SUDDEN VISUAL LOSS

Dr.Mohd. Mustafizur Rahman

Pakar Mata
Ophthalmology department
Queen Elizabeth Hospital
Objectives

• Have a clear DDx for causes of acute

vision loss

• Have a clear understanding of

immediate management steps to be
taken by the primary care provider
Acute loss of vision
Loss of vision

painful Painless

Prolonged Fleeting Prolonged

ACG embolic ION

Optic Neuritis migrain CRAO

GCA Raised ICP CRVO

Orbital cellulitis VIT.HGE

Endopthal Ret. Detach

Common causes of sudden
visual loss:
• Transient (< 24 hrs)
– Few seconds (usually bilateral):
Papilloedema
– Few minutes: Amaurosis fugax (TIA)
(unilateral), vertebrobasilar artery
insufficiency (bilateral)10-60 minutes:
– Migraine (with or without headache)
Visual loss (> 24 hrs)
Painless:
Retinal artery or vein occlusion,
Retinal detachment,
Ischaemic optic neuropathy
Giant cell arteritis,
Vitreous haemorrhage,

Painful: Acute angle-closure glaucoma,

optic neuritis
History
• Transient visual loss (suggestive of amaurosis fugax) 
• sudden onset floaters and flashing light (Retinal
detachment)  
• History of poorly controlled diabetes mellitus and laser
treatment to the retina (vitreous haemorrhage) 
• Headache +/- jaw claudication (pain in the jaw on
eating) in the elderly (giant cell arteritis) 
• Pain on eye movement in young patients (optic neuritis)
Examination

• Visual acuity 
• Visual field by confrontation
• pupil reaction for afferent pupillary
defect
• Retinal examination.
Retinal Artery Occlusion: Hx

• Central (CRAO) or branched (BRAO)

– May have macular sparing (cilioretinal
artery)
• Sudden, painless, unilateral
– Loss: central vision + one/more fields 
CRAO
– Loss: one (horiz) field loss  BRAO
– Transient loss, esp “curtain descending”
 amaurosis fugax = impending RAO
Retinal artery occlusion
Causes
• Arteriosclerotic changes,
• Embolus (from heart or carotid artery)
• Inflammation (rare) –periarteritis, SLE
• Haematological disorders – Protein c, s
deficiency, anti- thrombin 3 deficiency and
antiphospholipid antibody syndrome
Retinal Artery Occlusion: Signs

• Marcus-Gunn pupil (relative afferent

pupillary defect)
• Retinal edema (after 1st few hrs)
• The retinal arteries are narrow or collapsed
• Embolus may be seen at O.N. (CRAO)
or branch point (BRAO)
• Cherry red spot = ischemia & edema
of posterior retina
– w/in several hrs of occlusion
CRAO
BRAO
Retinal Artery Occlusion:
Etiology
• Carotid disease
• Valvular disease
• Giant Cell arteritis
– Jaw claudication, scalp tenderness, tongue
pain, PMR, H/A
• Thrombosis: hypercoagulable states
– Pregnancy, OCPs, lupus anticoag, factor V
Leiden, antithrombin III, ptn C/S deficiency
Retinal Artery Occlusion:
Etiology
• IV drug use (talc retinopathy)
• Lipid emboli from trauma
• DIC
• Sickle cell
• Polyarteritis nodosa
• Retinal migraine
Retinal Artery Occlusion: W/U

• Heart, Carotid exam

• TA tenderness
• Neuro exam
• Va, visual fields, pupil and retinal
exam
• Carotid u/s
• ECHO
Retinal Artery Occlusion: W/U

• Labs:
– ESR/CRP
– CBC w/ diff
– Coags
– Consider hypercoag w/u
Retinal Artery Occlusion: Mgmt

• EMERGENCY OPTHO REFERRAL!!

