Differential Diagnosis of Sudden Persistent Visual Loss. (a) Painful
| Cause | Features |
|---|---|
| Acute angle-closure glaucoma | Nausea and vomiting. Unwell, uncooperative. Congested eye with mid-dilated pupil. Iris details hazy due to corneal oedema. Periocular pain and headache. May be preceded by subacute attacks. High intraocular pressure, for example >35 mmHg. Clinical emergency. |
| Anterior uveitis | Brow ache, red eye, particularly perilimbal (around corneal limbus) injection. Pupil will likely be constricted. Hypopyon in severe cases. |
| Endophthalmitis | Post-operative endophthalmitis: within 2–14 days of surgery. Pain, lid swelling, loss of vision, hypopyon. Clinical emergency. Endogenous endophthalmitis: seek infective source, for example infected central venous cannula, septic focus. May be immunosuppressed. Less of a hot eye. Clinical emergency. |
| Optic neuritis | May affect one eye or both eyes. Pain is less of a feature than visual loss. Maybe pain on eye movements. RAPD, if unilateral. Subacute dramatic vision loss over 1–2 days. Swollen hyperaemic optic nerve when acute, optic disc pallor when established. Visual field loss. Uhthoff's sign – visual loss exacerbated by increased body temperature, for example hot bath. Frequently associated with multiple sclerosis (MS): 25–72% will develop MS at 15 years, depending on MRI findings. |
| (b) Painless | |
| Affecting one eye | |
| Cause | Features |
|---|---|
| Bilateral arteritic ischaemic optic neuropathy (AION) | Chalky white optic discs. Vision usually worse than NAION. Older age group >55, typically >75. May have associated symptoms and signs of giant-cell arteritis (but may be ‘silent’ GCA). If GCA suspected, treat with corticosteroid (see text). |
| Optic neuritis | May affect both eyes. Subacute visual loss with pain on ocular movement and RAPD with field loss. Colour vision profoundly affected. May have MS or develop MS. Neurology input required. |
| Acute chiasmal lesion | May be infectious, inflammatory or vascular lesion. Pituitary apoplexy may complicate pituitary adenoma (Chapter 93). Typically results in bi-temporal hemianopia. III, IV or VI nerve palsies may be present if lesion extends into cavernous sinus. |
| Acute lesion affecting optic tract, the lateral geniculate body, the optic radiations, or the visual cortex | May be due to cerebral infarction or haemorrhage, or haemorrhage into brain tumour. Results in homonymous hemianopia. |
| Bilateral occipital lobe infarction | Due to posterior circulation stroke (see Chapter 65). |
| Reversible posterior leukoencephalopathy syndrome | Typically presents with seizures. Other features include headache, altered consciousness and visual abnormalities (e.g. blurred vision, homonymous hemianopia, cortical blindness). |
| Psychogenic | Diagnosis of exclusion. |
| Cause | Features |
|---|---|
| Vitreous haemorrhage | Sudden onset of floaters and blurred vision. Red reflex may be absent if haemorrhage is significant. Will not cause RAPD. Caused by proliferative diabetic retinopathy, or retinal tear until proven otherwise in non-diabetics. |
| Central/branch retinal vein occlusion | Often presents in the morning with variable visual loss from mild to profound, depending on degree of ischaemia. RAPD if ischaemic. Dark blot haemorrhages in quadrants according to venous drainage involved, that is, supero-temporal if BRVO, whole fundus if CRVO; hemi-vein occlusion will cause haemorrhage in either superior or inferior retina. Respects horizontal meridian if not CRVO (in which case whole retinal involved). |
| Central/branch retinal artery occlusion | Retinal pallor and oedema with profound visual loss. May have cherry red spot if acute. Cattle trucking of blood cells in retinal arterioles (segmentation of blood column denoting impaired, sluggish circulation). RAPD. Must exclude giant cell arteritis. |
| Retinal detachment | May be preceded by flashes and floaters, symptomatic of posterior vitreous separation/detachment (PVD). PVD causes retinal tear(s) by traction on the retina, which may cause retinal detachment. Field loss commensurate with retinal elevation – supero-temporal detachment causing infero-nasal field loss. White billowing retina seen on ophthalmoscopy. Clinical emergency. |
| Proliferative diabetic retinopathy | May be asymptomatic until tractional retinal detachment or vitreous haemorrhage supervene. Venous new vessel proliferation at optic nerve or along arcades or in watershed (ischaemic) area nasal to the optic nerve. Other diabetic changes will be present. If markedly asymmetric, consider coexisting carotid disease. |
| Age-related macular degeneration (wet) | Central visual loss with haemorrhage +/- exudate in central macula. May be bilateral and may arise in dry macular degeneration. Variable visual loss from 6/6 to hand movement vision. |
| Non-arteritic ischaemic optic neuropathy (NAION) | Acute visual loss, typically in morning. Swollen disc with haemorrhagic component. RAPD and loss of colour vision and has associated field defect. Younger age group, 45–65. |
| Arteritic ischaemic optic neuropathy (AION) | As above but chalky white optic disc. Vision usually worse than NAION. Older age group >55, typically >75. May have associated symptoms and signs of giant-cell arteritis (but may be ‘silent’ GCA). If GCA suspected, treat with corticosteroid (see text). |
| Optic neuritis | May affect one eye or both eyes. Subacute visual loss with pain on ocular movement and RAPD with field loss. Colour vision profoundly affected. May have MS or develop MS. Neurology input required. |
| AION, anterior ischaemic optic neuropathy; CF, counting fingers; CWS, cotton wool spot; HM, hand movements; NPL, no perception of light; PL, perception of light; RAPD, relative afferent pupillary defect. | |
| Affecting both eyes | |