ACUTE VISUAL LOSS

Amy O’Regan
Ophthalmology Tutor
Email: amy.oregan@ucd.ie
 LOSS OF VISION- HISTORY

Metamorphopsia straight line appear

• Duration? Hours / days versus months / years? wavy - ask them to
lokat a door frame
• Nature of visual loss?
sudden vs gradual have v diff
• Complete or blurry? causes and indicates how
soon need to be see ie eye
• Central or peripheral? casuality or out patient
red eye
• Metamorphopsia (distortion)?
age related
• Painful or painless? macular
is stroke Central visual loss degeneraion
• Any associated symptoms?
• Systemic medical conditions?
 EXAMINATION- VISUAL
ACUITY

• Snellen chart
• Ask patient to wear distance glasses
• Test from 6 metres
• If patient can’t see anything from 6m then try from 3m, 1m
• If can’t see from 1m then try Counting Fingers, Hand
Movements, Perception of Light
at 6 m if done from
• One eye at a time
3 m - would be 3/X

• Record as 6/X
• 6/6 = normal last line

• 6/60 = The patient can only read those letters at 6 meters,

a normal person would be able to read it at 60 metres
• Pinhole improves sight if there is a refractive error or a
cataract
EXAMINATION- RELATIVE AFFERENT
PUPILLARY DEFECT (RAPD)

should both constrict

equally
if problem with retina or
nerve
appears to dilate when
should constrict see
wkshop
LOSS OF VISION
BLOOD SUPPLY

carry blood away

supply choroid

supply retina get

loss of vision if ob
with them
 BLOOD SUPPLY

Optic disc (optic nerve) fundus of eye

Central retinal vein

Central retinal artery

Macula central vision

Branch retinal vein

Branch retinal artery
conjoin at central retinal vein
4 branches and out through optic nerve
head
CENTRAL RETINAL ARTERY OCCLUSION
(CRAO)

• Abrupt reduction in blood flow through the central

retinal artery
• Severe enough to cause ischaemia of the inner retina
• Irreversible retinal damage after 90-100 minutes
painless leads to ischemia
dusky - loss of arteioroles - and 'cherry spot ---> redish
macula
 PRESENTATION OF CRAO

• History:
transient ischmic
• Sudden painless severe loss of vision attack - clot,
CRAO = effectively
• May be preceded by episodes of amaurosis fugax = temporary
a stroke visual
and these loss (10% cases)
patients need a
• Most patients >60, affects Men > Women stroke workup

• Ask for symptoms of Giant cell arteritis

scalp tenderness
• Previous vasculopathy/RFs or jaw
claucidication
• Exam:
• Visual acuity is very poor, typically 6/240 or worse
cant read cart prob
• Relative afferent pupillary defect only see hand
mvmts
• Swollen pale retina with a cherry red spot
• Arteriolar attenuation
 MACULAR SPARING

• A patent cilioretinal artery results in a small

area of central retina that appears normal, with
or without preserved central vision
• Occurs in 25% CRAOs
• Good visual prognosis in these patients

some lucky patients

only affects peripheral vision
better prognosis but usuLLY THE
prognosis is poor
 CAUSES OF CRAO

can be a clot in situ

Embolic Thrombotic Other important not to

miss this
• Carotid artery disease • Atherosclerosis • Vasculitis eg GCA

after valve
• Atrial fibrillation • Coagulopathies • Traumatic vessel damage
replacement
• Cardiac valve • Vasospasm
vegetations antiphospholipid
syndrome
 INVESTIGATIONS

• Rule out Giant Cell Arteritis

• Raised ESR, CRP
• Temporal artery biopsy
• Stroke work-up:
• Blood pressure
• FBC, HbA1c, Lipids, clotting screen
• Carotid doppler US
clotting screen
• Cardiac: ECG and Echo

looking at cardiac cause of embolis

GCA = older have raised ESR or CRP - if these are noraml can b
pretty sure dont have GCA unless sympts really suggestive of it
temporal artey biopsy but befire that do steroids
 MANAGEMENT

o Immediate- to try to reperfuse

the eye: usually present too late to reperfuse
manage the cause '
• Ocular massage for 15 mins optimize their stroke risk factors
if do present immediately can try to reperfuse th eye

