13th February 2025

Vascular

Retinal vein occlusion and retinal artery occlusion

Retinal vein occlusion is more common than retinal artery occlusion and less sudden. Both need to be managed as an emergency. Note that branch retinal vein or artery occlusions can occur and typically present with vision loss to a lesser extent, and the patient may not even be aware of the defect.

Table 1 Clinical features and management of CRVO and CRAO

Image Source: Wikimedia Commons (2019). Fondo de ojo Ostrucción Vena central, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Fondo_de_ojo_Ostrucción_Vena_central.png (Accessed: 18 January 2024).

Image Source: Wikimedia Commons (2014). Cherry Red Spot Fiess, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Cherry_Red_Spot_Fiess.jpg, via Wikimedia Commons svg (Accessed: 18 January 2024).

Retinal vein occlusions can be clinically characterised into two types: ischaemic (25%) and non-ischaemic (75%) according to the area of non-perfusion in the posterior pole. Ischaemic retinal vein occlusions present with more severe vision loss, relative afferent pupillary defect and more marked fundoscopy findings. Prognosis is poorer and secondary complications are more common in ischaemic presentations.

Amaurosis fugax

Amaurosis fugax describes transient, painless monocular loss of vision caused by a carotid artery atheroma or embolus into the central retinal artery. It is considered as a retinal transient ischaemic attack (TIA) and hence the precursor to a stroke. Management should address any underlying cardiac risk factors and consider a carotid endarterectomy.

Vitreous haemorrhage

Vitreous haemorrhage can occur secondary to neovascularisation, retinal tears, retinal detachment or trauma. Neovascularisation is particularly significant in patients with diabetes because they can develop new retinal blood vessels (proliferative diabetic retinopathy) which are fragile and bleed easily. It is important the underlying cause is identified, and this may require an ultrasound if the blood obstructs the fundoscopy. Management may involve observation or a vitrectomy.

Anterior ischaemic optic neuropathy

Anterior ischaemic optic neuropathy (AION) is the most common cause of optic neuropathy in older people. It results from inflammation (arteritic) or atheroma (non-arteritic) causing blockage to the vascular supply of the optic nerve.

Arteritic AION is most commonly caused by giant cell (temporal) arteritis (GCA). GCA is classified as a medium-to-large-vessel vasculitis. Symptoms include monocular vision loss possibly preceded by episodes of amaurosis fugax, diplopia, new headache, jaw claudication and scalp tenderness. Examination reveals reduced visual acuity, optic disc oedema and thickened temporal arteries, which may be pulseless. Diagnosis can be confirmed with a raised ESR, raised CRP and a positive temporal artery biopsy. Note that due to skip lesions the biopsy may be falsely negative. Management with high-dose steroids should be started without delay (i.e. a positive biopsy result should not be awaited) to prevent vision loss in the other eye.

Other rarer causes of arteritic AION include other types of vasculitis, such as polyarteritis nodosa or systemic lupus erythematosus.

Non-arteritic AION is more common. It is typically painless and noticed on waking. Risk factors include hypertension, hypercholesterolaemia, diabetes mellitus and smoking. Management is to control these risk factors to prevent occurrence in the other eye.