1. Acute visual loss: Emergency room perspective
Dr.Ehud Zamir

4. Acute visual loss: history
How acute?: seconds/minutes? Hours?
Is it really acute?

5. History Associated symptoms Underlying risk factors
Flashing lights, floaters, shadow/curtain
Jaw claudication, scalp tenderness , temple pain, loss of weight
Diplopia , other neurological symptoms
Underlying risk factors
Peripheral vascular disease, hypertension, diabetes, cholesterol
Known embolic sources
Risk factors for retinal detachment: myopia, family history
Complete ophthalmic, systemic, family and drug history

6. Acute unilateral visual loss

7. Retinal vascular occlusions
Central Retinal Artery Occlusion
Abrupt onset
Usually profound visual loss
If branch: field defect
Retinal pallor
“Cherry red spot”
Visible emboli
Usually embolic (carotid)
Young pts: consider valve
Old: consider GCA

8. BRAO Variable VF defect Or central visual loss Embolic Vasculitic
Other autoimmuune
Hematological

9. Examination Generally very poor vision RAPD
typically less than counting fingers vision
severe visual field constriction
RAPD
Retinal whitening and pallor
Compare with the other eye
Carotid bruit / murmurs?
Temporal artery tenderness

10. Treatment No treatment proven consistently to be of value
Theoretically should be given ASAP
Irreversible ischaemic damage probably after 90 minutes
Modalities:
AC paracenthesis
Ocular massage
Diamox
CO2 enriched oxygen (carbogen)
Hyperbaric oxygen
Selective ophthalmic artery catheterisation, TPA
Always consider GCA: Hx, ESR, CRP

11. Acute optic neuropathies
Diagnosis:
Acute visual loss or visual field loss
RAPD (must be present)
Normal examination or abnormal nerve only
retina and media usually OK

15. Optic neuritis 20-50 years old, more in females
Preceded/accompanied by pain on eye movements
Dyschromatopsia: red desaturation test
RAPD
Reduced brightness
VF defect
VA: ANY
Disc: 2/3 are normal (hence retrobulbar ON) or disc swelling. Haemorrhage is atypical.

16. Optic neuritis Diagnosed clinically Most commonly due to demyelination
DD: vasculitis, neoplasia, syphilis
MRI of prognostic value re: MS
Treatment with high dose I.V methylprednisolone has some early benefit 1 gram I.V. per day for 3d, then pred 1mg/kg/day for 11d then 4d taper
Oral prednisolone (previously standard Rx) associated with more attacks!
Treatment only hastens recovery; has no influence over long-term visual outcome
Usually untreated; even after treatment some deficit often remains

17. 90%

18. Non arteritic AION Diagnosis of exclusion: must exclude GCA Painless
Acute onset, usually when waking up
Altitudinal field loss
RAPD
Pallid swelling of disc (may be sectoral)
Crowded disc (see other eye)
Vascular risk factors (DM, HTN, hypotension)
No effective therapy

19. Arteritic AION Should always be considered in AION
Constitutional symptoms
Combined ESR and CRP very sensitive and specific (97% for ESR>47, CRP>2.45)
If suspected: admission for IV steroids and early temporal artery biopsy.
Contralateral involvement in 50-90% of untreated patients!

20. Vitreoretinal Vitreous haemorrhage: Retinal tear / detachment
Proliferative diabetic retinopathy
Retinal vein occlusion
Retinal macroaneurysms (hypertension)
Posterior vitreous detachment

23. Vitreous haemorrhage
The retina has to be evaluated through dilated fundoscopy
Ultrasound B-scan if no fundal view
If retinal detachment: urgent surgical repair may be required (macula on RD)
Otherwise: later treatment or surgery (vitrectomy) depending on aetiology of the vitreous haemorrhage

24. Retinal detachment Typically causing visual loss over days
Starts as a dark curtain over part of field
Often preceded by photopsias
Family history, myopia, trauma, intraocular surgery may be risk factors
Requires surgical repair
The longer the delay in surgery the less chance the retina will return to function normally

25. Acute retinal detachment caused by a retinal tear

26. Macula still attached (on)RD
“Macula-on” detachment

27. Chronic, total RD with proliferative vitreoretinopathy

28. Age related macular degeneration
Most common reason for blindness in Western world
Wet form: neovascular membrane bleeds/leaks, thus affecting macular function
Treatment with intravitreal anti-VEGF injections
Prognosis guarded
Monitor for distortion (metamorphopsia)

30. Questions?