• Dislodge embolus to move embolus
“downstream” (decr IOP, dilate vessels)
– Ocular massage: firm digital pr on globe x 10-15 sec,
followed by rapid release of pr (may repeat 2-3x)
– Diamox 500mg IV or PO
– Topical beta blocker (timolol 0.5%)
– NTG sl
• Antiocoagulation once w/u confirms embolism
• Hyperbaric O2 within 24hr
Retinal Vein Occlusion
• Central (CRVO) or branched (BRVO)
– CRVO: involves all 4 retinal quadrants
– BRVO: involves one quadrant in arcuate
pattern
• Fairly common in elderly
• As with RAOs, may only be noticed with
unaffected eye closed
• Impedes flow of blood from retinal
circulation
Retinal Vein Occlusion: Sx

• Sudden or gradual, painless blurry Va

or vision loss
• Unilateral (horiz) visual field loss
(BRVO)
• Rare: unilateral pain and redness w/
loss of vision (“neovascular
glaucoma” assoc w/ RVO)
Retinal Vein Occlusion: Signs

• Marcus-Gunn pupil
• “blood and thunder” fundus
• Dilated & tortuous veins
• Flame-shaped hemorrhage
• Cotton-wool spots
• Macular edema
• Exudates
CRVO: “blood & thunder”
CRVO: cotton wool spots
BRVO
Retinal Vein Occlusion: W/U

• Va, visual fields, pupil and retinal exam

• Systemic htn
• HCG? OCPs?
• h/o other thromboembolic events, fam hx
• Labs
– Hypercoagulable w/u as in RAO
– tsh to check for thyroid eye disease
– compression of CRV
Retinal Vein Occlusion: Mgmt

• Optho eval w/in 48-72 hrs

• Laser photocoagulation to reduce
macular edema and neovascular
complications
Retinal Detachment

• Fluid separates retina from underlying

retinal pigment epithelium
• Causes:
– Posterior vitreous detachment  retinal tear
liquefied vitreous dissects between retina
and pigment epithelium
– Serous fluid under retina
– Traction from scar tissue in vitreous (diabetic
retinopathy  repeated vitreous hem)
Retinal Detachment: Sx
• Flashing lights
• Floaters
• Visual field loss: “curtain, shadow or
bubble”
• Metamorphopsia
• Decreased Va
• Painless
Metamorphopsia
Retinal Detachment: Signs

• Marcus-Gunn
• Unilateral visual field loss
– Sectoral, quadrant, hemifield, total
• Retinal exam w/ direct
ophthalmoscope may be unrevealing
Retinal Detachment
Retinal Detachment
Retinal Detachment:
W/U & Mgmt
• Immediate Ophtho referral!!
– Surgical intervention
– If acute or progressive should be
referred to Ophthalmology <24h, if
chronic may be seen with 2-4 weeks
Vitreous Hemorrhage

• Due to underlying vascular process

• Painless, pt may complain of red
“shower” or “spots”
• May be slower in onset vs RAO, RVO
or retinal detachment
• Visualization of retina often
impossible
– Ophthalmic u/s done by eye docs
Vitreous Hemorrhage: Etiology

• Proliferative diabetic retinopathy

• Posterior vitreous detachment w/ an
avulsed vessel
• Retinal tear through vessel
• Trauma
• Retinal vascular lesion
• Management: ophtho referral & tx
underlying process
Vitreous Hemorrhage
Angle Closure Glaucoma

• Outflow of aqueous humor from

shallow anterior chamber is occluded
when pupil dilates
• F:M = 3-4:1, high incidence in asians
• Peak age: 55-70
• Shorter, smaller far-sighted eyes
Normal Angle
Narrow or Closed Angle
Angle Closure Glaucoma

• Precipitating factors:
– Enter darkened room
– Stress
– Dilating drugs
– Systemic rx
• Anticholinergics
• sympathomimetics
Angle Closure Glaucoma: Sx

