified in to three Papilitis
 Neuroretinitis
 Retrobulber neuritis
 Papilitis-
It is inflammation of optic disc.
Usually unilateral
Symptom
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Sudden profusal visual loss is hallmark of papilitis
Dark adaptation is depressed
Light brightness is depressed
Colour object may look wash away
Depth perception percularly for moving object may be impaird.
Signs Visual acuty reduced markly
 colour vision often severly impaired
 Pupil-ill-stained constriction to light
 Ophthalmoscope Hyperemia of disc
 Bluring of margin
 Disc become oedematous & physiological cup is
obliterated
 Retinal veins are congested
 Splinter haemorrhage is seen.
 Visual field change-
central or centroceacal scotoma.
the field defect are more marked to red colour than
white
 Visually evoked response (VER)shows reduced amplitude
& delayed in the transmission time.
Methyl alcohol amblyopia
Acute onset
Resulting in optic atrophy & permanent blindness
Etiology Intake of wood alcohol spirit in cheap adulterated
beverages
 Inhalation of fumes in industries
 Absorbed from skin following prolonged daily use
of linments
PathogenesisMethyl alcohol metabolized very slowly,
stay longer period
Oxidised in to formic acid & formaldehyde
oedema
Degenaration of ganglion cell of retina
Complete blindness
Clinical features Headache
 Dizziness
 Nausea
 Vomiting
 Abdominal pain
 Delirium
 Stupor
 Even death
Diagnostic signPresence of charecteristic
odour due to excretion of
formaldehyde
Occular featuresmild disc oedema
markedly narrowed
blood vessels
bilatral optic
atrophy
Treatment Gastric lavage
 Admission of alkali to overcame
acidosis.sodabicarb may be given orally or
IV
 Eliminative treatment by diaphoresis in the
form of peritoneal dialysis
 Prognosis is usually poor, death may occur.
The eye is the lamp of the body
If your eyes are good,
Your whole body will be full of light,
so
Take care of your eyes.