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    Anisman Acute Vision Loss

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    arnol3090
    Sudden visual loss can be caused by many factors. It is important to determine if the visual loss is transient or prolonged, painful or painless in order to establish a differential diagnosis. A thorough history and examination including visual acuity, visual fields, pupil examination, and retinal examination are needed. Common causes include retinal artery occlusion, retinal vein occlusion, retinal detachment, vitreous hemorrhage, angle closure glaucoma, corneal ulcer, uveitis, optic neuritis, and exudative macular degeneration. Emergent ophthalmology referral is needed for many of these conditions.

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    Anisman Acute Vision Loss

    Uploaded by

    arnol3090
    298 views68 pages
    Sudden visual loss can be caused by many factors. It is important to determine if the visual loss is transient or prolonged, painful or painless in order to establish a differential diagnosis. A thorough history and examination including visual acuity, visual fields, pupil examination, and retinal examination are needed. Common causes include retinal artery occlusion, retinal vein occlusion, retinal detachment, vitreous hemorrhage, angle closure glaucoma, corneal ulcer, uveitis, optic neuritis, and exudative macular degeneration. Emergent ophthalmology referral is needed for many of these conditions.

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    Sudden visual loss can be caused by many factors. It is important to determine if the visual loss is transient or prolonged, painful or painless in order to establish a differential diagnosis. A thorough history and examination including visual acuity, visual fields, pupil examination, and retinal examination are needed. Common causes include retinal artery occlusion, retinal vein occlusion, retinal detachment, vitreous hemorrhage, angle closure glaucoma, corneal ulcer, uveitis, optic neuritis, and exudative macular degeneration. Emergent ophthalmology referral is needed for many of these conditions.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    298 views68 pages

    Anisman Acute Vision Loss

    Uploaded by

    arnol3090
    Sudden visual loss can be caused by many factors. It is important to determine if the visual loss is transient or prolonged, painful or painless in order to establish a differential diagnosis. A thorough history and examination including visual acuity, visual fields, pupil examination, and retinal examination are needed. Common causes include retinal artery occlusion, retinal vein occlusion, retinal detachment, vitreous hemorrhage, angle closure glaucoma, corneal ulcer, uveitis, optic neuritis, and exudative macular degeneration. Emergent ophthalmology referral is needed for many of these conditions.

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    Download as ppt, pdf, or txt
    of 68

    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

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