Approach to Visual Loss

Visual loss is classified by tempo (sudden over seconds to hours, subacute over days to weeks, gradual over months to years), duration (transient lasting less than 24 hours, persistent), laterality (monocular or binocular), and the presence of pain.

• Anatomical localisation guides the differential:
  • Ocular surface and media: tear film, cornea (oedema, ulcer, scar), anterior chamber (hyphaema, hypopyon), lens (cataract), vitreous (haemorrhage, inflammation).
  • Retina: detachment, vascular occlusion, macular disease, retinitis, toxicity.
  • Optic nerve: neuritis, ischaemic neuropathy, compression, toxic and nutritional causes, glaucoma, trauma.
  • Chiasm: bitemporal field loss; retrochiasmal pathway: homonymous field loss; occipital cortex: cortical blindness.
  • Functional (non-organic) loss, and refractive error.
• Time-critical emergencies: giant cell arteritis with visual loss, central retinal artery occlusion, retinal detachment, acute angle closure, endophthalmitis, orbital compartment syndrome, chiasmal or optic nerve compression, stroke, and papilloedema with progressive visual loss.

• History: onset and tempo, laterality, associated pain (ocular movement pain in optic neuritis; eye pain with nausea and haloes in angle closure), floaters and flashes (retinal), curtain (detachment), distortion (macular), field loss pattern, transient obscurations lasting seconds (papilloedema), amaurosis fugax lasting minutes (carotid embolism, giant cell arteritis), photophobia, and trauma.
• Systemic review: headache, scalp tenderness, jaw claudication, malaise, weight loss and proximal stiffness (giant cell arteritis); neurological symptoms (weakness, speech, diplopia, vertigo); multiple sclerosis; hypertension, diabetes, vascular disease, atrial fibrillation; medications and toxins (ethambutol, amiodarone, tobacco, alcohol, methanol); diet; family history of optic neuropathy; HIV and sexual history; pregnancy.
• Examination clues: relative afferent pupillary defect points to retina or optic nerve (unilateral or asymmetric); a normal pupil with normal fundus and bilateral loss points to cortical disease; red desaturation points to optic nerve; a normal fundus with reduced vision and afferent defect points to retrobulbar optic neuritis; a pale swollen disc points to ischaemia.

• Visual acuity with pinhole, colour vision (Ishihara plates), contrast sensitivity, Amsler grid, confrontation fields, pupils (swinging flashlight test), motility, intraocular pressure, slit lamp, dilated fundus examination of disc and macula.
• Visual field testing (Humphrey 24-2 or 30-2, Goldmann for peripheral and neurological fields); optical coherence tomography of macula and retinal nerve fibre layer; fundus photography; fluorescein angiography; B-scan ultrasound.
• Electrophysiology when fundus is normal and vision is poor: visual evoked potentials (optic nerve and pathway), pattern electroretinogram, and full-field electroretinogram (retinal dystrophy).
• Blood tests as directed: ESR, CRP, platelets (giant cell arteritis, within the hour for suspected cases), glucose, HbA1c, full count, vitamin B12, folate, syphilis, HIV, tuberculosis test, ACE, ANA, ANCA, aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies.
• Neuroimaging: MRI brain and orbits with contrast and fat suppression for optic neuritis, compression, chiasmal and retrochiasmal lesions; MR venography and angiography; CT for trauma and bone; lumbar puncture with opening pressure when raised intracranial pressure or demyelination suspected.
• Cardiovascular work-up for retinal artery occlusion: carotid duplex, echocardiography, ECG and cardiac monitoring.

• Triage by urgency:
  • Same-day or emergency: suspected giant cell arteritis (age over 50 with headache, jaw claudication, scalp tenderness, raised inflammatory markers, or visual symptoms), central retinal artery occlusion (stroke pathway), retinal detachment, acute angle closure, endophthalmitis, orbital cellulitis with visual compromise, papilloedema with visual loss, new chiasmal syndrome, optic neuritis with atypical features, and acute neurological symptoms.
  • Within 1 to 2 weeks: optic neuritis, macular disease, retinal vein occlusion, vitreous haemorrhage, progressive visual loss.
• Suspected giant cell arteritis with visual loss: start 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 temporal artery biopsy or ultrasound within 2 weeks; add aspirin 75 mg, gastric and bone protection.
• Treat the specific cause: anti-VEGF injections for macular neovascularisation, laser or surgery for retinal breaks, pressure-lowering for angle closure, high-dose steroids for optic neuritis, and decompression for compressive lesions.
• Functional visual loss: confirm with objective tests (normal pupils, optokinetic nystagmus, mirror test, normal visual evoked potentials) and manage with reassurance and cognitive-behavioural therapy; avoid missing coexisting organic disease.
• Rehabilitation and support: low-vision aids, certification and registration of visual impairment, driving advice (visual requirements), occupational advice, and psychological support.
• Follow-up with repeated acuity, fields, optical coherence tomography and review of the diagnosis when course is atypical.