Sudden Vision Loss : Simplified Approach

Acute or sudden vision loss is due to one of the following causes:

  1. Opacification of normally transparent structures anterior to retina
  2. Retinal abnormalities
  3. Abnormalities of optic nerve and visual pathway

Systematic history and ocular examination is necessary.

Step 1: Unilateral or Bilateral Sudden vision loss ?

  • Monocular loss of vision: lesion anterior to optic chiasma
  • Binocular loss of vision: lesion posterior to optic chiasma

Step 2: Painful or Painless Sudden Vision loss?

  • Constant eye pain: Corneal lesion, Anterior chamber inflammation or Increased IOP
    • AACG - sudden vision lossFeatures of Acute congestive glaucoma:
      • Nausea and vomiting
      • Colored halos around lights
      • Unreactive and fixed mid-dilated pupils
      • Hyperemic conjunctiva
      • Corneal edema demonstrated by a dulled reflection of¬†light from the corneal surface
    • Features of Corneal lesion:
      • Ask for history of Contact lens¬†wear
      • Photophobia
      • Perform fluorescein¬†staining of¬†corneal defect
    • Features of Endophthalmitis:
      • History of recent intraocular surgery or trauma
      • Floaters
      • Conjunctival injection
      • Decreased red reflex
      • Hypopyon
  • Eye pain with movement: Optic neuritis
    • Additional features:¬†RAPD, central visual field defect, red¬†desaturation (abnormal color vision)

Step 3: If the condition is painless sudden vision loss:

A) Onset and duration ?

  • Transient visual loss: Vascular cause, Papilledema or Migraine
    • Headache: Giant cell Arteritis or Migraine
      • Migraine: Young patients; Scintillating scotomata, fortification spectra, or complete loss of vision lasting usually lasting less than an hour; Unilateral headache and aura
      • Giant cell arteritis: Elderly patients;¬†jaw claudication,¬†scalp tenderness, headache, malaise, anorexia,¬†and proximal joint or muscle aches, pulseless or thickened temporal artery
        gca - sudden vision loss
    • Features of raised ICP: Papilledema
    • Carotid bruit, Evidence of emboli, Atrial fibrillation: Amaurosis fugax
    • Recurrent episodes, Cerebellar signs, Hemiparesis, Hemisensory loss: Vertebro-basilar insufficiency
  • Persistent visual loss: Abnormality of cornea, vitreous, fundus, cortex or a functional cause

papilledema vs papillitis

B) Floaters?

  • Retinal detachment:¬†Photopsias¬†(brief monocular flashes of light), Curtain or shadow moving in the field of vision
  • Others: Intermediate and Posterior uveitis

C) Relative Afferent Pupillary Defect (RAPD) on Swinging light test ?


  • Altitudinal visual field defect: Anterior Ischemic Optic Neuropathy (AION)
  • Features of retinal detachment: Severe retinal detachment
    • ‚ÄúTobacco dust‚ÄĚ in vitreous on slit-lamp examination: Rhegamtogenous retinal detachment
  • Evidence of cardiovascular disease, diabetes, hypercoagulable state: Central retinal artery occlusion (CRAO) or Central retinal vein occlusion (CRVO)

AION types

Step 4: Findings in fundoscopy in sudden vision loss ?

A) Difficulty seeing red reflex: Opacification of transparent structures ahead of retina

B) No difficulty seeing red reflex:

  • Papilledema:¬†bilateral optic disc swelling, loss of spontaneous venous¬†pulsation (SVP), peripapillary hemorrhagespapilledema fundoscopic
  • CRAO: attenuated arterioles, box carring¬†of retina vessels, pale fundus, cherry-red spot,¬†Hollenhorst plaque (refractile object at the site of arterial occlusion)crao fundoscopy
  • CRVO:¬†dilated tortuous veins, hemorrhages in all¬†four quadrants, ¬Ī cotton wool spots, retinal edema
  • Rhegmatogenous retinal detachment:¬†corrugated elevated retina with (multiple) break(s)
  • Exudative retinal detachment: convex elevated retina with shifting¬†fluid, no break; tractional: concave elevated retina with tractional¬†membranesfundoscopy visuaal loss
  • Intermediate uveitis: macular¬†edema, optic nerve edema
  • Posterior uveitis: retinal/choroidal infiltrates, macular edema, vascular sheathing or occlusion,¬†hemorrhages.
  • Anterior ischemic optic neuropathy: pale edematous disc ¬Ī flameshaped¬†hemorrhages
  • Choroidal neovascular membrane (Wet ARMD): drusen,¬†subretinal membrane ¬Ī hemorrhage, exudate

Step 5:¬†If pupillary light reflexes are normal ‚Äď Check optokinetic nystagmus

If an optokinetic drum is unavailable, a mirror can be held near the patient’s eye and slowly moved. If the patient can see, the eyes usually track movement of the mirror.

