Acute visual loss: Emergency room perspective

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Presentation transcript:

Acute visual loss: Emergency room perspective Dr.Ehud Zamir

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

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

Acute unilateral visual loss

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

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

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

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

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

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.

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

90%

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

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!

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

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

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

Acute retinal detachment caused by a retinal tear

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

Chronic, total RD with proliferative vitreoretinopathy

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)

Questions?