Acute

visual loss

Types of acute visual loss

1) According to duration
2) Painful / painless

DDx of acute visual loss

According to duration

Transient
Seconds
Papilledema

Minutes

Amaurosis fugax
- Uni TIA
- Bil Vertebrobasilar A insuff
Impending CRVO
>24 hours to a few days (acute)
Painless

Painful

10 60 min
Migraine

Retinal detachment
Retinal vascular diseases (central retinal A / V occlusion)
Vitreous hemorrhage
Macular disease
(wet age-related macular degeneration a/x hemorrhage)
AION
Corneal ulcer
Corneal abrasion
Endophthalmitis, slceritis, uveitis
Optic neuritis (pain on eye movement)
IOP ( corneal edema pain)

A/x Sx
1) Flashes

A) Vitreoretinal traction
*If floaters, flashes chronic
Posterior vitreous detachment
e.g. more than 6 weeks less
Retinal break & rhegmatogenous retinal detachment
worrying,
B) Migraine

2) Floaters = grey/black specks or lines or cobwebs
Hyaloid A. remnants
Posterior uveitis
Vitreous
i) Syneresis ii) Condensations / debris (asteroid hyalosis)
iii) Hemorrhage iv) Detachment (PVD)
Retinal tear / detachment

Hx
Visual loss
1) Binocular or monocular?
2) Time onset (gradual or sudden?), duration of Sx (second, minute, hours, days..), progressive or stable
3) Vision normal before?
4) Precipitating factor Trauma, recent eye surgery
5) Past episode
A/x sx
1) Painful, painless pathology in back of eye
2) Flashes & floaters
3) Visual field defect
RF
1) DM
2) HT
Causes
- MS, trauma
Past ophthalmic hx
1) Ocular surgery/laster e.g. recent intraocular surg (endophthalmitis), barrier laser retinal detachment
2) Uveitis, glaucoma, high myopia, blepharitis
3) Predisposing factor for ocular surface infn (contact lens, use steroid)
Drug Hx aspirin, anti-coagulants
A/x Dz
- CAD / CVD
PE
AFROO (on dilated fundus)
IOP
Color vision
EOM
Slit lamp
Affected and then DO NOT forget the other eye!!!! As also predisposed to having pathology!
(AIFRO + Slit lamp + stain)

Cornea
1) Corneal edema


Vitreous humor
I) Vitreous syneresis
liquefaction of vitreous body
RF = aging, myopia, trauma, post intraocular surgery

II) Vitreous Condensation asteroid hyalosis = white Ca opacities seen in slit lamp

III) Posterior vitreous detachment
Etiology Vitreous body shrinks & liquefies (syneresis)
i.e. molecules that hold water condense (collagen fibres lose crosslinks form clumps)
= floaters
Liquid vitreous moves btw vitreous gel & retina (as cortex thins + pockets of liquid enlarged)
vitreous membrane peeled away and sep from internal limiting membrane of
neurosensory retina (at vitreous base)
this peeling process usu starts ard fovea, last around the optic disc at Weiss ring
and ora serrata
(Former and latter = 2nd and 1st strongest attachment to vitreous cortex in posterior
segment)
(Weiss ring = glial tissue around optic disc that stil remains attached to membrane
indicates vitreous nearly detached from optic nerve )

Clinical
Cx

Floaters
Flashes of light (Mechanical disruption of photorecptors stimulation AP)
More common in high myopes / ocular trauma (blunt/perforating)
1) Retinal tears/detachment
If there are areas of abnormally strong vitreoretinal adhesions (e.g. lattice degen)
Vitreous traction retinal hole / break liquefied vitreous flows subretinally RD
Clinical features: sudden dramatic increase in floaters (RPE) / flashes of light

2) Vitreous hemorrhage (caused by 1)
If bridging retinal blood vessel torn

PVD vs RD

Risk factors

PVD
High myopia
Trauma

Floaters
Flashes
Visual field defect
VA

Chronic
Acute
/
/

Shafers sign*
Retinal
break/subretinal fluid

/
/

RD
High myopia
Trauma
Previous Hx of retinal break/degen
Family Hx of retinal detachment

Progressive in days
Progressive (in days)
Affected if macula involved
(can be normal if without central part detach)
+ve Shaffers sign 75% RRD
+ve

*Shaffers sign = RPE in anterior vitreous (right behind lens) tear on retina
Aka tobacco dusting
Detected on slit lamp exam w/ a diopter, done when suspect rhegmat. RD

IV) Vitreous hemorrhage
Etiology
From new fragile vessels (any conditions that retinal ischemia neovascularizations)
1) Proliferative DM retinopathy (looks identical to radiation retinopathy!!!)
2) CRVO/branch
3) Chronic uveits, ocular ischemic syndrome etc rarer causes
From retinal vessels
4) RD,PVD vitreoretinal traction
Breakthrough hemorrhage
5) Wet AMD
6) Retinal macroaneurysm
Trauma/ subarachnoid hemorrhage

