24 Hour Ophthalmic Emergencies Part 3 – Sudden Vision Loss

Author: William Spackman, Adam Booth / Editor: Liz Herrievan / Codes:  / Published: 20/05/2025

Editors intro: This fab four-part blog has been written for us by an ophthalmology registrar. The aim is to highlight the eye conditions we ED folk should be aware of, particularly those we need to refer asap. Some of the slit-lamp examination findings described might elude some of us (me, at least) in many cases, but dont let that put you off! Ive also Googled some of the more unfamiliar terms so you dont have to.

Part 1 Acute Red Eye

Part 2 – Swollen Lids and Ocular Trauma

Introduction

There are a limited number of true ophthalmic emergencies, but it is important for emergency clinicians to be aware of ophthalmic conditions where immediate action needs to be taken. In many of the conditions discussed in this blog, prompt recognition and management can be sight-preserving and, in certain cases, life-preserving. This blog aims to guide emergency clinicians in the assessment and management of some of the most important emergency ophthalmic presentations.

Sudden Vision Loss

Vision loss should be characterised to establish timing, whether sudden or progressive, monocular or binocular, generalised or affecting a certain portion of the visual field, painful or painless and whether there were any other associated ocular symptoms. It is also important to screen for other systemic symptoms that may be relevant such as neurological symptoms or symptoms of Giant Cell Arteritis (GCA). The differential diagnosis for sudden vision loss is broad. This article will focus on some of the more common causes including vascular occlusions, macular pathology and acute optic neuropathies.

Vascular Occlusions

Retinal Artery Occlusions

Retinal artery occlusions can either be central or branch and usually occur due to an embolus or vasculitis.¹ A central retinal artery occlusion (CRAO) will cause sudden, profound, painless, unilateral vision loss. A branch retinal artery occlusion (BRAO) will cause an altitudinal field defect with superior retinal artery occlusions causing an inferior altitudinal defect and vice versa.¹

On clinical examination, visual acuity is usually counting fingers or worse in a CRAO.¹ A RAPD will usually be present and fundoscopy will reveal a pale retina with a cherry red spot at the fovea in CRAO and segmental pallor in BRAO.

Patients presenting with CRAO within 12-24 hours of onset should be treated as an emergency and referred as soon as possible to an ophthalmologist. If patients present in a timely manner, treatment options include ocular massage, intravenous acetazolamide and/or AC paracentesis.¹ There is however no good evidence for any of these interventions.²

It is of upmost importance to consider the aetiology of an arterial occlusion. GCA should be considered if the patient is aged over 50 presenting with CRAO (but not BRAO).¹ A focused history should be taken for any systemic symptoms of GCA and minimum investigations should include FBC, CRP and ESR.² If there is suggestion of GCA then patients should be started on high dose steroid to protect the fellow eye. Initial treatment is 1g IV Methylprednisolone for 3 days with referral to rheumatology to guide ongoing treatment.¹ A temporal artery ultrasound and/or temporal artery biopsy can be performed to confirm the diagnosis.

More commonly, a CRAO is secondary to atherosclerosis and thus cardiovascular risk factors must be investigated and managed for secondary prevention.¹ This is most appropriately worked up in a TIA clinic with ECG, carotid dopplers and echocardiogram if appropriate. Other more rare causes include haematological, infective and other inflammatory disease.¹

Retinal Vein Occlusions

Retinal vein occlusions can either be central (CRVO) or branch (BRVO). They cause a sudden, painless reduction in vision but is usually less profound than with an arterial occlusion. A BRVO will usually cause an altitudinal visual field defect depending on the location affected.¹

Clinically, visual acuity will usually be reduced and there may be a RAPD if the occlusion is ischaemic. In the posterior segment, retinal haemorrhages, vascular tortuosity, cotton wool spots and optic nerve swelling may be seen.¹

The majority of vein occlusions occur in elderly patients and are associated with cardiovascular risk factors. Around 15% may affect younger patients under 45 and are more likely to be related to underlying systemic disease including haematological and inflammatory disease.¹ Other risk factors include the oral contraceptive pill and ophthalmic disease including glaucoma.¹

Patients with retinal vein occlusions should be referred and seen promptly in the eye clinic.Management includes reviewing and optimising cardiovascular risk factors in conjunction with their general physician. Ophthalmic treatment may involve intravitreal anti-veg F or steroids to treat macula oedema and pan-retinal photocoagulation laser to areas of retinal ischaemia.¹,³ Management of intraocular pressure may be required, particularly in patients with an ischaemic vein occlusion who develop neovascular glaucoma.¹ This may require cyclodiode laser and/or surgery.

Wet Age-Related Macular Degeneration

Age-related macular degeneration (AMD) is a common cause of vision loss in the elderly population and can broadly be divided into the dry and wet types. Dry AMD typically causes a slow decay in vision and doesnt usually present as an emergency. On the other hand, wet AMD may cause a sudden reduction in vision and, as such, patients may present to the emergency department.