• Intense pain & photophobia

• Blurred vision, usually unilateral
• Halos around lights
• Vasovagal sx (diaphoresis, n/v)
Angle Closure Glaucoma: Signs

• Mid-dilated pupil
• Conjunctival injection w/ lid edema
• Corneal edema
– Blurring of corneal light reflex
• IOP markedly elevated (60-80 mm
Hg)
Angle Closure Glaucoma: Mgmt

• OPHTHO EMERGENCY!!!!
• Rx to lower IOP
– Topical beta-blocker (timolol 0.5% 1 drop)
– CA inhibitors (Diamox 500mg IV, or 250 mg PO
x2)
– Osmotic agents (mannitol 1-2g/kg IV over
45min)
• Laser iridectomy
Corneal Ulcer

• Risk factors:
– Recent trauma or contact lens wear
(may develop from corneal abrasion)
– Poor lid apposition
– Incr risk Gm neg bacteria (esp P’monas)
w/ soft contact lens wear
– Fungal: h/o trauma w/ vegetable matter
or chronic topical steroid use
Corneal Ulcer: Sx

• Pain
• Redness
• Decreased Va
• photophobia
Corneal Ulcer: Signs

• Dense corneal infiltrate w/ overlying

epithelial defect
• Hypopyon
• Corneal destruction and ocular
perforation
• Ulcer w/ feathery border: fungal
Corneal ulcer w/ hypopion
Corneal Ulcer: Tx

• Immediate Ophtho referral

• Corneal scraping for Gram’s stain &
Cx
• Abx: gent, cefazolin
• Contact lens removal
• Pt will require daily f/u until healed
Uveitis

• May be subacute in onset

• Pain, photophobia, decreased vision
• Exam:
– Small, sluggish pupil
– Circumlimbal flush
– Cell & flare in ant chamber on SLEx
• Ophtho eval before ocular steroids
Uveitis
Uveitis
Uveitis
Uveitis
Uveitis

• Etiol: most idiopathic; many systemic

causes
• W/U: careful H&P, looking for
systemic disease
– for unilateral, first-episode disease,
unremarkable hx and exam, no w/u
needed
– for bilateral, recurrent disease, systemic
w/u indicated
Uveitis

• Tx:
– ophtho referral w/in 24h
– cycloplegia (topical homatropine 5%
bid)
– topical steroid (Pred-Forte 1%) initiated
by an ophthalmologist
Optic Neuritis

• 15-45 y.o.
• Usually subacute (several days)
• Pain w/ eye movement (+/-)
• May have h/o transient neurological
disturbances
• Assoc w/ MS
Optic Neuritis

• Signs
– Optic Disc edema (unusual)
– Visual field cuts, esp. central
– Maracus-Gunn pupil (very common)
Optic Neuritis (pappiledema)
Optic Neuritis: Mgmt

• Ophtho referral
– eval for other ocular dz
– formal visual field testing
• MR of brain & orbits – confirmatory
and to look for early M.S.
Optic Neuritis

• MR: look for white matter plaques

– IV steroids if +
• Decreases further MS-related events
• Hastens visual recovery
• No change in final Va outcome
– If neg, IV steroids of no proven benefit
• Consider in single-eye patients
– Never use PO steroids
• Increased recurrence of O.N.
Exudative Macular Degeneration

• #1 Cause of blindness >65 y/o

• Worsen gradually or suddenly
• Metamorphopsia common
• Photopsia +/-
• Central scotoma +/-
• More commonly: subacute-
chronically progressive vision loss
Exudative Macular Degeneration:

Central Scotoma
Exudative Macular Degeneration

• Signs
– Decreased Va
– Drusen: yellowish deposits deep to
retina
• Limit nutritional/metabolic support to outer
retina
Exudative Macular Degeneration:
Drusen
Exudative Macular Degeneration

• Management
– Optho referral
• Amsler grid
• Fluoresscein angiography
• Tx: laser photocoagulation (selected cases)
 Miscellaneous

• CVA
• Functional