Clinical
Depends on location and amt of blood
i) Small extravasation floaters
ii) Large amt Acute visual loss + loss of red reflexes + retina not visible
Dx
Small amt Ophthalmoscopy on dilated pupil
Loss of red reflex but lens appears clear suspect VH Ultrasound (B-scan) to r/o RD, PDR
Tx
Vitrectomy RD repair retinal endolaser to possible bleeding sites/vessels

Retina ends peripherally at ora serrata (where the ciliary body begins),
Antomy
Nueorsensory retina (w/ photoreceptor) RPE choroid
Functions of RPE
Nourish retina by recycling vit A for use by retina, resorbs subretinal fluid
w/ melanin absorbs light and decreases light scatter within eye

Blood supply: Inner 2/3 = central retinal artery, outer 1/3 = choroid
Fovea only cones, the overlying layers not present
Retinal detachment
Intro
Cleavage in plane btw neurosensory retina and RPE
3 types
Rhegmatogenous
Tractional

Exudative

MOST COMMON!!!


Causes Full thickness tear / hole in Traction
Underlying condition
neurosensory retina
(from vitreous, epiretinal /
accumulation of fluid btw
fluid flows from vitreous subretinal membrane)
neurosensory retina & RPE
into subretinal space
pull neurosensory retina (usu due to damage of RPE)

from underlying RPE
Ex
PVD
PDR
Posterior Uveitis

Degen retinal changes
CRVO
Intraocular tumor

(Vitreous mem gliotic/
Trauma/iatrogenic e.g.

fibrous/vasulcar in response
cataract surgery

to proliferative xxx)


*Could also be progressed
ROP

from TRD
Ocular trauma

Tx
1) Scleral buckle procedure Vitrectomy
Treat underlying cause!

2) Pneumatic retinopexy
Injection of gas / silicone
(usu for smaller RD)
oil
1) + 2) + localization of
Scleral buckling
retinal tears/holes
Membrane removal
barrier

laser/cryotherapy to
*Pars plana vitrectomy:
make adhesions btw RPE insert needle through pars P
and neurosensory retina aspirate vitreous

**Pneumatic R: inject a gas
Recurrent cases:
bubble into eye btw retina and
Vitrectomy +
vitreous patient positioning
Injection of gas / silicone oil
Clinical features
4Fs
Flashes of light
Floaters
Field loss (peripheral) = curtain of blackness
Fall in VA / IOP

Others:
Loss of central vision if macula off
RAPD
Fundoscopy:
Shaeffers sign!!!! +ve when seeing clumps of brown/black pigments in anterior vitreous
on slit-lamp Rhegmatogenous RD
i) Loss of red reflex
ii) Bullous separation of retina: Detached retina look grey-white w/ surface blood vessels
OCT
Identify microscopic detachment of retina
Fovea status affects prognosis
B-scan
If large vitreous hemorrhage / severe cataract (significant media opacity)

Tx
Retinal tear:
Prophylactic: symptomatic tear
seal off with laser/cryotherapy prevent progression to RD

Retain detachment
Refer to above (principle: macula on: surgery asap, macula off: within a few days
Loss of vision, vitreous hemorrhage, recurrent RD

Cx
Retinal vascular
I) Branch / central retinal vein occlusion (CRVO) NOT a true ocular emergency
Intro
2nd most common vascular retinal disorder after DR
Usu manifestation of a systemic disease (HT, DM)
Thrombus within lumen of blood vessel
Predisposing factors 1) Arteriosclerosis

2) HT
Old ones look for
3) DM
vascular RF only is ok Others: Hypophospholipidemia
Young check blood
Open angle glaucoma
clotting for PV, etc
Hyperviscosity syndrome (PV, lymphoma, leukemia)
Drugs oral contraceptive pills, diuretics
Clinical
Sx
Signs

RAPD (+ve / -ve) +ve ischemic CRVO

Fundscopy
Blood and thunder appearance in all 4 quadrants!
Diffuse retinal hemorrhage
Cotton-wool spots
Dilated & tortuous veins (arteries WONT D & T!)
Macular edema
Swollen optic disc
Neovacularization
Hemorrhagic / ischemic retinopathy
Venous stasis / non-ischemic retinopathy
Significantly affected (20/200)
Less affected (20/80)
+ve
-ve
More hemorrhage & cotton wool spots Less
Higher risk
Lower
Poor visual prognosis
Resolves over months, may regain vision if

macula spared
Fundus fluorescein angiogram needed to determine degree of ischemia
(and thus risk of neovascularization)
Non-ischemic type 30% of conversion to ischemic, thus follow up needed
8 10 % of risk of B/CRVO in the other eye
No Tx available to restore vision loss
Treat underlying cause + prophylactic low dose aspirin
Reduce iris/retinal neovascularization Prevent neovascular glaucoma
- Retinal laser photocoagulation (PRP)

Macular edema in BRVO only
Macular grid laser photocoagulation
Macular edema in both BRVO AND CRVO
Intravitreal or slow-release biodegradable corticosteroid
Intravitreal anti-VEGF injection
Painless
Monocular
A/C visual loss