  • Absent: Occipital lesions
  • Present: Functional visual loss


Based on the disorder suspected from the history and clinical examination:

  1. ESR, CRP, Platelets: whenever Giant cell arteritis needs to be excluded as the possible cause (All increased in GCA)
    • If suggestive, temporal artery biopsy must be done within 7 days of starting steroids to confirm the diagnosis.
  2. MRI/CT: to rule out central lesions and demylenating lesions as a cause of optic neuritis
  3. Culture of anterior chamber and vitreous fluids: Endophthalmitis
  4. ECG, Carotid ultrasonography: Cardiovascular cause
  5. USG-B scan: Retinal detachment
  6. Gonioscopy: Acute congestive glaucoma (ACG)


1. Acute Congestive Glaucoma:

a. Immediate:

  • Systemic: acetazolamide 500 mg IV stat, then 250 mg PO 4x/day
  • Ipsilateral eye:
    • B-blocker e.g., timolol 0.5% stat, then 2/day
    • Sympathomimetic e.g., apraclonidine 1% stat
    • Steroid e.g., prednisolone 1% stat, then q30‚Äď60 min
    • Pilocarpine 2% Once IOP <50 mmHg; e.g., twice in first hour¬†then 4x/day
  • Consider corneal indentation with a 4-mirror goniolens, which may¬†help relieve pupillary block.
  • Laying the patient supine may allow the¬†lens to fall back away from the iris.
  • Analgesics and anti-emetics may¬†be necessary.
  • Promptly assess and treat contralateral eye with laser PI (LPI).

b. Intermediate:

  • Check IOP hourly until there is adequate control.
  • If IOP is not improving, consider systemic hyperosmotics (e.g.,¬†glycerol PO 1 g/kg of 50% solution in lemon juice or mannitol 20%¬†solution IV 1‚Äď1.5 g/kg).
  • If IOP is still not improving, consider acute LPI (can use topical¬†glycerine to temporarily reduce the corneal edema).
  • If IOP is still not improving, review the diagnosis (e.g., could this be¬†aqueous misdirection syndrome or neovascular glaucoma?), consider¬†repeating LPI, or proceeding to surgical PI or even emergency¬†trabeculectomy.

c. Definitive: Bilateral laser (e.g., Nd-YAG) or surgical PI

2. Anterior Ischemic Optic Neuropathy (AION):

a. Immediate:

  • IV Steroid treatment (e.g., 1 g methylprednisolone¬†IV 1x/day for 1‚Äď3 days)
  • Followed by oral prednisolone 1‚Äď2 mg/kg 1x/day)
  • Aspirin may have additional benefit.

b. Maintenance: Steroids may be titrated according to symptoms and inflammatory markers (CRP responds more quickly than ESR).

3. CRAO:

  • Medical emergency and the visual loss is irreversible
  • Attempt to reduce IOP in affected eye:
    • 500 mg IV acetazolamide, ocular massage ¬Ī
    • AC¬†paracentesis ocular
  • Selective ophthalmic artery catheterization with thrombolysis if available
  • Protect other eye, e.g., treat underlying GCA with systemic steroids immediately
  • Panretinal photocoagulation with argon, krypton, diode, etc. laser prevents neovascularisation

4. CRVO:

  • Reduce IOP: if elevated (in either eye)
  • Panretinal photocoagulation for neovascularization or high risk.
  • Intravitreal triamcinolone acetonide or intravitreal dexamethasone¬†implant for treatment of CME.
  • Intravitreal bevacizumab and ranibizumab for treatment of CME and¬†neovascularization.
  • Pars plana vitrectomy and endolaser for vitreous hemorrhage¬†secondary to neovascularization.
  • Treat underlying medical conditions

5. Optic neuritis:

  • IV steroid treatment may be¬†offered to those with poor vision in the other eye or with severe pain.
  • In those at high risk (>2 plaques on MRI), interferon B1a appears to¬†reduce or at least delay both the clinical diagnosis of MS

7. Giant cell arteritis:

  • Immediate high dose steroids (e.g. oral prednisolone 60 mg OD)¬†without delay. The aim is to prevent contralateral loss of vision.
  • Urgent rheumatology referral is warranted.
  • Steroids may be required for up to two years with doses based on¬†monitoring of symptoms and ESR.

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