Sudden Painless Loss of Vision

Sudden painless visual loss over seconds to hours is an emergency presentation in which several causes have treatment windows measured in hours, and others (giant cell arteritis) threaten the fellow eye.

• Causes by site:
  • Retinal vascular: central retinal artery occlusion (an ocular stroke), branch retinal artery occlusion, central retinal vein occlusion (ischaemic type), ocular ischaemic syndrome.
  • Vitreous and retina: vitreous haemorrhage, rhegmatogenous retinal detachment, macular haemorrhage from neovascular macular degeneration or macroaneurysm, retinal tear.
  • Optic nerve: anterior ischaemic optic neuropathy (non-arteritic and arteritic from giant cell arteritis), posterior ischaemic optic neuropathy, optic neuritis (can be painless), compressive and traumatic neuropathy.
  • Brain: occipital or posterior pathway stroke, pituitary apoplexy, migraine aura, cortical blindness.
  • Transient (resolving within 24 hours): amaurosis fugax from carotid embolism, giant cell arteritis, papilloedema obscurations, vasospasm, hyperviscosity.
• Common risk contexts: age over 50 years, hypertension, diabetes, atrial fibrillation, carotid disease, hyperlipidaemia, smoking, thrombophilia, sickle haemoglobinopathy, and recent surgery or injury.

• Central retinal artery occlusion: profound monocular loss (counting fingers to light perception), relative afferent pupillary defect, pale oedematous retina with a cherry red spot, box carring of vessels, possible visible emboli.
• Anterior ischaemic optic neuropathy: altitudinal field loss, swollen disc (pale and chalky with giant cell arteritis), relative afferent pupillary defect, with jaw claudication, scalp tenderness, headache, and weight loss in the arteritic form.
• Central retinal vein occlusion: dilated tortuous veins with widespread haemorrhages ("blood and thunder"), disc swelling, and cotton wool spots.
• Vitreous haemorrhage: floaters, red haze, loss of red reflex; retinal detachment: preceding flashes and floaters, curtain, positive tobacco dust.
• Macular haemorrhage: central dark scotoma with distortion in older patients.
• Stroke and pituitary apoplexy: homonymous or bitemporal field defect, normal fundus, normal pupils (postchiasmal), headache, ophthalmoplegia, hypotension.
• Transient loss: curtain descending over seconds to minutes with recovery (carotid), contralateral limb or speech deficits, scalp tenderness.

• Immediate assessment: visual acuity, pupils (relative afferent defect), colour vision, confrontation fields, intraocular pressure, dilated fundus examination, blood pressure, pulse (atrial fibrillation), glucose.
• Optical coherence tomography (retinal oedema, subretinal fluid, nerve fibre layer), fluorescein angiography, B-scan ultrasound when the view is blocked.
• Blood tests for everyone over 50: ESR, CRP, platelets (giant cell arteritis); full count, glucose, HbA1c, lipids, clotting, and thrombophilia and sickle screening in young patients; urgent blood work within the hour for suspected arteritic disease.
• Vascular and cardiac: ECG, carotid duplex or CT angiography, echocardiogram, and prolonged rhythm monitoring.
• Neuroimaging: MRI brain with diffusion weighted imaging for retinal artery occlusion (silent infarcts), pathway lesions and optic neuropathy; CT head for haemorrhage; MRI and MR angiography if pituitary apoplexy or aneurysm is suspected.
• Temporal artery biopsy or ultrasound within 2 weeks of starting steroids for suspected giant cell arteritis.

• Act within the treatment window:
  • Central retinal artery occlusion (symptoms under 4.5 hours, ideally under 24 hours in some centres): send immediately for emergency stroke assessment and transfer; intravenous alteplase 0.9 mg/kg (maximum 90 mg, 10 percent bolus, remainder over 60 minutes) or tenecteplase 0.25 mg/kg where protocols allow; supine positioning, ocular massage (10 seconds of pressure then release, repeated), anterior chamber paracentesis, acetazolamide 500 mg IV, timolol 0.5 percent drops, and rebreathing into a paper bag are used as adjuncts without proven benefit. Start aspirin 300 mg after imaging excludes haemorrhage, then secondary stroke prevention and carotid and cardiac management.
  • Giant cell arteritis (with any visual symptom): methylprednisolone 1 g IV daily for 3 days (or prednisolone 60 to 80 mg orally if IV is unavailable) without waiting for biopsy, then prednisolone 1 mg/kg daily with slow taper, aspirin 75 mg, proton pump inhibitor, and bone protection.
  • Rhegmatogenous retinal detachment: urgent repair within 24 hours for macula on disease and within 3 to 7 days for macula off (scleral buckle, vitrectomy, or pneumatic retinopexy).
  • Vitreous haemorrhage: head elevation at 30 to 45 degrees, B-scan to exclude a tear or detachment, laser or vitrectomy as indicated, and anti-VEGF for proliferative disease.
  • Central retinal vein occlusion and macular haemorrhage: intravitreal anti-VEGF (aflibercept 2 mg, ranibizumab 0.5 mg, or bevacizumab 1.25 mg) within days; submacular haemorrhage threatening the fovea: tissue plasminogen activator with gas.
  • Pituitary apoplexy: hydrocortisone 100 mg IV then 50 mg every 6 hours, fluids, and urgent neurosurgical review.
  • Posterior circulation stroke: stroke pathway with thrombolysis within the window and antiplatelet therapy.
  • Optic neuritis: methylprednisolone 1 g IV daily for 3 days after exclusion of mimics.
• Control vascular risk factors (blood pressure, diabetes, lipids with statin, stop smoking) and treat atrial fibrillation with anticoagulation.
• Document findings with times, and ensure follow up within 24 to 48 hours for all patients who are not admitted.
• Counselling on symptoms in the fellow eye (new loss, floaters, headache, jaw pain) and on driving.