2 types

VA
RAPD
RH
NeoV
Px
Evaluat

Tx

If ischemic


If old and no edema
no
If young no edema
still need anti-VEGF
Cx
So check IOP

*Main 2 Cx of CRVO

1) Degeneration of RPE
2) Neovascularization* of retina and iris (secondary rubeosis) II glaucoma
3) Vitreous hemorrhage
4) Macular edema* w/ permanent visual loss



II) Central Retinal Artery Occlusion OCULAR EMERGENCY!
Etiology
1) Emboli (from carotid A / Heart arrhythmia, IE, VHD)
2) Thrombus
3) Temporal arteritis (giant cell arteritis)
Clinical features
Sx
PE
RAPD +ve
AVL
Fundoscopy
Painless (except GCA)
Cherry red spot at macula
Previous amaurosis fugax
(visualization of unaffected highly vascular
before the acute episode
choroid beneath thin fovea)

(

Cotton wool spots (retinal infarct)


Retinal pallor



Narrowed A., boxcarring (segmentation of blood in A)

Cholesterol emboli Hollenhorst plaques

(usu at arterioles bifurcation)
Workup
Blood immediate ESR, CRP, Plt as GCA is a DDx
CBC w/ differential, clotting profile, FBG
+ lipid profile, ANA, RF, FTA-ABS, antiphospholipid Ab if <50yo
Imaging
Echocardiogram, ECG (maybe Holter)
Carotid duplex US
Remarks
Restore blood flow within 2h in order to restore vision!!!!

Tx

Effect not really
proven

BRAO

Sooner tx = better prognosis!!!

Irreversible retinal damage if complete CRAO > 90 min!!!

1) Immediate globe massage dislodge emboli

(Intermittent raise IOP stop and restart blood flow and hope the flow can dislodge)
(heel of hand compress eye for 10s, release for 10s, continue for 5min)
2) Decrease IOP
IV acetazolamide
IV mannitol
Drain aqueous liquid (anterior chamber paracentesis May endophthalmitis)
Topical beta-blocker
Inhaled O2 (95%) - CO2 (5%) mixture )
Rebreathing bag (dilatation of arteries)
3) Tx underlying cause to prevent CRAO in the other eye
Not AVL but visual field defect
Fundus: only a segmental pallor not whole macula
EMBOLIC!!!!! NEED SEARCH FOR SOURCE!
Ocular massage
No Proven effective Tx for BRAO though
CRAO lower cahce of neovascularization coz it causes anoxia but not hypoxia so no release
of VEGF




Optic Nerve
Types of acute optic neuropathy: Ischemic optic neuropathy, optic neuritis, traumatic,

I) Acute Ischemic Optic Neuropathy
Ocular signs
1) Devastating visual loss 2) RAPD
3) Pale swollen optic nerve (chalky white), often with flame shape hemorrhage
4) Optic atrophy as optic nerve edema resolves 5) Visual field defect

Types
Arteritic
- Giant cell arteritis
Non Arteritic
Vascular disorder DM, HT etc
Painless visual loss
Altitudinal visual field dfect upper or lower uniocular field affected
Arteritic AION
Intro
More common in F >50 y/o (60 according to Toronto)
Clinical
Abrupt severe monocular visual loss
feature
Painless, non-progressive (can rapidly become bilateral tho)
Non-ocular systemic s&s
Temporal headache/tenderness aggravated on pillow
Jaw claudication pain when chewing
Scalp tenderness (tenderness w/ hair combing)
Thickened + non-pulsatile temporal artery
Polymyalgia rheumatica (proximal MS and joints)
Anorexia, weight loss, fever
Ix
Immediate ESR, CRP, Plt (coz can have thrombocytosis Plt > 400)
Temporal A biopsy (biopsy contralateral if ipsi ve)
Tx
High dose systemic CS relieve pain + prevent further ischemic episodes
(main reason = 50% the other eye will get non-arteritic as well)
Start Tx upon clinical suspicion, DO NOT wait till biopsy results out






II) Optic neuritis
Intro
18 45 y/o, younger than AION
Ex
MS, neuromyelitis optica
Clinical features Ocular S&S
Other Sx
VL (hours to days), nadir 1 wk after Focal neurological Sx weakness, numbness
Lhermittes sign electrical sensation down back on
onset, subtle / profound
neck flexion
Eye pain on movement
Antecedent flu-like vrial syndrome
Impaired color vision
Uhtohffs phenomenon Worsening of Sx on Ex /
RAPD +ve
increasing body temp
Visual field defect

Usu uni, can be bil
Dx
Tx

Blood NMO Ab
Imaging MRI brain Unidentified bright objects (UBO)) hyperintense plaque
NMO +ve immunosuppressants
Poor VA
Good VA
ONTT optic nerve treatment trial
Observation
IV methylprednisolone 3d

 Oral prednisone 11 d
(as oral only may increase recurrence rate)

Direct ophthalmoscope to check pupil

Take night time antihypertensive, then woke up and cant see in one eye
Painless
PMH: HT

Coz at night blood pressure already lowest, then take anti-hypertensive hypotension AION

More
Non arteritic smaller cup
Disk at risk consideration + hypotension

Normal CDR, chalky white disc

Barrier laser?????