Anisman Acute Vision Loss

7/26/2019 Anisman Acute Vision Loss

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SUDDEN VISUAL LOSS

Dr.Mohd. Mustafizur Rahman

Pakar MataOphthalmology department

Queen Elizabeth Hospital



Objectives

• Have a clear DDx for causes of acutevision loss

• Have a clear understanding ofimmediate management steps to be

taken by the primary care provider



Acute loss of vision

Loss of vision

painful Painless

Prolonged

ACG

Optic Neuritis

GCA

Orbital cellulitis

Endopthal

Fleeting Prolonged

embolic

migrain

Raised ICP

ION

CRAO

CRVO

VIT.HGE

Ret. Detach



Common causes of suddenvisual loss:

• Transient (< 24 hrs)

– Few seconds (usually bilateral):Papilloedema

– Few minutes: Amaurosis fugax (TIA)(unilateral), vertebrobasilar arteryinsufficiency (bilateral)10-60 minutes:

–

Migraine (with or without headache)

http://www.eyecasualty.co.uk/maincontent1/centralretinalarteryocclusion.html






















Visual loss (> 24 hrs)

Painless:

Retinal artery or vein occlusion,

R etinal detachment,

Ischaemic optic neuropathy

Giant cell arteritis,

V itreous haemorrhage,

Painful: Acute angle-closure glaucoma,

optic neuritis

http://www.eyecasualty.co.uk/maincontent1/retinaldetachment.html

http://www.eyecasualty.co.uk/maincontent1/ischaemicopticneuropathy.html


http://www.eyecasualty.co.uk/maincontent1/vitreoushaemorrhage.html



































History

• Transient visual loss (suggestive of amaurosis fugax)

• sudden onset floaters and flashing light (Retinaldetachment)

• History of poorly controlled diabetes mellitus and lasertreatment to the retina (vitreous haemorrhage)

• Headache +/- jaw claudication (pain in the jaw oneating) 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 pupillarydefect

• 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 fieldsCRAO

– 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, antithrombin 3 deficiency andantiphospholipid antibody syndrome



Retinal Artery Occlusion: Signs

• Marcus-Gunn pupil (relative afferentpupillary 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 VLeiden, 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 retinalexam

• 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 withunaffected eye closed

• Impedes flow of blood from retinalcirculation



Retinal Vein Occlusion: Sx

• Sudden or gradual, painless blurry Vaor vision loss

• Unilateral (horiz) visual field loss(BRVO)

• Rare: unilateral pain and redness w/

loss of vision (“neovascularglaucoma” 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 neovascularcomplications



Retinal Detachment

• Fluid separates retina from underlyingretinal pigment epithelium

•

Causes: – Posterior vitreous detachment retinal tear

liquefied vitreous dissects between retinaand 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/ directophthalmoscope may be unrevealing



Retinal Detachment



Retinal Detachment:W/U & Mgmt

• Immediate Ophtho referral!!

– Surgical intervention

– If acute or progressive should bereferred to Ophthalmology <24h, ifchronic 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 oftenimpossible – 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 & txunderlying process



Vitreous Hemorrhage



Angle Closure Glaucoma

• Outflow of aqueous humor fromshallow 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 matteror chronic topical steroid use



Corneal Ulcer: Sx

• Pain

• Redness

• Decreased Va

• photophobia



Corneal Ulcer: Signs

• Dense corneal infiltrate w/ overlyingepithelial 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

• Etiol: most idiopathic; many systemiccauses

•

W/U: careful H&P, looking forsystemic 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%) initiatedby 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

E d ti M l D ti



Exudative Macular Degeneration:Central Scotoma




• Signs

– Decreased Va

– Drusen: yellowish deposits deep toretina

• Limit nutritional/metabolic support to outerretina

E d ti M l D ti



Exudative Macular Degeneration:Drusen




• Management

– Optho referral

•

Amsler grid• Fluoresscein angiography

• Tx: laser photocoagulation (selected cases)



Miscellaneous

• CVA

• Functional

Anisman Acute Vision Loss

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