• Decrease intraocular pressure- reduce interocular press - may cause more blood to
anterior chamber paracentesis, IV come to eye

acetazolamide increase CO2 level may cause vasodilatoin in eye to

reperfuse
• Rebreathing into a bag
• Manage cause and optomise risk
factors
 CENTRAL RETINAL VEIN OCCLUSION

blokcs drainage of
blood from the reina
and results in leakage
of fluid and blodd from
retinal vein
are dilated and tortuous
optic nerve head is
swollen
exudates, macular
oedema, retinal
hemorrhage in all 4
retinal quads
 RISK FACTORS AND ASSOCIATIONS OF
CENTRAL RETINAL VEIN OCCLUSION
arent considereed
same as stroke
dont need as an
extensive workup
• Age
• Hypertension
• Hyperlipidaemia
• Diabetes mellitus
• Smoking
• Raised IOP
in younger patients • Hypercoagulable states
• Myeloproliferative disorders, Antiphospholipid syndrome, Prooein C/S,
deficiency,, OCP
• Inflammatory conditions eg Behcets, GPA, Sarcoidosis
 PRESENTATION

History:
but can be in both
• Presents with acute painless onset of blurred vision, usually unilateral eyes in
inflammatory
condition
Clinical signs:
• Vision loss varies from mild to severe
isch crvo worse
• Worse VA in ischaemic CRVO
prognosis
• RAPD if ischaemic CRVO
• Retinal haemorrhages in all four quadrants
• Engorgement retinal vessels
• Macular oedema, optic nerve head swelling
• Cotton wool spots
• Neovascularisation in ischaemic CRVOs
 BRANCH RETINAL VEIN OCCLUSION

hemorrage and exudates only in

supero- temporal can result in
maculuar oedema like with
CRVO
 INVESTIGATIONS
branch or CRVO
not as urgent as artery

useful in CRVO to say • Blood pressure, HbA1c, Lipids

there is ischmia and if
will have neovasc and
poor prognosis
• If <40, investigate for hypercoagulable state
• Optical coherence tomography to assess macular oedema
• Fluorescein angiography can be useful in assessing ischaemia
 MANAGEMENT OF CRVO

• Establish cause and manage risk factors

• Treat complications
• Degree of ischaemia determines prognosis
 COMPLICATIONS OF CRVO

Macular oedema-
• Treated with intravitreal anti-VEGF or
steroid injections
usuLLY 3 INJECTIONS 6
WKS APART

bubbles - fluid dt
leakahe from veins
foveal dip in macula
 COMPLICATIONS OF CRVO

Neovascularisation in ischaemic CRVOs

EITHER ON ANTERIOR
CHAMPBER ON IRIS OR
RETINA
• Rubeosis iridis → 100 day glaucoma
• Managed with pan-retinal photocoagulation,
Intravitreal anti-VEGF injections

ON IRIS CAN RESULT I • Intra-ocular pressure lowering drops in rubeotic

GLAUMCOMA AS BLOCKS glaucoma
DRAINAGE OF AQ HUMOUR
THROUGH THE
TRABECULAR MESHWORK
100 DAYS AFTER CRVO

if there is neovas pan retinal

phototcoag - to destroy
ischmic retina and reduced
VEGF and can do anti vegf
iinjecions
 RETINAL DETACHMENT

detachment from
neuro sensory retina
from retinal pigment
epithelium - baloons
forward needs
surgical intervention v
quickly
 RISK FACTORS
minus 8 or 9 retina
is like wall paper -
when is very long
is much further
• High myopia stretched

• Peripheral retinal degeneration (eg lattice

degeneration)
• Family history of retinal detachment
• Ocular trauma
• Previous intraocular surgery
 THREE TYPES