Patients may describe an acute or sub-acute reduction in vision, distortion, metamorphopsia (vision dysfunction that causes objects, specifically straight lines, to appear warped, distorted or bent) or a scotoma in their visual field.¹ Posterior segment examination may reveal haemorrhages, grey lesions, exudates or pigmentary changes at the macula.¹

Patients with a suspected wet macular degeneration should be referred urgently to the eye clinic.⁴ Treatment for wet AMD is generally with intravitreal anti-VEGF injections to manage intraretinal and subretinal fluid.¹ Risk factors should be addressed including advising patients on lifestyle factors such as smoking cessation and a well-balanced diet.¹

Acute Optic Neuropathies

Ischaemic Optic Neuropathies

An anterior ischaemic optic neuropathy (AION) can be sub-divided into the more common non-arteritic category (NAION) or less common arteritic category (AAION), accounting for 5-10% of presentations.¹ Both occur when blood supply to the optic nerve is impaired leading to ischaemia.⁵

Patients are typically elderly and present with sudden, painless vision reduction and altitudinal field defect.¹ On examination there will almost certainly be a RAPD. Examining the posterior segment will reveal a swollen optic nerve that is typically pale in AAION and more hyperaemic in NAION. In NAION the disc may be small and crowded and thus predisposed to NAION.¹

AAION is caused by GCA and if missed can have significant ocular and systemic consequences. Therefore, all patients with suspected AION should be asked about symptoms of GCA and have bloods including FBC, CRP and ESR.

If an arteritic cause has been excluded and the patient has been diagnosed with NAION, treatment options are limited. Risk factors should be reviewed and optimised by a physician in order to protect the other eye. Systemic risk factors to be aware of include hypertension, diabetes, hyperlipidaemia, smoking and obstructive sleep apnoea.¹

Optic Neuritis

Optic neuritis is inflammation of the optic nerve and can be broken down into typical and atypical presentations. A typical optic neuritis presents in young adults with unilateral vision reduction and retrobulbar pain.¹ Symptoms tend to worsen over a period of hours to days and start improving at around 2 weeks.¹ These patients will have a RAPD and reduced colour vision. There may or may not be optic nerve swelling.¹ A typical optic neuritis is most commonly secondary to demyelination and thus may be associated with Multiple Sclerosis.¹

An atypical optic neuritis is where the presentation does not fit this pattern and, in these cases, further investigation is required. The differential includes compressive lesions, inflammatory, ischaemic, hereditary, toxic and nutritional causes. Neuromyelitis Optica Spectrum Disorders (NMOSD) is an important differential to consider.¹

In typical optic neuritis, visual recovery is usually spontaneous and occurs by around 3 months.¹ Neuroimaging in the form of MRI with contrast to look for white-matter lesions may be performed. Treatment is not necessarily indicated but there are differing opinions on this.⁶ The Optic Neuritis Treatment Trial showed that IV Methylprednisolone did speed up recovery from optic neuritis but had no effect on the long-term outcomes.⁷ Some neuro-ophthalmologists may advocate offering IV or oral methylprednisolone after counselling on the relative risks and benefits.⁶ 

Atypical optic neuritis should be investigated urgently and managed with neurology input. There is generally a lower threshold for high dose corticosteroid treatment in atypical cases where there is no suspected infective cause.⁶ In particular, patients with NMOSD should be given prompt high dose corticosteroids and may require plasma exchange.⁶

Other Causes

Other causes of sudden vision reduction include:

• Central Serous Chorioretinopathy
• Retinal Detachment
• Acute Angle Closure Glaucoma
• Macula Hole
• Cortical Stroke
• Papilledema

Conclusion

The role of the emergency clinician is to be able to recognise and distinguish serious ophthalmic pathology, initiate immediate investigation and management if appropriate and make a timely referral to ophthalmology. As discussed, prompt recognition of certain ophthalmic conditions is of great importance. Having a structured history and examination pattern will help narrow the differential considerably and ease discussion and referral to the ophthalmic team. Hopefully this article will act as an aide to recall the key considerations of varying presentations and give clinicians confidence in assessing patients with emergency ophthalmic presentations.

Part 4 – Flashes, Floaters and Double Vision

References

1. Denniston AKO, Murray PI, editors. Oxford handbook of ophthalmology. 4th ed. Oxford University Press; 2018.
2. American Academy of Ophthallmology. Retinal artery occlusion – EyeWiki. Eyewiki.org. 2024 Jun 10 [accessed 2024 Nov 19].
3. Royal College of Ophthalmology. Clinical Guidelines: Retinal Vein Occlusion (RVO). 2022.
4. National Institute for Health and Care Excellence (NICE). Macular degeneration – age-related: Scenario: Suspected age-related macular degeneration. NICE CKS, 2022.
5. American Academy of Ophthalmology. Non-arteritic anterior ischemic optic neuropathy (NAION) – EyeWiki. Eyewiki.org. 2024 May 16 [accessed 2024 Nov 19].
6. Laviers H, Petzold A, Braithwaite T. How far should I manage acute optic neuritis as an ophthalmologist? A United Kingdom perspective. Eye (Lond). 2024 Aug;38(12):2238-2245.
7. Royal College of Ophthalmology. The Management Of Angle-Closure Glaucoma. Rcophth.ac.uk. 2022 Jun [accessed 2024 Nov 19]