• Rhegmatogenous – due to a break/tear in the retina (eg due to

trauma, or a traumatic posterior vitreous detachment) full thickness hole/break - vitrious humor can leak
under retina pushing retina forward off the retinal
pigment epithelium

• Tractional – due to membranes on retinal surface that contract and

fibrous bAND ON RETINA PULL
cause traction on retina (eg in proliferative DR) IT FORWAR - USUALLY IN
SEVERE PROLIFERATIVE
DIABETIC RETINOPATHY

• Exudative/serous – due to inflammation or subretinal mass lesion

(eg with choroidal melanoma) FLUID PUSHES THE
SENSORINEURAL RETINA
PUSHED FORWARD OFF THE
RETINAL PIGMENT EPITELIUM
 RHEMATOGENOUS RD
ASSOCIATED WITH
BEING SHORT
SIGHTED AND IS
STRETCHED TO THE
EXTREME

IF POST VITRIOUS
DETACHMENT
OCCURS VITROUS
JELLY COMES
FORWARD - SEE
FLOATERS - PULLS
RETINA WITH IT - GET
RETINA TEAR
HAPPENS WHEN GET
OLDER
 TRACTIONAL RD

PROLIFERATIVE
DIABTETIC RETINOPTHY

TRACTION FROM
PROLIFERATING
MEMBRAN ON THE RETINA
PULLS THE RETINA
FORWARD OF RETINAL
PIGMETN EPI
 EXUDATIVE RD

DT CHOROIDAL MELANOMA -
PUSHING MEM FORWARD
 PRESENTATION

History:
• New floaters (“shower of black dots”)
• Flashing lights (photopsia)
• Dark shadow in visual field
OR VISUAL FIELD
Exam: DEFECT
SOMETIME LOSE
PERIPHERAL
• May have RAPD DEFECT

• “Tobacco dust” (pigment cells seen in vitreous)

• May have vitreous haemorrhage HEMOR - CANT SEE BACK OF
EYE AT ALL - DO US
 MANAGEMENT
LOCALISATION AND CLISURE OF BREAKS

• Identify and close any retinal tears/breaks (with laser

or cryotherapy)
BUCKLE
AROUNDEYE
MUSCLES TO
Surgical Techniques: SUPORT SCLERA
AND SUE
• Scleral buckle CRYOTHERAPY
(silicone buckle around globe to
relieve any traction and support retinal tears)

• Vitrectomy (removal of vitreous and flattening of

retina)
PUT IN SALT WHILE OPERATING THEN PUT IN
GAS OR OIL.. TO HOLD THE RETINA IN PLACE ?
PERMANENTLY?
• Pneumatic retinopexy (injecting a gas bubble to
tamponade the retinal tear)
GAS BUBLE
EXPANDS TO
HOLD THE
 RETINOPEXY

IDEALLY CATH PPL BEFORE

RETINA DETACHES CAN THEN
LASER THE TEAR IN er WITHOUT
THEATRE - YELLOW DOTS ARE
LASER BURNS TO HOLD IT IN
PLACE
 PROGNOSIS

• Depends on whether macular attached or detached at presentation

HAVE GOOD • Macula-on detachment – requires urgent repair and usually has a good
VISUAL AQUITY
WHEN PRESENT
visual prognosis
AND AFTER -
NEED TO BE • Macular-off detachment – repair can be not as urgent (within a few
OPEERATED ON
V ACUTELY
days usually) – and generally worse visual prognosis

THOUGH MOST
PPL GET IT BACK
AT 6/12 NEEDED
FOR DRIVING
 LOSS OF VISION

Acute Gradual
Painful Painless Painless

Keratitis CRVO Cataract

Uveitis CRAO Glaucoma (POAG)
Scleritis Retinal detachment Dry AMD
AACG Wet AMD Diabetic retinopathy
Optic neuritis Vitreous haemorrhage Refractive error
GCA NAION
CVA
Amaurosis fugax
THANK YOU Any Questions email me: amy.oregan@ucd.ie